FN Thomson Reuters Web of Science™ VR 1.0 PT J AU DANDREA, AD AF DANDREA, AD TI THE INTERACTION OF THE ERYTHROPOIETIN RECEPTOR AND GP55 SO CANCER SURVEYS LA English DT Article ID FOCUS-FORMING VIRUS; PROTEIN TYROSINE PHOSPHORYLATION; ERYTHROID PROGENITOR CELLS; COLONY-STIMULATING FACTOR; LONG TERMINAL REPEAT; ENVELOPE GENE; FRIEND-VIRUS; INTERLEUKIN-2 RECEPTOR; MEMBRANE GLYCOPROTEIN; TRANSMEMBRANE DOMAIN RP DANDREA, AD (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. NR 66 TC 15 Z9 15 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1992 VL 15 BP 19 EP 36 PG 18 WC Oncology SC Oncology GA JW675 UT WOS:A1992JW67500003 PM 1451111 ER PT J AU HABER, DA HOUSMAN, DE AF HABER, DA HOUSMAN, DE TI ROLE OF THE WT1 GENE IN WILMS-TUMOR SO CANCER SURVEYS LA English DT Article ID RETINOBLASTOMA SUSCEPTIBILITY GENE; EARLY GROWTH-RESPONSE; HUMAN CHROMOSOME-11; PHYSICAL MAP; WAGR REGION; CELL-CYCLE; BAND 11P13; SHORT ARM; ANIRIDIA; DELETION C1 MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02115 USA. RP HABER, DA (reprint author), MIT, CTR CANC RES, CAMBRIDGE, MA 02139 USA. NR 57 TC 33 Z9 33 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1992 VL 12 BP 105 EP 117 PG 13 WC Oncology SC Oncology GA HP484 UT WOS:A1992HP48400007 PM 1322241 ER PT J AU LIVINGSTON, DM AF LIVINGSTON, DM TI FUNCTIONAL-ANALYSIS OF THE RETINOBLASTOMA GENE-PRODUCT AND OF RB-SV40T-ANTIGEN COMPLEXES SO CANCER SURVEYS LA English DT Article ID LARGE T-ANTIGEN; VIRUS-40 LARGE-T; SV40 LARGE-T; SUSCEPTIBILITY GENE; ADENOVIRUS E1A; BINDING; REGIONS; PROTEIN; PHOSPHORYLATION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LIVINGSTON, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 14 TC 14 Z9 15 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1992 VL 12 BP 153 EP 160 PG 8 WC Oncology SC Oncology GA HP484 UT WOS:A1992HP48400010 PM 1638546 ER PT J AU DYSON, N HARLOW, E AF DYSON, N HARLOW, E TI ADENOVIRUS-E1A TARGETS KEY REGULATORS OF CELL-PROLIFERATION SO CANCER SURVEYS LA English DT Review ID RETINOBLASTOMA SUSCEPTIBILITY GENE; LARGE T-ANTIGEN; E2F TRANSCRIPTION FACTOR; DNA-BINDING ACTIVITY; SV40 LARGE-T; HOST-RANGE MUTANTS; REGION 1A PROTEINS; E1A PROTEINS; MESSENGER-RNA; FUNCTIONAL DOMAINS RP DYSON, N (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 154 TC 145 Z9 145 U1 2 U2 4 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0261-2429 J9 CANCER SURV JI Cancer Surv. PY 1992 VL 12 BP 161 EP 195 PG 35 WC Oncology SC Oncology GA HP484 UT WOS:A1992HP48400011 PM 1353412 ER PT J AU GARG, HG LIPPAY, EW NEAME, PJ AF GARG, HG LIPPAY, EW NEAME, PJ TI PROTEOGLYCANS IN HUMAN BURN HYPERTROPHIC SCAR FROM A PATIENT WITH EHLERS-DANLOS SYNDROME SO CARBOHYDRATE RESEARCH LA English DT Article ID DERMATAN SULFATE PROTEOGLYCAN; PROTEODERMATAN SULFATE; I COLLAGEN; CHONDROITIN; SKIN; PURIFICATION; INHIBITION; CARTILAGE; PROTEINS; POSTBURN AB Proteoglycans (PGs) from human bum hypertrophic scar of a patient with Ehlers-Danlos syndrome were extracted with 4M guanidinium chloride and purified by DEAE-cellulose chromatography. Differential ethanol precipitation of the PG fraction obtained after ion-exchange chromatography yielded two low mol.-wt. PGs, one rich in glucuronic acid (PG(GLCA); M(r) 66 kDa) and the other rich in iduronic acid (PG(IDOA); M(r) 48 kDa). In PG(GLCA), 84% of the glycosaminoglycan chains are composed of GlcA --> GalNAc(SO4) units, whereas in PG(IDOA) the chains contain 95% IdoA --> GalNAc(SO4) disaccharide units. Upon treatment with testicular hyaluronidase, the PGs gave different-sized oligosaccharides. Chondroitinase ABC digestion of PG(GLCA) or PG(IDOA) gave a single protein core (M(r) approximately 20 kDa). The presence of glucosamine and sialic acid in PG(GLCA) and PG(IDOA) suggests that both contain N-linked oligosaccharides. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. SHRINERS HOSP CRIPPLED CHILDREN, ORTHOPED RES LABS, TAMPA UNIT, TAMPA, FL 33612 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. RP GARG, HG (reprint author), SHRINERS BURN INST, 51 BLOSSOM ST, BOSTON, MA 02114 USA. NR 41 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JAN PY 1992 VL 223 BP 209 EP 220 DI 10.1016/0008-6215(92)80017-U PG 12 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HB800 UT WOS:A1992HB80000017 PM 1596919 ER PT J AU CRAWLEY, AP COHEN, MS YUCEL, EK PONCELET, B BRADY, TJ AF CRAWLEY, AP COHEN, MS YUCEL, EK PONCELET, B BRADY, TJ TI SINGLE-SHOT MAGNETIC-RESONANCE-IMAGING - APPLICATIONS TO ANGIOGRAPHY SO CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article DE MR ANGIOGRAPHY; INSTASCAN; ECHO PLANAR IMAGING AB Recently developed technologies that allow the collection of magnetic resonance imaging (MRI) in as little as 26 msec have been explored in their application to angiography. Advantages are demonstrated in scan time reduction, insensitivity to patient motion (especially in abdominal applications), flow quantification, and temporal resolution. We demonstrate that because such single-shot techniques are inherently resistant to flow dephasing during acquisition that allow for sustained high signal intensities to be achieved when images must be combined through the cardiac cycle. Such high temporal resolution scans may be utilized for the collection of time-resolved angiograms. With these techniques we demonstrate the collection of complete MR angiograms in the course of reasonable 10-25 sec breath holds. The relative simplicity of the technique, coupled with its overall short acquisition time, allows us to incorporate angiography into other imaging protocols without adding significant time burdens. Results to date are promising for further improvements in spatial resolution, without extension of scan time. C1 MASSACHUSSETTS GEN HOSP,CTR NMR,BLDG 149,13TH ST,BOSTON,MA 02129. RI Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [5T32CA09502]; NHLBI NIH HHS [R01 HL39371-04] NR 0 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0174-1551 J9 CARDIOVASC INTER RAD JI Cardiovasc. Interv. Radiol. PD JAN-FEB PY 1992 VL 15 IS 1 BP 32 EP 42 PG 11 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA HA824 UT WOS:A1992HA82400005 PM 1537063 ER PT J AU MURAGALELLI, MJ NARUSAWA, H SHIMADA, T IIJIMA, M AOBA, T AF MURAGALELLI, MJ NARUSAWA, H SHIMADA, T IIJIMA, M AOBA, T TI EFFECTS OF FLUORIDE ON PRECIPITATION AND HYDROLYSIS OF OCTACALCIUM PHOSPHATE IN AN EXPERIMENTAL-MODEL SIMULATING ENAMEL MINERALIZATION DURING AMELOGENESIS SO CELLS AND MATERIALS LA English DT Article DE FLUORIDE; OCTACALCIUM PHOSPHATES; APATITE; ENAMEL MINERALIZATION; AMELOGENESIS ID RESOLUTION ELECTRON-MICROSCOPY; PORCINE AMELOGENESIS; APATITE CRYSTALS; CALCIUM APATITES; GROWTH AB The present study was undertaken to investigate effects of fluoride at low concentrations on the precipitation of calcium phosphates on hydroxyapatite seeds in media resembling the enamel fluid composition. To this end, we used a new crystal growth model adopting a miniaturized reaction column. Experimental solutions had the composition similar to that found in the enamel fluid, except for calcium concentrations which were adjusted at 1.0 and 0.5 mM. Precipitation reactions taking place in the system at the higher supersaturation ([Ca] = 1 mM) were characterized by co-precipitation of plate-like OCP and rod-like apatite crystals, while the reaction at the lower supersaturation ([Ca] = 0.5 mM) was characterized by the precipitation and growth of apatitic crystals. Concerning threshold fluoride concentrations for OCP precipitation, the observation by scanning electron microscopy showed that precipitation of plate-like crystals occurred in media containing fluoride up to 0.3 ppm. More interestingly, neither analysis by X-ray diffraction nor Fourier transform infrared spectroscopy yielded characteristics of OCP for plate-like crystals exposed to fluoride at 0.05 ppm or higher concentrations. The results obtained in vitro support the contention that precipitation of OCP-like precursors and their rapid hydrolysis take place in enamel fluid microenvironment containing low concentrations of fluoride. C1 FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115. ASAHI UNIV,SCH DENT,GIFU,JAPAN. NR 21 TC 20 Z9 20 U1 1 U2 4 PU SCANNING MICROSCOPY INT PI CHICAGO PA PO BOX 66507, AMF O'HARE, CHICAGO, IL 60666 SN 1051-6794 J9 CELL MATER JI Cells Mat. PY 1992 VL 2 IS 3 BP 221 EP 230 PG 10 WC Cell Biology; Medicine, Research & Experimental; Materials Science, Biomaterials SC Cell Biology; Research & Experimental Medicine; Materials Science GA KC002 UT WOS:A1992KC00200005 ER PT J AU REISS, CS GAPUD, CP KEIL, W AF REISS, CS GAPUD, CP KEIL, W TI NEWLY SYNTHESIZED CLASS-II MHC CHAINS ARE REQUIRED FOR VSV-G PRESENTATION TO CTL CLONES SO CELLULAR IMMUNOLOGY LA English DT Article ID STOMATITIS-VIRUS GLYCOPROTEIN; MAJOR HISTOCOMPATIBILITY COMPLEX; CYTOLYTIC LYMPHOCYTES-T; VACCINIA VIRUS; INTRACELLULAR-TRANSPORT; RESTRICTED PRESENTATION; ENDOPLASMIC-RETICULUM; ENDOGENOUS ANTIGEN; INFECTED CELLS; G-PROTEIN C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV INFECT DIS,BOSTON,MA 02115. OI Reiss, Carol/0000-0003-4353-8882 FU NIAID NIH HHS [R01 AI18083, R37 AI20896] NR 36 TC 5 Z9 6 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 JAN PY 1992 VL 139 IS 1 BP 229 EP 238 DI 10.1016/0008-8749(92)90115-6 PG 10 WC Cell Biology; Immunology SC Cell Biology; Immunology GA GW213 UT WOS:A1992GW21300021 PM 1309489 ER PT J AU FRAGOSO, CAV KACMAREK, RM SYSTROM, DM AF FRAGOSO, CAV KACMAREK, RM SYSTROM, DM TI IMPROVEMENT IN EXERCISE CAPACITY AFTER NOCTURNAL POSITIVE PRESSURE VENTILATION AND TRACHEOSTOMY IN A POSTPOLIOMYELITIS PATIENT SO CHEST LA English DT Article ID RESPIRATORY MUSCLE AB Progressive neuromuscular symptoms years after recovery from acute paralytic poliomyelitis have been termed the PPS. We describe a 52-year-old man who contracted poliomyelitis at age 9 years who fully recovered and 33 years later developed progressive dyspnea. Neurologic evaluation revealed bilateral paralysis of the vocal cords, generalized weakness, and accentuated mouth occlusion pressure and ventilatory responses to hypercapnic, hyperoxic breathing. An EMG and muscle biopsy showed changes consistent with acute and chronic denervation. Cardiopulmonary exercise evaluation demonstrated a pulmonary mechanical limit with excessive ventilation relative to CO2 output. Tracheostomy and nocturnal positive pressure ventilation resulted in increased respiratory muscle strength, normalization of ventilatory drive and marked improvement in exercise capacity. C1 MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RESP CARE,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD JAN PY 1992 VL 101 IS 1 BP 254 EP 257 PG 4 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GX871 UT WOS:A1992GX87100051 ER PT J AU JELLINEK, MS MURPHY, JM POITRAST, F QUINN, D BISHOP, SJ GOSHKO, M AF JELLINEK, MS MURPHY, JM POITRAST, F QUINN, D BISHOP, SJ GOSHKO, M TI SERIOUS CHILD MISTREATMENT IN MASSACHUSETTS - THE COURSE OF 206 CHILDREN THROUGH THE COURTS SO CHILD ABUSE & NEGLECT LA English DT Article DE CHILD ABUSE AND NEGLECT; CARE AND PROTECTION PETITIONS; ADJUDICATION ID NEGLECT; ABUSE AB Two hundred and six severely abused and/or neglected children brought before the Boston Juvenile Court on care and protection petitions were followed prospectively for 4 years. Two thirds of all parents were found to be poor, 84% had one or more psychiatric disorders, and 81% had been known to the Department of Social Services prior to their court appearance. The average age of children at the start of the court process was 4.2 years, and the average length of temporary foster care was 2.3 years. Judges' decisions to return children to parental custody or to order permanent removal were most strongly predicted by parental compliance with court-order services. Of the 63 cases dismissed from court and thus returned to biological parents, 18 (29%) had substantiated reports of new mistreatment over an approximately 3-year follow-up period. We concluded that children are often poorly served by the current delays in the social service/legal system, and that further clinical research would provide needed empirical data on how best to protect mistreated children. C1 BOSTON JUVENILE COURT,BOSTON,MA. RP JELLINEK, MS (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,ACC725,BOSTON,MA 02114, USA. NR 24 TC 41 Z9 41 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2134 J9 CHILD ABUSE NEGLECT JI Child Abuse Negl. PY 1992 VL 16 IS 2 BP 179 EP 185 DI 10.1016/0145-2134(92)90026-N PG 7 WC Family Studies; Psychology, Social; Social Work SC Family Studies; Psychology; Social Work GA HL515 UT WOS:A1992HL51500003 PM 1559167 ER PT J AU NIGG, EA GALLANT, P KREK, W AF NIGG, EA GALLANT, P KREK, W TI REGULATION OF P34CDC2 PROTEIN-KINASE ACTIVITY BY PHOSPHORYLATION AND CYCLIN BINDING SO CIBA FOUNDATION SYMPOSIA LA English DT Article ID B-TYPE CYCLINS; CELL-CYCLE; SCHIZOSACCHAROMYCES-POMBE; CATALYTIC SUBUNIT; PROMOTING FACTOR; A-TYPE; CDC2; ACTIVATION; PHOSPHATASE-2A; DEGRADATION AB Activation of the protein kinase p34cdc2 is required for entry into meiotic or mitotic M phase in all eukaryotic cells. One important mechanism regulating the activity of p34cdc2 during the cell cycle is based on phosphorylation/dephosphorylation. Avian p34cdc2 is phosphorylated on threonine 14 (Thr14), tyrosine 15 (Tyr15), threonine 161 (Thr161) and serine 277 (Ser277). Dephosphorylation of both Thr14 and Tyr15 is required for activation of p34cdc2 at the G2/M transition, indicating that phosphorylation of these residues negatively regulates p34cdc2 activity. Conversely, phosphorylation of Thr161 is required for kinase activity. Whether modification of this residue is due to intramolecular autophosphorylation or to the action of an as yet unidentified kinase remains unresolved. Likewise, the role of phosphorylation of p34cdc2 on Ser277 during G1 phase of the cell cycle remains to be determined. The function of p34cdc2 is regulated also by cell cycle-dependent complex formation with cyclin proteins. We found that chicken cyclin B2 undergoes a striking redistribution from the cytoplasm to the nucleus just prior to the onset of mitosis. Expression of a nondestructible cyclin B2 mutant causes HeLa cells to arrest in mitosis. Frequently, arrested cells displayed multiple mitotic spindles. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP NIGG, EA (reprint author), SWISS INST EXPTL CANC RES,155 CHEMIN BOVERESSES,CH-1066 EPALINGES,SWITZERLAND. NR 36 TC 15 Z9 16 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 170 BP 72 EP 96 PG 25 WC Medicine, General & Internal SC General & Internal Medicine GA JQ182 UT WOS:A1992JQ18200006 PM 1483352 ER PT J AU HARLOW HUNTER NASMYTH HUNT KIRSCHNER BEACH PINES REED YANAGIDA LEHNER AF HARLOW HUNTER NASMYTH HUNT KIRSCHNER BEACH PINES REED YANAGIDA LEHNER TI THE CYCLIN-DEPENDENT KINASE FAMILY SO CIBA FOUNDATION SYMPOSIA LA English DT Discussion C1 SALK INST, MOLEC BIOL & VIROL LAB, SAN DIEGO, CA 92186 USA. RES INST MOLEC PATHOL, A-1030 VIENNA, AUSTRIA. UNIV CALIF SAN FRANCISCO, SCH MED, DEPT BIOCHEM & BIOPHYS, SAN FRANCISCO, CA 94143 USA. COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY 11724 USA. SCRIPPS RES INST, DEPT MOLEC BIOL, LA JOLLA, CA 92037 USA. KYOTO UNIV, FAC SCI, DEPT BIOPHYS, SAKYO KU, KYOTO 606, JAPAN. MAX PLANCK GESELL, FRIEDRICH MIESCHER LAB, BIOL ARBEITSGRP ABT, W-7400 TUBINGEN, GERMANY. RP HARLOW (reprint author), MASSACHUSETTS GEN HOSP, CTR CANC, BLDG 149, 13TH ST, CHARLESTON, MA 02129 USA. NR 2 TC 0 Z9 0 U1 0 U2 3 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 170 BP 205 EP 208 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA JQ182 UT WOS:A1992JQ18200013 ER PT J AU JARLAIS, DCD EDWARDS, G MOORE, MH ALMOND, B KLEBER, HD NEGRETE JONES, JC WOOLVERTON, WL MUSTO, DF KALANT, H ANTHONY, JC OBRIEN, CP KUHAR, MJ AF JARLAIS, DCD EDWARDS, G MOORE, MH ALMOND, B KLEBER, HD NEGRETE JONES, JC WOOLVERTON, WL MUSTO, DF KALANT, H ANTHONY, JC OBRIEN, CP KUHAR, MJ TI AIDS AND HIV-INFECTION IN COCAINE USERS SO CIBA FOUNDATION SYMPOSIA LA English DT Discussion ID INTRAVENOUS-DRUG-USERS; INJECTION C1 NATL ADDICT CTR,ADDICT RES UNIT,LONDON SE5 8AF,ENGLAND. HARVARD UNIV,JOHN F KENNEDY SCH GOVT,CAMBRIDGE,MA 02138. UNIV HULL,SOCIAL VALUES RES CTR,HULL HU6 7RX,N HUMBERSIDE,ENGLAND. OFF NATL DRUG CONTROL POLICY,EXECUT OFF PRESIDENT,WASHINGTON,DC 20500. MCGILL UNIV,MONTREAL GEN HOSP,DEPT PSYCHIAT,MONTREAL H3G 1A4,QUEBEC,CANADA. DRUG DEPENDENCE UNIT,MONTREAL H3G 1A4,QUEBEC,CANADA. UNIV CALIF SAN FRANCISCO,DEPT PSYCHIAT,LANGLEY PORTER PSYCHIAT INST,SAN FRANCISCO,CA 94143. UNIV CHICAGO,DRUG ABUSE RES CTR,DEPT PHARMACOL & PHYSIOL SCI,CHICAGO,IL 60637. YALE UNIV,SCH MED,CHILD STUDY CTR PSYCHIAT & HIST MED,NEW HAVEN,CT 06510. UNIV TORONTO,DEPT PHARMACOL,ADDICT RES GRP,TORONTO M5S 1A8,ONTARIO,CANADA. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MENTAL HLTH,BALTIMORE,MD 21205. UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. ADDICT RES CTR,NEUROSCI BRANCH,BALTIMORE,MD 21224. RP JARLAIS, DCD (reprint author), BETH ISRAEL MED CTR,NARCOT & DRUG RES INC,11 BEACH ST,NEW YORK,NY 10013, USA. NR 15 TC 0 Z9 0 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 166 BP 181 EP 194 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA HV055 UT WOS:A1992HV05500011 ER PT J AU OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR AF OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR TI PSYCHOTHERAPY FOR COCAINE DEPENDENCE SO CIBA FOUNDATION SYMPOSIA LA English DT Article AB Dependence on cocaine is a new disorder for contemporary US clinicians. Until the 1980s sufficient quantities of the drug were not available to produce a true dependence. Thus far the only models for pharmacological intervention involve an interaction between medication and psychotherapy; that is, medication may be able to facilitate a drug-free interval during which time the patient can be engaged in psychotherapy. Psychotherapy programmes for cocaine dependence have generally been modelled on group-oriented treatments of the type used by Alcoholics Anonymous. Controlled studies of therapy programmes for cocaine dependence are currently being conducted and one prospective random-assignment study comparing day hospital and in-patient rehabilitation shows generally good results. Behavioural treatments aimed at reducing or extinguishing conditioned responses in cocaine addicts have also shown efficacy in a controlled study. More general relapse prevention procedures including rehearsal and role-playing are also used in the treatment of cocaine dependence. Combinations of psychotherapy and pharmacotherapy have so far shown the most promise in the treatment of this disorder. RP OBRIEN, CP (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [R01 DA 000586, P50 DA 5186] NR 9 TC 6 Z9 6 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0300-5208 J9 CIBA F SYMP JI CIBA Found. Symp. PY 1992 VL 166 BP 207 EP 223 PG 17 WC Medicine, General & Internal SC General & Internal Medicine GA HV055 UT WOS:A1992HV05500013 PM 1638915 ER PT J AU RUSKIN, JN AF RUSKIN, JN TI ROLE OF INVASIVE ELECTROPHYSIOLOGICAL TESTING IN THE EVALUATION AND TREATMENT OF PATIENTS AT HIGH-RISK FOR SUDDEN CARDIAC DEATH SO CIRCULATION LA English DT Article; Proceedings Paper CT SYMP ON CURRENT PERSPECTIVES ON THE PROBLEM OF SUDDEN CARDIAC DEATH CY SEP 24-25, 1990 CL DALLAS, TX SP AMER HEART ASSOC DE SUDDEN CARDIAC DEATH; ELECTROPHYSIOLOGICAL TESTING; PROGRAMMED ELECTRICAL STIMULATION; VENTRICULAR TACHYCARDIA; VENTRICULAR FIBRILLATION ID ACUTE MYOCARDIAL-INFARCTION; NONSUSTAINED VENTRICULAR-TACHYCARDIA; CORONARY-ARTERY DISEASE; PROGRAMMED ELECTRICAL-STIMULATION; IDIOPATHIC DILATED CARDIOMYOPATHY; TERM FOLLOW-UP; RECURRENT UNEXPLAINED SYNCOPE; UNDERLYING HEART-DISEASE; HYPERTROPHIC CARDIOMYOPATHY; PROGNOSTIC-SIGNIFICANCE AB Invasive electrophysiological testing has contributed importantly to the objective evaluation and management of patients at high risk for sudden cardiac death. The clinical application of the technique is based on the hypothesis that the reproducible induction of ventricular arrhythmias by programmed cardiac stimulation constitutes a marker of risk for spontaneous ventricular arrhythmias and sudden death as well as an objective end point to guide the selection of antiarrhythmic therapy. The value of electrophysiological testing is well established in patients with ischemic heart disease and a history of sustained ventricular tachycardia or fibrillation and in some subsets of patients with unexplained syncope. More recently, the technique has been used by some investigators to identify individuals at high risk for sudden death among patients with recent myocardial infarction and those with left ventricular dysfunction and recurrent nonsustained ventricular tachycardia. The predictive value of the technique in patients with nonischemic heart disease is unknown. In addition to its use as an objective end point in the selection of antiarrhythmic drug therapy, invasive electrophysiological testing has advanced our knowledge of the mechanisms of life-threatening ventricular arrhythmias and contributed importantly to the development of new therapies, such as implantable arrhythmia control devices and catheter ablation techniques. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NR 98 TC 17 Z9 17 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 PY 1992 VL 85 IS 1 SU S BP 152 EP 159 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HA414 UT WOS:A1992HA41400023 ER PT J AU POLLOCK, SG ABBOTT, RD BOUCHER, CA BELLER, GA KAUL, S AF POLLOCK, SG ABBOTT, RD BOUCHER, CA BELLER, GA KAUL, S TI INDEPENDENT AND INCREMENTAL PROGNOSTIC VALUE OF TESTS PERFORMED IN HIERARCHICAL ORDER TO EVALUATE PATIENTS WITH SUSPECTED CORONARY-ARTERY DISEASE - VALIDATION OF MODELS BASED ON THESE TESTS SO CIRCULATION LA English DT Article DE CORONARY ARTERY DISEASE; TI-201; EXERCISE; STRESS; TESTING; ANGIOGRAPHY ID CHEST PAIN; MYOCARDIAL-INFARCTION; BAYES THEOREM; EXERCISE ELECTROCARDIOGRAPHY; CARDIAC-CATHETERIZATION; AMBULATORY PATIENTS; STRESS TEST; TL-201; SCINTIGRAPHY; DIAGNOSIS AB Background. The additive prognostic value of tests done in a hierarchical order for the detection of coronary artery disease (CAD) is not always known. The principal goal of this study, therefore, was to assess the incremental prognostic value of data obtained in succession (clinical, exercise stress testing, Tl-201 imaging, and coronary angiography) in patients with suspected CAD. A second goal was to develop models for determining prognosis based on results of these tests and to test the clinical validity of these models in unrelated patients. Methods and Results. Data from two groups of patients who had undergone such evaluation and had been followed for a mean of 4.4 years were analyzed. There were 204 patients from Massachusetts General Hospital (MGH) and 299 from the University of Virginia (UVA). There were 20 deaths and 21 nonfatal infarctions in the MGH group and 41 deaths and nine infarctions in the UVA group. Both univariate and multivariate Cox regression analyses were performed to assess the individual and incremental prognostic value of these tests. In both groups, Tl-201 imaging provided significant additional prognostic information compared with clinical and exercise stress test data (p < 0.05). At MGH, where the lung/heart Tl-201 ratio had been analyzed, coronary angiography did not provide additional prognostic information. In this group of patients, the combination of clinical and exercise Tl-201 variables provided greater prognostic information than the combination of clinical and angiographic data (p < 0.001). In the UVA cohort, in which the lung/heart ratio had not been analyzed, coronary angiography provided incremental prognostic information compared with clinical and exercise Tl-201 data alone (p < 0.05). When models developed using data from either sample were applied to the other unrelated sample, there was often close agreement between the overall observed rates and those predicted by the models. This was also true for the low-risk and high-risk subgroups. Some models, however, did not perform as well as other models, which suggests that models that do well in one sample may not always be generalized to other groups. Conclusions. Tests performed in hierarchical order for the evaluation of suspected CAD provide additional prognostic information. Models developed using clinically relevant combinations of test results obtained from different patient populations are frequently able to predict absolute levels of survival in unrelated but similar samples. C1 UNIV VIRGINIA,DEPT MED,DIV CARDIOL,BOX 158,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,DEPT MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22908. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [KO8-HL-01833, R01-HL-26215, R01-HL-26205] NR 45 TC 140 Z9 141 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 PY 1992 VL 85 IS 1 BP 237 EP 248 PG 12 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA GY582 UT WOS:A1992GY58200029 PM 1728455 ER PT J AU LEINBACH, RC AF LEINBACH, RC TI THROMBOLYSIS IN UNSTABLE ANGINA SO CIRCULATION LA English DT Editorial Material DE EDITORIAL COMMENTS; UNSTABLE ANGINA; THROMBOLYSIS ID TISSUE PLASMINOGEN-ACTIVATOR; PLACEBO-CONTROLLED TRIAL; THROMBIN INHIBITION; PECTORIS; STREPTOKINASE; INFARCTION; THERAPY C1 MASSACHUSETTS GEN HOSP,DEPT MED,DIV CARDIOL,BOSTON,MA 02114. NR 13 TC 8 Z9 8 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 PY 1992 VL 85 IS 1 BP 376 EP 377 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA GY582 UT WOS:A1992GY58200048 PM 1728474 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI KINETICS OF RESTITUTION OF LEFT-VENTRICULAR RELAXATION SO CIRCULATION RESEARCH LA English DT Article DE DIASTOLE; EXTRASYSTOLE; INTRACELLULAR CALCIUM; PRESSURE DECAY ID MECHANICAL RESTITUTION; PRESSURE; MYOCARDIUM; RYANODINE; DOGS AB Although the kinetics of cardiac systolic force restitution have been well described, the restitution kinetics of left ventricular relaxation have not been examined. To define relaxation restitution behavior, we studied seven dogs chronically instrumented with left ventricular high-fidelity micromanometers and piezoelectric dimension crystals. After a priming period at a basic cycle length of 375 msec, test extrastimuli were introduced after a range of extrasystolic intervals (ESIs). Relaxation behavior of control and extrasystolic beats was characterized by the time constant of isovolumic relaxation, tau. Relaxation restitution can be described by two concatenated monoexponential curves, an early phase described by a rapid time constant and a late phase described by a slower time constant (TC1, 36.21 +/- 7.90 msec; TC2, 75.94 +/- 10.65 msec; p < 0.05). The first phase of relaxation restitution parallels systolic force restitution over the same range and displays faster recovery (TC(s), 58.93 +/- 10.01 msec, p < 0.05). Postextrasystolic restitution of test pulses after beats at fixed ESIs depends on the initial ESI. Relaxation recovery of postextrasystolic beats proceeds faster with smaller initial ESIs (TC1 for ESI of 300 msec, 13.27 +/- 4.05 msec; TC1 for ESI of 450 msec, 72.85 +/- 21.72 msec; p < 0.0001). The monoexponential pattern of restitution was seen with model-independent descriptors of relaxation as well as with tau. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Prabhu, Sumanth/D-5223-2009 NR 27 TC 14 Z9 14 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD JAN PY 1992 VL 70 IS 1 BP 29 EP 38 PG 10 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA HE089 UT WOS:A1992HE08900004 PM 1370136 ER PT J AU TUCKER, RM DENNING, DW HANSON, LH RINALDI, MG GRAYBILL, JR SHARKEY, PK PAPPAGIANIS, D STEVENS, DA AF TUCKER, RM DENNING, DW HANSON, LH RINALDI, MG GRAYBILL, JR SHARKEY, PK PAPPAGIANIS, D STEVENS, DA TI INTERACTION OF AZOLES WITH RIFAMPIN, PHENYTOIN, AND CARBAMAZEPINE - INVITRO AND CLINICAL OBSERVATIONS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID COCCIDIOIDES-IMMITIS; AMPHOTERICIN-B; ITRACONAZOLE INTERACTION; CYCLOSPORIN; THERAPY; KETOCONAZOLE; FLUCONAZOLE; ANTIFUNGAL; SERUM; SUSCEPTIBILITY AB Twelve patients receiving therapy with an azole agent (ketoconazole, itraconazole, and/or fluconazole) for systemic mycoses experienced drug interactions with rifampin, phenytoin, and/or carbamazepine resulting in substantial decreases in azole concentrations in serum. All four patients receiving azoles and concurrent phenytoin and/or carbamazepine failed to respond to treatment or suffered a relapse of their fungal infection. Four of five patients with cryptococcosis who received itraconazole and rifampin responded despite decreases in their serum itraconazole concentrations; synergy between itraconazole and rifampin was documented by in vitro analysis of inhibition and of killing of Cryptococcus neoformans isolates from all patients receiving this combination. In contrast, two patients with coccidioidomycosis failed to respond to itraconazole/rifampin. Moreover, two patients with cryptococcosis suffered a relapse or persistence of seborrheic dermatitis while receiving itraconazole/rifampin. The latter combination showed synergy in vitro in the inhibition of the mycelial phase of Coccidioides immitis and, to a lesser extent, of the pathogenic spherule phase of this fungus; synergy in the killing of C. immitis was not noted, nor was synergy seen against Malassezia furfur, the purported etiologic agent of seborrheic dermatitis. These findings illustrate several drug interactions that may affect clinical outcome and that must be considered in the management of antifungal therapy. C1 SANTA CLARA VALLEY MED CTR,DEPT MED,DIV INFECT DIS,751 S BASCOM,SAN JOSE,CA 95128. CALIF INST MED RES,SAN JOSE,CA. STANFORD UNIV,MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,STANFORD,CA 94305. WENATCHEE VALLEY CLIN,DEPT INFECT DIS,DIV INTERNAL MED,WENATCHEE,WA. UNIV WASHINGTON,DEPT INTERNAL MED,SEATTLE,WA 98195. UNIV CALIF DAVIS,SCH MED,DEPT MED MICROBIOL,DAVIS,CA 95616. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,MYCOL TESTING LAB,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. OI Denning, David/0000-0001-5626-2251 NR 40 TC 141 Z9 142 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1992 VL 14 IS 1 BP 165 EP 174 PG 10 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HD517 UT WOS:A1992HD51700026 PM 1315160 ER PT J AU SHAPIRO, CL HAFT, RF GANTZ, NM DOERN, GV CHRISTENSON, JC OBRIEN, R OVERALL, JC BROWN, BA WALLACE, RJ AF SHAPIRO, CL HAFT, RF GANTZ, NM DOERN, GV CHRISTENSON, JC OBRIEN, R OVERALL, JC BROWN, BA WALLACE, RJ TI TSUKAMURELLA-PAUROMETABOLUM - A NOVEL PATHOGEN CAUSING CATHETER-RELATED BACTEREMIA IN PATIENTS WITH CANCER SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID GORDONA-AURANTIACA RHODOCOCCUS; IDENTIFICATION; NOV AB Tsukamurella paurometabolum is a weakly acid-fast, pleomorphic gram-positive bacterium found in soil. Human infection due to this organism has rarely been described, and there are no published accounts of bacteremia. Three cases of bacteremia due to T. paurometabolum and related to long-term use of a central venous catheter in patients with cancer who were receiving chemotherapy are described. C1 BRIGHAM & WOMENS HOSP,DIV INFECT DIS,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,DIV INFECT DIS,AMHERST,MA 01003. UNIV MASSACHUSETTS,MED CTR,DEPT CLIN MICROBIOL,AMHERST,MA 01003. UNIV UTAH,DIV PEDIAT INFECT DIS,SALT LAKE CITY,UT 84112. UNIV UTAH,DIV PEDIAT HEMATOL ONCOL,SALT LAKE CITY,UT 84112. UNIV TEXAS,HLTH SCI CTR,DEPT MICROBIOL,TYLER,TX. RP SHAPIRO, CL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [2-T32-AI07061-12AI] NR 10 TC 29 Z9 29 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD JAN PY 1992 VL 14 IS 1 BP 200 EP 203 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HD517 UT WOS:A1992HD51700032 PM 1571430 ER PT J AU HARRIS, WH AF HARRIS, WH TI THE 1ST 32 YEARS OF TOTAL HIP-ARTHROPLASTY - ONE SURGEONS PERSPECTIVE SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT 19TH OPEN SCIENTIFIC MEETING OF THE HIP SOC CY MAR 09, 1991 CL ANAHEIM, CA SP HIP SOC ID LOCALIZED BONE-RESORPTION; 10-YEAR FOLLOW-UP; CEMENT INTERFACE; KNEE REPLACEMENT; COMPONENT; IMPLANT AB During the first 32 years of total hip arthroplasty, high risk of sepsis, improved prevention of infection, problems of loosening, new disease of bone lysis secondary to particulate debris, and the complexities of cementless fixation have taught orthopedic surgeons many lessons. These lessons include the following: (1) In cemented THA, bone cement can be made five-times stronger just by porosity reduction; the critical interface in a cemented femoral stem is the cement-metal interface, not the cement-bone interface; and no one has solved the long-term fixation problem in cemented sockets. (2) In cementless implants, the disuse osteoporosis that occurs around cementless femoral components can be severe; the use of cementless implants does not eliminate bone lysis; only small amounts of bone ingrowth occur in many cementless implants, particularly in revision cases; and little or no bone ingrowth occurs from grafts. Today, however, some of these lessons are ignored by surgeons. If progress is to be made in arthroplasty, these lessons from the past should be learned and warning signs of the present should be heeded. RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,1126A JACKSON TOWERS,BOSTON,MA 02114, USA. NR 41 TC 34 Z9 36 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1992 IS 274 BP 6 EP 11 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GY549 UT WOS:A1992GY54900003 PM 1729023 ER PT J AU SCHMALZRIED, TP KWONG, LM JASTY, M SEDLACEK, RC HAIRE, TC OCONNOR, DO BRAGDON, CR KABO, JM MALCOLM, AJ PATH, MRC HARRIS, WH AF SCHMALZRIED, TP KWONG, LM JASTY, M SEDLACEK, RC HAIRE, TC OCONNOR, DO BRAGDON, CR KABO, JM MALCOLM, AJ PATH, MRC HARRIS, WH TI THE MECHANISM OF LOOSENING OF CEMENTED ACETABULAR COMPONENTS IN TOTAL HIP-ARTHROPLASTY - ANALYSIS OF SPECIMENS RETRIEVED AT AUTOPSY SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT 19TH OPEN SCIENTIFIC MEETING OF THE HIP SOC CY MAR 09, 1991 CL ANAHEIM, CA SP HIP SOC ID 10-YEAR FOLLOW-UP; STRESS DISTRIBUTIONS; BONE-RESORPTION; REPLACEMENT; WEAR; POLYETHYLENE; PROSTHESES; REGION; SOCKET AB Late aseptic loosening of cemented acetabular components is governed by the progressive, three-dimensional resorption of the bone immediately adjacent to the cement mantle. This process begins circumferentially at the intraarticular margin and progresses toward the dome of the implant. Evidence of bone resorption at the cement-bone interface was present even in the most well-fixed implants before the appearance of lucent lines on standard roentgenographic views. The mechanical stability of the implant was determined by the three-dimensional extent of bone resorption and membrane formation at the cement-bone interface. The leading edge of the membrane is a transition zone from regions of membrane interposition between the cement and the bone to regions of intimate cement-bone contact. Histologic analysis revealed that progressive bone resorption is fueled by small particles of high density polyethylene (HDP) migrating along the cement-bone interface and bone resorption occurs as a result of the macrophage inflammatory response to the particulate HDP. Evidence in support of a mechanical basis for failure of fixation was lacking. The mechanism of late aseptic loosening of a cemented acetabular component is therefore biologic in nature, not mechanical. This is exactly opposite to the mechanism of loosening on the femoral side of a cemented total hip replacement, which is mechanical in nature. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. UNIV CALIF LOS ANGELES,DIV ORTHOPAED SURG,BIOMECH SECT,LOS ANGELES,CA 90024. ROYAL VICTORIA INFIRM,DEPT PATHOL,NEWCASTLE TYNE NE1 4LP,TYNE & WEAR,ENGLAND. NR 60 TC 1 Z9 1 U1 1 U2 10 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1992 IS 274 BP 60 EP 78 PG 19 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GY549 UT WOS:A1992GY54900009 ER PT J AU HARRIS, WH AF HARRIS, WH TI WILL STRESS SHIELDING LIMIT THE LONGEVITY OF CEMENTED FEMORAL COMPONENTS OF TOTAL HIP-REPLACEMENT SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article; Proceedings Paper CT 19TH OPEN SCIENTIFIC MEETING OF THE HIP SOC CY MAR 09, 1991 CL ANAHEIM, CA SP HIP SOC AB One must acknowledge the speculative nature of evaluating whether stress shielding will limit the longevity of cemented femoral components. One can, however, evaluate the data available from patients studied up to 20 years. Stress shielding does lead to disuse osteoporosis, particularly in the proximal medial cortex, and also more slowly and to a lesser extent elsewhere. Concern also exists that progressive endosteal enlargement will lead to failure of many or all cemented femoral stems. No evidence exists that disuse osteoporosis has limited the longevity of cemented femoral stems up to 20 years. Moreover, new data show that what has been described as the normal process of endosteal enlargement after inserting a cemented femoral component is a misinterpretation. What actually happens is that (1) neocortex develops around the cement mantle, (2) the original cortex thins, (3) the trabeculae in the zone of decreased density that develops between them maintain the structural integrity between those two bony masses, and (4) the implant remains rigidly fixed. RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,BOSTON,MA 02114, USA. NR 11 TC 34 Z9 34 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD JAN PY 1992 IS 274 BP 120 EP 123 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GY549 UT WOS:A1992GY54900013 PM 1728997 ER PT J AU LITZ, BT AF LITZ, BT TI EMOTIONAL NUMBING IN COMBAT-RELATED POSTTRAUMATIC-STRESS-DISORDER - A CRITICAL-REVIEW AND REFORMULATION SO CLINICAL PSYCHOLOGY REVIEW LA English DT Article ID DSM-III CRITERIA; VIETNAM VETERANS; EXPERIENCE; MEMORY; INFORMATION; ADJUSTMENT; VALIDITY; SYMPTOMS; SYSTEM; THREAT AB Emotional numbing symptoms are considered in the clinical literature as cardinal signs of Post-Traumatic Stress Disorder (PTSD) and have been formally codified in DSM-III-R. However, the term has not been consistently defined nor adequately researched. The present paper critically reviews the extant empirical and theoretical literature in combat-related PTSD that has explored emotional numbing symptoms. A theoretical framework, based on Levonthal's (1984) perceptual-motor theory of emotion, is posited to account for the parameters of emotional processing in PTSD, and specific hypotheses concerning selective or differential emotional processing deficits in PTSD are described in order to clarify empirical issues about the development and maintenance of emotional processing deficits in PTSD and to stimulate future research in this underexplored, yet clinically important area. C1 TUFTS UNIV,SCH MED,BOSTON,MA 02111. RP LITZ, BT (reprint author), VET ADM MED CTR JAMAICA PLAIN,NATL CTR PTSD,116-B,150 S HUNTINGTON AVE,BOSTON,MA 02130, USA. NR 79 TC 118 Z9 121 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0272-7358 J9 CLIN PSYCHOL REV JI Clin. Psychol. Rev. PY 1992 VL 12 IS 4 BP 417 EP 432 DI 10.1016/0272-7358(92)90125-R PG 16 WC Psychology, Clinical SC Psychology GA HV764 UT WOS:A1992HV76400003 ER PT J AU SOBER, AJ KANG, S BARNHILL, RL AF SOBER, AJ KANG, S BARNHILL, RL TI DISCERNING INDIVIDUALS AT ELEVATED RISK FOR CUTANEOUS MELANOMA SO CLINICS IN DERMATOLOGY LA English DT Article RP SOBER, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BARTLETT 410,BOSTON,MA 02114, USA. NR 0 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0738-081X J9 CLIN DERMATOL JI Clin. Dermatol. PD JAN-MAR PY 1992 VL 10 IS 1 BP 15 EP 20 DI 10.1016/0738-081X(92)90053-2 PG 6 WC Dermatology SC Dermatology GA JG979 UT WOS:A1992JG97900004 PM 1504924 ER PT J AU YAREMCHUK, MJ AF YAREMCHUK, MJ TI CHANGING CONCEPTS IN THE MANAGEMENT OF SECONDARY ORBITAL DEFORMITIES SO CLINICS IN PLASTIC SURGERY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 25 Z9 26 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0094-1298 J9 CLIN PLAST SURG JI Clin. Plast. Surg. PD JAN PY 1992 VL 19 IS 1 BP 113 EP 124 PG 12 WC Surgery SC Surgery GA LA245 UT WOS:A1992LA24500010 PM 1537213 ER PT B AU OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR AF OBRIEN, CP MCLELLAN, AT ALTERMAN, A CHILDRESS, AR BE BOCK, GR WHELAN, J TI PSYCHOTHERAPY FOR COCAINE DEPENDENCE SO COCAINE : SCIENTIFIC AND SOCIAL DIMENSIONS SE CIBA FOUNDATION SYMPOSIA LA English DT Proceedings Paper CT SYMP ON COCAINE : SCIENTIFIC AND SOCIAL DIMENSIONS CY JUL 20-22, 1991 CL CIBA FDN, LONDON, ENGLAND SP CIBA FDN HO CIBA FDN RP OBRIEN, CP (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT PSYCHIAT,3900 CHESTNUT ST,PHILADELPHIA,PA 19104, USA. FU NIDA NIH HHS [R01 DA 000586, P50 DA 5186] NR 0 TC 6 Z9 6 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI CHICHESTER PA CHICHESTER BN 0-471-93179-9 J9 CIBA F SYMP PY 1992 VL 166 BP 207 EP 223 PG 17 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry; Psychology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry; Psychology GA BV65D UT WOS:A1992BV65D00013 PM 1638915 ER PT J AU ROMEO, C KOLANUS, W AMIOT, M SEED, B AF ROMEO, C KOLANUS, W AMIOT, M SEED, B TI ACTIVATION OF IMMUNE-SYSTEM EFFECTOR FUNCTION BY T-CELL OR FC RECEPTOR INTRACELLULAR DOMAINS SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; ANTIGEN RECEPTOR; ZETA-CHAIN; MOLECULAR-CLONING; ETA-CHAIN; TRANSFECTED CELLS; TRIGGER MOLECULES; CYTO-TOXICITY; LYMPHOCYTES-T; CD3 COMPLEX RP ROMEO, C (reprint author), MASSACHUSETTS GEN HOSP,DEPT MICROBIOL & IMMUNOL,BOSTON,MA 02114, USA. NR 59 TC 17 Z9 17 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1992 VL 57 BP 117 EP 125 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LV416 UT WOS:A1992LV41600013 PM 1339650 ER PT J AU HEMLER, ME KASSNER, PD CHAN, BMC AF HEMLER, ME KASSNER, PD CHAN, BMC TI FUNCTIONAL ROLES FOR INTEGRIN ALPHA-SUBUNIT CYTOPLASMIC DOMAINS SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; LEUKOCYTE ADHESION GLYCOPROTEIN; COMPLEMENT RECEPTOR TYPE-3; FIBRONECTIN RECEPTOR; MEMBRANE GLYCOPROTEIN; MOLECULAR-CLONING; CELL-ADHESION; GPIIB-IIIA; TYROSINE PHOSPHORYLATION; ONCOGENIC TRANSFORMATION RP HEMLER, ME (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM-38903, GM-46526] NR 64 TC 25 Z9 25 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1992 VL 57 BP 213 EP 220 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LV416 UT WOS:A1992LV41600024 PM 1339660 ER PT J AU HARRISON, SC WANG, J YAN, Y GARRETT, T LIU, J MOEBIUS, U REINHERZ, E AF HARRISON, SC WANG, J YAN, Y GARRETT, T LIU, J MOEBIUS, U REINHERZ, E TI STRUCTURE AND INTERACTIONS OF CD4 SO COLD SPRING HARBOR SYMPOSIA ON QUANTITATIVE BIOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; CLASS-II MHC; RECOMBINANT SOLUBLE CD4; TOXIC LYMPHOCYTES-T; BINDING-SITE; ENVELOPE GLYCOPROTEIN; OLIGOMERIC STRUCTURE; MONOCLONAL-ANTIBODY; ATOMIC-STRUCTURE; TYPE-1 C1 HOWARD HUGHES MED INST,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP HARRISON, SC (reprint author), HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138, USA. FU NIAID NIH HHS [AI-30361, AI-27336]; NIGMS NIH HHS [GM-39589] NR 52 TC 13 Z9 14 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0091-7451 J9 COLD SPRING HARB SYM JI Cold Spring Harbor Symp. Quant. Biol. PY 1992 VL 57 BP 541 EP 548 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA LV416 UT WOS:A1992LV41600057 PM 1339691 ER PT J AU LEES, S PAGE, EA AF LEES, S PAGE, EA TI A STUDY OF SOME PROPERTIES OF MINERALIZED TURKEY LEG TENDON SO CONNECTIVE TISSUE RESEARCH LA English DT Article DE TURKEY LEG TENDON; COLLAGEN; DENSITY; SONIC VELOCITY; ELASTIC MODULI; DIMENSIONAL CHANGES ON DRYING ID NEUTRON-DIFFRACTION; X-RAY; COLLAGEN FIBRILS; BONE; CRYSTALS; WATER; TISSUES; MODEL AB Several macroscopic physical properties of mineralized turkey leg tendon were measured including wet density, composition, volume fractions of the major components, sonic velocity in three axes, longitudinal modulus and dimensional changes on drying. Where possible the properties were related to density. Typically the wet density of unmineralized tissue is 1.09 g/cc, where for fully mineralized tissue it is 1.6 g/cc (compared with 2.06 to 2.10 g/cc for compact cow bone). Longitudinal sonic velocity axially is 3.22 km/sec, 2.57 km/sec transversely and 2.21 km/sec in thickness. The axial longitudinal modulus is 16.7 GPa compared to the axial Young's modulus of 8.53 GPa. MTLT shrinks 0.5% axially, 4.75% transversely and 4.15% in thickness. The anisotropy is equally exhibited in its microscopic structure when observed optically. Least squares second order curves were fitted to the water, mineral and organic component experimental values. Apparently the water in MTLT is replaced by mineral, unlike the process in bone where there is less organic matter as the mineral content increases and the water fraction changes much less. The generalized packing model for collagen was used to relate the data to the ultrastructure. The distribution of the major components between the intrafibrillar and extrafibrillar volumes as a function of the density was calculated. The results show the intrafibrillar volume fraction increases with density, the water content of the intrafibrillar volume remains almost constant, but the water fraction of the extrafibrillar volume decreases from 51 to 8% of the water in the tissue. It is concluded that the mineralization process in MTLT differs from that in bone. C1 NORTHEASTERN UNIV,BOSTON,MA 02115. RP LEES, S (reprint author), FORSYTH DENT CTR,DEPT BIOENGN,140 FENWAY,BOSTON,MA 02115, USA. NR 40 TC 45 Z9 45 U1 1 U2 6 PU GORDON BREACH SCI PUBL LTD PI READING PA C/O STBS LTD PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 0300-8207 J9 CONNECT TISSUE RES JI Connect. Tissue Res. PY 1992 VL 28 IS 4 BP 263 EP 287 DI 10.3109/03008209209016820 PG 25 WC Cell Biology; Orthopedics SC Cell Biology; Orthopedics GA KV176 UT WOS:A1992KV17600003 PM 1304442 ER PT J AU DEFRONZO, RA AF DEFRONZO, RA TI INSULIN RESISTANCE, HYPERINSULINEMIA, AND CORONARY-ARTERY DISEASE - A COMPLEX METABOLIC WEB SO CORONARY ARTERY DISEASE LA English DT Review DE INSULIN RESISTANCE; HYPERINSULINISM; CORONARY DISEASE; CHOLESTEROL; HYPERTENSION; DIABETES-MELLITUS; NON-INSULIN-DEPENDENT; OBESITY ID IMPAIRED GLUCOSE-TOLERANCE; DEPENDENT DIABETES-MELLITUS; CARDIOVASCULAR RISK-FACTORS; SODIUM-LITHIUM COUNTERTRANSPORT; HIGH-DENSITY LIPOPROTEIN; BLOOD-PRESSURE REGULATION; HEART-DISEASE; ESSENTIAL-HYPERTENSION; PIMA-INDIANS; FOLLOW-UP C1 UNIV TEXAS, HLTH SCI CTR, DIV NEPHROL, SAN ANTONIO, TX 78284 USA. AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX USA. RP DEFRONZO, RA (reprint author), UNIV TEXAS, HLTH SCI CTR, DIV DIABET, SAN ANTONIO, TX 78284 USA. NR 120 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0954-6928 EI 1473-5830 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD JAN PY 1992 VL 3 IS 1 BP 11 EP 25 DI 10.1097/00019501-199201000-00003 PG 15 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HE751 UT WOS:A1992HE75100003 ER PT J AU TODRES, ID AF TODRES, ID TI ETHICAL DILEMMAS IN PEDIATRIC CRITICAL CARE SO CRITICAL CARE CLINICS LA English DT Article RP TODRES, ID (reprint author), MASSACHUSETTS GEN HOSP,NEONATAL UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 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 0749-0704 J9 CRIT CARE CLIN JI Crit. Care Clin. PD JAN PY 1992 VL 8 IS 1 BP 219 EP 227 PG 9 WC Critical Care Medicine SC General & Internal Medicine GA GX301 UT WOS:A1992GX30100015 PM 1732030 ER PT J AU CONN, AKT AF CONN, AKT TI COWLEY,R,ADAMS SO CRITICAL CARE MEDICINE LA English DT Editorial Material RP CONN, AKT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD JAN PY 1992 VL 20 IS 1 BP 4 EP 4 DI 10.1097/00003246-199201000-00004 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA GZ015 UT WOS:A1992GZ01500004 ER PT J AU SMITH, DJ TAUBMAN, MA AF SMITH, DJ TAUBMAN, MA TI ONTOGENY OF IMMUNITY TO ORAL MICROBIOTA IN HUMANS SO CRITICAL REVIEWS IN ORAL BIOLOGY & MEDICINE LA English DT Article DE SECRETORY IGA; SALIVARY DEFENSES; ONTOGENY; CARIOGENIC STREPTOCOCCI AB This article reviews the ontogeny of immune systems in the human oral cavity that may influence the colonization, accumulation, or pathogenesis of oral microbiota. The prenatal development of cellular components associated with the secretory immune system reveals that the initial organization of tissue into Peyer's patches can first be detected immunohistologically at 11 weeks gestation. Epithelial cells positive for secretory component and immunocytes positive for IgM can be detected in salivary gland tissue by 19 to 20 weeks and continue to predominate during gestation. After birth, immunocytes containing IgA begin to dominate. Essentially, no IgA can be detected in saliva at birth. However, salivary IgA and IgM often appear soon thereafter, presumably in response to environmental antigenic and mitogenic challenges. Salivary IgA in young infants has molecular characteristics of secretory IgA and becomes the quantitatively predominate Ig in saliva. Both IgA subclasses are present in proportions characteristic of adult pure glandular salivas in many 1- to 2-month-old infants, although the appearance of IgA2 is delayed in some subjects. Many innate, antibody, and cellular immune components are found in maternal colostrum and breast milk. The antibacterial properties of these maternal factors are diverse and can exert multifaceted protective effects on the infant's alimentary tract. The infant apparently can mount mucosal immune responses quite early in life. For example, salivary antibody activity to organisms that originally colonize the gut (e.g., E. coli) or the oral cavity (e.g., S. mitis, S. salivarius) can be detected by 1 to 2 months of age. Most of this antibody activity has characteristics of secretory IgA, although some IgM antibody can also be initially detected. Salivary IgA1 and IgA2 antibody specificities to S. mitis and S. salivarius components increase qualitatively and quantitatively during the first few years of life. Salivary IgA antibody to components of streptococci that require hard surfaces for colonization (e.g., S. sanguis and mutans streptococci) generally appear after tooth eruption. The loss of placentally derived maternal IgG antibody specificities to these microbiota in the circulation is replaced by de novo synthesis, presumably as a result of the teething process. These IgG antibodies can enter the oral cavity in the gingival crevicular fluid and by the process of teething. The collective contributions in the oral cavity of innate and antibody-based immune elements from the saliva, gingival crevicular fluid (and milk if breast feeding) may be considered together with diet, infectious dose, salivary receptors, and tooth integuments, as factors that can determine the outcome of initial colonization events on erupting tooth surfaces. RP SMITH, DJ (reprint author), FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-04733, DE-06153] NR 0 TC 47 Z9 49 U1 0 U2 3 PU INT AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314-3406 SN 1045-4411 J9 CRIT REV ORAL BIOL M JI Crit. Rev. Oral Biol. Med. PY 1992 VL 3 IS 1-2 BP 109 EP 133 PG 25 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA GU916 UT WOS:A1992GU91600006 PM 1730067 ER PT J AU MOTOKURA, T YI, HF KRONENBERG, HM MCBRIDE, OW ARNOLD, A AF MOTOKURA, T YI, HF KRONENBERG, HM MCBRIDE, OW ARNOLD, A TI ASSIGNMENT OF THE HUMAN CYCLIN-D3 GENE (CCND3) TO CHROMOSOME 6P-]Q13 SO CYTOGENETICS AND CELL GENETICS LA English DT Article ID CANDIDATE ONCOGENE; CELL; RETINOBLASTOMAS; ABNORMALITIES; LYMPHOMA; BCL-1 AB The PRAD1/cyclin D1 gene (CCND 1), a member of the D-type cyclin gene family, has been implicated as a protooncogene in parathyroid, lymphoid, and mammary tumors. We cloned and mapped another member of this family, the human cyclin D3 gene (CCND3), to chromosome 6p --> q13 using human x rodent hybrids. This assignment raises the hypothesis that cyclin D3 may be involved in the pathogenesis of human neoplasms with abnormalities of chromosome 6. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 5,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NCI,BIOCHEM LAB,BETHESDA,MD 20892. FU NCI NIH HHS [CA55909]; NIDDK NIH HHS [DK11794] NR 16 TC 13 Z9 13 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1992 VL 61 IS 1 BP 5 EP 7 DI 10.1159/000133359 PG 3 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA JL517 UT WOS:A1992JL51700002 PM 1387066 ER PT J AU MITCHISON, HM WILLIAMS, RE MCKAY, TR CALLEN, DF THOMPSON, A MULLEY, JC STALLINGS, RL HILDEBRAND, CE MOYZIS, RK JARVELA, I PELTONEN, L HAINES, J SUTHERLAND, GR GARDINER, RM AF MITCHISON, HM WILLIAMS, RE MCKAY, TR CALLEN, DF THOMPSON, A MULLEY, JC STALLINGS, RL HILDEBRAND, CE MOYZIS, RK JARVELA, I PELTONEN, L HAINES, J SUTHERLAND, GR GARDINER, RM TI LINKAGE ANALYSIS OF NEURONAL CEROID LIPOFUSCINOSIS - REFINED MAPPING OF CLN3 AND EVIDENCE OF LOCUS HETEROGENEITY OF CLN3 AND CLN2 SO CYTOGENETICS AND CELL GENETICS LA English DT Meeting Abstract C1 UNIV LONDON UNIV COLL,DEPT PAEDIAT,LONDON WC1E 6BT,ENGLAND. UNIV LONDON MIDDLESEX HOSP,LONDON,ENGLAND. ADELAIDE CHILDRENS HOSP INC,DEPT CYTOGENET & MOLEC GENET,ADELAIDE,SA 5006,AUSTRALIA. LOS ALAMOS NATL LAB,LOS ALAMOS,NM 87544. NATL PUBL HLTH INST,MOLEC GENET LAB,SF-00280 HELSINKI 28,FINLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Sutherland, Grant/D-2606-2012; Callen, David/G-1975-2012 NR 1 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1992 VL 60 IS 3-4 BP 173 EP 173 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA JK230 UT WOS:A1992JK23000017 ER PT J AU HAINES, JL TROFATTER, JA TANZI, RE WATKINS, P WEXLER, NS CONNEALLY, PM GUSELLA, JF AF HAINES, JL TROFATTER, JA TANZI, RE WATKINS, P WEXLER, NS CONNEALLY, PM GUSELLA, JF TI CHROMOSOME-21 GENETIC-LINKAGE DATA SET BASED ON THE VENEZUELAN REFERENCE PEDIGREE SO CYTOGENETICS AND CELL GENETICS LA English DT Article; Proceedings Paper CT 7TH GENETIC ANALYSIS WORKSHOP : ISSUES IN GENE MAPPING AND DETECTION OF MAJOR GENES ( GAW 7 ) CY OCT 14-16, 1990 CL DAYTON, OH SP NATL INST GEN MED SCI ID MAP C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. LIFECODES INC,GAITHERSBURG,MD. COLUMBIA UNIV,SCH MED,DEPT NEUROL,NEW YORK,NY 10032. COLUMBIA UNIV,SCH MED,DEPT PSYCHOL,NEW YORK,NY 10032. INDIANA UNIV,SCH MED,DEPT MOLEC & MED GENET,INDIANAPOLIS,IN 46202. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00169, HG00324]; NINDS NIH HHS [NS22031] NR 7 TC 2 Z9 2 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1992 VL 59 IS 2-3 BP 88 EP 89 DI 10.1159/000133208 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HF049 UT WOS:A1992HF04900007 PM 1346592 ER PT J AU HAINES, JL TROFATTER, JA AF HAINES, JL TROFATTER, JA TI GENETIC-LINKAGE AND AFFECTED PEDIGREE MEMBER ANALYSIS IN MALIGNANT-MELANOMA SO CYTOGENETICS AND CELL GENETICS LA English DT Article; Proceedings Paper CT 7TH GENETIC ANALYSIS WORKSHOP : ISSUES IN GENE MAPPING AND DETECTION OF MAJOR GENES ( GAW 7 ) CY OCT 14-16, 1990 CL DAYTON, OH SP NATL INST GEN MED SCI C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [R01-HG00324] NR 5 TC 2 Z9 2 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0171 J9 CYTOGENET CELL GENET JI Cytogenet. Cell Genet. PY 1992 VL 59 IS 2-3 BP 206 EP 207 DI 10.1159/000133247 PG 2 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA HF049 UT WOS:A1992HF04900046 PM 1737502 ER PT J AU BRUIJN, JA SALASCHE, S SOBER, AJ MIHM, MC BARNHILL, RL AF BRUIJN, JA SALASCHE, S SOBER, AJ MIHM, MC BARNHILL, RL TI DESMOPLASTIC MELANOMA - CLINICOPATHOLOGICAL ASPECTS OF 6 CASES SO DERMATOLOGY LA English DT Article DE MELANOMA; DESMOPLASTIC MELANOMA; MALIGNANT MELANOMA ID MALIGNANT-MELANOMA; NEUROTROPIC MELANOMA; SPINDLE CELL; ELECTRON-MICROSCOPY; VARIANT; TUMORS; HEAD; NECK AB We report 6 cases of desmoplastic melanoma. Upon removal and histologic examination, each lesion consisted of a dermal nodule of fascicles of spindle cells, many of which showed pleomorphic and hyperchromatic nuclei. Fascicles, as well as single cells, were seen infiltrating the dermal collagen. Lentiginous hyperplasia of melanocytes with varying but usually slight cellular atypia overlay the dermal proliferations in all cases. Melanophages and some pigmented cells, albeit few in number, were present in the infiltrate, whereas mitotic figures were also noted. These features are most consistent with desmoplastic melanoma, a rare tumor of which a limited number of cases has been described. The clinical and histopathologic features of the lesions presented exemplify the diagnostic and therapeutic dilemma associated with desmoplastic melanoma. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. LEIDEN UNIV,DEPT PATHOL,LEIDEN,NETHERLANDS. NR 24 TC 17 Z9 17 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1992 VL 185 IS 1 BP 3 EP 8 PG 6 WC Dermatology SC Dermatology GA JE284 UT WOS:A1992JE28400002 PM 1638068 ER PT J AU ALBERT, VA BARNHILL, R SOBER, AJ AF ALBERT, VA BARNHILL, R SOBER, AJ TI LEUKODERMA IN ASSOCIATION WITH GIANT CONGENITAL NEVI - REPORT OF 2 CASES SO DERMATOLOGY LA English DT Article DE MELANOMA; LEUKODERMA; VITILIGO; GIANT CONGENITAL NEVUS; CONGENITAL NEVI ID MALIGNANT-MELANOMA; VITILIGO; HYPOPIGMENTATION AB Two patients are presented in whom giant congenital nevi were associate wit hypopigmentation. One patient has had no associated melanoma. The second patient developed hypopigmentation years before a melanoma was excised, and increased hypopigmentation was noted years later without evidence of melanoma recurrence. While the mechanism for the development of the hypopigmentation noted in these two patients is uncertain, an immunologically mediated systemic process may be responsible. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BARTLETT 410,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DERMATOPATHOL UNIT,BOSTON,MA 02114. NR 27 TC 13 Z9 14 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1992 VL 185 IS 2 BP 140 EP & PG 0 WC Dermatology SC Dermatology GA JK178 UT WOS:A1992JK17800015 PM 1421627 ER PT J AU SHAFFER, D WALKER, K WEISS, GR AF SHAFFER, D WALKER, K WEISS, GR TI MALIGNANT-MELANOMA IN A HISPANIC MALE WITH NEVUS OF OTA SO DERMATOLOGY LA English DT Article DE MALIGNANT MELANOMA; OCULODERMAL MELANOCYTOSIS; NEVUS OF OTA; BLADDER ID OCULODERMAL MELANOCYTOSIS; BLUE NEVUS AB Nevus of Ota is uncommon in the non-Oriental population. We report a case of malignant melanoma with metastasis to the genitourinary tract in a Hispanic male with nevus of Ota. Thirty-six prior cases of nevus of Ota with malignant melanoma reported in the English language are reviewed. Sixty-eight percent were women; 76% were Caucasians. Metastatic disease was reported in 16%. Three patients had liver metastases. Our case was the first involving the genito-urinary tract. All but one patient with metastatic disease died within 1 month of presentation. Despite the increased frequency of nevus of Ota in the Japanese, only 4 cases of malignant melanoma have been reported. Nevus of Ota would appear to be a risk factor for developing malignant melanoma in the Caucasian population. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. NR 44 TC 20 Z9 22 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1018-8665 J9 DERMATOLOGY JI Dermatology PY 1992 VL 185 IS 2 BP 146 EP 150 PG 5 WC Dermatology SC Dermatology GA JK178 UT WOS:A1992JK17800017 PM 1421629 ER PT J AU SMITH, TH MILLER, JB AF SMITH, TH MILLER, JB TI DISTINCT MYOGENIC PROGRAMS OF EMBRYONIC AND FETAL MOUSE MUSCLE-CELLS - EXPRESSION OF THE PERINATAL MYOSIN HEAVY-CHAIN ISOFORM INVITRO SO DEVELOPMENTAL BIOLOGY LA English DT Article ID PRENATAL RAT HINDLIMB; SKELETAL-MUSCLE; SLOW MYOSIN; NUCLEAR DOMAINS; CLONAL ANALYSIS; FIBER TYPES; GENE; DIFFERENTIATION; CULTURES; LINEAGES C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP SMITH, TH (reprint author), MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 51 TC 46 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JAN PY 1992 VL 149 IS 1 BP 16 EP 26 DI 10.1016/0012-1606(92)90260-N PG 11 WC Developmental Biology SC Developmental Biology GA GX896 UT WOS:A1992GX89600003 PM 1728586 ER PT J AU WABER, DP BERNSTEIN, JH KAMMERER, BL TARBELL, NJ SALLAN, SE AF WABER, DP BERNSTEIN, JH KAMMERER, BL TARBELL, NJ SALLAN, SE TI NEUROPSYCHOLOGICAL DIAGNOSTIC PROFILES OF CHILDREN WHO RECEIVED CNS TREATMENT FOR ACUTE LYMPHOBLASTIC-LEUKEMIA - THE SYSTEMIC APPROACH TO ASSESSMENT SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID LONG-TERM SURVIVORS; ACUTE LYMPHOCYTIC-LEUKEMIA; CRANIAL IRRADIATION; INTRATHECAL METHOTREXATE; DEVELOPMENTAL-PSYCHOLOGY; CHILDHOOD LEUKEMIA; HUMAN-BRAIN; PROPHYLAXIS; SEX; BEHAVIOR AB A systemic developmental neuropsychological approach (Bernstein & Waber, 1990) was applied in a controlled fashion to evaluate its reliability and validity. Specifically, we examined the impact of central nervous system (CNS) treatment on behavioral development of children treated for acute lymphoblastic leukemia (ALL). A blind structured clinical rating procedure yielded severity ratings and neuropsychological diagnoses for 49 ALL patients and 15 Wilm's tumor (WT) patients. The ALL patients were more severely affected than the WT patients and females more affected than males. Neuropsychological diagnostic profiles were systematically related to age at CNS treatment: Children treated before 36 months of age exhibited inefficiencies of right-hemisphere brain systems; those treated at older ages showed left-hemisphere related inefficiencies. The findings are discussed in relation to processes of human postnatal neurobehavioral development, as well as to the status of the systemic approach. C1 CHILDRENS HOSP MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. RP WABER, DP (reprint author), CHILDRENS HOSP MED CTR,DEPT PSYCHIAT,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 87 TC 19 Z9 19 U1 1 U2 1 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 8756-5641 J9 DEV NEUROPSYCHOL JI Dev. Neuropsychol. PY 1992 VL 8 IS 1 BP 1 EP 28 PG 28 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA HH904 UT WOS:A1992HH90400001 ER PT J AU BONNERWEIR, S AF BONNERWEIR, S TI 2 PATHWAYS OF BETA-CELL GROWTH IN THE REGENERATING RAT PANCREAS - IMPLICATIONS FOR ISLET TRANSPLANTATION SO DIABETES NUTRITION & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON ISLET TRANSPLANTATION CY SEP 26-29, 1991 CL GUBBIO, ITALY ID B-CELLS; GLUCOSE; PANCREATECTOMY; EXPRESSION AB Islet mass increases considerably from the embryo to the adult. There are two major pathways for this increase: new islet formation by budding from ductules and replication of existing islet cells. We have recently reported both of these pathways in regenerating adult rat pancreas after partial pancreatectomy. These two modes of growth in the adult pancreas suggest a schema that beta-cells have a finite lifespan and a population turnover occurs. The implications of such a schema on islet transplantation are discussed. RP BONNERWEIR, S (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02115, USA. NR 19 TC 5 Z9 5 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-3402 J9 DIABETES NUTR METAB JI Diabetes Nutr. Metab. PY 1992 VL 5 IS 3 SU 1 BP 21 EP 24 PG 4 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA JX595 UT WOS:A1992JX59500005 ER PT J AU MONTANA, E WEIR, GC BONNERWEIR, S AF MONTANA, E WEIR, GC BONNERWEIR, S TI CHANGES IN BETA-CELL REPLICATION RATE AND MASS IN TRANSPLANTED ISLETS SO DIABETES NUTRITION & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON ISLET TRANSPLANTATION CY SEP 26-29, 1991 CL GUBBIO, ITALY ID PANCREATECTOMY; TYPE-1; GROWTH AB Beta-cell replication rate and mass were measured in transplanted islet tissue. Streptozocin diabetic mice were either given 300 islets to normalize glucose values or 150 islets, an inadequate number, to allow transplanted beta-cells to be exposed to hyperglycemia. Beta-cell replication was assessed by immunostaining of incorporated 5-bromo-2'deoxyuridine (BrdU) and determination of beta-cell mass by point counting morphometry. The inadequate number of grafted beta-cells exposed to hyperglycemia had an early increase in replication rate, but this could not be sustained and was accompanied by a severe decline in beta-cell mass, thus providing evidence for a deleterious effect of hyperglycemia upon transplanted beta-cells. In addition, 300 islets were transplanted into normal mice. In this circumstance, a marked reduction in mass was also observed, presumably being a downregulation to compensate for the excess in total beta-cell mass imposed by the graft. These data indicate that transplantation of either an insufficient or an excessive number of beta-cells is followed by a reduction of the beta-cell mass of the graft, this reduction resulting from different mechanisms. C1 JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 14 TC 0 Z9 0 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-3402 J9 DIABETES NUTR METAB JI Diabetes Nutr. Metab. PY 1992 VL 5 IS 3 SU 1 BP 25 EP 27 PG 3 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA JX595 UT WOS:A1992JX59500006 ER PT J AU PIETROPAOLO, M EISENBARTH, GS AF PIETROPAOLO, M EISENBARTH, GS TI PREDICTION OF TYPE-I DIABETES-MELLITUS SO DIABETES NUTRITION & METABOLISM LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON ISLET TRANSPLANTATION CY SEP 26-29, 1991 CL GUBBIO, ITALY ID GENETIC SUSCEPTIBILITY; INSULIN AUTOANTIBODIES; IDENTIFICATION; RELATIVES; HETEROZYGOTES; AUTOIMMUNITY; ASSOCIATION; PROGRESSION; HYPOTHESIS; RESISTANCE AB Concepts concerning the natural history of Type I diabetes mellitus (IDDM) have radically changed over the last few years. What was considered an acute disease is instead the outcome of a progressive autoimmune process occurring in genetically susceptible individuals. In Islet Cell Antibody body (ICA) positive individuals developing IDDM we do not believe there is a "long latency period" without beta-cell destruction, but rather a long period preceding diabetes of asymptomatic beta-cell destruction. Autoantibodies targeted against all islet cells are currently found years prior to the overt disease and have become useful markers for predicting IDDM. In particular a number of cellular proteins of the neuroendocrine system such as glutamic acid decarboxylase (GAD) and other proteins, such as insulin, are considered autoantigens related to IDDM. The humoral immunity associated with IDDM is heterogeneous and in part immunogenetically determined. For first degree relatives of patients with IDDM it is now possible to predict the development of diabetes and even to estimate the approximate time of onset of the disease. In the near future it will be extremely important to determine which antigens(s) are related to pathogenesis, which will provide reliable markers for prediction, and which antigen specific therapies can be candidates for safe prevention of IDDM. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 33 TC 1 Z9 1 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0394-3402 J9 DIABETES NUTR METAB JI Diabetes Nutr. Metab. PY 1992 VL 5 IS 3 SU 1 BP 105 EP 110 PG 6 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA JX595 UT WOS:A1992JX59500022 ER PT J AU THOR, AD AF THOR, AD TI PROGNOSTIC FACTORS IN BREAST-CANCER - INTEGRATING THE CYTOLOGY LABORATORY SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Editorial Material RP THOR, AD (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PY 1992 VL 8 IS 4 BP 319 EP 321 DI 10.1002/dc.2840080402 PG 3 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA JH252 UT WOS:A1992JH25200001 PM 1638930 ER PT J AU FILOMENA, CA JORDAN, AG EHYA, H AF FILOMENA, CA JORDAN, AG EHYA, H TI NEEDLE ASPIRATION CYTOLOGY OF THE IRRADIATED BREAST SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Article DE BREAST; FINE-NEEDLE ASPIRATION BIOPSY; RADIATION; CYTOLOGY; BREAST CARCINOMA AB During a 3-year period (1987-1989), 60 fine-needle aspiration biopsies (FNAs) were obtained from new breast lesions in patients previously treated by radiation and surgery for breast carcinoma. The lesions occurred at or near the site of previous excision, 3-117 months after initiation of radiotherapy. FNAs were classified as follows: acellular (11); negative (29); atypical (13); suspicious (4); and positive (3). For statistical analysis, acellular, negative, and atypical diagnoses were considered negative findings, and suspicious and positive diagnoses were considered positive findings. On the basis of subsequent biopsy and/or patient follow-up, FNA yielded a sensitivity of 86%, a specificity of 98%, a positive predictive value of 86%, a negative predictive value of 98%, and an efficiency of 97%. Excluding cystic lesions, the most reliable criterion for distinguishing malignant from benign lesions was the abundance of epithelial cells, both singly and in large clusters. Cellular characteristics were less helpful, since nuclear atypia was seen in both benign and malignant lesions. It is concluded that (1) FNA is a reliable technique in the evaluation of the irradiated breast; (2) when performed by an experienced operator, an acellular aspirate may be interpreted as evidence against recurrent carcinoma; and (3) epithelial atypia must be interpreted with caution to avoid a false-positive diagnosis. RP FILOMENA, CA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 0 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 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PY 1992 VL 8 IS 4 BP 327 EP 332 DI 10.1002/dc.2840080404 PG 6 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA JH252 UT WOS:A1992JH25200003 PM 1638932 ER PT J AU PITMAN, MB THOR, AD GOODMAN, ML ROSENBERG, AE AF PITMAN, MB THOR, AD GOODMAN, ML ROSENBERG, AE TI BENIGN METASTASIZING PLEOMORPHIC ADENOMA OF SALIVARY-GLAND - DIAGNOSIS OF BONE-LESIONS BY FINE-NEEDLE ASPIRATION BIOPSY SO DIAGNOSTIC CYTOPATHOLOGY LA English DT Note DE PLEOMORPHIC ADENOMA; BONE METASTASES; FINE-NEEDLE ASPIRATION AB Two cases of benign salivary gland pleomorphic adenomas metastatic to bone (benign-metastasizing pleomorphic adenomas) diagnosed by fine-needle aspiration biopsy are presented. Both primary tumors were slightly atypical cytologically but neither case demonstrated features of carcinoma. The metastatic lesions contained benign epithelial myoepithelial, and stromal components. In both cases the clinical history was either not known by the radiologist or not communicated to the cytopathologist interpreting the case, and a primary tumor of bone was the leading clinical diagnosis. Obtaining pertinent clinical history and comparing the cytomorphology of the bone aspirate with the primary parotid tumor allowed for an accurate diagnosis in both cases. The differential diagnosis with primary bone tumors is discussed and the importance of clinical history is emphasized. RP PITMAN, MB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114, USA. NR 0 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 8755-1039 J9 DIAGN CYTOPATHOL JI Diagn. Cytopathol. PY 1992 VL 8 IS 4 BP 384 EP 387 DI 10.1002/dc.2840080417 PG 4 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA JH252 UT WOS:A1992JH25200016 PM 1322265 ER PT J AU FOSTER, CS NEUMANN, R TAUBER, J AF FOSTER, CS NEUMANN, R TAUBER, J TI LONG-TERM RESULTS OF SYSTEMIC CHEMOTHERAPY FOR OCULAR CICATRICIAL PEMPHIGOID SO DOCUMENTA OPHTHALMOLOGICA LA English DT Article DE AZATHIOPRINE; CYCLOPHOSPHAMIDE; CYCLOSPORINE; DAPSONE; IMMUNOSUPPRESSIVE THERAPY; OCULAR CICATRICIAL PEMPHIGOID; PROGNOSIS ID IMMUNOSUPPRESSIVE THERAPY AB Ocular cicatricial pemphigoid (OCP) is a chronic, progressive, blinding, autoimmune disease that scars mucous membranes. We studied the long-term outcome in 104 consecutive patients (average follow-up: 4 years) to determine whether complete remission could be achieved following a course of treatment with immunosuppressive drugs. We found that prolonged periods of remission off therapy are maintained in about one third of OCP patients. Follow-up must be continued for life as relapse occurs in approximately one third of cases. Those who relapsed regained disease control readily upon reinstitution of therapy and did not deteriorate to more advanced cicatrization. Sex, age, initial degree of inflammation and the incidence of extraocular involvement did not bear a prognostic significance. The mechanism which underlies the differing responses to therapy is not yet known. C1 MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. RP FOSTER, CS (reprint author), MASSACHUSETTS EYE & EAR INFIRM,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 9 TC 35 Z9 37 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0012-4486 J9 DOC OPHTHALMOL JI Doc. Ophthalmol. PY 1992 VL 82 IS 3 BP 223 EP 229 DI 10.1007/BF00160769 PG 7 WC Ophthalmology SC Ophthalmology GA KZ197 UT WOS:A1992KZ19700006 PM 1303858 ER PT J AU FOSTER, CS BARNEY, NP AF FOSTER, CS BARNEY, NP TI SYSTEMIC ACYCLOVIR AND PENETRATING KERATOPLASTY FOR HERPES-SIMPLEX KERATITIS SO DOCUMENTA OPHTHALMOLOGICA LA English DT Article DE ACYCLOVIR; CORNEAL TRANSPLANTATION; HERPES KERATITIS; REJECTION ID ORAL ACYCLOVIR; MANAGEMENT; PROGNOSIS; VIRUS AB Corneal graft survival in 13 patients (14 eyes) receiving oral acyclovir following corneal transplantation for herpes simplex keratitis was compared to that in nine patients (9 eyes) who underwent penetrating keratoplasty for herpes simplex keratitis without receiving postoperative acyclovir. Mean age, duration of disease, and time of follow-up did not differ in the two groups. There were no recurrences of herpes simplex keratitis in any patient receiving acyclovir during a mean follow-up of 16.5 months compared to a 44% (4/9) recurrence rate in patients without acyclovir during a mean follow-up of 20.6 months (p < 0.01). Graft failure occurred in 14% (2/14) of acyclovir treatment eyes and in 56% (5/9) of the grafts in patients not receiving acyclovir. Long term prophylactic oral acyclovir significantly decreased the recurrence of herpes simplex keratitis and reduced corneal graft failure in patients with a history of recurrent herpes simplex keratitis who underwent corneal transplantation. RP FOSTER, CS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 16 TC 23 Z9 23 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0012-4486 J9 DOC OPHTHALMOL JI Doc. Ophthalmol. PY 1992 VL 80 IS 4 BP 363 EP 369 DI 10.1007/BF00154385 PG 7 WC Ophthalmology SC Ophthalmology GA JZ159 UT WOS:A1992JZ15900010 PM 1473452 ER PT J AU LEE, JM WEINSTEIN, DA KOWALL, NW BEAL, MF AF LEE, JM WEINSTEIN, DA KOWALL, NW BEAL, MF TI INABILITY OF BETA-AMYLOID (25-35) TO BIND TO CENTRAL-NERVOUS-SYSTEM NEUROKININ-1 RECEPTORS SO DRUG DEVELOPMENT RESEARCH LA English DT Article DE SUBSTANCE-P; ALZHEIMERS DISEASE; NEUROTOXICITY ID SUBSTANCE-P; PROTEIN AB Beta-amyloid (1-40) has recently been shown to exhibit both neurotoxic and neurotrophic properties. The putatively active moiety is beta-(25-35), which has a structural homology to the human tachykinin substance P. Substance P, which preferentially binds to neurokinin 1 (NK1) receptors in the central nervous system (CNS), has been shown to block the neurotoxic effects of beta-amyloid (1-40). These data suggest that effects of beta-amyloid may be mediated by an NK1 receptor-mediated process. However, in the present study, we demonstrate that beta-(25-35) is unable to competitively inhibit the binding of 0.15 nM I-125-substance P from rat CNS NK1 receptors. Therefore, the mechanisms of action of beta-amyloid neurotoxic effects are probably not to be mediated through a NK1 receptor-mediated process. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 6 TC 7 Z9 7 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 0272-4391 J9 DRUG DEVELOP RES JI Drug Dev. Res. PY 1992 VL 27 IS 4 BP 441 EP 444 DI 10.1002/ddr.430270412 PG 4 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA KE859 UT WOS:A1992KE85900011 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI INSULINOTROPIC HORMONE GLUCAGON-LIKE PEPTIDE-I(7-37) STIMULATION OF PROINSULIN GENE-EXPRESSION AND PROINSULIN BIOSYNTHESIS IN INSULINOMA BETA-TC-1 CELLS SO ENDOCRINOLOGY LA English DT Article ID PERFUSED RAT PANCREAS; PEPTIDE-I; BINDING-PROTEINS; ISOLATED ISLETS; RINM5F CELLS; GLUCOSE; LINE; SECRETION; ENDOCRINE; RELEASE AB Glucagon-like peptide-I(7-37) [GLP-I(7-37)] is an intestinal peptide hormone that is released in response to oral nutrients and that potently augments glucose-mediated insulin secretion. GLP-I(7-37) has potent insulin-releasing activities in vivo in response to oral nutrients, in situ in the isolated perfused pancreas, and in vitro in cultured pancreatic B-cells. As such GLP-I(7-37) is a potent hormonal mediator in the enteroinsular axis involved in the regulation of glucose homeostasis. We now show that in addition to stimulating the release of insulin, GLP-I(7-37) stimulates proinsulin gene expression at the levels of gene transcription and cellular levels of proinsulin messenger RNA as well as the translational biosynthesis of proinsulin. These findings of the positive anabolic actions of GLP-I(7-37) on the synthesis of insulin in B-cells support the notion that GLP-I(7-37) may be of therapeutic use in stimulating the production of insulin in patients with noninsulin-dependent diabetes mellitus and that overproduction of insulin with subsequent hypoglycemia will not occur in response to the administration of GLP-I(7-37). Furthermore, these positive actions of GLP-I(7-37) on insulin production obviate the possibility of B-cell exhaustion in response to such a potent secretagogue. RP FEHMANN, HC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK30834] NR 52 TC 260 Z9 272 U1 1 U2 10 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1992 VL 130 IS 1 BP 159 EP 166 DI 10.1210/en.130.1.159 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HH370 UT WOS:A1992HH37000024 PM 1309325 ER PT J AU WEISS, J CROWLEY, WF JAMESON, JL AF WEISS, J CROWLEY, WF JAMESON, JL TI PULSATILE GONADOTROPIN-RELEASING-HORMONE MODIFIES POLYADENYLATION OF GONADOTROPIN SUBUNIT MESSENGER RIBONUCLEIC-ACIDS SO ENDOCRINOLOGY LA English DT Article ID GENE-EXPRESSION INVIVO; LUTEINIZING-HORMONE; FEMALE RATS; RNA; STIMULATION; INVITRO; FREQUENCY; INCREASES; PROTEIN AB Gonadotropin subunit mRNA levels rise after castration, coincident with a period of increased GnRH input to the pituitary. In addition to increased levels of gonadotropin mRNAs, we observed that the sizes of the alpha and LH-beta mRNAs were increased after ovariectomy (OVX) of rats. To determine whether these changes occurred in the 5' (alternate transcriptional start site or splicing)- or 3' (altered polyadenylation)-end of the molecules, mRNAs were cleaved using oligonucleotide-directed RNase-H digestion, and the fragments were analyzed by Northern blot, using probes specific to the 5'- and 3'-segments of each transcript. After OVX, there was no change in the sizes of the 5'-segments of LH-beta, FSH-beta, and alpha-subunit mRNAs. However, the LH-beta and alpha-subunit 3'-fragments were increased in size, indicating a shift to more adenylated forms of the LH-beta and alpha transcripts. For FSH-beta, the 3'-fragment bands were more diffuse than for LH-beta or alpha-subunit, and no alteration in the lengths of FSH-beta poly(A) tails were detected. A perifused pituitary cell system was used to determine whether pulses of GnRH were sufficient to cause modifications of polyadenylation. GnRH was administered as hourly 10-nM pulses for 4-12 h. Time-dependent increases in the sizes of LH-beta and alpha-subunit mRNAs were observed in GnRH-treated cells compared to cells receiving no GnRH. Changes in the lengths of LH-beta and alpha-subunit mRNAs were shown to be due to increased polyadenylation, and there was no observable change in polyadenylation of FSH-beta mRNA. In addition, no changes were observed in the size of the 3'-fragments of PRL or beta-actin mRNAs. These data demonstrate that pulsatile GnRH administered in vitro elicits specific increases in the lengths of the LH-beta and alpha-subunit mRNA poly(A) tails. Similar changes occur after OVX. Thus, in addition to transcriptional stimulation of the gonadotropin gene, GnRH modifies gonadotropin mRNAs at a posttranscriptional level. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,THYROID UNIT,BOSTON,MA 02114. RP WEISS, J (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,REPROD ENDOCRINE UNIT,BHX-5,BOSTON,MA 02114, USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-23262, HD-15788, R01 HD015788, U54 HD029164] NR 18 TC 41 Z9 41 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JAN PY 1992 VL 130 IS 1 BP 415 EP 420 DI 10.1210/en.130.1.415 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HH370 UT WOS:A1992HH37000056 PM 1345779 ER PT J AU McIntire, WS AF McIntire, William S. TI Wither PQQ SO ESSAYS IN BIOCHEMISTRY, VOL 27 SE ESSAYS IN BIOCHEMISTRY LA English DT Review ID QUINONE BIOSYNTHESIS GENES; PYRROLOQUINOLINE QUINONE; METHYLAMINE DEHYDROGENASE; AMINE OXIDASES; ACTIVE-SITE; COFACTOR; ENZYMES; OXIDOREDUCTASES; 6-HYDROXYDOPA; QUINOPROTEINS C1 [McIntire, William S.] US Dept Vet Affairs, Div Mol Biol, Med Ctr, San Francisco, CA 94121 USA. [McIntire, William S.] Univ Calif San Francisco, Dept Biochem, San Francisco, CA 94143 USA. [McIntire, William S.] Univ Calif San Francisco, Dept Anesthesia, San Francisco, CA 94143 USA. RP McIntire, WS (reprint author), US Dept Vet Affairs, Div Mol Biol, Med Ctr, San Francisco, CA 94121 USA. NR 33 TC 15 Z9 15 U1 0 U2 1 PU PORTLAND PRESS LTD PI LONDON PA 59 PORTLAND PL, LONDON W1N 3AJ, ENGLAND SN 0071-1365 J9 ESSAYS BIOCHEM PY 1992 VL 27 BP 119 EP 134 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA BHO25 UT WOS:000254740200009 PM 1330543 ER PT J AU ROSENBLATT, KA THOMAS, DB NOONAN, EA BERRY, G MACLENNAN, R SHEARMAN, R JELIHOVSKY, T BOOTH, JC MOLINA, R MARTINEZ, L SALAS, O DABANCENS, A CHEN, ZH TAO, Y HU, YW MODAN, B RON, E ALFANDARY, E CUEVAS, HR SALAZAR, SB PALET, A ONTIVER, P APELO, RA DELACRUZ, JR BAENS, J JAVIER, B SILPISORNKOSOL, S PARDTHAISONG, T MARTIN, N THEETRANONT, C BOOSIRI, B CHUTIVONGSE, S VIAUTAMASEN, P WONGSRICHANALAI, C JIMAKORN, P KOETSAWANG, S RACHAWAT, D CHANTARAKUL, N SCULLY, RE YOUNG, RH THOMAS, DB ROSENBLATT, KA NOONAN, EA HOLCK, S FARLEY, T MEIRIK, O AF ROSENBLATT, KA THOMAS, DB NOONAN, EA BERRY, G MACLENNAN, R SHEARMAN, R JELIHOVSKY, T BOOTH, JC MOLINA, R MARTINEZ, L SALAS, O DABANCENS, A CHEN, ZH TAO, Y HU, YW MODAN, B RON, E ALFANDARY, E CUEVAS, HR SALAZAR, SB PALET, A ONTIVER, P APELO, RA DELACRUZ, JR BAENS, J JAVIER, B SILPISORNKOSOL, S PARDTHAISONG, T MARTIN, N THEETRANONT, C BOOSIRI, B CHUTIVONGSE, S VIAUTAMASEN, P WONGSRICHANALAI, C JIMAKORN, P KOETSAWANG, S RACHAWAT, D CHANTARAKUL, N SCULLY, RE YOUNG, RH THOMAS, DB ROSENBLATT, KA NOONAN, EA HOLCK, S FARLEY, T MEIRIK, O TI HIGH-DOSE AND LOW-DOSE COMBINED ORAL-CONTRACEPTIVES - PROTECTION AGAINST EPITHELIAL OVARIAN-CANCER AND THE LENGTH OF THE PROTECTIVE EFFECT SO EUROPEAN JOURNAL OF CANCER LA English DT Article ID PITUITARY; STIMULATION; ESTROGEN; POTENCY; RISK AB The relations between use of high-dose and low-dose combined oral contraceptives and epithelial ovarian cancer were compared in an international hospital-based case-control study. 393 cases from seven countries were compared with 2561 matched controls. The odds ratio (OR) was somewhat lower for women who used high-dose oestrogen oral contraceptives (OR = 0.68) than for women who used low-dose preparations (OR = 0.81) although the difference could have occurred by chance. After controlling for time since last use, risk was slightly lower for long-term users of high-dose preparations than for long-term users of low-dose pills. Both high-dose and low-dose oral contraceptives protect against ovarian cancer, but the degree of protection may be slightly weaker for the newer, low-dose products. C1 FRED HUTCHINSON CANC RES CTR, 1123 COLUMBIA ST, SEATTLE, WA 98104 USA. WHO, SPECIAL PROGRAMME RES DEV & RES TRAINING HUMAN REP, CH-1211 GENEVA 27, SWITZERLAND. UNIV SYDNEY, DEPT PUBL HLTH, SYDNEY, NSW 2006, AUSTRALIA. UNIV CHILE, HOSP JOSE JOAQUIN AGUIRRE, FAC MED, DEPT OBSTET & GYNECOL, SANTIAGO, CHILE. MINIST SALUD, HOSP SALVADOR, DEPT OBSTET & GYNECOL, SANTIAGO, CHILE. SHANGHAI INST PLANNED PARENTHOOD RES, SHANGHAI, PEOPLES R CHINA. CHAIM SHEBA MED CTR, DEPT CLIN EPIDEMIOL, IL-52621 TEL HASHOMER, ISRAEL. HOSP GEN MEXICO CITY, MEXICO CITY, MEXICO. UNIV PHILIPPINES, COLL MED, MANILA, PHILIPPINES. CHIANG MAI UNIV, FAC MED, CHIANG MAI, THAILAND. CHULALONGKORN UNIV, FAC MED, DEPT OBSTET & GYNECOL, WHO COLLABORATING CTR RES HUMAN REPROD, BANGKOK 5, THAILAND. MAHIDOL UNIV, SIRIRAJ HOSP,FAC MED,DEPT OBSTET & GYNAECOL, FAMILY PLANNING RES UNIT, BANGKOK 10700, THAILAND. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. FRED HUTCHINSON CANC RES CTR, DIV PUBL HLTH SCI, SEATTLE, WA 98104 USA. FU NCIPC CDC HHS [NICHD-CE-84-16] NR 25 TC 32 Z9 33 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PY 1992 VL 28A IS 11 BP 1872 EP 1876 DI 10.1016/0959-8049(92)90026-X PG 5 WC Oncology SC Oncology GA JK747 UT WOS:A1992JK74700026 PM 1389530 ER PT J AU AKINS, CW AF AKINS, CW TI REVIEW OF THE GLOBAL EXPERIENCE WITH THE MEDTRONIC-HALL VALVE SO EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY LA English DT Article; Proceedings Paper CT SYMP ON MEDTRONIC CARDIOVASCULAR TECHNOLOGY CY OCT 24-27, 1991 CL TURNBERRY, SCOTLAND DE HEART VALVE PROSTHESIS; MEDTRONIC-HALL VALVE; VALVE-RELATED COMPLICATIONS AND CONSEQUENCES AB The Medtronic-Hall cardiac valvular prosthesis has been available for insertion since 1977. This report reviews the English language literature concerning that valve published during the last 14 years. The review is focused on three modes of assessment. First, experience with valve implantation techniques and their results has demonstrated that with careful attention to education of the implanting cardiac surgeon and increasing experience in the clinical use of the prosthesis, the incidence of occluder impingements has steadily fallen to 0.2% of total valve implantations in the United States in 1989. Secondly, hemodynamic assessment of the prosthesis with both invasive catheterization and Doppler echocardiography has demonstrated rest and exercise transvalve gradients and functional valve areas that are as good or better than those in other mechanical cardiac valvular prostheses. Finally, review of the long-term follow-up reports of the Medtronic-Hall prosthesis has demonstrated an acceptably low incidence of late vatve-related complications and their consequences. RP AKINS, CW (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC SURG UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1010-7940 J9 EUR J CARDIO-THORAC JI Eur. J. Cardio-Thorac. Surg. PY 1992 VL 6 SU 1 BP S68 EP S74 DI 10.1016/1010-7940(92)90026-T PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA JN115 UT WOS:A1992JN11500012 PM 1389283 ER PT J AU BAUME, DM ROBERTSON, MJ LEVINE, H MANLEY, TJ SCHOW, PW RITZ, J AF BAUME, DM ROBERTSON, MJ LEVINE, H MANLEY, TJ SCHOW, PW RITZ, J TI DIFFERENTIAL RESPONSES TO INTERLEUKIN-2 DEFINE FUNCTIONALLY DISTINCT SUBSETS OF HUMAN NATURAL-KILLER-CELLS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN PERIPHERAL-BLOOD; FC-GAMMA RECEPTOR; MONOCLONAL-ANTIBODIES; LYMPHOKINE GENES; NK CELLS; EXPRESSION; LYMPHOCYTES; ACTIVATION; CD16; ANTIGEN AB Human natural killer (NK) cells can be subdivided into two populations based on the density of cell surface CD56 antigen. The great majority (approximately 90%) of NK cells express CD56 at low levels (the CD56dim phenotype), whereas a small NK cell subset (approximately 10%) exhibits approximately fivefold greater density of surface CD56. Exposure to exogenous interleukin 2 (IL 2) induces tenfold greater proliferation of CD56bright cells compared to CD56dim lymphocytes, even though both subsets constitutively express similar levels of intermediate affinity IL 2 receptor (IL 2R) p75 chains. Incubation with IL 2 alone or irradiated target cells alone could induce expression of the IL 2R p55 chain by both CD56bright and CD56dim NK cells; a combination of both stimuli was most effective. IL 2R p55 induction was evident after co-culture of NK cells with both NK-sensitive and NK-resistant cell lines or with antibody-coated target cells. Activation of NK cells with IL 2 plus target cells resulted in enhanced proliferation compared to activation with IL 2 alone; target cells alone did not induce significant proliferation. Although both NK cell subsets appeared to express high-affinity IL 2R p75/p55 heterodimers after stimulation with target cells and IL 2, proliferation of CD56dim cells remained minimal after such activation; activated CD56dim cells consistently demonstrated less proliferation to IL 2 than did resting CD56bright cells. In contrast, CD56bright NK cells exhibited even greater proliferation after stimulation with target cells. Almost all CD56dim NK cells expressed CD16 (Fc-gamma-R III) as well as the NK zeta chain, whereas < 50% of CD56bright cells express either CD16 or zeta. CD56bright and CD56dim lymphocytes, thus, appear to represent distinct subpopulations of NK cells with different functional activities. Unlike CD56bright cells, CD56dim NK cells do not proliferate optimally to IL 2, even after the latter have been stimulated to express both IL-2R p55 and IL 2R p75. Efficient proliferation of CD56dim NK cells may, thus, require additional or alternative signals. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619] NR 30 TC 89 Z9 94 U1 0 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1992 VL 22 IS 1 BP 1 EP 6 DI 10.1002/eji.1830220102 PG 6 WC Immunology SC Immunology GA HB026 UT WOS:A1992HB02600001 PM 1370410 ER PT J AU BAMEZAI, A GOLDMACHER, VS ROCK, KL AF BAMEZAI, A GOLDMACHER, VS ROCK, KL TI INTERNALIZATION OF GLYCOSYL-PHOSPHATIDYLINOSITOL (GPI)-ANCHORED LYMPHOCYTE PROTEINS .2. GPI-ANCHORED AND TRANSMEMBRANE MOLECULES INTERNALIZE THROUGH DISTINCT PATHWAYS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; CYTOPLASMIC DOMAIN; COATED PITS; CELL-SURFACE; MONOCLONAL-ANTIBODY; HUMAN FIBROBLASTS; PLASMA-MEMBRANE; RECEPTOR; ENDOCYTOSIS; ACTIVATION AB Ly-6A.2 (T-cell-activating protein, TAP) and Thy-1 are glycosyl-phosphatidylinositol (GPI)-anchored proteins expressed on the surface of murine T lymphocytes. We have found that Ly-6A.2 (TAP) and Thy-1 are internalized by T cells. In the present study we have investigated whether these GPI-anchored proteins enter cells by endocytosis through coated pits. Two lines of evidence argue against the involvement of coated pits in the internalization of Ly-6A.2 (TAP) and Thy-1. First, drugs that effectively blocked the endocytosis of transferrin receptor and H-2 class I molecules, (which are known to be internalized via coated pits) did not inhibit the internalization of the GPI-anchored proteins. Second, in ultrastructural analyses, Ly-6A2 (TAP) and Thy-1, in contrast to the transferrin receptor, were rarely found in coated pits or vesicles. These observations suggest that the GPI-anchored proteins on T lymphocytes are internalized by a distinct pathway that does not involve endocytosis through coated pits. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. IMMUNOGEN INC,CAMBRIDGE,MA. RP BAMEZAI, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 40 TC 57 Z9 57 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1992 VL 22 IS 1 BP 15 EP 21 DI 10.1002/eji.1830220104 PG 7 WC Immunology SC Immunology GA HB026 UT WOS:A1992HB02600003 PM 1346109 ER PT J AU KANSAS, GS CAMBIER, JC TEDDER, TF AF KANSAS, GS CAMBIER, JC TEDDER, TF TI CD4 BINDING TO MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II ANTIGENS INDUCES LFA-1-DEPENDENT AND LFA-1-INDEPENDENT HOMOTYPIC ADHESION OF LYMPHOCYTES-B SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID MHC CLASS-II; T-CELLS; MONOCLONAL-ANTIBODIES; MOLECULE ICAM-1; HIV GP120; ACTIVATION; EXPRESSION; LFA-1; DIFFERENTIATION; RECEPTORS AB T helper cells recognize processed antigen (Ag) in the context of major histocompatibility complex (MHC) class II antigens present on the surface of B cells and other Ag-presenting cells. This interaction is mediated through the T cell receptor complex with associate recognition of class II molecules by the CD4 molecule. In this study, the binding of a soluble recombinant CD4/Ig heavy chain fusion protein (CD4-gamma(3)) or monoclonal antibody (mAb) to class II antigens on human B cells was shown to induce rapid and specific homotypic adhesion of B cells and most B lymphoblastoid cell lines. mAb reactive with CD4 inhibited CD4-gamma(3)-induced adhesion and a mutant B lymphoblastoid cell line deficient in class II antigens failed to respond. Induction of homotypic adhesion was dependent on energy metabolism and a functional cytoskeleton, and class II+ pre-B cells did not exhibit adhesion in response to these stimuli, suggesting that cross-linking of class II molecules generated a transmembrane signal and did not simply aggregate cells. In addition, MHC class II-induced adhesion was Fc receptor independent, as 15 mAb of different Ig isotypes reactive with HLA-D or HLA-DQ gene products induced adhesion. Anti-class II mAb and CD4-gamma(3) were able to induce adhesion at concentrations as low as 10 ng/ml and 100 ng/ml, respectively. Suboptimal stimulation of B cell lines through HLA-D antigens induced homotypic adhesion that was dependent on the activation of LFA-1 (CD11a/CD18), and which could be blocked by specific mAb. However, at greater signal strengths, adhesion was not blocked by mAb against the known adhesion receptors, suggesting the induction of a novel adhesion pathway. Consistent with this, homotypic adhesion induced by engagement of MHC class II antigens was observed with LFA-1-deficient B cell lines, and was independent of CD49d or CD18 expression. Thus, the direct engagement of B cell class II antigens by CD4 is likely to generate transmembrane signals which trigger both LFA-1-dependent and LFA-1-independent adhesion pathways. C1 NATL JEWISH CTR IMMUNOL & RESP MED,DIV BASIC SCI,DENVER,CO. NATL JEWISH CTR IMMUNOL & RESP MED,DEPT PEDIAT,DENVER,CO. RP KANSAS, GS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 34183]; NIAID NIH HHS [AI 26872] NR 46 TC 46 Z9 46 U1 0 U2 2 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD JAN PY 1992 VL 22 IS 1 BP 147 EP 152 DI 10.1002/eji.1830220122 PG 6 WC Immunology SC Immunology GA HB026 UT WOS:A1992HB02600021 PM 1730248 ER PT J AU NITSCH, RM SLACK, BE WURTMAN, RJ GROWDON, JH AF NITSCH, RM SLACK, BE WURTMAN, RJ GROWDON, JH TI SECRETION OF ALZHEIMER AMYLOID PRECURSOR IS STIMULATED BY ACTIVATION OF MUSCARINIC M1 AND M3 RECEPTORS IN TRANSFECTED HUMAN CELL-LINES SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1992 SU 5 BP 19 EP 19 PG 1 WC Neurosciences SC Neurosciences & Neurology GA KC682 UT WOS:A1992KC68200058 ER PT J AU BEAL, MF AF BEAL, MF TI MPP+ PRODUCES EXCITOTOXIC LESIONS IN RAT STRIATUM DUE TO IMPAIRMENT OF OXIDATIVE-METABOLISM SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PY 1992 SU 5 BP 238 EP 238 PG 1 WC Neurosciences SC Neurosciences & Neurology GA KC682 UT WOS:A1992KC68200894 ER PT J AU ALPER, CA AWDEH, Z YUNIS, EJ AF ALPER, CA AWDEH, Z YUNIS, EJ TI CONSERVED, EXTENDED MHC HAPLOTYPES SO EXPERIMENTAL AND CLINICAL IMMUNOGENETICS LA English DT Review DE MAJOR HISTOCOMPATIBILITY COMPLEX; HLA; EXTENDED HAPLOTYPES; AUTOIMMUNE DISEASES; IMMUNE RESPONSE ID HISTOCOMPATIBILITY COMPLEX HAPLOTYPES; DEPENDENT DIABETES-MELLITUS; HEPATITIS-B VACCINE; BONE-MARROW TRANSPLANTATION; DISEASE ASSOCIATIONS; PEMPHIGUS-VULGARIS; JEWISH PATIENTS; POLYMORPHISMS; COMPLOTYPES; INDIVIDUALS AB Extended major histocompatibility complex (MHC) haplotypes are fixed conserved regions of the short arm of the sixth human chromosome defined by their HLA-B, complotype (BF, C2, C4A, C4B), HLA-DR alleles. The regions of conservation may extend further. At least a third of normal MHC haplotypes in Caucasians are extended, and they are largely responsible for previously observed linkage disequilibrium in the region. They are relatively population-specific. Their presence has major implications for tissue transplantation, and particularly for the identification of unrelated donor-recipient pairs, since matching for extended haplotypes probably optimizes engraftment in individuals who have them. Even for those who do not, extended haplotypes provide the means for identifying likely MLR-I-negative donor-recipients, and for identifying the genes involved in this function. Extended haplotypes provide most of the markers for HLA-associated autoimmune diseases; like the MHCs of inbred and inbred recombinant strains of mice, they have aided in the analysis of the contribution of specific genes in this region to disease susceptibility and immune functions, particularly the antibody response. Finally, extended haplotypes must be taken into account when considering population genetic questions and when using HLA markers to identify individuals in forensic applications. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ALPER, CA (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT PEDIAT,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 29583]; NIAID NIH HHS [AI 14157]; NIDDK NIH HHS [DK 26844] NR 44 TC 48 Z9 50 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-9670 J9 EXP CLIN IMMUNOGENET JI Exp. Clin. Immunogenet. PY 1992 VL 9 IS 2 BP 58 EP 71 PG 14 WC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology SC Biochemistry & Molecular Biology; Genetics & Heredity; Immunology GA KB310 UT WOS:A1992KB31000001 PM 1489551 ER PT J AU CHENG, HM KUAN, WP GARRIDO, L XIONG, J CHANG, C AF CHENG, HM KUAN, WP GARRIDO, L XIONG, J CHANG, C TI HIGH-RESOLUTION MR IMAGING OF WATER DIFFUSION IN THE RABBIT LENS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE LENS; GALACTOSEMIC CATARACT; MAGNETIC RESONANCE IMAGING; DIFFUSION IMAGING; PROTON DENSITY; (H2O)-O-17 ID NUCLEAR MAGNETIC-RESONANCE; SENILE CATARACTOUS LENSES; TISSUES; STATE; NMR C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR IMAGING,BOSTON,MA 02114. RP CHENG, HM (reprint author), HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. RI Chang, Chen/B-5079-2009; Garrido, Leoncio/K-3092-2014 OI Garrido, Leoncio/0000-0002-7587-1260 FU NCRR NIH HHS [RR03264]; NEI NIH HHS [EY07620] NR 17 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JAN PY 1992 VL 54 IS 1 BP 127 EP 132 DI 10.1016/0014-4835(92)90076-5 PG 6 WC Ophthalmology SC Ophthalmology GA HD241 UT WOS:A1992HD24100015 PM 1541330 ER PT J AU TOKSOZ, D WILLIAMS, D SMITH, KA ZSEBO, K BIRKETT, N AF TOKSOZ, D WILLIAMS, D SMITH, KA ZSEBO, K BIRKETT, N TI EXPRESSION OF 2 DISTINCT CDNAS OF THE STEEL GENE (SCF) IN DEFICIENT MURINE STROMAL CELL-LINES SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. AMGEN CORP,THOUSAND OAKS,CA. NR 0 TC 1 Z9 1 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 JAN PY 1992 VL 20 IS 1 BP 138 EP 139 PG 2 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA GX273 UT WOS:A1992GX27300097 ER PT J AU ISACSON, O PESCHANSKI, M AF ISACSON, O PESCHANSKI, M TI IS THERE CAPACITY FOR ANATOMICAL AND FUNCTIONAL REPAIR IN THE ADULT SOMATOSENSORY THALAMUS SO EXPERIMENTAL NEUROLOGY LA English DT Article ID RAT THALAMUS; NEURONS; NEOCORTEX; AFFERENTS; STRIATUM C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, DEPT NEUROL, PROGRAM NEUROSCI, BOSTON, MA 02114 USA. INSERM, U161, UNITE RECH NEUROPHYSIOL PHARMACOL, F-75014 PARIS, FRANCE. RP HARVARD UNIV, MCLEAN HOSP, SCH MED, NEUROREGENERAT LAB, MRC 119, BELMONT, MA 02178 USA. NR 12 TC 6 Z9 6 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0014-4886 EI 1090-2430 J9 EXP NEUROL JI Exp. Neurol. PD JAN PY 1992 VL 115 IS 1 BP 173 EP 176 DI 10.1016/0014-4886(92)90244-K PG 4 WC Neurosciences SC Neurosciences & Neurology GA GX804 UT WOS:A1992GX80400035 PM 1728564 ER PT J AU DRYJA, TP AF DRYJA, TP TI RHODOPSIN AND AUTOSOMAL DOMINANT RETINITIS-PIGMENTOSA SO EYE LA English DT Article ID CYSTIC-FIBROSIS GENE; RETINALDEHYDE-BINDING-PROTEIN; CYCLIC-GMP PHOSPHODIESTERASE; OUTER SEGMENT MEMBRANES; OCULAR FINDINGS; TRANSVERSION MUTATION; ALPHA-TRANSDUCIN; GAMMA-SUBUNIT; 2 FAMILIES; S-ANTIGEN C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 67 TC 55 Z9 55 U1 0 U2 3 PU ROYAL COLL OPHTHALMOLOGISTS PI LONDON PA 17 CORNWALL TERRACE, LONDON, ENGLAND NW1 4QW SN 0950-222X J9 EYE JI Eye PY 1992 VL 6 BP 1 EP 10 PN 1 PG 10 WC Ophthalmology SC Ophthalmology GA KC831 UT WOS:A1992KC83100002 PM 1358680 ER PT J AU BONINI, S BARNEY, NP SCHIAVONE, M CENTOFANTI, M BERRUTO, A BONINI, S ALLANSMITH, MR AF BONINI, S BARNEY, NP SCHIAVONE, M CENTOFANTI, M BERRUTO, A BONINI, S ALLANSMITH, MR TI EFFECTIVENESS OF NEDOCROMIL SODIUM 2-PERCENT EYEDROPS ON CLINICAL SYMPTOMS AND TEAR FLUID CYTOLOGY OF PATIENTS WITH VERNAL CONJUNCTIVITIS SO EYE LA English DT Article DE ALLERGIC CONJUNCTIVITIS; NEDOCROMIL SODIUM EYE DROPS; TEAR FLUID CYTOLOGY; VERNAL CONJUNCTIVITIS ID TILADE; ASTHMA AB A double-masked, randomised, placebo-controlled study was conducted to evaluate the effectiveness of nedocromil 2% eyedrops, a mast cell stabiliser, in 20 symptomatic patients with vernal conjunctivitis. A 1-week baseline period was followed by 6 weeks of treatment. Clinical examination and cytological evaluation of tear fluid were performed weekly, and the patients recorded their subjective assessment on a daily diary card. The nedocromil group showed significantly less hyperaemia in the course of treatment than did the placebo group, and significantly less itching at all visits compared with baseline itching. In the nedocromil-treated group, but not in the placebo group, the number of neutrophils, eosinophils and lymphocytes in tears decreased significantly during some treatment weeks when compared with baseline. The overall assessment of treatment efficacy by both clinician and patient was significantly in favour of nedocromil treatment over placebo. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. UNIV ROME LA SAPIENZA,FONDAZ A CESALPINO,DEPT MED,I-00185 ROME,ITALY. HARVARD UNIV,SCH MED,EYE RES INST,BOSTON,MA 02115. BIETTI EYE FDN,ROME,ITALY. RP BONINI, S (reprint author), UNIV ROME TOR VERGATA,DEPT OPHTHALMOL,VIA CASSIA ANTICA 35,I-00191 ROME,ITALY. RI Bonini, Stefano/A-2250-2012; OI Bonini, Stefano/0000-0002-7787-2144; Bonini, Sergio/0000-0003-0079-3031 NR 19 TC 29 Z9 30 U1 0 U2 0 PU ROYAL COLL OPHTHALMOLOGISTS PI LONDON PA 17 CORNWALL TERRACE, LONDON, ENGLAND NW1 4QW SN 0950-222X J9 EYE JI Eye PY 1992 VL 6 BP 648 EP 652 PN 6 PG 5 WC Ophthalmology SC Ophthalmology GA KF777 UT WOS:A1992KF77700022 PM 1337745 ER PT J AU ANDERSON, WM DELINCK, DL BENNINGER, L WOOD, JM SMILEY, ST CHEN, LB AF ANDERSON, WM DELINCK, DL BENNINGER, L WOOD, JM SMILEY, ST CHEN, LB TI ANTICARCINOMA ACTIVITY OF THIACARBOCYANINE DYES MAY RELATE TO INHIBITION OF MITOCHONDRIAL NADH-UBIQUINONE REDUCTASE-ACTIVITY VIA A ROTENONE-TYPE MECHANISM SO FASEB JOURNAL LA English DT Meeting Abstract C1 INDIANA UNIV,SCH MED,NWCME,GARY,IN 46408. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A198 EP A198 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44001136 ER PT J AU ARYSTARKHOVA, EA GASPARIAN, M SWEADNER, KJ AF ARYSTARKHOVA, EA GASPARIAN, M SWEADNER, KJ TI EXTRACELLULAR ANTIBODY VG4 ENHANCES OUABAIN BINDING TO NA,K-ATPASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Chernyak, Boris/D-9917-2012 NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A121 EP A121 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44000702 ER PT J AU AUSIELLO, DA PRAT, AG CANTIELLO, HF AF AUSIELLO, DA PRAT, AG CANTIELLO, HF TI REGULATION OF APICAL EPITHELIAL NA+ CHANNELS BY G PROTEINS, PHOSPHOLIPIDS AND ACTIN-FILAMENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A1 EP A1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44000003 ER PT J AU BAENZIGER, JE MILLER, KW ROTHSCHILD, KJ AF BAENZIGER, JE MILLER, KW ROTHSCHILD, KJ TI CONFORMATIONAL-CHANGES ASSOCIATED WITH THE DESENSITIZATION OF THE NICOTINIC ACETYLCHOLINE-RECEPTOR PROBED AT THE AMINO-ACID RESIDUE LEVEL SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. BOSTON UNIV,DEPT PHYS,BOSTON,MA 02215. BOSTON UNIV,DEPT PHYSIOL,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A260 EP A260 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44001496 ER PT J AU BERGELSON, JM SHEPLEY, MP CHAN, BMC HEMLER, ME FINBERG, RW AF BERGELSON, JM SHEPLEY, MP CHAN, BMC HEMLER, ME FINBERG, RW TI IDENTIFICATION OF AN INTEGRIN RECEPTOR FOR ECHOVIRUS-1 SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A264 EP A264 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44001521 ER PT J AU CANTIELLO, HF KIM, DS AF CANTIELLO, HF KIM, DS TI EPITHELIAL ION CHANNELS ARE LINKED BY CYTOSKELETAL-NETWORK SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A123 EP A123 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44000708 ER PT J AU EWEN, M KAELIN, WG CHITTENDEN, T SHIRODKAR, S DECAPRIO, J FLEMINGTON, E GRIFFIN, JD AJCHENBAUM, F SHERR, C LIVINGSTON, DM AF EWEN, M KAELIN, WG CHITTENDEN, T SHIRODKAR, S DECAPRIO, J FLEMINGTON, E GRIFFIN, JD AJCHENBAUM, F SHERR, C LIVINGSTON, DM TI FUNCTIONAL-ANALYSIS OF THE RB GENE-PRODUCT AND RELATED PROTEINS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. ST JUDE HOSP & RES INST,MEMPHIS,TN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A1 EP A1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44000004 ER PT J AU HUDSON, NW NEAR, RI AF HUDSON, NW NEAR, RI TI THR TO GLU MUTATION IN THE L-CHAIN OF ANTIDIGOXIN 26-10 RESULTS IN AFFINITY AND SPECIFICITY CHANGES SO FASEB JOURNAL LA English DT Meeting Abstract C1 INDIANA UNIV,SCH MED,NW CTR,GARY,IN 46408. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A208 EP A208 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44001191 ER PT J AU MARGOSSIAN, SS WHITE, HD CAULFIELD, JB NORTON, P TAYLOR, S SLAYTER, HS AF MARGOSSIAN, SS WHITE, HD CAULFIELD, JB NORTON, P TAYLOR, S SLAYTER, HS TI STRUCTURE AND ACTIVITY OF HUMAN CARDIAC MYOSIN DURING CARDIOMYOPATHY SO FASEB JOURNAL LA English DT Meeting Abstract C1 MONTEFIORE MED CTR,BRONX,NY 10467. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. EASTERN VIRGINIA MED SCH,NORFOLK,VA 23501. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A434 EP A434 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44002488 ER PT J AU MARGOSSIAN, SS TAYLOR, S CAULFIELD, JB NORTON, P SLAYTER, HS AF MARGOSSIAN, SS TAYLOR, S CAULFIELD, JB NORTON, P SLAYTER, HS TI PARTIAL-PURIFICATION OF A LC2-SPECIFIC PROTEASE FROM MYOPATHIC HUMAN HEARTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MONTEFIORE MED CTR,BRONX,NY 10467. UNIV ALABAMA,BIRMINGHAM,AL 35294. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A434 EP A434 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44002486 ER PT J AU PRAT, AG KIM, DS AUSIELLO, DA CANTIELLO, HF AF PRAT, AG KIM, DS AUSIELLO, DA CANTIELLO, HF TI VASOPRESSIN AND ITS CAMP-DEPENDENT PATHWAY ACTIVATE APICAL G-PROTEIN CONTROLLED EPITHELIAL NA+ CHANNELS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JAN 1 PY 1992 VL 6 IS 1 BP A391 EP A391 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA GY440 UT WOS:A1992GY44002244 ER PT B AU CAVINESS, VS FILIPEK, PA KENNEDY, DN AF CAVINESS, VS FILIPEK, PA KENNEDY, DN BE FUKUYAMA, Y SUZUKI, Y KAMOSHITA, S CASAER, P TI MAGNETIC-RESONANCE-IMAGING - PERSPECTIVE FOR DEVELOPMENTAL DISORDERS OF THE CENTRAL-NERVOUS-SYSTEM SO FETAL AND PERINATAL NEUROLOGY LA English DT Proceedings Paper CT 5TH INTERNATIONAL CHILD NEUROLOGY CONGRESS / 3RD ASIAN AND OCEANIAN CONGRESS OF CHILD NEUROLOGY CY NOV 04-09, 1990 CL TOKYO, JAPAN SP INT CHILD NEUROL ASSOC, ASIAN & OCEANIAN ASSOC CHILD NEUROL RP CAVINESS, VS (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,DIV CHILD NEUROL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5398-6 PY 1992 BP 137 EP 143 PG 7 WC Neurosciences; Pathology; Pediatrics SC Neurosciences & Neurology; Pathology; Pediatrics GA BV29L UT WOS:A1992BV29L00012 ER PT J AU COLLEN, D MASUDA, M LU, HR FLAMENG, W VERHEYEN, A DECLERCK, F GOLD, HK AF COLLEN, D MASUDA, M LU, HR FLAMENG, W VERHEYEN, A DECLERCK, F GOLD, HK TI EFFECT OF RIDOGREL, A COMBINED THROMBOXANE A2 SYNTHASE INHIBITOR PROSTAGLANDIN ENDOPEROXIDE RECEPTOR ANTAGONIST, ON THE LYSIS OF PLATELET-RICH CORONARY ARTERIAL THROMBI WITH RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN A CANINE MODEL SO FIBRINOLYSIS LA English DT Article ID STREPTOKINASE-INDUCED THROMBOLYSIS; ACUTE MYOCARDIAL-INFARCTION; SYNTHETASE INHIBITION; ONE MOLECULE; INVIVO; REOCCLUSION; RECANALIZATION; SULOTROBAN; ANTIBODY; THERAPY AB The effect of ridogrel, a combined thromboxane A2 synthase inhibitor/prostaglandin endoperoxide receptor antagonist, on the lysis of platelet-rich thrombi with recombinant tissue-type plasminogen activator (rt-PA) was studied in everted (inside-out) femoral arterial grafts inserted in the left anterior descending coronary arteries of heparinised dogs. Thrombotic occlusion of the everted segment graft with a platelet-rich thrombus, persisting for at least 30 min, occurred spontaneously within 4.3 +/- 3.9 min (mean +/- SD). These dogs were then heparinised and randomised to 1 of 4 blinded treatment groups: double placebo infusion, bolus injections of 0.5 mg/kg rt-PA, repeated at 15 min intervals until recanalisation occurred or up to 4 doses, ridogrel infusion (5 mg/kg bolus followed by continuous infusion of 5 mg/kg over 150 min), or the combination of rt-PA and ridogrel. In the control group, stable occlusion as measured with an electromagnetic flow probe was maintained throughout the observation period. rt-PA produced reperfusion in 3 of 5 dogs, associated with cyclic reocclusion and reflow in 1 dog. Ridogrel administration did not produce recanalisation in any of the animals. The combined administration of ridogrel and rt-PA produced stable reperfusion without reocclusion in all of 5 dogs (p < 0.003 vs control groups), within 41 +/- 17 min. Coronary blood flow after recanalisation was significantly higher (p < 0.05) in dogs given rt-PA and ridogrel (29 +/- 6 ml/min after 10 min and 30 +/- 9 ml/min after 60 min) than in dogs given rt-PA alone (10 +/- 5 ml/min after 10 min and 14 +/- 6 ml/min after 60 min). Ridogrel, alone or in combination with rt-PA, prolonged the template bleeding time from approximately 3.5 min to more than 20 min, whereas rt-PA alone did not significantly affect the bleeding time. The results indicate that ridogrel enhances and sustains recanalisation of platelet-rich arterial thrombosis with rt-PA. C1 CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,B-3000 LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,CTR EXPTL SURG & ANESTHESIOL,B-3000 LOUVAIN,BELGIUM. JANSSEN RES FDN,DEPT HEMATOL,BEERSE,BELGIUM. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 35 TC 12 Z9 12 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0268-9499 J9 FIBRINOLYSIS JI Fibrinolysis PD JAN PY 1992 VL 6 IS 1 BP 7 EP 15 DI 10.1016/0268-9499(92)90042-G PG 9 WC Hematology SC Hematology GA HA957 UT WOS:A1992HA95700002 ER PT B AU POLAK, M BLEICH, D EISENBARTH, GS JACKSON, RA AF POLAK, M BLEICH, D EISENBARTH, GS JACKSON, RA BE Laron, Z Karp, M TI OCCURRENCE OF MATERNAL TYPE-1 DIABETES AFTER AGE 12 DECREASES THE TRANSMISSION RATE OF DISEASE TO OFFSPRING SO GENETIC AND ENVIRONMENTAL RISK FACTORS FOR TYPE I DIABETES (IDDM) INCLUDING A DISCUSSION ON THE AUTOIMMUNE BASIS LA English DT Proceedings Paper CT 8th Beilinson Symposium on Childhood Diabetes CY OCT 20-25, 1991 CL HERZLIYYA, ISRAEL C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FREUND PUBL HOUSE LTD PI LONDON PA SUITE 500, CHESHAM HOUSE, 150 REGENT ST, LONDON, ENGLAND W1R 5FA BN 965-094-080-1 PY 1992 BP 31 EP 32 PG 2 WC Endocrinology & Metabolism; Genetics & Heredity; Immunology SC Endocrinology & Metabolism; Genetics & Heredity; Immunology GA BZ85S UT WOS:A1992BZ85S00004 ER PT J AU SMALLEY, SL WOLKENSTEIN, BH LARUE, A WOODWARD, JA JARVIK, LF MATSUYAMA, SS AF SMALLEY, SL WOLKENSTEIN, BH LARUE, A WOODWARD, JA JARVIK, LF MATSUYAMA, SS TI COMMINGLING ANALYSIS OF MEMORY PERFORMANCE IN OFFSPRING OF ALZHEIMER PATIENTS SO GENETIC EPIDEMIOLOGY LA English DT Article DE ALZHEIMER; COMMINGLING ANALYSIS; HERITABILITY; MEMORY PERFORMANCE ID NEUROPATHOLOGICAL FINDINGS; 1ST-DEGREE RELATIVES; CLINICAL-DIAGNOSIS; GENETIC-LINKAGE; DISEASE; DEMENTIA; AGE; CHROMOSOME-21; SEGREGATION; MARKERS AB Dementia of the Alzheimer type (DAT) is a neurodegenerative disorder which afflicts approximately 3% of the population. Genetic influences are indicated from twin and family studies although genetic heterogeneity has been suggested from both pedigree analyses and linkage investigations. Autosomal dominant inheritance with age-dependent penetrance has been suggested in at least some families with DAT. In the present investigation, we examine memory and nonmemory task performance in 106 asymptomatic offspring (mean age 40.6 years) of 54 DAT probands. Intraclass sibling correlations revealed little evidence of sibling similarity for performance on three memory tasks which have been reported to be relatively sensitive to the memory losses accompanying DAT. Subsequent investigations of the distributions of the cognitive task scores in the offspring revealed evidence for a commingling of two distributions for the three memory tasks but not for the nonmemory measures. These findings are consistent with a hypothesis that these distributions reflect genotypic subgroups, carriers, and noncarriers, of a presumed DAT gene. C1 UNIV CALIF LOS ANGELES,DEPT PSYCHOL,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. RP SMALLEY, SL (reprint author), UNIV CALIF LOS ANGELES,SCH MED,NPI,DEPT PSYCHIAT,ROOM 48-241,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NCRR NIH HHS [1 P41 RR03655]; NIMH NIH HHS [MH 36205] NR 41 TC 11 Z9 12 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PY 1992 VL 9 IS 5 BP 333 EP 345 DI 10.1002/gepi.1370090505 PG 13 WC Genetics & Heredity; Mathematical & Computational Biology SC Genetics & Heredity; Mathematical & Computational Biology GA JW004 UT WOS:A1992JW00400004 PM 1427022 ER PT J AU KONRADI, C OZELIUS, L BREAKEFIELD, XO AF KONRADI, C OZELIUS, L BREAKEFIELD, XO TI HIGHLY POLYMORPHIC (GT)N REPEAT SEQUENCE IN INTRON-II OF THE HUMAN MAOB GENE SO GENOMICS LA English DT Note ID MONOAMINE-OXIDASE; DNA-POLYMERASE C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP KONRADI, C (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROBIOL,BOSTON,MA 02129, USA. FU NIAAA NIH HHS [AA08683]; NINDS NIH HHS [NS21921] NR 12 TC 50 Z9 52 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JAN PY 1992 VL 12 IS 1 BP 176 EP 177 DI 10.1016/0888-7543(92)90426-S PG 2 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA GV797 UT WOS:A1992GV79700029 PM 1733859 ER PT J AU OUM, BS DAMICO, DJ KWAK, HW WONG, KW AF OUM, BS DAMICO, DJ KWAK, HW WONG, KW TI INTRAVITREAL ANTIBIOTIC-THERAPY WITH VANCOMYCIN AND AMINOGLYCOSIDE - EXAMINATION OF THE RETINAL TOXICITY OF REPETITIVE INJECTIONS AFTER VITREOUS AND LENS SURGERY SO GRAEFES ARCHIVE FOR CLINICAL AND EXPERIMENTAL OPHTHALMOLOGY LA English DT Article ID ENDOPHTHALMITIS; GENTAMICIN; VITRECTOMY; CLEARANCE AB The combination of vancomycin and an aminoglycoside antibiotic is frequently injected into aphakic/vitrectomized eyes for the treatment of endophthalmitis. At 2 weeks after lens and vitreous removal, rabbit eyes received an injection of a combination of 1 mg vancomycin and either 400-mu-g amikacin or 100-mu-g gentamicin. Furthermore, the effects of repeating the same combination a second and third time at intervals of 48 h were examined by light and transmission electron microscopy at 7 days to 4 months after the last injection. A single injection of either combination produced no toxicity. After 2 or 3 sets of injections of either combination, 13 of 16 eyes displayed retinal toxicity manifested by macrophages in the subretinal space, disorganization of the outer segments and retinal pigment epithelium, and discontinuities in Bruch's membrane. These results indicate that whereas a single injection of these combinations is not toxic to aphakic/vitrectomized eyes, repetitive injections may result in increasing toxicity. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [EY04474] NR 20 TC 18 Z9 19 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-832X J9 GRAEF ARCH CLIN EXP JI Graefes Arch. Clin. Exp. Ophthalmol. PD JAN PY 1992 VL 230 IS 1 BP 56 EP 61 DI 10.1007/BF00166763 PG 6 WC Ophthalmology SC Ophthalmology GA HA122 UT WOS:A1992HA12200010 PM 1547968 ER PT J AU BORODIC, GE PEARCE, LB SMITH, K JOSEPH, M AF BORODIC, GE PEARCE, LB SMITH, K JOSEPH, M TI BOTULINUM A TOXIN FOR SPASMODIC TORTICOLLIS - MULTIPLE VS SINGLE INJECTION POINTS PER MUSCLE SO HEAD AND NECK-JOURNAL FOR THE SCIENCES AND SPECIALTIES OF THE HEAD AND NECK LA English DT Article ID CERVICAL DYSTONIA; A TOXIN; BLEPHAROSPASM AB Eighty-six injections in 49 patients with adult onset spasmodic torticollis were evaluated for efficacy with respect to single point per muscle versus multiple point per muscle injection techniques. Parameters of the syndrome assessed were pain, posture deformity, range of cervical motion, disfigurement, cervical muscle hypertrophy, activity limitation, and degree of involuntary movement. The multiple point per muscle injection strategy appeared superior to the single injection per muscle technique with respect to pain (p < 0.002, chi-square), posture deformity (p < 0.001), range of motion (p < 0.001), and improvement in activity endurance (p < 0.001). No significant differences were noted with respect to cervical muscle hypertrophy or degree of involuntary movements, although the injections were considered beneficial in both groups to these syndrome components. C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. RP BORODIC, GE (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,100 CHARLES RIVER PLAZA,BOSTON,MA 02114, USA. NR 17 TC 50 Z9 51 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1043-3074 J9 HEAD NECK-J SCI SPEC JI Head Neck-J. Sci. Spec. Head Neck PD JAN-FEB PY 1992 VL 14 IS 1 BP 33 EP 37 DI 10.1002/hed.2880140108 PG 5 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA GW884 UT WOS:A1992GW88400007 PM 1624292 ER PT J AU POLONSKY, WH DAVIS, CL JACOBSON, AM ANDERSON, BJ AF POLONSKY, WH DAVIS, CL JACOBSON, AM ANDERSON, BJ TI CORRELATES OF HYPOGLYCEMIC FEAR IN TYPE-I AND TYPE-II DIABETES-MELLITUS SO HEALTH PSYCHOLOGY LA English DT Note DE FEAR OF HYPOGLYCEMIA; DIABETES; ANXIETY; FREQUENCY OF HYPOGLYCEMIA AB We examined whether fear of hypoglycemia in insulin-dependent diabetes mellitus was associated with (a) higher levels of trait anxiety and general fearfulness, (b) difficulty in differentiating symptoms of anxiety and hypoglycemia, and (c) past experience with hypoglycemia. Joslin Diabetes Center outpatients with Type I and Type II diabetes (N = 232), all requiring insulin, were surveyed. Type I patients experienced significantly more fear of hypoglycemia than Type II patients. For the Type I and Type II groups, higher scores on the Worry subscale of the Hypoglycemia Fear Survey (HFS-W) were associated with higher levels of trait anxiety and fear. Higher scores on the Behavior subscale (HFS-B) were associated with higher levels of fear. Among Type I subjects only, HFS-W scores were also positively associated with past hypoglycemic experience and with difficulty in differentiating anxiety and hypoglycemic symptoms. These latter relations remained significant even after the variance resulting from trail anxiety and fear was removed. Other significant associations with HFS-B scores were not observed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP POLONSKY, WH (reprint author), JOSLIN DIABETES CTR,PSYCHOSOCIAL UNIT,1 JOSLIN PL,BOSTON,MA 02215, USA. OI Davis, Catherine Lucy/0000-0002-2942-8233 NR 8 TC 60 Z9 60 U1 0 U2 4 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0278-6133 J9 HEALTH PSYCHOL JI Health Psychol. PY 1992 VL 11 IS 3 BP 199 EP 202 DI 10.1037/0278-6133.11.3.199 PG 4 WC Psychology, Clinical; Psychology SC Psychology GA HW017 UT WOS:A1992HW01700007 PM 1618174 ER PT J AU ELIAS, AD AF ELIAS, AD TI FUTURE-DIRECTIONS IN THE MANAGEMENT OF SOFT-TISSUE SARCOMAS SO HEMATOLOGICAL ONCOLOGY LA English DT Article; Proceedings Paper CT CONF ON CURRENT CANCER THERAPY CY OCT, 1990 CL TAMPA, FL SP UNIV S FLORIDA, H LEE MOFFITT CANC CTR & RES INST ID GYNECOLOGIC ONCOLOGY GROUP; PHASE-II TRIAL; ADJUVANT CHEMOTHERAPY; RANDOMIZED TRIAL; COMBINATION CHEMOTHERAPY; NONOSSEOUS SARCOMAS; UTERINE SARCOMAS; IFOSFAMIDE; DOXORUBICIN; ADRIAMYCIN RP ELIAS, AD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115, USA. NR 60 TC 5 Z9 5 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0278-0232 J9 HEMATOL ONCOL JI Hematol. Oncol. PD JAN-FEB PY 1992 VL 10 IS 1 BP 53 EP 60 DI 10.1002/hon.2900100110 PG 8 WC Oncology; Hematology SC Oncology; Hematology GA HP549 UT WOS:A1992HP54900009 PM 1563704 ER PT J AU RIVKEES, SA REPPERT, SM AF RIVKEES, SA REPPERT, SM TI PERINATAL-DEVELOPMENT OF DAY-NIGHT RHYTHMS IN HUMANS SO HORMONE RESEARCH LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON ENDOCRINOLOGY AND DEVELOPMENT : BASIC AND CLINICAL ASPECTS CY OCT 12-14, 1990 CL ATHENS, GREECE DE CIRCADIAN RHYTHM ID FETAL BIOLOGICAL CLOCK; LAST 10 WEEKS; CIRCADIAN-RHYTHMS; SUPRACHIASMATIC NUCLEUS; MELATONIN RECEPTORS; HUMAN HYPOTHALAMUS; BODY MOVEMENTS; HEART-RATE; CORTISOL; PATTERNS AB Evidence suggests that the suprachiasmatic nuclei function as a circadian pacemaker in humans. The development of the circadian timing systems may be similar to that described in rodents and nonhuman primates. Awareness of circadian rhythmicity during development should improve infant care and increase the understanding of several disease states. RP RIVKEES, SA (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,BOSTON,MA 02114, USA. NR 49 TC 16 Z9 16 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0301-0163 J9 HORM RES JI Horm. Res. PY 1992 VL 37 SU 3 BP 99 EP 104 DI 10.1159/000182409 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JV001 UT WOS:A1992JV00100016 PM 1427650 ER PT S AU REPPERT, SM SWAAB, DF CORNER, MA REPASKE, DR MIRMIRAN, M AF REPPERT, SM SWAAB, DF CORNER, MA REPASKE, DR MIRMIRAN, M BE Swaab, DF Hofman, MA Mirmiran, M Ravid, R Vanleeuwen, FW TI PRENATAL DEVELOPMENT OF A HYPOTHALAMIC BIOLOGICAL CLOCK SO HUMAN HYPOTHALAMUS IN HEALTH AND DISEASE SE PROGRESS IN BRAIN RESEARCH LA English DT Review CT 17TH INTERNATIONAL SUMMER SCHOOL OF BRAIN RESEARCH ON THE HUMAN HYPOTHALAMUS IN HEALTH AND DISEASE CY AUG 26-30, 1991 CL UNIV AMSTERDAM, AMSTERDAM, NETHERLANDS SP ROYAL NETHERLANDS ACAD SCI, UNIV AMSTERDAM, NEUROSCI AMSTERDAM, CIBA GEIGY, SAAL VAN ZWANENBERG FDN, MERCK SHARP & DOHME, MERRELL DOW RES INST, NETHERLANDS SOC ADV NAT SCI MED & SURG, ORGANON INT, REMMERT ADRIAAN LAANFONDS HO UNIV AMSTERDAM RP REPPERT, SM (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,32 FRUIT ST,BOSTON,MA 02114, USA. RI Repaske, David/E-3939-2011 NR 0 TC 34 Z9 35 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL B V PI AMSTERDAM PA AMSTERDAM SN 0079-6123 BN 0-444-89538-8 J9 PROG BRAIN RES PY 1992 VL 93 BP 119 EP 132 PG 14 WC Endocrinology & Metabolism; Neurosciences; Pathology; Physiology SC Endocrinology & Metabolism; Neurosciences & Neurology; Pathology; Physiology GA BX13F UT WOS:A1992BX13F00010 PM 1480745 ER PT J AU HOMMA, S JONES, R QVIST, J ZAPOL, WM REID, L AF HOMMA, S JONES, R QVIST, J ZAPOL, WM REID, L TI PULMONARY VASCULAR-LESIONS IN THE ADULT RESPIRATORY-DISTRESS SYNDROME CAUSED BY INHALATION OF ZINC-CHLORIDE SMOKE - A MORPHOMETRIC STUDY SO HUMAN PATHOLOGY LA English DT Article DE PULMONARY VASCULAR LESIONS; ADULT RESPIRATORY DISTRESS SYNDROME; ZINC CHLORIDE; MORPHOMETRY; FATAL CASES ID CELL-PROLIFERATION; HYPERTENSION; EXPOSURE; TOXICITY; ARTERIES; FAILURE; LUNG C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV COPENHAGEN,HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. UNIV COPENHAGEN,FAC MED,DK-2100 COPENHAGEN,DENMARK. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP HOMMA, S (reprint author), CHILDRENS HOSP MED CTR,DEPT PATHOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HLBI 23591] NR 29 TC 23 Z9 26 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JAN PY 1992 VL 23 IS 1 BP 45 EP 50 DI 10.1016/0046-8177(92)90010-Z PG 6 WC Pathology SC Pathology GA HC345 UT WOS:A1992HC34500009 PM 1544669 ER PT J AU ZHOU, LJ ORD, DC OMORI, SA TEDDER, TF AF ZHOU, LJ ORD, DC OMORI, SA TEDDER, TF TI STRUCTURE OF THE GENES ENCODING THE CD19 ANTIGEN OF HUMAN AND MOUSE LYMPHOCYTES-B SO IMMUNOGENETICS LA English DT Article ID EXON INTRON ORGANIZATION; PRE-B; DIFFERENTIATION ANTIGEN; CELL DIFFERENTIATION; DNA FRAGMENTS; IMMUNOGLOBULIN; HYBRIDIZATION; EXPRESSION; PROMOTER; ENHANCER AB CD19 is a B lymphocyte cell-surface marker that is expressed early during pre-B-cell differentiation with expression persisting until terminal differentiation into plasma cells, CD19 is a member of the Ig gene superfamily with two extracellular Ig-like domains separated by a non-Ig-like domain, and with an extensive approximately 240 amino acid cytoplasmic domain. In this study, Southern blot analysis revealed that the human and mouse CD19 genes were compact single copy genes. Both the human and mouse CD19 genes were isolated and the nucleotide sequences flanking each exon were determined. Both genes were composed of 15 exons and spanned approximately 8 kilobases (kb) of DNA in human and approximately 6 kb in mouse. The positions of exon-intron boundaries were identical between human and mouse and correlated with the putative functional domains of the CD 19 protein. The 200 bp region 5' of the putative translation initiation AUG codon was well conserved in sequence between human and mouse and contained potential transcription regulatory elements. In addition, the 3' untranslated regions (UT) of the CD19 genes following the termination codon were conserved in sequence. The high level of conservation of nucleotide sequences between species in all exons and 5' and 3' UT suggests that expression of the CD19 gene may be regulated in a similar fashion in human and mouse. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-26872] NR 37 TC 26 Z9 29 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JAN PY 1992 VL 35 IS 2 BP 102 EP 111 PG 10 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA HA799 UT WOS:A1992HA79900004 PM 1370948 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI THE NEXT HUMAN-LEUKOCYTE DIFFERENTIATION ANTIGEN WORKSHOP SO IMMUNOLOGY TODAY LA English DT Article RP SPRINGER, TA (reprint author), CTR BLOOD RES,BOSTON,MA 02115, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD JAN PY 1992 VL 13 IS 1 BP 6 EP 6 DI 10.1016/0167-5699(92)90196-E PG 1 WC Immunology SC Immunology GA GY441 UT WOS:A1992GY44100003 ER PT J AU GRAVENSTEIN, S MILLER, BA DRINKA, P AF GRAVENSTEIN, S MILLER, BA DRINKA, P TI PREVENTION AND CONTROL OF INFLUENZA-A OUTBREAKS IN LONG-TERM CARE FACILITIES SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID NURSING-HOME; ELDERLY PEOPLE; IMMUNIZATION; AMANTADINE; VACCINATION; REDUCTION; VIRUS; H3N2; PROPHYLAXIS; MORTALITY C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. WISCONSIN VET HOME,KING,WI. RP GRAVENSTEIN, S (reprint author), UNIV WISCONSIN,INST AGING & ADULT LIFE,DEPT MED,GERIATR SECT,425 HENRY MALL,MADISON,WI 53706, USA. RI Gravenstein, Stefan/G-1681-2011 FU NIA NIH HHS [AG00548, AG09632] NR 34 TC 26 Z9 26 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD JAN PY 1992 VL 13 IS 1 BP 49 EP 54 PG 6 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA GZ076 UT WOS:A1992GZ07600007 PM 1545112 ER PT B AU FOSTER, CS AF FOSTER, CS BE BOKE, WRF MANTHEY, KF NUSSENBLATT, RB TI MEDICAL-TREATMENT OF INTERMEDIATE UVEITIS SO INTERMEDIATE UVEITIS SE DEVELOPMENTS IN OPHTHALMOLOGY LA English DT Proceedings Paper CT INTERNATIONAL WORKSHOP ON INTERMEDIATE UVEITIS CY JUL 05-06, 1990 CL GUTERSLOH, GERMANY SP UNIV KIEL, DEPT OPHTHALMOL, BERTELSMANN FDN RP FOSTER, CS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5436-2 J9 DEV OPHTHALMOL PY 1992 VL 23 BP 156 EP 157 PG 2 WC Medicine, Research & Experimental; Ophthalmology; Pharmacology & Pharmacy SC Research & Experimental Medicine; Ophthalmology; Pharmacology & Pharmacy GA BU53U UT WOS:A1992BU53U00026 PM 1730350 ER PT B AU FOSTER, CS AF FOSTER, CS BE BOKE, WRF MANTHEY, KF NUSSENBLATT, RB TI CATARACT-SURGERY AND INTRAOCULAR-LENS IMPLANTATION IN PATIENTS WITH INTERMEDIATE UVEITIS SO INTERMEDIATE UVEITIS SE DEVELOPMENTS IN OPHTHALMOLOGY LA English DT Proceedings Paper CT INTERNATIONAL WORKSHOP ON INTERMEDIATE UVEITIS CY JUL 05-06, 1990 CL GUTERSLOH, GERMANY SP UNIV KIEL, DEPT OPHTHALMOL, BERTELSMANN FDN RP FOSTER, CS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5436-2 J9 DEV OPHTHALMOL PY 1992 VL 23 BP 212 EP 218 PG 7 WC Medicine, Research & Experimental; Ophthalmology; Pharmacology & Pharmacy SC Research & Experimental Medicine; Ophthalmology; Pharmacology & Pharmacy GA BU53U UT WOS:A1992BU53U00035 PM 1730360 ER PT J AU CLAYTON, LK LERNER, A DIENER, AC HUSSEY, RE KOYASU, S REINHERZ, EL AF CLAYTON, LK LERNER, A DIENER, AC HUSSEY, RE KOYASU, S REINHERZ, EL TI T-CELL-RECEPTOR ISOFORMS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT CONF ON BISPECIFIC ANTIBODIES AND TARGETED CELLULAR CYTOTOXICITY CY JUN 13-17, 1992 CL OSTUNI, ITALY SP EUROPEAN COMMUNITY CONCERTED ACT, CULTURAL ASSOC FRONTIERE SCI, CILAG ID NATURAL-KILLER-CELLS; ZETA-CHAIN; ANTIGEN RECEPTOR; TYROSINE PHOSPHORYLATION; SIGNAL TRANSDUCTION; MOLECULAR-CLONING; GAMMA-SUBUNIT; FC-EPSILON; ETA-CHAIN; ACTIVATION AB Early work on T-cell hybridomas lacking the T-cell-receptor (TCR) sub-unit CD3eta had suggested a correlation between the presence of CD3zeta-eta heterodimers and signalling leading to phosphatidyl-inositol (PI) turnover as well as activation-induced cell death. The cloning of CD3eta has now allowed thorough and direct analysis of the signal transduction properties of CD3zeta-zeta-, CD3zeta-eta- and CD3eta-eta-containing TCRs. We have found that all forms of the TCR are capable of transducing signals leading to PI turnover, Ca2+ mobilization, IL-2 production and cell-cycle arrest. CD3zeta and CD3eta utilize the same promoter which yields coordinate expression of both products, so that restricted CD3eta expression in a sub-population of thymocytes is unlikely. Immunohistochemical methods employing an anti-CD3eta-specific monoclonal antibody (MAb) show no detectable staining of thymic sections from adult mice, implying at best a low level of constitutive CD3eta expression. In contrast, CD3eta expression is readily detected in the majority of cortical thymocytes of CD3eta transgenic mice using a Thy-I promoter construct. However, over-expression of CD3eta in mice transgenic for this polypeptide does not result in increased negative selection in vivo, consistent with the in vitro findings that induction of cell death is not strictly dependent on CD3eta. Despite earlier reports of the detection of human CD3eta protein, we find no CD3eta message in human thymus or T cells. Cloning of the human CDzeta-eta genomic locus has demonstrated approximately 70% homology between the mouse and human genomic sequence, corresponding to the mouse CD3eta-specific exon. However, translation of the DNA sequence does not result in a homologous amino acid sequence. Thus, there does not appear to be a CD3eta protein in humans. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 NR 51 TC 1 Z9 1 U1 0 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PY 1992 SU 7 BP 1 EP 5 PG 5 WC Oncology SC Oncology GA JY980 UT WOS:A1992JY98000001 ER PT J AU VIVIER, E ACKERLY, M ROCHET, N ANDERSON, P AF VIVIER, E ACKERLY, M ROCHET, N ANDERSON, P TI STRUCTURE AND FUNCTION OF THE CD16-ZETA-GAMMA COMPLEX EXPRESSED ON HUMAN NATURAL-KILLER-CELLS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article; Proceedings Paper CT CONF ON BISPECIFIC ANTIBODIES AND TARGETED CELLULAR CYTOTOXICITY CY JUN 13-17, 1992 CL OSTUNI, ITALY SP EUROPEAN COMMUNITY CONCERTED ACT, CULTURAL ASSOC FRONTIERE SCI, CILAG ID IGG FC-RECEPTOR; SINGLE AMINO-ACID; EPSILON-RI-GAMMA; T-CELL; ANTIGEN RECEPTOR; TYROSINE PHOSPHORYLATION; ZETA-CHAIN; ACTIVATION; CD16; SUBUNIT AB Natural-killer (NK) cells are large granular lymphocytes involved in host defense against tumor cells and virally-infected cells. In addition to natural cytotoxicity, NK cells can effect antibody-dependent cytoxicity mediated by CD16 (FcgammaRIIIAalpha). It has recently been shown that CD16 is associated with disulfide-linked dimers composed of 2 homologous sub-units, zeta and gamma. These transducing molecules are also associated with other multimeric cell-surface receptors such as the T-cell antigen receptor (CD3:TCR) complex (zeta and gamma) and the high-affinity Fc receptor for IgE (FcepsilonRI) expressed on basophils and mast cells (gamma). These results show that distinct cell-surface receptors utilize common transducing sub-units, and emphasize the homology between the CD16, FcepsilonRI and CD3:TCR complexes. However within the lymphoid cells, the gamma-gamma homodimer is preferentially expressed in NK cells and cytotoxic T cells, suggesting that specific combinations of these transducing dimers might sub-serve distinct signal-transducing functions, and contribute to lymphocyte heterogeneity. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. RP VIVIER, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 45 TC 0 Z9 0 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PY 1992 SU 7 BP 11 EP 14 PG 4 WC Oncology SC Oncology GA JY980 UT WOS:A1992JY98000003 ER PT J AU ELIAS, A MAZANET, R ANDERSON, K AYASH, L WHEELER, C SCHWARTZ, G TEPLER, I HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, K AF ELIAS, A MAZANET, R ANDERSON, K AYASH, L WHEELER, C SCHWARTZ, G TEPLER, I HUNT, M CRITCHLOW, J SCHNIPPER, L FREI, E ANTMAN, K TI GM-CSF MOBILIZED PERIPHERAL-BLOOD STEM-CELL AUTOGRAFTS - THE DFCI BIH EXPERIENCE SO INTERNATIONAL JOURNAL OF CELL CLONING LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL SYMP ON PERIPHERAL BLOOD STEM CELL AUTOGRAFTS CY SEP 29-OCT 02, 1991 CL MULHOUSE, FRANCE SP IMMUNOTECH, INST PASTEUR MERIEUX, LAB ROCHE, SANDOZ PHARMA, LAB SARGET, DIV ONCOL, LAB SCHERING PLOUGH ID AUTOLOGOUS BONE-MARROW; NON-HODGKINS LYMPHOMA; TRANSPLANTATION; DISEASE C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. RP ELIAS, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 5 TC 3 Z9 3 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 0737-1454 J9 INT J CELL CLONING PD JAN PY 1992 VL 10 SU 1 BP 149 EP 151 PG 3 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HD137 UT WOS:A1992HD13700048 ER PT J AU RUTAN, JS AF RUTAN, JS TI PSYCHODYNAMIC GROUP-PSYCHOTHERAPY SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article AB The author provides an overview of critical factors in the working phase of group psychotherapy from the perspective of psychodynamic theory. The discussion is organized around a clinical vignette to illustrate various types of intervention such as past, here and now future; individual, interpersonal, group as a whole; in group-out of group; affect-cognition; and understanding-corrective emotional experience. The critical "windows into the unconscious," transference, counter-transference, and free association, are also discussed in terms of the clinical example. The author concludes his article with a few thoughts about the future of psychodynamic theory in relationship to group treatments. RP RUTAN, JS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR GRP PSYCHOTHERAPY,15 PARKMAN AVE,SUITE 805,BOSTON,MA 02114, USA. NR 18 TC 6 Z9 6 U1 0 U2 1 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD JAN PY 1992 VL 42 IS 1 BP 19 EP 35 PG 17 WC Psychology, Clinical SC Psychology GA GZ797 UT WOS:A1992GZ79700002 PM 1563902 ER PT J AU GANS, JS AF GANS, JS TI MONEY AND PSYCHODYNAMIC GROUP-PSYCHOTHERAPY SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article AB Money may be the most upsetting and therefore the most avoided topic in group psychotherapy. To overcome this resistance, the leader must secure prospective members' willingness to speak openly about financial matters. Financial issues particular to group therapy emerge when money is normalized as a topic for discussion. These include lowering or not raising fees, rescheduling, leaves of absence, combined and conjoint therapy, and nonverbal behaviors. Several case examples are provided. Members' strong feelings toward the leader around financial transactions often find expression in angry accusations. Suggestions for dealing therapeutically with countertransference reactions to these accusations are offered. C1 MASSACHUSETTS GEN HOSP,PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PSYCHIAT,BOSTON,MA 02115. NR 16 TC 14 Z9 14 U1 1 U2 1 PU GUILFORD PUBLICATIONS INC PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0020-7284 J9 INT J GROUP PSYCHOTH JI Int. J. Group Psychother. PD JAN PY 1992 VL 42 IS 1 BP 133 EP 152 PG 20 WC Psychology, Clinical SC Psychology GA GZ797 UT WOS:A1992GZ79700008 PM 1563901 ER PT J AU POLLACK, MH REITER, S HAMMERNESS, P AF POLLACK, MH REITER, S HAMMERNESS, P TI GENITOURINARY AND SEXUAL ADVERSE-EFFECTS OF PSYCHOTROPIC MEDICATION SO INTERNATIONAL JOURNAL OF PSYCHIATRY IN MEDICINE LA English DT Review DE GENITOURINARY; SEXUAL; LIBIDO; ERECTION; EJACULATION; ORGASM; PRIAPISM; INFERTILITY; ADVERSE EFFECTS; PSYCHOTROPICS ID ANTIPSYCHOTIC DRUG-THERAPY; ANTIDEPRESSANT MEDICATION; URINARY-INCONTINENCE; ORGASMIC INHIBITION; ERECTILE IMPOTENCE; INDUCED ANORGASMIA; PENILE CORPORA; L-DEPRENYL; DYSFUNCTION; PRIAPISM AB Objective: We review the adverse effects on genitourinary and sexual function associated with antidepressants, neuroleptics, lithium, and benzodiazepines, and suggest treatment strategies that may be used for their management. Method: This article is based on systematic review of the existing literature, including more than 130 relevant articles on genitourinary and sexual effects of psychotropic medications. Results: We find that genitourinary function, including effects on continence and flow, and sexual function, including libido, erection, ejaculation and orgasm, may be altered by psychotropic administration. Many of these effects may be consequent to the impact of these medications on neurophysiologic systems. Conclusions: Genitourinary and sexual adverse effects associated with psychotropic therapy are important areas of study and clinical concern that may affect patient comfort and compliance with treatment. C1 SUMMIT PSYCHIAT ASSOCIATES,SUMMIT,NJ. RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,15 PARKMAN ST,ACC-815,BOSTON,MA 02114, USA. NR 128 TC 60 Z9 61 U1 1 U2 1 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 1992 VL 22 IS 4 BP 305 EP 327 PG 23 WC Psychiatry SC Psychiatry GA KN858 UT WOS:A1992KN85800001 PM 1363418 ER PT J AU SCHOENTHALER, R ALBRIGHT, NW WARA, WM PHILLIPS, TL WILSON, CB LARSON, DA AF SCHOENTHALER, R ALBRIGHT, NW WARA, WM PHILLIPS, TL WILSON, CB LARSON, DA TI REIRRADIATION OF PITUITARY-ADENOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE PITUITARY ADENOMA; RADIATION; REIRRADIATION; TEMPORAL LOBE NECROSIS; OPTIC NERVE INJURY; PITUITARY CARCINOMA ID RADIATION-THERAPY; BRAIN-TUMORS; IRRADIATION; FRACTIONATION; CRANIOPHARYNGIOMAS; COMPLICATIONS; RADIONECROSIS; TIME AB Fifteen patients initially irradiated for pituitary adenoma were subsequently treated with a second course of radiotherapy at the University of California at San Francisco between 1961 and 1989. The reirradiation followed surgery in all but two cases. The median time to recurrence was 9 years (range 2-17) and median follow-up after the second course of radiotherapy was 10 years (range 1-30). The median initial radiation dose was 4084 cGy; that at recurrence was 4200 cGy. Local control has been maintained in 12 patients. One failed locally with a benign adenoma that was surgically salvaged. Two developed pituitary carcinomas which were poorly controlled. Of the patients who presented with visual abnormalities at the time of recurrence, 50% improved and the remainder stabilized after reirradiation. There are no long-term visual complications. Hypopituitarism was present in nine patients prior to the second course of radiotherapy and developed in the remaining six patients after reirradiation. Temporal lobe injury was seen in two patients. Careful analysis of each patient's pituitary and temporal lobe doses, intervals between treatments, treatment volume, neurets, relative decay factors, absolute decay factors, TDF and modified LQF values, and dose-volume relationships, revealed no correlation with complication or likelihood of local control. Repeat radiotherapy for recurrent pituitary adenoma with the doses used in these patients appears to carry acceptable risk with good local control. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BLOSSOM ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. NR 30 TC 29 Z9 29 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 24 IS 2 BP 307 EP 314 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JP784 UT WOS:A1992JP78400016 PM 1526869 ER PT J AU ROACH, M KRALL, J KELLER, JW PEREZ, CA SAUSE, WT DOGGETT, RLS ROTMAN, M RUSS, H PILEPICH, MV ASBELL, SO SHIPLEY, W AF ROACH, M KRALL, J KELLER, JW PEREZ, CA SAUSE, WT DOGGETT, RLS ROTMAN, M RUSS, H PILEPICH, MV ASBELL, SO SHIPLEY, W TI THE PROGNOSTIC-SIGNIFICANCE OF RACE AND SURVIVAL FROM PROSTATE-CANCER BASED ON PATIENTS IRRADIATED ON RADIATION-THERAPY ONCOLOGY GROUP PROTOCOLS (1976-1985) SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE RACE AND PROSTATE CANCER; BLACKS AND PROSTATE CANCER; CANCER SURVIVAL AND RACE ID DEFINITIVE RADIOTHERAPY; BREAST-CANCER; CARCINOMA; BLACK; MORTALITY; DISEASE; CARE AB A number of studies have identified race as a prognostic factor for survival from prostate cancer. To evaluate the prognostic significance of race in a controlled setting, we evaluated 1294 patients treated on three prospective randomized trials conducted by the Radiation Therapy Oncology Group between 1976 to 1985. One-hundred and twenty (9%) of the patients were coded as black, while 1077 (83%) of the patients were coded as white. Protocol 7506 included 607 patients with clinical Stage T3-T4Nx or T1b-T2N1-2. Protocol 7706 included 484 patients with clinical Stage T1b or T2 who were node negative. Protocol 8307 included 203 Stage T2b-T4 patients with no lymph node involvement beyond the pelvis. Univariate and multivariate analyses were used to assess the possible independent significance of race and other prognostic factors, including Gleason score, serum acid phosphatase, nodal status, and hormonal status. Protocols 7706 and 8307 revealed that race was not of prognostic significance for disease-free or overall survival by either univariate or multivariate analysis. Univariate analysis of Protocol 7506 revealed that the median survival for blacks was somewhat shorter (5.4 years vs. 7.1 years, p = 0.02). This difference persisted after a multivariate analysis. A higher percentage of blacks treated on 7506 had an abnormally elevated serum acid phosphatase compared to whites (p = 0.006), and the time to distant failure tended to be shorter (p = 0.07). These findings suggest that blacks treated on 7506 may have had more extensive disease at presentation. Based on these prospective randomized trials, it is most likely that the lower survival noted for black Americans with prostate cancer reflects the tendency for blacks to present with more advanced disease. Differences in access to care, the quality of care received, and the impact of co-morbid conditions may explain the lower survival reported for black Americans elsewhere in the literature. C1 RADIAT THERAPY ONCOL GRP HEADQUARTERS,PHILADELPHIA,PA. UNIV ROCHESTER,ROCHESTER,NY 14627. WASHINGTON UNIV,ST LOUIS,MO 63130. LATTER DAY ST HOSP,SALT LAKE CITY,UT 84143. RADIAT ONCOL CTR,SACRAMENTO,CA. SUNY DOWNSTATE MED CTR,BROOKLYN,NY. MARSHFIELD CLIN FDN MED RES & EDUC,MARSHFIELD,WI 54449. C MCAULEY HLTH CTR,ANN ARBOR,MI. ALBERT EINSTEIN MED CTR,NO DIV,PHILADELPHIA,PA 19141. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ROACH, M (reprint author), UNIV CALIF SAN FRANCISCO,DEPT RADIAT ONCOL,505 PARNASSUS AVE,SAN FRANCISCO,CA 94143, USA. NR 25 TC 51 Z9 52 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 24 IS 3 BP 441 EP 449 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JU040 UT WOS:A1992JU04000007 PM 1399729 ER PT J AU WEICHSELBAUM, RR HALLAHAN, DE SUKHATME, VP KUFE, DW AF WEICHSELBAUM, RR HALLAHAN, DE SUKHATME, VP KUFE, DW TI GENE-THERAPY TARGETED BY IONIZING-RADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE GENE THERAPY; X-RAYS; TRANSCRIPTION ID TUMOR-NECROSIS-FACTOR; CELLS; INVITRO; BETA AB Gene therapy used for the treatment of neoplastic diseases is not well localized. Ionizing radiation can be used to activate the transcription of exogenous genes that encode cytotoxic proteins. This may be accomplished through the use of radiation responsive elements distal to the transcription start site of such genes. We discuss this concept and describe a technique which can be used to amplify the signal initiated by localized radiation therapy. These techniques may be used to target gene therapy during the treatment of human neoplasms. C1 UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MED,CHICAGO,IL 60637. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP WEICHSELBAUM, RR (reprint author), UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,5841 S MARYLAND,BOX 442,CHICAGO,IL 60637, USA. FU NCI NIH HHS [CA-42596, CA-41068] NR 11 TC 54 Z9 69 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 24 IS 3 BP 565 EP 567 PG 3 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JU040 UT WOS:A1992JU04000024 PM 1399745 ER PT J AU SMITH, AR AF SMITH, AR TI RADIATION PHYSICS INSTRUCTION FOR RESIDENTS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article RP SMITH, AR (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,COX BLDG,BOSTON,MA 02114, USA. NR 6 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 24 IS 5 BP 851 EP 852 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KA570 UT WOS:A1992KA57000011 PM 1447015 ER PT J AU FLYNN, DF HUSSEY, DH AF FLYNN, DF HUSSEY, DH TI REVIEW OF THE MANPOWER ISSUE IN RADIATION ONCOLOGY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV IOWA,COLL MED,DEPT RADIOL,DIV RADIAT ONCOL,IOWA CITY,IA 52242. RP FLYNN, DF (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 4 TC 7 Z9 7 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 24 IS 5 BP 909 EP 912 PG 4 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA KA570 UT WOS:A1992KA57000029 PM 1447033 ER PT J AU URIE, MM FULLERTON, B TATSUZAKI, H BIRNBAUM, S SUIT, HD CONVERY, K SKATES, S GOITEIN, M AF URIE, MM FULLERTON, B TATSUZAKI, H BIRNBAUM, S SUIT, HD CONVERY, K SKATES, S GOITEIN, M TI A DOSE-RESPONSE ANALYSIS OF INJURY TO CRANIAL NERVES AND OR NUCLEI FOLLOWING PROTON-BEAM RADIATION-THERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CRANIAL NERVES; DOSE RESPONSE; CNS TOLERANCE; NORMAL TISSUE TOLERANCE; COMPLICATIONS; OPTIC NERVE TOLERANCE; 3-D TREATMENT PLANNING; PROTON THERAPY ID CENTRAL NERVOUS-SYSTEM; SPINAL-CORD; BRAIN INJURY; OPTIC-NERVE; IRRADIATION; COMPLICATIONS; RADIOTHERAPY; EYE; TOLERANCE AB The low tolerance of the central nervous system (CNS) limits the radiation dose which can be delivered in the treatment of many patients with brain and head and neck tumors. Although there are many reports concerning the tolerance of the CNS, few have examined individual substructures of the brain and fewer still have had detailed dose information. This study has both. A three dimensional planning system was used to develop the combined proton beam/photon beam treatments for 27 patients with skull-base tumors. The cranial nerves and their related nuclei were delineated on the planning CT scans and the radiation dose to each was determined from three dimensional dose distributions. In the 594 CNS structures (22 structures/patient in 27 patients), there have been 17 structures (in 5 patients) with clinically manifest radiation injury, after a mean follow-up time of 74 months (range 40-110 months). From statistical analyses, dose is found to be a significant predictor of injury. Using logistic regression analysis, we find that, for each cranial nerve, at 60 Cobalt Gray Equivalent (CGE) the complication rate is 1% (0.5-3% with 95% confidence) and that the 5% complication rate occurs at 70 CGE (64-81 CGE with 95% confidence). The slope of the dose response curve (at 50%) is 3.2 (2.2-5.4 with 95% confidence). No significant relationship between dose and latency period for nerve injury was found. C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP URIE, MM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239] NR 49 TC 58 Z9 58 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 1 BP 27 EP 39 PG 13 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HR986 UT WOS:A1992HR98600004 PM 1572828 ER PT J AU TAGHIAN, A SUIT, H PARDO, F GIOIOSO, D TOMKINSON, K DUBOIS, W GERWECK, L AF TAGHIAN, A SUIT, H PARDO, F GIOIOSO, D TOMKINSON, K DUBOIS, W GERWECK, L TI INVITRO INTRINSIC RADIATION SENSITIVITY OF GLIOBLASTOMA-MULTIFORME SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE INTRINSIC RADIOSENSITIVITY; SF2; MALIGNANT GLIOMA ID GLIOMA CELL-LINES; SURVIVAL CURVES; MALIGNANT-MELANOMA; INITIAL SLOPE; HUMAN-TUMORS; RADIOSENSITIVITY; RADIOTHERAPY; RADIORESPONSIVENESS; ASTROCYTOMA; CARCINOMA AB Glioblastoma multiforme is one of the most resistant of human tumors to radiation whether used alone or in combination with surgery and/or chemotherapy. This resistance may be caused by one or more of several different factors. These include inherent cellular radiation sensitivity, an efficient repair of radiation damage, an increased number of clonogens per unit of volume, a high hypoxic fraction, high [GSH] concentration, and rapid proliferation between fractions. In the present study, we evaluate the intrinsic radiation sensitivity (surviving fraction at 2 Gy or mean inactivation dose) of malignant human glioma cells in vitro. The in vitro radiation sensitivity of 21 malignant glioma cell lines (early and long term passages) has been measured using colony formation as the end-point of cell viability. The survival curve parameters (SF2 measured and calculated, alpha, beta, D0, n approximately, and MID) have been determined for single dose irradiations of exponential phase cells (18-24 hr after plating) under aerobic conditions and growing on plastic. The mean SF2 of the 21 cell lines is 0.51 +/- 0.14 (with a range of 0.19 to 0.76). This value may be compared to the mean SF2 of 0.43-0.47 for SCC, 0.43 for melanoma, and 0.52 for glioblastoma as reported from other authors when using colony formation of cells in exponential phase on plastic. Although glioblastoma is almost invariably fatal, our data demonstrate a very wide range of intrinsic radiosensitivities. These broadly overlap the radiation sensitivities of cell lines from tumors that are often treated successfully. We conclude that standard in vitro measurements of cellular radiation sensitivity (SF2) do not yield values that track in a simple manner with local control probability at the clinical level and that, for at least some of the tumors, other parameters and/or physiological factors are more important. RP TAGHIAN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA13311] NR 36 TC 85 Z9 85 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 1 BP 55 EP 62 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HR986 UT WOS:A1992HR98600007 PM 1315313 ER PT J AU NIEMIERKO, A AF NIEMIERKO, A TI RANDOM SEARCH ALGORITHM (RONSC) FOR OPTIMIZATION OF RADIATION-THERAPY WITH BOTH PHYSICAL AND BIOLOGICAL END-POINTS AND CONSTRAINTS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE OPTIMIZATION; MODELING; TREATMENT PLANNING ID DOSE-VOLUME RESTRICTIONS; INVERSE PROBLEM; RADIOTHERAPY TREATMENT; BEAM WEIGHTS; VERIFICATION AB A new algorithm for the optimization of 3-dimensional radiotherapy plans is presented. The RONSC algorithm (Random Optimization with Non-linear Score functions and Constraints) is based on the idea of random search in the space of fesible solutions. RONSC takes advantage of some specific properties of the dose distribution and derivable information such as dose-volume histograms and calculated estimates of tumor control and normal tissue complication probabilities. The performance of the algorithm for clinical and test cases is discussed and compared with the performance of the simulated annealing algorithm, which is also based on the idea of random search. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,DIV RADIAT BIOPHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 50628, CA 21239] NR 33 TC 39 Z9 39 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 1 BP 89 EP 98 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HR986 UT WOS:A1992HR98600011 PM 1572834 ER PT J AU NIEMIERKO, A URIE, M GOITEIN, M AF NIEMIERKO, A URIE, M GOITEIN, M TI OPTIMIZATION OF 3D RADIATION-THERAPY WITH BOTH PHYSICAL AND BIOLOGICAL END-POINTS AND CONSTRAINTS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE OPTIMIZATION; BIOPHYSICAL MODELS; RADIOTHERAPY PLANNING ID TREATMENT PLANNING SYSTEM; DOSE-VOLUME HISTOGRAMS; COMPLICATION PROBABILITY; TREATMENT PLANS; MODEL AB A new optimization model is described and its clinical usefulness is demonstrated. The optimization technique was developed to allow computer optimization of 3-dimensional radiation therapy plans with biological models of tumor and normal tissue response to radiation as well as with scores based on physical dose. The emphasis was placed on the optimization model, which should describe, as closely as possible, the goal of the radiation treatment, which is eradication of the tumor while sparing normal tissues. Since the statement of the goals may vary from case to case, a technique that allows a variety of objective functions and types of constraints was developed. The optimization algorithm is capable of handling nonlinear and even discrete score (objective) functions and constraints and effectively explores the vast space of feasible solutions in a relatively short time (minutes of Micro Vax 3200 CPU time). An example of computer optimization of radiation therapy of a chordoma of the sphenoid bone using x-ray and proton beams is shown and compared with the best plans achieved by an experienced planner. Directions for future development of the algorithm, allowing optimization of beam orientation, are presented. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP NIEMIERKO, A (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,DIV RADIAT BIOPHYS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239, CA 50628] NR 22 TC 74 Z9 75 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 1 BP 99 EP 108 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HR986 UT WOS:A1992HR98600012 PM 1572836 ER PT J AU COIA, LR AARONSON, N LINGGOOD, R LOEFFLER, J PRIESTMAN, TJ AF COIA, LR AARONSON, N LINGGOOD, R LOEFFLER, J PRIESTMAN, TJ TI A REPORT OF THE CONSENSUS WORKSHOP PANEL ON THE TREATMENT OF BRAIN METASTASES SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE BRAIN METASTASES; PALLIATIVE RADIATION THERAPY; STEREOTAXIC RADIOSURGERY ID THERAPY-ONCOLOGY-GROUP; CENTRAL NERVOUS-SYSTEM; RADIATION-THERAPY; CEREBRAL METASTASES; LINEAR-ACCELERATOR; DOSE IRRADIATION; 1ST 2; RADIOTHERAPY; PALLIATION; MANAGEMENT AB The consensus workshop on management of brain metastases focused on several broad issues concerning the patient with brain metastases. These issues included: What are the goals of treatment? Who should not be treated with radiation? What are the optimal treatment regimens? What are the areas of controversy where future investigations may be useful? The brain consensus panel attempted to develop guidelines for radiation oncologists through use of a decision tree format. Existing data to support management decisions, particularly those regarding radiation treatment, were reviewed. Data regarding cost of treatment as well as data regarding explicit quality of life measures were felt to be very important but were largely not available and therefore played little scientific role in the guideline development. Areas where controversy existed and where consensus could not be reached were identified. C1 NETHERLANDS CANC INST,DIV PSYCHOSOCIAL RES & EPIDEMIOL,1066 CX AMSTERDAM,NETHERLANDS. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,BOSTON,MA 02115. WOLVERHAMPTON ROYAL HOSP,DEPT RADIOTHERAPY,WOLVERHAMPTON,ENGLAND. RP COIA, LR (reprint author), UNIV PENN,FOX CHASE CANC CTR,DEPT RADIAT ONCOL,7701 BURHOLME AVE,PHILADELPHIA,PA 19111, USA. NR 28 TC 62 Z9 63 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 1 BP 223 EP 227 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HR986 UT WOS:A1992HR98600030 PM 1572820 ER PT J AU GERWECK, LE KOUTCHER, JA ZAIDI, STH SENEVIRATNE, T AF GERWECK, LE KOUTCHER, JA ZAIDI, STH SENEVIRATNE, T TI ENERGY STATUS IN THE MURINE FSAII AND MCAIV TUMORS UNDER AEROBIC AND HYPOXIC CONDITIONS - AN INVIVO AND INVITRO ANALYSIS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE ENERGY STATUS; HYPOXIC CELL FRACTION; P-31-NMR ID P-31 NMR-SPECTROSCOPY; CELL FRACTION; X-IRRADIATION; FIBRO-SARCOMA; HYPERTHERMIA; OXYGEN; RADIOTHERAPY; SENSITIVITY; METABOLISM; PERFUSION AB The relationship between energy status and hypoxia was examined in two murine tumors with substantially different hypoxic cell fractions in situ and in cells derived from these tumors in vitro. Parameters of tumor energy status were NTP/P(i) and PCr/P(i) obtained by P-31-NMR spectroscopy and adenylate energy charge and energy status obtained by high-pressure liquid chromatographic analysis of tumor extracts. Adenylate energy charge and rates of high-energy phosphate degradation were determined on cells obtained from both tumor types (MCaIV and FSaII) under identical nutrient and oxygen conditions, that is, air and nitrogen for various durations (0-6 hr). No consistent or substantial differences were noted in the various parameters of tumor energy status obtained by nuclear magnetic resonance analysis or analysis of tumor extracts, even though the MCaIV contains a substantially larger hypoxic fraction (49% vs 12%). Under in vitro conditions, the two cell lines exhibited different responses to oxygen deprivation, the MCaIV being substantially more refractory to energy changes secondary to hypoxia. Noting with caution that this study is based on only two tumor types, our results suggest that differences in cellular capacity for energy maintenance preclude quantitative inferences regarding tumor oxygen status from energy status between tumor types. RP GERWECK, LE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-22860] NR 19 TC 16 Z9 16 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 3 BP 557 EP 561 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JA074 UT WOS:A1992JA07400010 PM 1612956 ER PT J AU SUIT, HD AF SUIT, HD TI LOCAL-CONTROL AND PATIENT SURVIVAL SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE LOCAL CONTROL; DISTANT METASTASIS; DISEASE FREE SURVIVAL ID RADIATION-THERAPY; CONSERVATIVE TREATMENT; BLADDER-CANCER; UTERINE CERVIX; UVEAL MELANOMA; SURGERY; CARCINOMA; ADENOCARCINOMA; SENSITIVITIES; IRRADIATION AB Consideration is given to the concern that future improvements in radiation therapy which achieve increases of local control probabilities will fail to yield gains in survival, in that the new local control patients will ultimately fail because of the development of distant metastasis. The concept is that the local failure merely represents a marker of the exceptionally malignant nature of the tumor; hence, elimination of the local tumor will not affect the ultimate outcome, viz distant failure. This would mean that all tumors which fail locally after the current best radiation therapy will have established distant metastasis (subclinical) at the time of treatment of the primary tumor in stage M0 patients. Thus, a more effective local treatment would not impact on the ultimate fate of the patient. Several lines of evidence are discussed which document that tumor free survival is greater after treatment which yields higher local control probabilities than those achieved by conventional external beam radiation therapy. That is, not all of the new local control patients develop distant metastasis. Consider the following points: (a) survival rates have increased during the history of radiation therapy as technical development provided the means of administering higher doses to the tumor involved tissues, for example, the shift from 140-180 kVp x-ray units of the 1920's to linear accelerators combined with complex treatment planning systems and modern imaging techniques of current standards of treatment; (b) the use of surgery in place of radiation for tumors for which conventional radiation therapy alone is quite ineffective has improved survival, for example, carcinoma of the gastrointestinal tract, kidney, ovary, squamous and adenocarcinoma of the lung, sarcoma of bone and soft tissues, etc.; (c) the addition of surgery to conventional external beam radiation therapy has also raised survival rates, for example, adenocarcinoma of the endometrium, Stage T III and IV carcinoma of the glottis and supraglottis; (d) the use of special techniques to administer higher radiation dose levels than is feasible with conventional fractionated radiation therapy alone have yielded higher survival rates in some instances, for example, external beam radiation therapy + brachytherapy for carcinoma of the uterine cervix, trans-anal 50 kVp x-ray beams for early stage carcinoma of the rectum (Papillon technique), proton beam therapy or radioactive plaques for uveal melanoma, proton beam techniques for sarcomas of the skull base, external beam radiation therapy + intraoperative electron beam radiation therapy for locally advanced carcinoma of the rectum, etc.; (e) long term disease free survivors are obtained by salvage surgery for local failures after radiation therapy in a worthwhile proportion of patients for many tumor categories; (f) the frequency of distant metastasis does not track "radiocurability" for example, seminoma versus glioblastoma multiforme; and (g) the limited evidence from laboratory studies shows no correlation between radiation sensitivity in vitro and spontaneous metastatic activity in vivo. These clinical findings do not suggest that the tumors which fail locally after conventional radiation therapy have established distant metastasis at the start of their local therapy. RP SUIT, HD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA113311] NR 38 TC 110 Z9 112 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 3 BP 653 EP 660 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JA074 UT WOS:A1992JA07400024 PM 1612967 ER PT J AU PERNOT, M MALISSARD, L TAGHIAN, A HOFFSTETTER, S LUPORSI, E FORCARD, JJ ALETTI, P BEY, P AF PERNOT, M MALISSARD, L TAGHIAN, A HOFFSTETTER, S LUPORSI, E FORCARD, JJ ALETTI, P BEY, P TI VELOTONSILLAR SQUAMOUS-CELL CARCINOMA - 277 CASES TREATED BY COMBINED EXTERNAL IRRADIATION AND BRACHYTHERAPY - RESULTS ACCORDING TO EXTENSION, LOCALIZATION, AND DOSE-RATE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 33RD MEETING OF THE AMERICAN SOC FOR THERAPEUTIC RADIOLOGY AND ONCOLOGY CY NOV 04-08, 1991 CL WASHINGTON, DC SP AMER SOC THERAPEUT RADIOL & ONCOL DE OROPHARYNX; RADIATION THERAPY; BRACHYTHERAPY; RESULTS; COMPLICATIONS ID RADIATION-THERAPY; SOFT PALATE; TONSILLAR REGION; OROPHARYNGEAL CARCINOMA; RADIOTHERAPY; FOSSA; UVULA; CANCER; TONGUE AB From 1977 to 1987, 277 patients with velotonsillar cancer (oropharyngeal cancer excluding base of tongue and valleculae) were treated by brachytherapy either alone (14 patients) or combined with external beam irradiation (263 patients) using a new afterloading Iridium-192 technique. The distribution of patients according to the localisation was as follows: 106 tonsillar region, 98 soft palate, 45 anterior pillar, 8 posterior pillar and 20 pharyngoglossal sulcus. According to the UICC TNM classification of 1979, the patients were staged as follows: 65 Tl, 103 T2, 101 T3, 8 TX. 172 patients were NO, 74 N1, 3 N2, 20 N3 et 8 NX. According to the tumor extension, the 5 year actuarial local control, locoregional control, specific survival* and overall survival by T stage (T1 165 pts], T2 [103 pts.], T3 1101 pts]) were respectively: local control: 89%, 86%, 69%; locoregional control: 84%, 80%, 67%; specific survival (excluding patients dead with intercurrent disease or second cancer): 78%, 62%, 46%; overall survival: 62%, 53%, 43%. No local recurrence was detected after 3 years. According to the localization, the tumors arising from the tonsillar region, the soft palate and the posterior pillars (A Group) had a better prognosis than the tumors arising from the anterior pillars and glossotonsillar sulcus (B Group). The complications were classified into four grades according to their extension and duration: Grade 1 (minor) with very small tissue ulcer which healed within 2 months with medical treatment (20%). Grade 2 (moderate) (5%), grade 3 (severe) (1.4%), grade 4 (fatal) (0.4%). The dose rate seemed to be relatively higher in patients with grade 2 and 3 complications (70 cGy per hour on average) versus the dose rate of patients without complications (50 cGy per hour) but the difference was not significant. In conclusion, the brachytherapy boost after external irradiation can be performed under favourable conditions with an acceptable rate of complications. It was set out in order to attempt to improve the local control of the tumor while preserving the salivary function and lessening the muscular fibrosis. It shows how experienced the team is, however only a randomized study would allow to state whether this technique brings about a real improvement especially as for tumors T2 or T3. C1 CTR ALEXIS VAUTRIN,DEPT RADIAT THERAPY,F-54500 VANDOEUVRE NANCY,FRANCE. CTR ALEXIS VAUTRIN,DEPT BIOSTAT,F-54500 VANDOEUVRE NANCY,FRANCE. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. RP PERNOT, M (reprint author), CTR ALEXIS VAUTRIN,DEPT BRACHYTHERAPY,F-54500 VANDOEUVRE NANCY,FRANCE. NR 53 TC 28 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 4 BP 715 EP 723 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JD828 UT WOS:A1992JD82800003 PM 1618663 ER PT J AU GALVIN, JM SMITH, AR MOELLER, RD GOODMAN, RL POWLIS, WD RUBENSTEIN, J SOLIN, LJ MICHAEL, B NEEDHAM, M HUNTZINGER, CJ KLIGERMAN, MM AF GALVIN, JM SMITH, AR MOELLER, RD GOODMAN, RL POWLIS, WD RUBENSTEIN, J SOLIN, LJ MICHAEL, B NEEDHAM, M HUNTZINGER, CJ KLIGERMAN, MM TI EVALUATION OF MULTILEAF COLLIMATOR DESIGN FOR A PHOTON-BEAM SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article AB Various aspects of multileaf collimator (MLC) design are examined relative to clinical requirements. The characteristics studied included: (a) irregular field edge definition or "effective" penumbra, (b) optimum field coverage for the multileaf portion of the field, and (c) leaf velocity. A film dosimetry technique was developed to measure the rapid 2-dimensional change in dose at an edge defined by a multileaf collimator with the segments staggered. The method applies a correction factor which allows for the changing ratio of scattered to primary photons at the field edge so that the energy dependence of the film is corrected. Stepped lead alloy blocks were irradiated with 6 MV photons to obtain films simulating a double-focused multileaf collimator, and the results were compared to films of fields shaped with standard divergent blocks. The effect of the shape of the leaf face (the end of the leaf) on penumbra was also studied. Proper shaping of the leaf ends may eliminate the need to exactly match beam divergence so that the mechanical mechanism of the collimator system is simplified. Leaves having several different end shapes and moving horizontally to intercept a vertical beam were compared to the divergent design where a straight face moves along an arc. The measurements showed that the "effective" penumbra (measured as the distance from the 80 to 20% isodose lines) for the multileaf collimator is a function of the angle between the direction of leaf motion and the edge defined by the leaves. In addition, all leaf end shapes showed some increase in penumbra compared to standard divergent blocking and also had increasing penumbra width as they moved over or back from the field center line. A total of 459 treatment fields and six disease sites were examined to determine the percentage of fields potentially shaped by multileaf segments of specified length. This study showed 93% of the fields had lengths of 30 cm or less and 99% had widths of 25 cm or less. A study conducted to determine the required leaf velocity to shape various target volume configurations during complete rotation (at 1 RPM) showed that a leaf speed of at least 1.5 cm/sec at isocenter is needed for dynamic comformal treatment. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. VARIAN ASSOCIATES INC,DIV RADIAT,PALO ALTO,CA 94303. HOSP UNIV PENN,SCH MED,DEPT RADIAT ONCOL,PHILADELPHIA,PA 19104. RADIAT THERAPY REG CTR,FT MYERS,FL. FOX CHASE CANC INST,DEPT RADIAT THERAPY,PHILADELPHIA,PA 19111. RP GALVIN, JM (reprint author), NYU,TISCH HOSP,SCH MED,DEPT RADIAT ONCOL,DIV RADIAT ONCOL,566 1ST AVE,NEW YORK,NY 10016, USA. NR 4 TC 66 Z9 66 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 4 BP 789 EP 801 PG 13 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JD828 UT WOS:A1992JD82800012 PM 1618672 ER PT J AU BAUMANN, M DUBOIS, W PU, A FREEMAN, J SUIT, HD AF BAUMANN, M DUBOIS, W PU, A FREEMAN, J SUIT, HD TI RESPONSE OF XENOGRAFTS OF HUMAN-MALIGNANT GLIOMAS AND SQUAMOUS-CELL CARCINOMAS TO FRACTIONATED-IRRADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE HUMAN TUMOR XENOGRAFTS; MALIGNANT GLIOMA; SQUAMOUS CELL CARCINOMA; FRACTIONATED RADIOTHERAPY; TCD50; GROWTH DELAY; SF2 ID LOCAL TUMOR-CONTROL; NCR/SED NUDE-MICE; RADIATION SENSITIVITY; RADIOSENSITIVITY; GLIOBLASTOMA; RADIORESPONSIVENESS; RADIOTHERAPY; INVIVO; MURINE; LINES AB The response of xenografts of five human malignant glioma cell lines and two human squamous cell carcinomas to fractionated irradiation was studied. For this, the tumors were transplanted into nude mice which had been further immunosuppressed by 6 Gy whole-body irradiation. Radiation was given as 30 fractions applied under normal blood flow conditions in two sessions per day over 15 days. Absolute and specific tumor growth delay after 48 Gy, and tumor control dose 50% (TCD50) were evaluated. Using local tumor control as experimental endpoint, four out of five malignant gliomas were more resistant to fractionated radiation therapy than the two squamous cell carcinomas. The TCD50s of these four gliomas ranged from 73 Gy to more than 120 Gy, whereas the TCD50s of the squamous cell carcinomas were 51 and 60 Gy. Absolute tumor growth delay correlated well with TCD50, but no correlation was obtained between specific growth delay and TCD50. The response of the human tumor xenografts in vivo did not correlate with the surviving fractions at 2 Gy of the same cell lines in vitro which have been previously obtained in our laboratory. The results suggest that the unique radioresistance observed in malignant gliomas in patients is at least in part reflected in human tumor xenografts. The lack of correlation between the surviving fraction at 2 Gy in vitro and the tumor response in vivo could be a consequence of an immune response by the host, a difference in cell radiation sensitivity between cell lines and xenografted tumors, or of differences of parameters such as hypoxic fraction, rate of repopulation, and cell cycle effects between the different tumor lines studied. It illustrates the difficulties which might be involved in the prediction of the response of individual tumors to radiation therapy based solely on the intrinsic radiosensitivity of the tumor cells as assayed by in vitro assays of colony formation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114. FU NCI NIH HHS [CA 13311] NR 36 TC 41 Z9 42 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 4 BP 803 EP 809 PG 7 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JD828 UT WOS:A1992JD82800013 PM 1319979 ER PT J AU URANO, M ABE, Y AF URANO, M ABE, Y TI LATE REACTION FOLLOWING TWICE-A-DAY IRRADIATIONS IN THE MURINE FOOT - POSSIBLE REPOPULATION OR CONSEQUENTIAL LATE EFFECT SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE LATE RADIATION EFFECT; FOOT REACTION; FRACTIONATION; FIBROSIS; CONSEQUENTIAL LATE EFFECT; REPOPULATION; C3H MOUSE ID RAT SPINAL-CORD; NECK-CANCER; MOUSE LUNG; ACCELERATED FRACTIONATION; DOSE FRACTIONATION; RADIATION RESPONSE; INCOMPLETE REPAIR; LOCAL-CONTROL; X-RAYS; RADIOTHERAPY AB The effect of twice-a-day irradiation on the foot reaction was studied in C3Hf/Sed mice. A numerical scoring system was used to evaluate the foot reaction that became visible shortly after irradiation. Peak reaction occurred on the 21st to 23rd day and reappeared after approximately the 200th postirradiation day. These reactions are called early- and late-appearing reactions, respectively. Animals studied for early-appearing reactions were continuously scored for more than 600 days after irradiation. The late-appearing reaction increased continuously or remained constant, but never decreased during the course of the experiments. Animal feet were irradiated with a fraction size from 1.0 to 5.0 Gy twice-a-day daily with a treatment interval of 6 and 18 hours, and varying numbers of fractions were given. A top-up dose of 20 Gy was given as the last dose. The late-appearing foot reaction following a fraction size of 1.5 Gy or greater increased with increasing total dose. However, the increase in the late reaction score with increasing total dose was trivial following multiple doses with a fraction size of 1.0 Gy, suggesting a possible repopulation during prolonged irradiation or that the observed reaction was a consequential late effect. The Fe-plot based on doses which induced fibrosis in one-half of the irradiated animals, showed an alpha/beta ratio of 6.57 +/- 0.62 Gy, and the presence of a breaking point at approximately 1.5 Gy. The alpha/beta ratios calculated by Joiner 's method and Thames direct analysis were identical. The slope of the Fe-plot below 1.5 Gy was significantly steeper than that above 1.5 Gy. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. RP URANO, M (reprint author), UNIV KENTUCKY,MED CTR,DEPT RADIAT MED,800 ROSE ST,LEXINGTON,KY 40536, USA. FU NCI NIH HHS [CA 26350] NR 36 TC 1 Z9 1 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 23 IS 4 BP 847 EP 852 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA JD828 UT WOS:A1992JD82800018 PM 1618676 ER PT J AU SUIT, HD AF SUIT, HD TI NCI PROTON WORKSHOP - POTENTIAL CLINICAL GAINS BY USE OF SUPERIOR RADIATION-DOSE DISTRIBUTION - EDITORS NOTE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material ID THERAPY RP SUIT, HD (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 2 BP 233 EP 234 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GX876 UT WOS:A1992GX87600001 PM 1310960 ER PT J AU TATSUZAKI, H URIE, MM LINGGOOD, R AF TATSUZAKI, H URIE, MM LINGGOOD, R TI COMPARATIVE TREATMENT PLANNING - PROTON VS X-RAY-BEAMS AGAINST GLIOBLASTOMA-MULTIFORME SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT WORKSHOP ON POTENTIAL CLINICAL GAINS BY USE OF SUPERIOR RADIATION DOSE DISTRIBUTION CY APR 27-29, 1989 CL NCI, BETHESDA, MD HO NCI DE GLIOBLASTOMA MULTIFORME; PROTON BEAM THERAPY; COMPARATIVE TREATMENT PLANNING ID MALIGNANT GLIOMAS; RADIATION-THERAPY; RANDOMIZED COMPARISONS; FINAL REPORT; RADIOTHERAPY; SURGERY; PROCARBAZINE; CARMUSTINE; ANATOMY; TRIAL AB The survival of patients with glioblastoma multiforme is extremely poor, the 5-year survival rate being almost zero. The cause of failure is almost exclusively local progression of tumor, the remainder is due to complications of treatment. Although this tumor is clearly radiation resistant, there is evidence of a dose response relationship. Using a thin slice CT scan of the entire head of a patient with glioblastoma mutiforme, 3-dimensional radiation treatment plans were developed for treatment to a dose of 90 cobalt-Gray-equivalent (CGE). Dose distributions using protons were compared to those using x-rays. The results showed advantages for the proton beam technique. Namely the proton plan irradiated less non-target brain than the x-ray plan; this was especially so in the decrease of coverage of deep-seated structures. The volume of non-target brain that received more than 70 CGE was 175 ml for the x-ray plan and 94 ml for the proton plan. This study indicates that for a subpopulation of patients with glioblastoma multiforme, at least 90 CGE could be delivered with proton beam techniques to the target with only small volumes of normal brain structures receiving more than 70 CGE. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. FU NCI NIH HHS [CA-21239] NR 26 TC 28 Z9 28 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 2 BP 265 EP 273 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GX876 UT WOS:A1992GX87600007 PM 1310962 ER PT J AU MIRALBELL, R CROWELL, C SUIT, HD AF MIRALBELL, R CROWELL, C SUIT, HD TI POTENTIAL IMPROVEMENT OF 3 DIMENSION TREATMENT PLANNING AND PROTON THERAPY IN THE OUTCOME OF MAXILLARY SINUS CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT WORKSHOP ON POTENTIAL CLINICAL GAINS BY USE OF SUPERIOR RADIATION DOSE DISTRIBUTION CY APR 27-29, 1989 CL NCI, BETHESDA, MD HO NCI DE MAXILLARY SINUS; PROTON BEAM THERAPY; COMPARATIVE TREATMENT PLANNING ID RADIATION-THERAPY; MALIGNANT-TUMORS; NASAL CAVITY; OPTIC-NERVE; CARCINOMA; RADIOTHERAPY; IRRADIATION; ANTRUM; SURGERY; EYE AB Carcinomas arising in the maxillary sinus are challenging technical problems for radiotherapists due to the complexity of the regional anatomy and the close relations of the tumor to dose-limiting critical structures (eyes, optic nerves, optic chiasm, and brain stem). This study shows that an improvement in the dose distribution can be achieved with the use of three dimensional treatment planning and a combination of x-ray and proton beam arrangements. Although tumor coverage was identical when comparing dose distributions of X rays alone to X rays plus proton beam boost, the critical structures received less dose in the X rays plus proton beam plan. Because a superior dose distribution should yield an improved local control and reduced morbidity, a benefit in survival could be expected. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,CYCLOTRON LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA21239-12] NR 26 TC 29 Z9 29 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 2 BP 305 EP 310 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GX876 UT WOS:A1992GX87600011 PM 1310965 ER PT J AU TATSUZAKI, H URIE, MM WILLETT, CG AF TATSUZAKI, H URIE, MM WILLETT, CG TI 3-D-COMPARATIVE STUDY OF PROTON VS X-RAY-RADIATION THERAPY FOR RECTAL-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT WORKSHOP ON POTENTIAL CLINICAL GAINS BY USE OF SUPERIOR RADIATION DOSE DISTRIBUTION CY APR 27-29, 1989 CL NCI, BETHESDA, MD HO NCI DE PROTON RADIATION THERAPY; RECTAL CARCINOMA; COMPARATIVE TREATMENT PLANNING ID POSTOPERATIVE RADIOTHERAPY; CURATIVE SURGERY; ADENOCARCINOMA; COMPLICATIONS; CARCINOMA; CERVIX AB To assess the usefulness of proton beams for treatment of patients with rectal cancer, we have performed comparative 3D treatment planning for proton beam and x-ray beam therapy. Three common x-ray techniques (AP-PA, 3-field, and 4-field box), a proton beam only plan, and a proton boost plan were compared. The plan which would have been treated without the aid of the 3D planning system was also simulated. Dose distributions were analyzed and dose-volume histograms computed for the target volumes and critical normal tissues. Analyses of these plans demonstrate that the proton beam techniques reduce the volume of small bowel irradiated. This may allow higher doses to be delivered to the tumor, with a probable increase in local control, or a reduction in normal tissue complications probability. All the plans developed with the 3D planning system treated significantly less bowel than the one planned without it. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. FU NCI NIH HHS [CA-21239] NR 29 TC 31 Z9 31 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 2 BP 369 EP 374 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA GX876 UT WOS:A1992GX87600020 PM 1310972 ER PT J AU BUMP, EA COLEMAN, CN CERCE, BA MCGINNIS, DJ AF BUMP, EA COLEMAN, CN CERCE, BA MCGINNIS, DJ TI SENSITIZATION OF CHINESE-HAMSTER OVARY CELLS TO MELPHALAN BY ETANIDAZOLE UNDER INTERMITTENT HYPOXIA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE SR-2508; ETANIDAZOLE; MELPHALAN; HYPOXIA; SENSITIZERS ID CYTO-TOXICITY; CHEMOTHERAPEUTIC-AGENTS; SOLID TUMORS; MISONIDAZOLE; CHEMOSENSITIZATION; RADIOSENSITIZER; GLUTATHIONE; SR-2508; 1-METHYL-2-NITROSOIMIDAZOLE; ENHANCEMENT AB Incubation of Chinese hamster ovary cells with etanidazole under hypoxic conditions increases cell killing by subsequent treatment with melphalan under aerobic conditions. We report here that this sensitization can be achieved even if periods of hypoxia are interrupted by reoxygenation. Preincubation under hypoxia in the absence of etanidazole also results in sensitization to melphalan. Intermittent hypoxia is less effective than continuous hypoxia as a single sensitizing factor. Glutathione depletion does not appear to have more than an additive effect on chemosensitization by etanidazole. These results suggest that prolonged treatment with low doses of etanidazole may be a more effective strategy for clinical chemosensitization than a short exposure to a higher dose, in order to target intermittently as well as chronically hypoxic cells. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP HARVARD UNIV, SCH MED, JOINT CTR RADIAT THERAPY, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA 42391] NR 31 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 EI 1879-355X J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 4 BP 731 EP 735 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HJ377 UT WOS:A1992HJ37700022 PM 1531977 ER PT J AU MAJIMA, H URANO, M SOUGAWA, M KAHN, J AF MAJIMA, H URANO, M SOUGAWA, M KAHN, J TI RADIATION AND THERMAL SENSITIVITIES OF MURINE TUMOR (FSA-II) CELLS RECURRENT AFTER A HEAVY IRRADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE RADIOSENSITIVITY; THERMAL SENSITIVITY; RECURRENT TUMOR; FSA-II TUMOR ID SURVIVAL CURVES; INITIAL SLOPE; BREAST-CANCER; HYPERTHERMIA; MELANOMA; RADIORESPONSIVENESS; RADIOSENSITIVITY; RADIOTHERAPY; INVIVO; CARCINOMAS AB Radiation and thermal sensitivities, and cell doubling times (Tds) of C3Hf/Sed mouse FSa-II cells recurring after a heavy irradiation were examined in vitro. Tumors in the leg were irradiated with gamma-rays and observed for late recurrence (in vivo clones), or removed immediately after irradiation and single cell suspensions were plated for colony formation (in vitro clones). Five subclones were selected from original cells in vitro. Survival curves were fitted to the multi-target and linear quadratic models. Surviving fractions at 2 (SF2) and 10 Gy (SF10) irradiations, and those at 30 and 60 min heatings at 44-degrees-C (SF30 and SF60), were obtained for each clone. Although, Tds of subclones were slightly longer than those of the parental cells, those of recurrent clones were prolonged substantially with an exception of one cell line. Radiosensitivities of FSa-II parental cells tested in vitro and in vivo were equally radioresistant. Thermal sensitivities of parental cells tested in vitro and in vivo were also identical. All subclones were more radiosensitive compared to the parental cells. The in vitro recurrent clones showed smaller D0 (radiation dose to reduce survival from S to S/e in the exponential portion of survival curve) than the D0 of the parental cells. The SF2 values of four in vitro recurrent clones were greater than that of the parental cells whereas those of two lines were smaller. It was of interest that the in vivo recurrent tumor cells showed a wide variation in the radiation sensitivity. Among 9 tumor cell lines examined, 4 lines were more sensitive and 4 were more resistant compared to the original. FSa-II subclones as well as both in vitro and in vivo recurrent clones showed a wide variation in thermal sensitivity. No consistent changes in the shoulder or in the slope were found. The SF30 or SF60 showed that 5 out of 9 in vivo recurrent clones and 4 out of 9 in vitro clones were more resistant compared to the original cells. No correlation was observed between thermal and radiation sensitivities. The Td was not related with radiation or thermal sensitivity. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,EDWIN L STEEL LAB,BOSTON,MA 02114. FU NCI NIH HHS [CA 26350] NR 40 TC 10 Z9 10 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 5 BP 1019 EP 1028 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HN407 UT WOS:A1992HN40700027 PM 1555947 ER PT J AU WANG, CC AF WANG, CC TI UNNECESSARY MORBIDITY FOLLOWING IRRADIATION OF LATERALIZED HEAD AND NECK-CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material RP WANG, CC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 4 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 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 5 BP 1155 EP 1156 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HN407 UT WOS:A1992HN40700048 PM 1555968 ER PT J AU CHOI, NC AF CHOI, NC TI CONTROVERSIES IN THE ROLE OF POSTOPERATIVE RADIOTHERAPY IN STAGE-II AND STAGE-IIIA RESECTED NON-SMALL-CELL LUNG-CARCINOMA - REPLY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Letter ID BRONCHOGENIC-CARCINOMA; IRRADIATION; CANCER RP CHOI, NC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PY 1992 VL 22 IS 5 BP 1162 EP 1163 PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HN407 UT WOS:A1992HN40700053 ER PT J AU LEE, A PHILLIPS, MW OROURKE, JL PASTER, BJ DEWHIRST, FE FRASER, GJ FOX, JG SLY, LI ROMANIUK, PJ TRUST, TJ KOUPRACH, S AF LEE, A PHILLIPS, MW OROURKE, JL PASTER, BJ DEWHIRST, FE FRASER, GJ FOX, JG SLY, LI ROMANIUK, PJ TRUST, TJ KOUPRACH, S TI HELICOBACTER-MURIDARUM SP-NOV, A MICROAEROPHILIC HELICAL BACTERIUM WITH A NOVEL ULTRASTRUCTURE ISOLATED FROM THE INTESTINAL-MUCOSA OF RODENTS SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID CAMPYLOBACTER-PYLORIDIS; SPIRAL BACTERIUM; GASTRIC-MUCOSA; GASTROENTERITIS; MICROORGANISMS; INFECTION; ABORTION; MUSTELAE AB Helical organisms with novel ultrastructural characteristics were isolated from the intestinal mucosa of rats and mice. These bacteria were characterized by the presence of 9 to 11 periplasmic fibers which appeared as concentric helical ridges on the surface of each cell. The cells were motile with a rapid corkscrewlike motion and had bipolar tufts of 10 to 14 sheathed flagella. The bacteria were microaerophilic, nutritionally fastidious, and physiologically similar to Helicobacter species and Wolinella succinogenes but could be differentiated from these organisms by their unique cellular ultrastructure. Using 16S rRNA sequencing, we found that strain ST1T (T = type strain) was related to previously described Helicobacter species, "Flexispira rappini," and W. succinogenes. The closest relatives of strain ST1T were Helicobacter mustelae and "F. rappini" (average similarity value, 96%). On the basis of phylogenetic data, strain ST1T (= ATCC 49282T) represents a new species of the genus Helicobacter, for which we propose the name Helicobacter muridarum. C1 UNIV NEW S WALES,ELECTRON MICROSCOPY UNIT,KENSINGTON,NSW 2033,AUSTRALIA. FORSYTH DENT CTR,BOSTON,MA 02115. MIT,CAMBRIDGE,MA 02139. UNIV QUEENSLAND,DEPT MICROBIOL,ST LUCIA,QLD 4067,AUSTRALIA. UNIV VICTORIA,DEPT BIOCHEM & MICROBIOL,VICTORIA V8W 2Y2,BC,CANADA. RP LEE, A (reprint author), UNIV NEW S WALES,SCH MICROBIOL & IMMUNOL,KENSINGTON,NSW 2033,AUSTRALIA. RI Romaniuk, Ryszard/B-9140-2011 OI Romaniuk, Ryszard/0000-0002-5710-4041 NR 44 TC 150 Z9 153 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD JAN PY 1992 VL 42 IS 1 BP 27 EP 36 PG 10 WC Microbiology SC Microbiology GA GZ716 UT WOS:A1992GZ71600005 PM 1736969 ER PT J AU SHOWERS, MO DANDREA, AD AF SHOWERS, MO DANDREA, AD TI SUBUNIT STRUCTURE AND TRANSMEMBRANE SIGNALING OF THE ERYTHROPOIETIN RECEPTOR SO INTERNATIONAL REVIEW OF CYTOLOGY-A SURVEY OF CELL BIOLOGY LA English DT Review ID COLONY-STIMULATING FACTOR; FOCUS-FORMING VIRUS; RECOMBINANT HUMAN ERYTHROPOIETIN; MURINE ERYTHROLEUKEMIA-CELLS; ERYTHROID PROGENITOR CELLS; TYROSINE KINASE-ACTIVITY; BETA-CHAIN; INTERLEUKIN-2 RECEPTOR; EXPRESSION CLONING; MOLECULAR-CLONING C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. NR 95 TC 5 Z9 5 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 0074-7696 J9 INT REV CYTOL JI Int.Rev.Cytol. PY 1992 VL 137B BP 99 EP 120 PG 22 WC Cell Biology SC Cell Biology GA ME105 UT WOS:A1992ME10500004 PM 1336006 ER PT J AU HARRIS, NL AF HARRIS, NL TI DIFFERENTIAL-DIAGNOSIS BETWEEN HODGKINS-DISEASE AND NON-HODGKINS-LYMPHOMA SO INTERNATIONAL REVIEW OF EXPERIMENTAL PATHOLOGY LA English DT Review ID REED-STERNBERG CELLS; RECEPTOR GENE REARRANGEMENTS; TRANSFORMED GERMINAL-CENTERS; T-CELL; MONOCLONAL-ANTIBODIES; NODULAR PARAGRANULOMA; CD30 EXPRESSION; ANTIGEN; PREDOMINANCE; IMMUNOHISTOCHEMISTRY RP HARRIS, NL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114, USA. NR 40 TC 9 Z9 10 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 0074-7718 J9 INT REV EXP PATHOL JI Int. Rev. Exp. Pathol. PY 1992 VL 33 BP 1 EP 25 PG 25 WC Pathology SC Pathology GA MC968 UT WOS:A1992MC96800001 PM 1733868 ER PT J AU CALONGE, M NG, B ALLANSMITH, MR BLOCH, KJ AF CALONGE, M NG, B ALLANSMITH, MR BLOCH, KJ TI VASCULAR-PERMEABILITY DURING THE EARLY AND LATE PHASES OF OCULAR ANAPHYLAXIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE EARLY-PHASE REACTION; GUINEA PIG IMMUNOGLOBULIN G1 ANTIBODY; LATE-PHASE REACTION; OCULAR ANAPHYLAXIS; VASCULAR PERMEABILITY ID GUINEA-PIGS; ANTIGEN CHALLENGE; RAT; RESPONSES; ANTIBODIES; HISTAMINE; IMMEDIATE; ALLERGY; INVIVO; SKIN AB The role of enhanced vascular permeability in a model of ocular anaphylaxis was investigated during both early- and late-phase reactions (EPR and LPR). Vascular permeability was assessed by measuring the extravascular retention of I-125-bovine serum albumin (I-125-BSA) in ocular tissues. Ten groups of guinea pigs (n = 5-12 per group) were injected with dinitrophenylated (DNP) bovine gamma globulin emulsified in Freund's adjuvants and challenged after a 4-week interval by topical application of di-DNP-lysine to one eye and phosphate-buffered saline to the other eye. Thereafter, the eyes were examined and the animals were killed at different intervals after topical challenge. They were injected intravenously with I-125-BSA 0.5 hr before death. Retained radioactivity was measured separately in four tissues. The EPR (period between 0.5-1.5 hr after challenge) was characterized by enhanced retention of radioactivity in lids, conjunctiva, and orbital content. There was no significant retention of extravascular radioactivity in the globe and lacrimal gland. Thereafter (period between 2-3.5 hr after challenge), retained radioactivity was significantly diminished. The subsequent period, between 4.5-6.5 hr (LPR), was characterized by a smaller, although significant, increment of radioactivity retained in lids and conjunctiva but not in the other tissues examined. These findings indicate that enhanced microvascular permeability occurs during two phases in actively immunized guinea pigs challenged topically with di-DNP-lysine and that these phases correspond to the clinical signs that constitute the EPR and LPR of ocular anaphylaxis. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GEN MED SERV,CLIN IMMUNOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,RETINA FDN,EYE RES INST,IMMUNOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED SERV,ALLERGY UNIT,BOSTON,MA 02114. RI Calonge, Margarita/K-2839-2014 OI Calonge, Margarita/0000-0001-8178-4836 FU NEI NIH HHS [EY02099]; NIADDK NIH HHS [AM33506] NR 26 TC 2 Z9 2 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD JAN PY 1992 VL 33 IS 1 BP 55 EP 59 PG 5 WC Ophthalmology SC Ophthalmology GA HA137 UT WOS:A1992HA13700008 PM 1730548 ER PT J AU LAWRENCE, V MATTHAI, W HARTMAIER, S AF LAWRENCE, V MATTHAI, W HARTMAIER, S TI COMPARATIVE SAFETY OF HIGH-OSMOLALITY AND LOW-OSMOLALITY RADIOGRAPHIC CONTRAST AGENTS - REPORT OF A MULTIDISCIPLINARY WORKING GROUP SO INVESTIGATIVE RADIOLOGY LA English DT Article ID ACUTE RENAL DYSFUNCTION; HIGH-RISK PATIENTS; CARDIAC ANGIOGRAPHY; CORONARY ANGIOGRAPHY; ADVERSE REACTIONS; INTRAVENOUS UROGRAPHY; EXCRETORY UROGRAPHY; PROSPECTIVE TRIAL; MEDIA; COMPLICATIONS C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. COOPER HOSP UNIV MED CTR,ROBERT WOOD JOHNSON MED SCH,CAMDEN,NJ. UNIV N CAROLINA,SCH PUBL HLTH,DEPT EPIDEMIOL,CHAPEL HILL,NC 27514. RP LAWRENCE, V (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 85 TC 54 Z9 55 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD JAN PY 1992 VL 27 IS 1 BP 2 EP 28 DI 10.1097/00004424-199201000-00002 PG 27 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GX894 UT WOS:A1992GX89400002 PM 1733876 ER PT S AU SWEADNER, KJ ARYSTARKHOVA, E AF SWEADNER, KJ ARYSTARKHOVA, E BE Scarpa, A Carafoli, E Papa, S TI CONSTRAINTS ON MODELS FOR THE FOLDING OF THE NA,K-ATPASE SO ION-MOTIVE ATPASES : STRUCTURE, FUNCTION, AND REGULATION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON ION-MOTIVE ATPASES : STRUCTURE, FUNCTION, AND REGULATION CY JUN 13-17, 1992 CL CLEVELAND, OH SP NEW YORK ACAD SCI, ICI ITALIA, INT UNION BICHEM & MOLEC BIOL, INT UNION PURE & APPL BIOPHYS, ABBOTT LABS, AMER CANC SOC, CUYAHOGA CTY DIV, AMER CYANAMID, CLEVELAND CLIN FDN, CLEVELAND FDN, CASE W RESEARVE UNIV SCH MED RP SWEADNER, KJ (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN 4,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 20 Z9 20 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-770-0 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1992 VL 671 BP 217 EP 227 DI 10.1111/j.1749-6632.1992.tb43798.x PG 11 WC Biochemistry & Molecular Biology; Physiology SC Biochemistry & Molecular Biology; Physiology GA BX33M UT WOS:A1992BX33M00020 PM 1283814 ER PT J AU BENNETT, CL PASCAL, A CVITANIC, M GRAHAM, V KITCHENS, A DEHOVITZ, JA AF BENNETT, CL PASCAL, A CVITANIC, M GRAHAM, V KITCHENS, A DEHOVITZ, JA TI MEDICAL-CARE COSTS OF INTRAVENOUS-DRUG-USERS WITH AIDS IN BROOKLYN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE INPATIENT CHARGES; MEDICAID; MEDICAL COSTS; OUTPATIENT CHARGES ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; FORECASTS AB This article reports on a study of medical costs of intravenous drug users (IVDUs) with acquired immune deficiency syndrome (AIDS) in Brooklyn, NY, U.S.A. Sociodemographic and clinical data as well as information on medical resource use was gathered for 38 IVDUs with AIDS, all of whom belonged to minority racial/ethnic groups and were covered by Medicaid insurance. Data obtained through patient interviews and review of medical records indicated that the sample had mean annual medical charges of $33,002 per patient per year. Average inpatient charges were $24,171, with an average of 1.13 hospitalizations and 38.5 days of in-hospital care. Significantly more in-hospital care and higher inpatient changes on average were noted among patients who did not have a stable housing environment. Outpatient charges averaged $8,831, with 80% for pharmaceuticals. This estimate of medical charges and resource use, one of the first developed in a cohort of nonwhite individuals with i.v. drug use as a risk factor for human immunodeficiency virus infection, is about one third less than recent estimates reported from studies of cohorts of white homosexual men. C1 RAND CORP,SANTA MONICA,CA 90406. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM HOSP,SCH MED,DEPT MED,LOS ANGELES,CA 90024. VET ADM,WESTERN REG SPECIAL STUDIES GRP,LOS ANGELES,CA. SUNY HLTH SCI CTR,DEPT PREVENT MED,BROOKLYN,NY. KINGS CTY HOSP CTR,BROOKLYN,NY 11203. SUNY HLTH SCI CTR,DEPT COMMUNITY HLTH & MED,BROOKLYN,NY. RI Bennett, Charles/C-2050-2008 FU AHRQ HHS [1R01HS06494-01]; PHS HHS [6130] NR 22 TC 68 Z9 68 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN PY 1992 VL 5 IS 1 BP 1 EP 6 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GW913 UT WOS:A1992GW91300001 PM 1738078 ER PT J AU LEKUTIS, C OLSHEVSKY, U FURMAN, C THALI, M SODROSKI, J AF LEKUTIS, C OLSHEVSKY, U FURMAN, C THALI, M SODROSKI, J TI CONTRIBUTION OF DISULFIDE BONDS IN THE CARBOXYL TERMINUS OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-I GP120 GLYCOPROTEIN TO CD4 BINDING SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE GP120 GLYCOPROTEIN; CARBOXYL TERMINUS; CD4 RECEPTOR; DISULFIDE BONDS; CYSTEINE RESIDUES ID ENVELOPE GLYCOPROTEIN; RECEPTOR-BINDING; HTLV-III; T4 MOLECULE; HIV; RESIDUES; AIDS; SITE; IDENTIFICATION; RETROVIRUS AB The carboxyl half of the HIV-1 gp120 glycoprotein, which has been implicated in binding to the CD4 receptor, contains two disulfide bonds linking cysteine residues 378-445 and 385-418. To examine the necessity of these disulfide bonds for the formation and/or maintenance of a gp120 glycoprotein competent for CD4 binding, we created mutants of a soluble form of gp120 in which combinations of these cysteine residues were altered. The mutant glycoproteins were examined for export from the expressing cell and for CD4 binding ability. Mutant gp120 molecules lacking both disulfide bonds were not stably expressed or exported. However, mutants for which either disulfide bond could form were exported and were fully competent for CD4 binding. In some cases, the presence of one of the pair of linked cysteines exerted more detrimental effects on export or CD4 binding than did alteration of both cysteines. Thus, the evaluation or the contribution of a particular disulfide bond to a phenotype should include studies in which both cysteines involved in the bond are simultaneously altered. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,JF 621,44 BINNEY ST,BOSTON,MA 02115. FU NIAID NIH HHS [AI 24755] NR 35 TC 13 Z9 14 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JAN PY 1992 VL 5 IS 1 BP 78 EP 81 PG 4 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA GW913 UT WOS:A1992GW91300013 PM 1738091 ER PT J AU OTTO, MW POLLACK, MH SACHS, GS ROSENBAUM, JF AF OTTO, MW POLLACK, MH SACHS, GS ROSENBAUM, JF TI HYPOCHONDRIACAL CONCERNS, ANXIETY SENSITIVITY, AND PANIC DISORDER SO JOURNAL OF ANXIETY DISORDERS LA English DT Article ID DSM-III HYPOCHONDRIASIS; PSYCHOMETRIC PROPERTIES; BEHAVIORAL TREATMENT; AGORAPHOBIA; ATTACKS; FEARS; DEPRESSION; BELIEFS; HYPERVENTILATION; INVENTORY AB Many panic disorder patients have significant levels of hypochondriacal concerns. The present study investigated the relationship between specific symptom characteristics and hypochondriacal concerns in a sample of 50 panic disorder patients at different stages of treatment and recovery. Of the symptom characteristics examined -- anxious mood, depressed mood, anxiety sensitivity, current number of panic attacks, and degree of phobic avoidance -- hypochondriacal concerns were most highly associated with anxiety sensitivity. This finding is discussed in relation to the role of catastrophic interpretations of somatic symptoms in panic disorder and hypochondriasis. Treatment implications are discussed. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,BOSTON,MA 02114, USA. NR 53 TC 68 Z9 69 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PY 1992 VL 6 IS 2 BP 93 EP 104 DI 10.1016/0887-6185(92)90008-U PG 12 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA HP125 UT WOS:A1992HP12500001 ER PT J AU STEINBERG, BD GELBERMAN, RH MANKIN, HJ ROSENBERG, AE AF STEINBERG, BD GELBERMAN, RH MANKIN, HJ ROSENBERG, AE TI EPITHELIOID SARCOMA IN THE UPPER EXTREMITY SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID LIGHT AB Eighteen patients who had epithelioid sarcoma in the upper extremity were divided into two groups on the basis of treatment: marginal resection of the tumor or wide or radical resection of the tumor. Historical, demographic, histological, and staging data were recorded and were correlated with the type of treatment and the outcome. Marginal resection (excision through the reactive zone or pseudocapsule surrounding the tumor, with confirmation of a negative margin by a pathologist), with or without adjuvant therapy, led to a dismal outcome in patients who had been treated in this manner initially or secondarily (fifteen failures after seventeen procedures). Disease-free survival at ten years was significantly improved when wide resection (intracompartmental en bloc excision with a cuff of normal tissue of more than three centimeters) or radical resection was either the initial or the secondary treatment; success then was noted in nine of thirteen operations. Of twelve patients in whom a marginal resection had been done initially, three had had a recurrence, three had had a metastasis, and five had died, at a mean follow-up of seven years (range, twenty-seven months to sixteen years). At a mean follow-up of six years (range, two to fifteen years), only one of five patients in whom a secondary lesion had been treated with marginal resection was free of disease. Of the six patients who had been treated with wide or radical resection initially, none had died, one had had a recurrence, and one had had a metastasis, at a mean follow-up of seven years (range, twenty-two months to fourteen years). Of seven patients in whom a wide or radical resection had been performed secondarily for recurrence or metastasis, five had survived without additional evidence of disease at a mean follow-up of 4.7 years (range, thirty months to fourteen years). C1 MASSACHUSETTS GEN HOSP,WACC-527,BOSTON,MA 02114. NR 19 TC 27 Z9 28 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD JAN PY 1992 VL 74A IS 1 BP 28 EP 35 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA HD476 UT WOS:A1992HD47600005 PM 1734011 ER PT J AU KWONG, LM JASTY, M MULROY, RD MALONEY, WJ BRAGDON, C HARRIS, WH AF KWONG, LM JASTY, M MULROY, RD MALONEY, WJ BRAGDON, C HARRIS, WH TI THE HISTOLOGY OF THE RADIOLUCENT LINE SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID TOTAL JOINT-REPLACEMENT; BONE-CEMENT INTERFACE AB The radiographic and histological features of radiolucent areas at the cement-bone interface were correlated in 15 specimens retrieved at post-mortem from patients who had undergone cemented total hip arthroplasty, two weeks to 15 years prior to death. All but one of the components were securely fixed, as demonstrated by direct measurements of micromotion. Extensive radiolucencies were present in all but one case. In 11 of the 14 specimens with radiolucencies, histological examination showed that the radiolucent areas represented regions of osteoporosis and bone remodelling. The remodelling changes were characterised by osteoporosis, cancellisation and thinning of the endosteal cortex, and osteopenia of the trabecular bone. In two specimens the appearance of radiolucency was found to be due to fibrous tissue at the cement-bone interface and in one specimen there was a mixed picture of osteolysis and fibrosis. The study demonstrates that radiolucent lines can occur with well-fixed components and that they may commonly represent osteoporosis rather than the presence of a fibrous membrane at the cement-bone interface. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 23 TC 68 Z9 69 U1 0 U2 2 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JAN PY 1992 VL 74 IS 1 BP 67 EP 73 PG 7 WC Orthopedics; Surgery SC Orthopedics; Surgery GA HA168 UT WOS:A1992HA16800017 PM 1732269 ER PT J AU ZUSMAN, RM AF ZUSMAN, RM TI LEFT-VENTRICULAR HYPERTROPHY AND PERFORMANCE - THERAPEUTIC OPTIONS AMONG THE ANGIOTENSIN-CONVERTING ENZYME-INHIBITORS SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE LEFT VENTRICULAR HYPERTROPHY; ACE-INHIBITORS; MYOCARDIAL RENIN-ANGIOTENSIN CASCADE ID CONGESTIVE-HEART-FAILURE; CORONARY-ARTERY DISEASE; ANTIHYPERTENSIVE THERAPY; DIASTOLIC FUNCTION; ESSENTIAL-HYPERTENSION; SYSTOLIC FUNCTION; MOLECULAR-BASIS; CARDIOMYOPATHY; VERAPAMIL; BLOCKING AB The goal of antihypertensive therapy is the reduction in morbidity and mortality associated with high blood pressure. Despite our ability to reduce blood pressure, ''standard'' antihypertensive therapy has not produced a general decrease in coronary heart disease. This failure might be related to the adverse metabolic consequences of diuretics and beta-adrenergic receptor-blocking agents used in most clinical trials. In the hypertensive patient population, however, the principal physiologic abnormality is increased systemic vascular resistance. This increase in vascular tone leads to compensatory changes in cardiac function that result in left ventricular hypertrophy and diastolic filling abnormalities. Diastolic ventricular dysfunction is present in approximately 50% of asymptomatic hypertensive patients and might be a precursor of the syndrome of congestive heart failure with normal systolic ventricular function. In view of the prevalence of diastolic filling abnormalities in the hypertensive patient population, one should consider the effect of an antihypertensive drug on left ventricular function. In a comparison of the angiotensin-converting enzyme (ACE) inhibitors, captopril, lisinopril, and fosinopril, only fosinopril increased stroke volume, peak ejection rate, and peak filling rate, and decreased time to peak ejection rate. These favorable inotropic and lusitropic responses to fosinopril may reflect an effect on the myocardial renin-angiotensin cascade which is dependent upon the unique chemical structure of the fosinopril molecule. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,DIV HYPERTENS & VASC MED,15 PARKMAN ST,ACC 482,BOSTON,MA 02114, USA. NR 31 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PY 1992 VL 20 SU 10 BP S21 EP S28 DI 10.1097/00005344-199200101-00005 PG 8 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA KE593 UT WOS:A1992KE59300005 PM 1283427 ER PT J AU BAST, BJEG ZHOU, LJ FREEMAN, GJ COLLEY, KJ ERNST, TJ MUNRO, JM TEDDER, TF AF BAST, BJEG ZHOU, LJ FREEMAN, GJ COLLEY, KJ ERNST, TJ MUNRO, JM TEDDER, TF TI THE HB-6, CDW75, AND CD76 DIFFERENTIATION ANTIGENS ARE UNIQUE CELL-SURFACE CARBOHYDRATE DETERMINANTS GENERATED BY THE BETA-GALACTOSIDE ALPHA-2,6-SIALYLTRANSFERASE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID HUMAN LYMPHOCYTES-B; NH2-TERMINAL SIGNAL ANCHOR; MONOCLONAL-ANTIBODIES; TERMINAL GLYCOSYLATION; ERYTHROCYTE RECEPTOR; LYMPHOID-CELLS; SIALIC ACIDS; EXPRESSION; ACTIVATION; DNA AB Expression of the beta-galactoside alpha-2,6-sialyltransferase (alpha-2,6-ST) was shown to regulate the generation of multiple cell-surface differentiation antigens (Ags) that may be necessary for lymphocyte function. A new mAb was produced, termed HB-6, that was shown to identify a novel neuraminidase-sensitive cell-surface Ag expressed by subpopulations of human lymphocytes and erythrocytes. In attempting to isolate a cDNA encoding the HB-6 antigen by expression cloning, a cDNA encoding the alpha-2,6-ST (EC 2.4.99.1) was obtained. Since expression of the alpha-2,6-ST protein was shown to be limited to the Golgi apparatus, the cell-surface HB-6 Ag was demonstrated to be the product of alpha-2,6-ST activity. Interestingly, alpha-2,6-ST expression also generated two other neuraminidase-sensitive lymphocyte cell-surface differentiation Ags, CDw75, and CD76. The HB-6, CDw75, and CD76 mAb identified distinct Ags that were differentially expressed by different B cell lines and exhibited different patterns of expression in tissue sections. These results indicate that alpha-2,6-ST expression is a critical regulatory step in the formation of the Ags that are recognized by these mAb, and that an alpha-2,6-linked sialic acid residue is an essential component of each Ag. Thus, expression of a single ST can result in the generation of multiple distinct antigenic determinants on the cell surface which can be distinguished by mAb and may have regulatory roles in lymphocyte function. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOL CHEM,LOS ANGELES,CA 90024. CYTEL CORP,LA JOLLA,CA 92121. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-26872] NR 69 TC 97 Z9 98 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1992 VL 116 IS 2 BP 423 EP 435 DI 10.1083/jcb.116.2.423 PG 13 WC Cell Biology SC Cell Biology GA GZ963 UT WOS:A1992GZ96300017 PM 1730763 ER PT J AU MOSSER, DM SPRINGER, TA DIAMOND, MS AF MOSSER, DM SPRINGER, TA DIAMOND, MS TI LEISHMANIA PROMASTIGOTES REQUIRE OPSONIC COMPLEMENT TO BIND TO THE HUMAN-LEUKOCYTE INTEGRIN MAC-1 (CD11B/CD18) SO JOURNAL OF CELL BIOLOGY LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; MACROPHAGE-DERIVED COMPLEMENT; RECEPTOR TYPE-3 CR3; MONOCLONAL-ANTIBODIES; HUMAN-MONOCYTES; POLYMORPHONUCLEAR LEUKOCYTES; GLYCOPROTEIN FAMILY; HUMAN-NEUTROPHILS; SURFACE-ANTIGENS; LFA-1 AB Previous reports have suggested that Leishmania spp. interact with macrophages by binding to Mac-I (CD11b/CD18), a member of the leukocyte integrin family. To better define this interaction, we tested the ability of leishmania promastigotes to bind to purified leukocyte integrins and to cloned integrins expressed in COS cells. We show that leishmania promastigotes bind to cellular or purified Mac-1 but not lymphocyte function-associated antigen-1 in a specific, dose-dependent manner that requires the presence of serum. Binding is inhibited with specific monoclonal antibodies to Mac-1. In the absence of complement opsonization, three different species of leishmania tested fail to bind directly to any of the three leukocyte integrins. We show that binding to Mac-1 requires the third component of complement (C3). Organisms incubated in heat-inactivated serum or serum that has been immunologically depleted of C3 fail to bind to Mac-1. Because the addition of purified C3 to C3-depleted serum restores leishmania binding to Mac-1, we suggest that parasites gain entry into macrophages by fixing complement and subverting a well-characterized adhesive interaction in the immune system between Mac-1 and iC3b. C1 HARVARD UNIV, SCH MED, COMM CELL & DEV BIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. RP MOSSER, DM (reprint author), TEMPLE UNIV, HLTH SCI CTR, SCH MED, DEPT MICROBIOL & IMMUNOL, PHILADELPHIA, PA 19140 USA. RI Mosser, David/I-6697-2016 OI Mosser, David/0000-0002-9503-4187 FU NCI NIH HHS [CA31799]; NIAID NIH HHS [AI24313]; NIGMS NIH HHS [T32 GM007753, T32GM07753-11] NR 61 TC 91 Z9 91 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 950 THIRD AVE, 2ND FLR, NEW YORK, NY 10022 USA SN 0021-9525 EI 1540-8140 J9 J CELL BIOL JI J. Cell Biol. PD JAN PY 1992 VL 116 IS 2 BP 511 EP 520 DI 10.1083/jcb.116.2.511 PG 10 WC Cell Biology SC Cell Biology GA GZ963 UT WOS:A1992GZ96300024 PM 1730765 ER PT J AU GOLDSTEIN, BJ AF GOLDSTEIN, BJ TI PROTEIN-TYROSINE PHOSPHATASES AND THE REGULATION OF INSULIN ACTION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE PROTEIN-TYROSINE PHOSPHATASES; PHOSPHOPROTEIN PHOSPHATASES; PROTEIN PHOSPHORYLATION; INSULIN RECEPTOR; INSULIN RESISTANCE ID LEUKOCYTE COMMON ANTIGEN; GROWTH-FACTOR RECEPTORS; KINASE-ACTIVITY; HUMAN-PLACENTA; PHOSPHOTYROSINE PHOSPHATASE; BETA-SUBUNIT; XENOPUS OOCYTES; DIABETIC RATS; PHOSPHORYLATION; DEPHOSPHORYLATION AB Protein-tyrosine phosphatases (PTPases) play an important role in the regulation of insulin action by dephosphorylating the active (autophosphorylated) form of the insulin receptor and attenuating its tyrosine kinase activity. PTPases can also modulate post-receptor signalling by catalyzing the dephosphorylation of cellular substrates of the insulin receptor kinase. Dramatic advances have recently been made in our understanding of PTPases as an extensive family of transmembrane and intracellular proteins that are involved in a number of pathways of cellular signal transduction. Identification of the PTPase(s) which act on various components of the insulin action cascade will not only enhance our understanding of insulin signalling but will also clarify the potential involvement of PTPases in the pathophysiology of insulin-resistant disease states. This brief review provides a summary of reversible tyrosine phosphorlyation events in insulin action and available data on candidate PTPases in liver and skeletal muscle that may be involved in the regulation of insulin action. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP GOLDSTEIN, BJ (reprint author), JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK43396] NR 89 TC 87 Z9 87 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD JAN PY 1992 VL 48 IS 1 BP 33 EP 42 DI 10.1002/jcb.240480107 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HA504 UT WOS:A1992HA50400006 PM 1316360 ER PT J AU COOPER, G AF COOPER, G TI GENETIC ALTERATIONS AS INTERMEDIATE BIOMARKERS - OVERVIEW SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Editorial Material RP COOPER, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1992 SU 16G BP 129 EP 130 PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JY991 UT WOS:A1992JY99100021 ER PT J AU COOPER, GM AF COOPER, GM TI ONCOGENES AS MARKERS FOR EARLY DETECTION OF CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE ABL; CHEMOPREVENTION; COLORECTAL CARCINOMA; INTERMEDIATE BIOMARKER; LEUKEMIA; ONCOGENES; POLYMERASE CHAIN REACTION; RAS; TUMOR SUPPRESSOR GENES ID CHRONIC MYELOGENOUS LEUKEMIA; PROTO-ONCOGENE; RAS ONCOGENES; ACTIVATION; GENES; TRANSLOCATIONS; RECEPTOR AB Oncogenes are formed in human tumors as a result of mutations or DNA rearrangements leading to the abnormal expression or function of proto-oncogenes. Approximately 20 different oncogenes are reproducibly activated in malignancies of several types, including breast, colon, lung, pancreatic, and thyroid carcinomas, leukemias, and lymphomas. The potential utility of these oncogenes as markers for early defection of cancer is dependent on the stage of tumor development at which they are activated, and on whether the mutated oncogenes are readily distinguished from the corresponding proto-oncogenes by assays that are sufficiently sensitive to detect precancerous lesions. RP COOPER, GM (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. NR 22 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1992 SU 16G BP 131 EP 136 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JY991 UT WOS:A1992JY99100022 ER PT J AU PROUT, GR BARTON, BA AF PROUT, GR BARTON, BA TI 13-CIS-RETINOIC ACID IN CHEMOPREVENTION OF SUPERFICIAL BLADDER-CANCER SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Article DE 13-CIS-RETINOIC ACID; BLADDER CARCINOMA; CHEMOPREVENTION ID URINARY-BLADDER; CELL CARCINOMA; CARCINOGENESIS; RETINOIDS AB Animal studies indicate that 13-cis-retinoic acid (CRA) inhibits bladder tumor growth and is effective in treating patients with serious dermatologic disorders. A trial of CRA in patients at high risk for recurrent Ta, T1 tumors was initiated at an experimental dose of 0.5 mg/kg/d in three divided doses, increasing to 1 mg/kg/d at four weeks. Treatment of twenty eligible patients lasted for six months with an additional 24 month follow-up period. One patient was later excluded due to toxicity resulting in an early dose reduction. Eight patients stopped treatment before three months; of these five, had recurrences within three months, one developed pulmonary metastasis, and one developed a T2G3 tumor. Four patients stopped treatment between three and six months; three of them had recurrences before one year and one had no evidence of disease at seven years. Seven patients completed the course; of these three had recurrences within six months, and three more had recurrences at 8, 15, and 45 months, respectively. Toxicity was nearly universal; cheilosis, conjunctivitis, pruritus, joint and eye pain, flashing lights, and erythrocyte sedimentation rate (ESR) over 60 were all noted. The lack of positive results and the frequency and severity of toxicity led to termination of the study. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,UROL SERV,BOSTON,MA 02114. MARYLAND MED RES INST,BALTIMORE,MD. NR 11 TC 6 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PY 1992 SU 16I BP 148 EP 152 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA KV875 UT WOS:A1992KV87500027 ER PT J AU HAUGUELDEMOUZON, S CSERMELY, P ZOPPINI, G KAHN, CR AF HAUGUELDEMOUZON, S CSERMELY, P ZOPPINI, G KAHN, CR TI QUANTITATIVE DISSOCIATION BETWEEN EGF EFFECTS ON C-MYC AND C-FOS GENE-EXPRESSION, DNA-SYNTHESIS, AND EPIDERMAL GROWTH-FACTOR RECEPTOR TYROSINE KINASE-ACTIVITY SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID PROTO-ONCOGENE EXPRESSION; 3T3 CELLS; BINDING SITE; A431 CELLS; PHOSPHORYLATION; INDUCTION; TRANSCRIPTION; STIMULATION; ACTIVATION; INSULIN AB The exact relationship between EGF-stimulated tyrosine phosphorylation, induction of the cellular proto-oncogenes c-myc and c-fos, and DNA synthesis remains uncertain. Madin-Darby Canine Kidney (MDCK) cells possess EGF receptor sites with high binding capacity, and in contrast to A431 cells, respond to EGF by increasing DNA synthesis. Following EGF stimulation of intact MDCK cells, there was a rapid and marked increase in the autophosphorylation of the EGF receptor. This was associated with an increase in the tyrosine phosphorylation of a 120 kDa phosphoprotein believed to be an endogenous substrate of this receptor kinase. The ED50 for stimulation of phosphorylation of pp 120 was approximately 0.05 nM versus 1.0 nM for receptor autophosphorylation, consistent with amplification of signalling at this step in EGF action. Stimulation of DNA synthesis occurred after 12 to 24 hours and revealed even further amplification with an ED50 of about 0.1 nM. Intermediate between these events was a time-dependent activation of c-fos and c-myc gene expression. However, the ED50 for these processes was approximately 10 nM, indicating a relatively lower sensitivity of EGF for stimulation of proto-oncogene expression. Tyrphostin (RG 50864), a compound reported to inhibit specifically the EGF receptor kinase, completely blocked EGF stimulation of proto-oncogene induction. Interestingly, under the same experimental conditions, EGF receptor autophosphorylation was decreased only 60%. These data, along with the dose-response studies, indicate that proto-oncogene induction requires near maximal stimulation of EGF receptor autophosphorylation. They also suggest that, in MDCK cells, the EGF dependent induction of the c-fos and c-myc genes is not strictly correlated to the extent of EGF receptor autophosphorylation or EGF-stimulated DNA synthesis, and that EGF stimulation of DNA synthesis likely involves additional rate-limiting intermediate steps. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. FU FIC NIH HHS [1F05 TW04319-01 B1-5]; NIDDK NIH HHS [DK 33201] NR 43 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD JAN PY 1992 VL 150 IS 1 BP 180 EP 187 DI 10.1002/jcp.1041500124 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA GZ889 UT WOS:A1992GZ88900023 PM 1730782 ER PT J AU ROODMAN, GD KURIHARA, N OHSAKI, Y KUKITA, A HOSKING, D DEMULDER, A SMITH, JF SINGER, FR AF ROODMAN, GD KURIHARA, N OHSAKI, Y KUKITA, A HOSKING, D DEMULDER, A SMITH, JF SINGER, FR TI INTERLEUKIN-6 - A POTENTIAL AUTOCRINE PARACRINE FACTOR IN PAGETS-DISEASE OF BONE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INTERLEUKIN-6; OSTEOCLASTS; PAGETS DISEASE; PRECURSORS ID OSTEOCLAST-LIKE CELLS; HUMAN MARROW CULTURES; MONOCLONAL-ANTIBODIES; PARATHYROID-HORMONE; MEASLES-VIRUS; GROWTH-FACTOR; INVITRO; TISSUE; ULTRASTRUCTURE; STIMULATE AB Pagetic osteoclasts are greatly increased in number and size and have increased numbers of nuclei per cell compared to normal osteoclasts. The mechanisms responsible for enhanced osteoclast formation in Paget's disease are unknown. We have used our recently described model system for pagetic osteoclast formation to evaluate culture media conditioned by these atypical multinucleated cells (MNC) to determine if pagetic osteoclasts produce an autocrine or paracrine factor that enhances osteoclast formation. Conditioned media from long-term bone marrow cultures from patients with Paget's disease stimulated osteoclast-like MNC formation in normal marrow cultures. At least part of this activity could be ascribed to interleukin 6 (IL-6). In contrast, conditioned media from normal marrow cultures contained lower levels of IL-6 and did not stimulate formation of osteoclast-like MNC. 7 of 8 bone marrow plasma samples taken from involved bones and 18 of 27 peripheral blood serum samples from Paget's patients had high levels of IL-6. Normal marrow plasma and peripheral blood serum had no or very low levels of IL-6. These results suggest that IL-6 produced by marrow and/or bone cells in patients with Paget's disease may be an autocrine/paracrine factor for pagetic osteoclasts. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NOTTINGHAM HLTH AUTHOR,NOTTINGHAM NG5 1PB,ENGLAND. CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90048. FU NCI NIH HHS [CA-40035]; NIAMS NIH HHS [AR-35188, AR-39539] NR 34 TC 275 Z9 280 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JAN PY 1992 VL 89 IS 1 BP 46 EP 52 DI 10.1172/JCI115584 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GY561 UT WOS:A1992GY56100006 PM 1729280 ER PT J AU RON, D BRASIER, AR MCGEHEE, RE HABENER, JF AF RON, D BRASIER, AR MCGEHEE, RE HABENER, JF TI TUMOR NECROSIS FACTOR-INDUCED REVERSAL OF ADIPOCYTIC PHENOTYPE OF 3T3-L1 CELLS IS PRECEDED BY A LOSS OF NUCLEAR CCAAT ENHANCER BINDING-PROTEIN (C/EBP) SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ACUTE PHASE; ADIPOCYTES; CYTOKINES; CACHEXIA ID ANGIOTENSINOGEN GENE-EXPRESSION; PHASE RESPONSE ELEMENT; SERUM-ALBUMIN GENE; MOLECULAR-CLONING; CYCLIC-AMP; DIFFERENTIATION; FAMILY; CACHECTIN; CACHEXIA; TRANSACTIVATION AB Tumor necrosis factor (TNF)-treated 3T3-L1 adipocytes were used as a model for studying the effects of systemic inflammation on adipose tissue. Lipopolysaccharide-treated monocyte-conditioned medium or recombinant human TNF-alpha induced morphological dedifferentiation of the adipocytes and led to loss of adipocyte specific gene expression. Gel shift, Southwestern and Western immunoblot analysis demonstrated that dedifferentiation was preceded by a decrease in the DNA binding activity and protein level of the transcription factor CCAAT/enhancer binding protein (C/EBP). Liver activating protein, a related protein that binds identical DNA sequences, increased during cytokine treatment. Both proteins activate specific enhancer elements located in the promoter region of many genes whose transcription is altered during systemic inflammation. Pulse-chase labeling followed by immunoprecipitation demonstrated that C/EBP is a rapidly turning over protein in adipocytes and that cytokine treatment led to a specific, time dependent decrease in its rate of synthesis. Because C/EBP binding sites have been shown to play an important role in regulating the expression of genes involved in adipocyte metabolism, we propose that the TNF-induced changes in the complement of transcription factors binding those sites may be important in the pathogenesis of inflammation-induced atrophy of adipose tissue. RP RON, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 25532, DK 30457] NR 43 TC 131 Z9 133 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 JAN PY 1992 VL 89 IS 1 BP 223 EP 233 DI 10.1172/JCI115566 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GY561 UT WOS:A1992GY56100029 PM 1729273 ER PT J AU CHONG, JK CANTRELL, L HUSAIN, M RIESING, S MILLER, BE WANDS, J DELAMONTE, S GHANBARI, HA AF CHONG, JK CANTRELL, L HUSAIN, M RIESING, S MILLER, BE WANDS, J DELAMONTE, S GHANBARI, HA TI AUTOMATED MICROPARTICLE ENZYME-IMMUNOASSAY FOR NEURAL THREAD PROTEIN IN CEREBROSPINAL-FLUID FROM ALZHEIMERS-DISEASE PATIENTS SO JOURNAL OF CLINICAL LABORATORY ANALYSIS LA English DT Article DE ALZHEIMERS DISEASE; CEREBROSPINAL FLUID; ANTEMORTEM ALZHEIMERS DISEASE MARKER; MICROPARTICLE ENZYME IMMUNOASSAY (MEIA) ID HUMAN BRAIN-TISSUE; SECRETORY PROTEIN; DIAGNOSIS; ASSAY AB An automated microparticle enzyme immunoassay (MEIA) with the IMx(R) analyzer for the detection of neural thread protein (NTP) in cerebrospinal fluid (CSF) from Alzheimer's disease (AD) patients was developed. This assay uses monoclonal antibodies produced against the purified pancreatic form of the protein. The assay employs one monoclonal antibody covalently coupled to the microparticle to capture immunoreactive material in CSF or brain tissue. The second monoclonal antibody was conjugated to alkaline phosphatase and serves as detection antibody. The assay provides results in approximately 45 minutes with a sensitivity of 60 pg/ml (3 fmoles/ml). The titration curve of both normal and AD CSF resulted in a linear relationship with respect to the volume of CSF used. A similar relationship was observed when normal and AD brain tissue extracts were serially diluted. The molecular weight of NTP in CSF was approximately 20 kD as determined by gel filtration method under non-denaturing conditions. The recovery for pancreatic thread protein (PTP) spiked in either normal or AD CSF was 104% and 108%, respectively. Intra-, inter-, and total assay CVs (coefficient of variation) for controls were less than 2.9%, 3.3% and 3.0%, respectively. This assay will provide a useful tool in the study of the Alzheimer's disease and may help research in diagnosis and prognosis of Alzheimer's disease and related disorder's. C1 ABBOTT LABS,ABBOTT DIAGNOST DIV,DEPT APPL IMMUNOCHEM,ABBOTT PK,IL 60064. MASSACHUSETTS GEN HOSP,MASSACHUSETTS ALZHEIMERS DIS RES CTR,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP CHONG, JK (reprint author), ABBOTT LABS,ABBOTT DIAGNOST DIV,NEUROPSYCHIAT MARKERS RES & DEV,D-90J,AP20-4,ABBOTT PK,IL 60064, USA. NR 9 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0887-8013 J9 J CLIN LAB ANAL JI J. Clin. Lab. Anal. PY 1992 VL 6 IS 6 BP 379 EP 383 DI 10.1002/jcla.1860060608 PG 5 WC Medical Laboratory Technology SC Medical Laboratory Technology GA JU790 UT WOS:A1992JU79000007 PM 1432364 ER PT J AU CARLONE, GM FRASCH, CE SIBER, GR QUATAERT, S GHEESLING, LL TURNER, SH PLIKAYTIS, BD HELSEL, LO DEWITT, WE BIBB, WF SWAMINATHAN, B ARAKERE, G THOMPSON, C PHIPPS, D MADORE, D BROOME, CV AF CARLONE, GM FRASCH, CE SIBER, GR QUATAERT, S GHEESLING, LL TURNER, SH PLIKAYTIS, BD HELSEL, LO DEWITT, WE BIBB, WF SWAMINATHAN, B ARAKERE, G THOMPSON, C PHIPPS, D MADORE, D BROOME, CV TI MULTICENTER COMPARISON OF LEVELS OF ANTIBODY TO THE NEISSERIA-MENINGITIDIS GROUP-A CAPSULAR POLYSACCHARIDE MEASURED BY USING AN ENZYME-LINKED-IMMUNOSORBENT-ASSAY SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID INFLUENZAE TYPE-B; CEREBROSPINAL-FLUID; LATEX AGGLUTINATION; BINDING ASSAY; RADIOIMMUNOASSAY; ANTIGENS; IMMUNIZATION; QUANTITATION; VACCINE AB There is no standard immunoassay for evaluating immune responses to meningococcal vaccines. We developed an enzyme-linked immunosorbent assay to measure total levels of antibody to Neisseria meningitidis group A capsular polysaccharide. Five laboratories measured the antibody levels in six paired pre- and postvaccination serum samples by using the enzyme-linked immunosorbent assay. Methylated human serum albumin was used to bind native group. A polysaccharide to microtiter plate surfaces. The between-laboratory coefficients of variation for pre- and postvaccination sera had ranges of 31 to 91 and 17 to 31, respectively. The mean laboratory coefficients of variation for pre- and postvaccination sera, respectively, were 17 and 11 (Molecular Biology Laboratory, Centers for Disease Control), 12 and 15 (Immunodiagnostic Methods Laboratory, Centers for Disease Control), 22 and 19 (Dana-Farber Cancer Institute), 38 and 38 (Bacterial Polysaccharide Laboratory, U.S. Food and Drug Administration), and 11 and 10 (Praxis Biologics, Inc.). Standardization of this enzyme-linked immunosorbent assay should allow interlaboratory comparison of meningococcal vaccine immunogenicity, thus providing a laboratory-based assessment tool for evaluating meningococcal vaccines. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. US FDA,CTR BIOL EVALUAT & RES,BETHESDA,MD 20892. PRAXIS BIOL INC,ROCHESTER,NY 14623. CTR DIS CONTROL,CTR INFECT DIS,NATL CTR INFECT DIS,BIOSTAT & INFORMAT MANAGEMENT BRANCH,ATLANTA,GA 30333. RP CARLONE, GM (reprint author), CTR DIS CONTROL,CTR INFECT DIS,NATL CTR INFECT DIS,MENINGITIS & SPECIAL PATHOGENS BRANCH,ATLANTA,GA 30333, USA. NR 25 TC 92 Z9 97 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 JAN PY 1992 VL 30 IS 1 BP 154 EP 159 PG 6 WC Microbiology SC Microbiology GA GV355 UT WOS:A1992GV35500025 PM 1734048 ER PT J AU HOCHSTER, HS KIM, K GREEN, MD MANN, RB NEIMAN, RS OKEN, MM CASSILETH, PA STOTT, P RITCH, P OCONNELL, MJ AF HOCHSTER, HS KIM, K GREEN, MD MANN, RB NEIMAN, RS OKEN, MM CASSILETH, PA STOTT, P RITCH, P OCONNELL, MJ TI ACTIVITY OF FLUDARABINE IN PREVIOUSLY TREATED NON-HODGKINS LOW-GRADE LYMPHOMA - RESULTS OF AN EASTERN COOPERATIVE ONCOLOGY GROUP-STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NERVOUS-SYSTEM TOXICITY; PHASE-I; 9-BETA-D-ARABINOFURANOSYL-2-FLUOROADENINE 5'-MONOPHOSPHATE; PHOSPHATE; LEUKEMIA; TRIAL C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV PENN,PHILADELPHIA,PA 19104. BORGESS MED CTR,KALAMAZOO,MI 49001. MED COLL WISCONSIN,MILWAUKEE,WI 53226. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RP HOCHSTER, HS (reprint author), NYU MED CTR,KAPLAN CANC CTR,530 1ST AVE,NEW YORK,NY 10016, USA. FU NCI NIH HHS [CA 23318, CA 16395, CA 21115] NR 13 TC 159 Z9 160 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 JAN PY 1992 VL 10 IS 1 BP 28 EP 32 PG 5 WC Oncology SC Oncology GA GW592 UT WOS:A1992GW59200006 PM 1727921 ER PT J AU ANTMAN, K AYASH, L ELIAS, A WHEELER, C HUNT, M EDER, JP TEICHER, BA CRITCHLOW, J BIBBO, J SCHNIPPER, LE FREI, E AF ANTMAN, K AYASH, L ELIAS, A WHEELER, C HUNT, M EDER, JP TEICHER, BA CRITCHLOW, J BIBBO, J SCHNIPPER, LE FREI, E TI A PHASE-II STUDY OF HIGH-DOSE CYCLOPHOSPHAMIDE, THIOTEPA, AND CARBOPLATIN WITH AUTOLOGOUS MARROW SUPPORT IN WOMEN WITH MEASURABLE ADVANCED BREAST-CANCER RESPONDING TO STANDARD-DOSE THERAPY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID INDUCTION CHEMOTHERAPY; AUTO-TRANSPLANTATION; RANDOMIZED TRIAL; ONCOLOGY-GROUP; SOLID TUMORS; COMBINATION; INTENSIFICATION; ADRIAMYCIN; CISPLATIN; RESCUE C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT STAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT CANC PHARMACOL, BOSTON, MA 02115 USA. BETH ISRAEL HOSP, DEPT MED & SURG, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP ANTMAN, K (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT MED, 44 BINNEY ST, BOSTON, MA 02115 USA. FU NCI NIH HHS [P01CA-38493] NR 67 TC 376 Z9 376 U1 0 U2 0 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JAN PY 1992 VL 10 IS 1 BP 102 EP 110 PG 9 WC Oncology SC Oncology GA GW592 UT WOS:A1992GW59200016 PM 1727912 ER PT J AU VANKERCKHOVE, C RUSSELL, GJ DEUSCH, K REICH, K BHAN, AK DERSIMONIAN, H BRENNER, MB AF VANKERCKHOVE, C RUSSELL, GJ DEUSCH, K REICH, K BHAN, AK DERSIMONIAN, H BRENNER, MB TI OLIGOCLONALITY OF HUMAN INTESTINAL INTRAEPITHELIAL T-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID AUREUS TOXIN SUPERANTIGENS; RECEPTOR BETA-CHAIN; ANTIGEN RECEPTOR; LYMPHOCYTES; EXPRESSION; GENES AB T cells bearing the T cell receptor alpha/beta (TCR-alpha/beta) are the predominant lymphocyte population in the human intestinal epithelium. To examine if normal intestinal intraepithelial lymphocytes (IEL) have a TCR repertoire distinct from the TCR-alpha/beta-repertoire in peripheral blood lymphocytes (PBL), comparative analysis of relative V-beta-gene usage in IEL and PBL was performed by quantitative polymerase chain reaction. In each of the six individuals examined, one to three V-beta-families made up more than 40% of the total V-beta-transcripts detected in the IEL, whereas there was a more even distribution of V-beta-gene usage in the paired PBL. The predominant V-beta-families, especially V-beta-l, V-beta-2, V-beta-3, and V-beta-6, were frequently shared among IEL of different individuals. PCR cloning and sequence analysis of the predominant V-beta-6 family in two individuals revealed an identical V-D-J-C sequence in 13 of 21 clones obtained from one donor, and a different repeated sequence in 18 of 27 clones examined in the second donor. These data suggest that the V-beta-skewing in IEL is due to an oligoclonal T cell expansion and may reflect the response of the intestinal mucosal immune system to a restricted set of as yet undefined antigens present in the gut. C1 HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. TECH UNIV MUNICH,DEPT INTERNAL MED,W-8000 MUNICH 80,GERMANY. RP VANKERCKHOVE, C (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 25 TC 135 Z9 135 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1992 VL 175 IS 1 BP 57 EP 63 DI 10.1084/jem.175.1.57 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GY436 UT WOS:A1992GY43600008 PM 1730926 ER PT J AU DEFOUGEROLLES, AR SPRINGER, TA AF DEFOUGEROLLES, AR SPRINGER, TA TI INTERCELLULAR-ADHESION MOLECULE-3, A 3RD ADHESION COUNTER-RECEPTOR FOR LYMPHOCYTE FUNCTION ASSOCIATED MOLECULE-1 ON RESTING LYMPHOCYTES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; CELL-ADHESION; SUPERGENE FAMILIES; IMMUNE-SYSTEM; ICAM-1; LFA-1; EXPRESSION; DEFICIENCY; LIGAND; ADHERENCE AB Recent studies suggest that some T and B lymphocyte cell lines bind to the integrin lymphocyte function-associated molecule 1 (LFA-1) chiefly through a pathway independent of its two known counter-receptors, intercellular adhesion molecules (ICAMs)-l and -2. A monoclonal antibody (mAb) was raised that, in combination with blocking mAb to ICAM-1 and ICAM-2, can completely inhibit binding of these cell lines to purified LFA-1. This third ligand, designated ICAM-3 based on its functional relatedness to ICAM-1 and -2, is a highly glycosylated protein of 124,000 M(r). It is well expressed on all leukocytes and absent from endothelial cells. In assays of adhesion of resting lymphocytes to purified LFA-1, ICAM-3 is by far the most functionally important ICAM, implying an important role for ICAM-3 in the generation of immune responses. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,COMM IMMUNOL,BOSTON,MA 02115. NR 38 TC 424 Z9 425 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1992 VL 175 IS 1 BP 185 EP 190 DI 10.1084/jem.175.1.185 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GY436 UT WOS:A1992GY43600023 PM 1730916 ER PT J AU KOYASU, S DADAMIO, L ARULANANDAM, ARN ABRAHAM, S CLAYTON, LK REINHERZ, EL AF KOYASU, S DADAMIO, L ARULANANDAM, ARN ABRAHAM, S CLAYTON, LK REINHERZ, EL TI T-CELL RECEPTOR COMPLEXES CONTAINING FC-EPSILON-RI-GAMMA HOMODIMERS IN LIEU OF CD3-ZETA AND CD3-ETA COMPONENTS - A NOVEL ISOFORM EXPRESSED ON LARGE GRANULAR LYMPHOCYTES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NATURAL-KILLER-CELLS; AFFINITY IGE RECEPTOR; ANTIGEN RECEPTOR; ZETA-CHAIN; ETA-CHAIN; MOLECULAR-CLONING; TRANSFECTED CELLS; SUBUNIT; GENE; CD16 AB CD3-zeta and CD3-eta-form disulfide-linked homo- or heterodimers important in targeting partially assembled Ti-alpha-beta/CD3-gamma-delta-epsilon-T cell receptor (TCR) complexes to the cell surface and transducing stimulatory signals after antigen recognition. Here we identify a new TCR isoform expressed on splenic CD2+, CD3/Ti-alpha-beta+, CD4-, CD8-, CD16+, NK1.1+ mouse large granular lymphocytes (LGL), which are devoid of CD3-zeta and CD3-eta proteins. The TCRs of this subset contain homodimers of the gamma-subunit of the high affinity receptor for IgE (Fc-epsilon-RI-gamma) in lieu of CD3-zeta and/or CD3-eta-proteins. The LGL display natural killer-like activity and are cytotoxic for B cell hybridomas producing anti-CD3-epsilon and anti-CD16 monoclonal antibodies, demonstrating the signaling capacity of both TCR and CD16 in this cell type. These findings provide evidence for an additional level of complexity of TCR signal transduction isoforms in naturally occurring T cell subsets. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP KOYASU, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 FU NIAID NIH HHS [AI-19807, AI-21226, AI-31269] NR 39 TC 74 Z9 75 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1992 VL 175 IS 1 BP 203 EP 209 DI 10.1084/jem.175.1.203 PG 7 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GY436 UT WOS:A1992GY43600025 PM 1530959 ER PT J AU DASGUPTA, JD GRANJA, C DRUKER, B LIN, LL YUNIS, EJ RELIAS, V AF DASGUPTA, JD GRANJA, C DRUKER, B LIN, LL YUNIS, EJ RELIAS, V TI PHOSPHOLIPASE-C-GAMMA-1 ASSOCIATION WITH CD3 STRUCTURE IN T-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID TYROSINE PHOSPHORYLATION; ANTIGEN RECEPTOR; SIGNAL TRANSDUCTION; C-GAMMA; ACTIVATION; KINASE; COMPLEX; BINDING; PDGF AB Recently, we and others have reported tyrosine phosphorylation of phospholipase C-gamma-1 (PLC-gamma-1) enzyme after CD3 activation of T cells, and have proposed that PLC-gamma-1 mediates signal transduction through the T cell receptor (TCR/CD3). Here, using immunoblotting and immune complex PLC assays, we show that CD3 stimulation of Jurkat cells induces the association of PLC-gamma-1 enzyme with CD3 complex. PLC activity is also found to co-precipitate with the CD3-zeta-chain from activated cells. In addition, in vitro PLC assays show that CD3 activation leads to about 10-fold stimulation of PLC-gamma-1 activity. These results, along with the observation that Jurkat cells preferentially express PLC-gamma-1, indicate that PLC-gamma-1 participates in CD3 signaling. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. GENET INST,CAMBRIDGE,MA 02140. RP DASGUPTA, JD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,ROOM 740,44 BINNEY ST,BOSTON,MA 02115, USA. NR 21 TC 61 Z9 61 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JAN 1 PY 1992 VL 175 IS 1 BP 285 EP 288 DI 10.1084/jem.175.1.285 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GY436 UT WOS:A1992GY43600034 PM 1370531 ER PT J AU GALUN, E OFFENSPERGER, WB VONWEIZSACKER, F OFFENSPERGER, S WANDS, JR BLUM, HE AF GALUN, E OFFENSPERGER, WB VONWEIZSACKER, F OFFENSPERGER, S WANDS, JR BLUM, HE TI HUMAN NON-HEPATOCYTES SUPPORT HEPADNAVIRAL REPLICATION AND VIRION PRODUCTION SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID HEPATITIS-B VIRUS; HEPATOMA-CELL LINES; DNA; PARTICLES; INFECTION; HYBRIDIZATION; SYSTEM; LIVER AB The competence of non-hepatocytes to support hepatitis B virus (HBV) gene expression and replication was studied by transient transfection of various human cell lines with a head-to-tail dimer of HBV DNA. Independent of their neuroectodermal, mesenchymal or epithelial origin, all non-hepatocyte cell lines tested synthesized and secreted hepatitis B surface antigen (HBsAg) and hepatitis B core/e antigen (HBc/eAg). Further analyses of two of these cell lines (LS 180 and COLO 320) identified the two major HBV transcripts of 3.6 and 2.2/2.4 kb length, respectively. LS 180 cells were permissive for HBV and duck hepatitis B virus (DHBV) DNA replication and secretion of infectious virions. COLO 320 cells also supported HBV DNA replication, but did not appear to export complete viral particles. These findings provide direct evidence that both HBV and DHBV can replicate in non-hepatic tumour cell lines, one of which is shown also to produce infectious virions. ; C1 UNIV FREIBURG,DEPT MED,W-7800 FREIBURG,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666, AA-00048] NR 31 TC 11 Z9 12 U1 0 U2 1 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD JAN PY 1992 VL 73 BP 173 EP 178 DI 10.1099/0022-1317-73-1-173 PN 1 PG 6 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA HA165 UT WOS:A1992HA16500020 PM 1730939 ER PT J AU STEINBERG, DR GELBERMAN, RH RYDEVIK, B LUNDBORG, G AF STEINBERG, DR GELBERMAN, RH RYDEVIK, B LUNDBORG, G TI THE UTILITY OF PORTABLE NERVE-CONDUCTION TESTING FOR PATIENTS WITH CARPAL-TUNNEL SYNDROME - A PROSPECTIVE CLINICAL-STUDY SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB The usefulness and accuracy of a portable instrument, the electroneurometer, for measuring distal motor latencies was determined in a prospective study of 28 patients (51 hands) with carpal tunnel syndrome and 10 controls (18 hands). There was a close correlation of distal motor latencies from the electroneurometer with those from formal electrodiagnostic testing. The average distal motor latency of controls was 3.3 +/- 0.4 msec, compared with a mean value of 5.2 +/- 1.8 msec in symptomatic hands. The sensitivity of the neurometer test alone was 69% (9 false-negatives); when combined with quantitative sensibility testing, sensitivity increased to 84%. Specificity of the neurometer test alone was 100% (no false-positives). The portable electroneurometer is a convenient, painless, inexpensive device for screening patients with carpal tunnel syndrome. Formal electrodiagnostic testing is indicated for differentiation of lesions present at different levels, for detection of subtle sensory changes, and for use in those patients in whom surface electrode usage is ineffective. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC-527,BOSTON,MA 02114. NR 0 TC 13 Z9 13 U1 0 U2 2 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JAN PY 1992 VL 17A IS 1 BP 77 EP 81 DI 10.1016/0363-5023(92)90117-8 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GZ888 UT WOS:A1992GZ88800014 PM 1538114 ER PT J AU PAGE, RD HARRINGER, W HODAKOWSKI, GT GUERRERO, JL LARAIA, PJ AUSTEN, WG VLAHAKES, GJ AF PAGE, RD HARRINGER, W HODAKOWSKI, GT GUERRERO, JL LARAIA, PJ AUSTEN, WG VLAHAKES, GJ TI DETERMINANTS OF MAXIMAL RIGHT VENTRICULAR-FUNCTION SO JOURNAL OF HEART AND LUNG TRANSPLANTATION LA English DT Article; Proceedings Paper CT 11TH ANNUAL MEETING AND SCIENTIFIC SESSIONS OF THE INTERNATIONAL SOC FOR HEART TRANSPLANTATION CY APR 07-09, 1991 CL PARIS, FRANCE SP INT SOC HEART TRANSPLANTAT AB After heart transplantation, right ventricular failure can occur because of increased afterload. Previous studies have suggested that the maximal pressure the right ventricle can develop is determined primarily by right ventricular perfusion pressure. However, the interaction of the left ventricle and the pericardium as functional co-determinants of maximal right ventricular function is unknown. This study was undertaken to determine the interaction of the pericardium, left ventricular pressure, and right coronary artery perfusion pressure as potential determinants of maximal right ventricular function. In an acute canine preparation, with progressive pulmonary artery constriction, maximal generated right ventricular pressure was determined over a range of left ventricular systolic pressures. Additional groups of dogs were studied with the right coronary artery cannulated and were maintained at constant perfusion pressure. In all preparations, the maximal pressure the right ventricle could generate was linearly related to left ventricular systolic pressure. Having a closed pericardium markedly enhanced this effect; some effect was present with an open pericardium, although the magnitude of the influence of left ventricular pressure on maximal right ventricular pressure was much less. Maintaining constancy of right coronary artery perfusion pressure, either at high or low values, did not alter these findings nor did it alter the influence of the pericardium. These results suggest that right ventricular perfusion may not be the sole determinant of maximal right ventricular function. Furthermore, with the pericardium open, such as in the posttransplantation state, the left ventricular contribution to maximal right ventricular function may be diminished, increasing vulnerability for right ventricular failure caused by increased afterload. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 0 TC 24 Z9 24 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1053-2498 J9 J HEART LUNG TRANSPL JI J. Heart Lung Transplant. PD JAN-FEB PY 1992 VL 11 IS 1 BP 90 EP 98 PN 1 PG 9 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery; Transplantation SC Cardiovascular System & Cardiology; Respiratory System; Surgery; Transplantation GA HC249 UT WOS:A1992HC24900013 PM 1540618 ER PT J AU GRANT, EP ROCK, KL AF GRANT, EP ROCK, KL TI MHC CLASS-I-RESTRICTED PRESENTATION OF EXOGENOUS ANTIGEN BY THYMIC ANTIGEN-PRESENTING CELLS-INVITRO AND INVIVO SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TOXIC LYMPHOCYTES-T; SOLUBLE-PROTEIN; DENDRITIC CELLS; TOLERANCE; MOLECULES; PATHWAY; SPECIFICITY; SELECTION; MICE; H-2 AB We have used a T-T hybridoma, RF33.70, to detect the MHC class I-restricted presentation of exogenous native OVA by thymic APC in vitro. Presentation of OVA with class I molecules by thymic APC requires intracellular processing. Phenotypic analyses indicated that low bouyant density, MHC class II+, FcR+ cells are capable of using this presentation pathway. In order to determine whether thymic APC have this function in vivo, thymic APC were isolated from mice after i.v. injection of native OVA. We find that OVA is presented in association with MHC class I, but not class II, molecules in the thymus. in contrast to splenic APC, which present exogenous OVA with both class I and class II molecules under these conditions. Our findings have implications for the repertoire of self-peptides that might be presented by thymic APC to developing T lymphocytes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-20248, AI-31337] NR 42 TC 58 Z9 58 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1992 VL 148 IS 1 BP 13 EP 18 PG 6 WC Immunology SC Immunology GA GX162 UT WOS:A1992GX16200003 PM 1727862 ER PT J AU LACLETTE, JP SHOEMAKER, CB RICHTER, D ARCOS, L PANTE, N COHEN, C BING, D NICHOLSONWELLER, A AF LACLETTE, JP SHOEMAKER, CB RICHTER, D ARCOS, L PANTE, N COHEN, C BING, D NICHOLSONWELLER, A TI PARAMYOSIN INHIBITS COMPLEMENT C1 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID SCHISTOSOMA-MANSONI; TAENIA-SOLIUM; 1ST COMPONENT; ANTIGEN-B; PURIFICATION; PROTEINS; CLQ; COLLAGEN; SUBCOMPONENT; ANTIBODIES AB We report here the results of studies showing that inhibition of C is a property of several invertebrate paramyosins. Paramyosins from Taenia solium, Schistosoma mansoni, and the mussel Mytilus edulis bind polymeric collagen and can be isolated from crude extracts of tissues by collagen affinity. These paramyosins inhibit C1 function whether the C1 is isolated or present in C2-deficient serum. Because T. solium paramyosin was the best inhibitor, we concentrated further studies on this molecule. T. solium paramyosin binds purified C1q in solution with a dose/response similar to C1r2S2. Fur-ther studies of the C1-paramyosin interaction indicate that: 1) C4 is not activated, 2) C4b2a decay is not affected, and 3) there is no effect on the efficiency of C3-9, as provided in EDTA-chelated guinea pig serum, in lysing SRBC. Thus, paramyosin inhibition is directed at the initiation of the classical pathway. The results suggest that paramyosins of helminthic parasites may have a role as modulators of the host immune response through C inhibition at C1. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT TROP PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CHARLES A DANA RES INST,DEPT MED,HARVARD THORNDIKE LABS,BOSTON,MA 02215. NATL AUTONOMOUS UNIV MEXICO,INST INVEST BIOMED,DEPT IMMUNOL,MEXICO CITY 04510,DF,MEXICO. BRANDEIS UNIV,ROSENSTIEL CTR,WALTHAM,MA 02254. CTR BLOOD RES,BOSTON,MA 02115. RP LACLETTE, JP (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CHARLES A DANA RES INST,DIV INFECT DIS,BOSTON,MA 02215, USA. FU NHLBI NIH HHS [HL33768]; NIAMS NIH HHS [AR17346] NR 33 TC 113 Z9 124 U1 5 U2 6 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1992 VL 148 IS 1 BP 124 EP 128 PG 5 WC Immunology SC Immunology GA GX162 UT WOS:A1992GX16200019 PM 1727860 ER PT J AU SIMMONS, DL SATTERTHWAITE, AB TENEN, DG SEED, B AF SIMMONS, DL SATTERTHWAITE, AB TENEN, DG SEED, B TI MOLECULAR-CLONING OF A CDNA-ENCODING CD34, A SIALOMUCIN OF HUMAN HEMATOPOIETIC STEM-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN KINASE-C; MONOCLONAL-ANTIBODY; PROGENITOR CELLS; LEUKOSIALIN CD43; SURFACE-ANTIGEN; BONE-MARROW; AMINO-ACIDS; GM-CSF; SEQUENCE; GENE AB CD34 is a 115-kDa transmembrane glycoprotein of unknown function that is expressed on human hematopoietic progenitor cells and the small vessel endothelium of a variety of tissues. We have isolated a CD34 cDNA clone from a KG-1 cell library following three rounds of transient expression in COS cells and enrichment by panning with the anti-CD34 mAb MY10 and BI-3C5. The 5' and 3' ends of the full-length cDNA were subsequently amplified by polymerase chain reaction from KG-1 RNA; the final cDNA clone contained 2615 bp and ended in a poly(A) tail. COS cells transfected with the cDNA clone expressed a surface protein of approximately 110 kDa that was immunoprecipitated by MY10. Southern blot analysis suggested that CD34 is a single copy gene. A 2.7-kb CD34 transcript was observed in the hematopoietic cell lines KG-1, KMT-2, AML-1, RPMI 8402, and MOLT 13 and the endothelial cells BAE and EAhy926, but not in monocytes, resting T cells, or the cell lines Laz 509, HL-60, U937, K562, and HeLa. The cDNA sequence predicts a 40-kDa type I integral membrane protein with nine potential N-linked and numerous potential O-linked glycosylation sites in its extracellular domain. There are two consensus protein kinase C phosphorylation sites and one potential tyrosine kinase phosphorylation site in the cytoplasmic portion of CD34. CD34 has no significant sequence homology to any known protein but has some structural similarities to the heavily glycosylated leukocyte surface molecule CD43. C1 BETH ISRAEL HOSP,DIV HEMATOL ONCOL,RES & ROOM 219,330 BROOKLINE AVE,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CELL & DEV BIOL PROGRAM,BOSTON,MA 02115. FU NCI NIH HHS [CA34183] NR 43 TC 200 Z9 207 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JAN 1 PY 1992 VL 148 IS 1 BP 267 EP 271 PG 5 WC Immunology SC Immunology GA GX162 UT WOS:A1992GX16200040 PM 1370171 ER PT J AU TOONE, JR APPLEGARTH, DA LEVY, HL AF TOONE, JR APPLEGARTH, DA LEVY, HL TI PRENATAL-DIAGNOSIS OF NONKETOTIC HYPERGLYCINEMIA SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID GLYCINE CLEAVAGE SYSTEM; NONKETOTIC HYPERGLYCINEMIA; AMNIOTIC-FLUID; SERINE RATIO; PROTEIN AB Non-ketotic hyperglycinaemia (NKH) is a devastating neurological disease for which there is no effective therapy. Consequently, most couples with a pregnancy known to be at risk for NKH request prenatal diagnosis. We have applied the combination of chorionic villus (CVS) assay for glycine cleavage enzyme activity and determination of amniotic fluid glycine concentration to increase the reliability of prenatal diagnosis for this disorder beyond that of each of these methods alone. All 15 of the at-risk pregnancies monitored had CVS glycine cleavage assay and five also had amniotic fluid glycine measurements. Two cases had no detectable cleavage activity in CVS and one gave uninterpretable enzyme results. Amniotic fluid glycine concentration was increased in all three and NKH was confirmed by abortus tissue assays for cleavage activity and amino acids. The remaining 12 case had activity in CVS (two also had normal amniotic fluid glycine levels) and delivered unaffected infants. Four of these 12 cases had cleavage activities below or at the low end of the normal range, perhaps indicating carrier status. We believe that the combination of CVS glycine cleavage assay and amniotic fluid glycine measurement is currently the best approach to the prenatal diagnosis of NKH. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JOSEPH P KENNEDY JR LABS,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02129. RP TOONE, JR (reprint author), BRITISH COLUMBIA CHILDRENS HOSP,DEPT PATHOL,BIOCHEM DIS LAB,4480 OAK ST,VANCOUVER V6H 3V4,BC,CANADA. NR 14 TC 9 Z9 9 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PY 1992 VL 15 IS 5 BP 713 EP 719 DI 10.1007/BF01800011 PG 7 WC Endocrinology & Metabolism; Genetics & Heredity; Medicine, Research & Experimental SC Endocrinology & Metabolism; Genetics & Heredity; Research & Experimental Medicine GA JP565 UT WOS:A1992JP56500004 PM 1434509 ER PT J AU ODDS, FC ARAI, T DISALVO, AF EVANS, EGV HAY, RJ RANDHAWA, HS RINALDI, MG WALSH, TJ AF ODDS, FC ARAI, T DISALVO, AF EVANS, EGV HAY, RJ RANDHAWA, HS RINALDI, MG WALSH, TJ TI NOMENCLATURE OF FUNGAL DISEASES - A REPORT AND RECOMMENDATIONS FROM A SUB-COMMITTEE OF THE INTERNATIONAL-SOCIETY-FOR-HUMAN-AND-ANIMAL-MYCOLOGY (ISHAM) SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article AB The ISHAM Mycoses Nomenclature Committee has considered the present status of fungal disease names. It suggests that the traditional approach to mycoses nomenclature in which the name of a causative taxon is suffixed with '-asis', '-iasis', '-osis' or '-mycosis' leads to names that are frequently unstable with respect to subsequent taxonomic and clinico-epidemiological changes. It is therefore recommended that individual mycoses should be named as often as possible in the form 'pathology A due to/caused by fungus X' or '[adjectival] fungus X pathology A' in preference to construction of names based solely on fungal taxa. A list of recommended mycosis names retained for their long tradition or intrinsic convenience is provided, together with a combined index and list of rejected names. C1 BIOTHERAPY RES ASSOC,BUNKYO KU,TOKYO,JAPAN. DEPT PATHOL & LAB MED 350,RENO,NV. VALLABH BHAI PATEL CHEST INST,DEPT MED MYCOL,DELHI,INDIA. UNIV LEEDS,DEPT MICROBIOL,REG MYCOL LAB,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. AUDIE L MURPHY MEM VET ADM MED CTR,AUDIE L MURPHY MEM VET ADM HOSP,LAB SERV 113,SAN ANTONIO,TX 78284. NIH,BETHESDA,MD 20892. GUYS HOSP,DEPT DERMATOL,LONDON SE1 9RT,ENGLAND. RP ODDS, FC (reprint author), JANSSEN RES FDN,DEPT BACTERIOL & MYCOL,B-2430 BEERSE,BELGIUM. NR 3 TC 40 Z9 42 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1992 VL 30 IS 1 BP 1 EP 10 PG 10 WC Mycology SC Mycology GA HJ744 UT WOS:A1992HJ74400001 PM 1573518 ER PT J AU GALGIANI, JN RINALDI, MG POLAK, AM PFALLER, MA AF GALGIANI, JN RINALDI, MG POLAK, AM PFALLER, MA TI STANDARDIZATION OF ANTIFUNGAL SUSCEPTIBILITY TESTING SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article; Proceedings Paper CT 11TH CONGRESS OF THE INTERNATIONAL SOC FOR HUMAN AND ANIMAL MYCOLOGY CY JUN 24-28, 1991 CL MONTREAL, CANADA SP INT SOC HUMAN & ANIM MYCOL ID INVITRO SUSCEPTIBILITY; CANDIDA-ALBICANS; AMPHOTERICIN-B; INOCULUM SIZE; 5-FLUOROCYTOSINE; YEASTS; KETOCONAZOLE; AGENTS; FLUCYTOSINE; FLUCONAZOLE C1 UNIV ARIZONA,TUCSON,AZ 85721. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. F HOFFMANN LA ROCHE & CO LTD,CH-4002 BASEL,SWITZERLAND. UNIV OREGON,EUGENE,OR 97403. RP GALGIANI, JN (reprint author), VET ADM MED CTR,MED SERV 111,TUCSON,AZ 85723, USA. NR 39 TC 22 Z9 23 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1992 VL 30 SU 1 BP 213 EP 224 PG 12 WC Mycology SC Mycology GA KC681 UT WOS:A1992KC68100022 PM 1474447 ER PT J AU DOLAN, MJ LATTUADA, CP MELCHER, GP ZELLMER, R ALLENDOERFER, R RINALDI, MG AF DOLAN, MJ LATTUADA, CP MELCHER, GP ZELLMER, R ALLENDOERFER, R RINALDI, MG TI COCCIDIOIDES-IMMITIS PRESENTING AS A MYCELIAL PATHOGEN WITH EMPYEMA AND HYDROPNEUMOTHORAX SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID COCCIDIOIDES-IMMITIS; IDENTIFICATION; CULTURES AB A previously healthy Caucasian male developed hydropneumothorax and a pleural peel filled with pleomorphic, septate hyphae. The only organism grown from cultures of the lung and pleural fluid was Coccidioides immitis, confirmed by exoantigen testing. Spherule-endospore forms were produced, however, following injection of the arthroconidial tissue isolate into BALB/c mice. The patient had a positive immunodiffusion complement-fixation test and developed a positive coccidioidin skin test during therapy. He recovered following thoracotomy and wedge resection of the ruptured coccidioidal cavity, and therapy with amphotericin B followed by fluconazole. The sole presence of the mycelial form of the dimorphic fungus C. immitis in the pleural space may have been due to a low CO2 partial pressure at that site secondary to a bronchopleural fistula. The case shows a distinctive and uncommon presentation of coccidioidomycosis which demonstrates the specificity of both the immunodiffusion complement-fixation assay in diagnosing this disease and the exoantigen test in confirming culture results. C1 AUDIE L MURPHY MEM VET ADM MED CTR,MYCOL REFERENCE LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MICROBIOL,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,DEPT PATHOL,LACKLAND AFB,TX 78236. RP DOLAN, MJ (reprint author), WILFORD HALL USAF MED CTR,DEPT INFECT DIS,LACKLAND AFB,TX 78236, USA. NR 20 TC 14 Z9 14 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1992 VL 30 IS 3 BP 249 EP 255 PG 7 WC Mycology SC Mycology GA JG322 UT WOS:A1992JG32200008 PM 1517961 ER PT J AU ALLENDOERFER, R YATES, RR SUN, SH GRAYBILL, JR AF ALLENDOERFER, R YATES, RR SUN, SH GRAYBILL, JR TI COMPARISON OF AMPHOTERICIN-B LIPID COMPLEX WITH AMPHOTERICIN-B AND SCH-39304 IN THE TREATMENT OF MURINE COCCIDIOIDAL MENINGITIS SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article AB To assess the efficacy of amphotericin B lipid complex (ABLC) in the treatment of coccidioidal meningitis, we compared a wide range of doses (0.35-15 mg kg-1, intravenously (IV)) of ABLC with amphotericin B deoxycholate (AmB) (0.3-7 mg kg-1, intraperitoneally (IP)) and (IV) and a new triazole, SCH 39304 (SCH), in an experimental murine model. Survival data showed high dose ABLC to be of equal efficacy to IV and high dose IP AmB and SCH. Quantitative studies confirmed this outcome. No acute toxicity with ABLC, at the doses employed, was found. We conclude that ABLC is effective in the treatment of murine coccidioidal meningitis. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78242. RP ALLENDOERFER, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV INFECT DIS,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 15 TC 23 Z9 23 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PY 1992 VL 30 IS 5 BP 377 EP 384 PG 8 WC Mycology SC Mycology GA JW048 UT WOS:A1992JW04800004 PM 1469539 ER PT J AU MAROTTA, CA MAJOCHA, RE TATE, B AF MAROTTA, CA MAJOCHA, RE TATE, B TI MOLECULAR AND CELLULAR BIOLOGY OF ALZHEIMER AMYLOID SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Review ID BETA-PROTEIN-PRECURSOR; NERVE GROWTH-FACTOR; PAIRED HELICAL FILAMENTS; HEREDITARY CEREBRAL-HEMORRHAGE; PLAQUE CORE PROTEIN; BLOOD-BRAIN-BARRIER; X-RAY-DIFFRACTION; MESSENGER-RNA; NEUROFIBRILLARY TANGLES; SENILE DEMENTIA AB Alzheimer's Disease (AD), a disorder of unknown etiology, is the most common form of adult-onset dementia and is characterized by severe intellectual deterioration. The definitive diagnosis of AD is made by postmortem examination of the brain, which reveals large quantities of neurofibrillary tangles (NFT) and senile plaques within the parenchyma. The NFF are composed of paired helical filaments associated with several cytoskeletal proteins. The primary protein component of senile plaques is beta/A4 amyloid, a 42-43 amino acid peptide derived from a much larger molecule, the amyloid precursor protein (APP). Vascular beta/A4 amyloidosis is also prevalent in the disease. The mechanism by which beta/A4 amyloid accumulates in the AD brain is unknown. Recent research has demonstrated that the precursor molecule, APP, is a transmembrane protein with a large extracytoplasmic domain, a membrane spanning region that includes the portion that gives rise to beta/A4 amyloid, and a short intracytoplasmic domain. The precursor has multiple forms among which are those that differ by a variable length insert within the extracytoplasmic domain. The insert has sequence homology to the family of Kunitz protease inhibitor proteins. Cellular and animal models have been developed to study the nature of APP processing and the biological and behavioral consequences of beta/A4 amyloidosis. The results of such studies indicate that the normal processing of APP involves enzymatic cleavage of the molecule within the beta/A4 amyloid region, thus preventing the accumulation of beta/A4 in the normal brain. The factors leading to abnormal processing of APP, and consequent beta/A4 amyloid accumulation within the AD brain, have yet to be identified. In cell culture, the biological effects associated with beta/A4 amyloid include neurotrophic and neurotoxic activities, while the peptide has also been shown to have dramatic behavioral effects in animal models. C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP MAROTTA, CA (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115, USA. FU NIA NIH HHS [P01 AG02126] NR 144 TC 35 Z9 35 U1 0 U2 3 PU HUMANA PRESS INC PI TOTOWA PA 999 RIVERVIEW DRIVE SUITE 208, TOTOWA, NJ 07512 SN 0895-8696 J9 J MOL NEUROSCI JI J. Mol. Neurosci. PY 1992 VL 3 IS 3 BP 111 EP 125 DI 10.1007/BF02919403 PG 15 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HD908 UT WOS:A1992HD90800001 PM 1627458 ER PT J AU BARSKY, AJ CLEARY, PD WYSHAK, G SPITZER, RL WILLIAMS, JBW KLERMAN, GL AF BARSKY, AJ CLEARY, PD WYSHAK, G SPITZER, RL WILLIAMS, JBW KLERMAN, GL TI A STRUCTURED DIAGNOSTIC INTERVIEW FOR HYPOCHONDRIASIS - A PROPOSED CRITERION STANDARD SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID DSM-III; CLASSIFICATION; RELIABILITY; DEPRESSION; DISORDERS; ISSUES AB We developed a structured diagnostic interview for DSM-III-R hypochondriasis (SDIH) that is the first such clinician-administered instrument. The SDIH was administered to 88 general medical outpatients who scored above a predetermined cutoff on a hypochondriacal symptom questionnaire, and to 100 comparison patients randomly chosen from among those below the cutoff. Using the joint assessment method, interrater agreement on the DSM-III-R diagnostic criteria was 88% to 97% and agreement on the diagnosis was 96%. Concurrent validity was suggested by a significant correlation between the interview and the primary care physicians' ratings of hypochondriasis. A measure of external validity was demonstrated in that several clinical characteristics thought to be ancillary features of hypochondriasis were significantly more prevalent in interview-positive patients than in interview-negative patients. Finally, the SDIH appeared to have discriminant validity in that patients diagnosed as hypochondriacal had several other clinical features that distinguished them from the patients who scored above the cutoff on hypochondriacal symptomatology, but failed to be diagnosed as hypochondriacal with the SDIH. C1 MASSACHUSETTS GEN HOSP,PRIMARY CARE PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SOCIAL MED,BOSTON,MA 02115. NEW YORK STATE PSYCHIAT INST & HOSP,NEW YORK,NY 10032. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,CTR POPULAT STUDIES,BOSTON,MA 02115. COLUMBIA UNIV COLL PHYS & SURG,DEPT PSYCHIAT,NEW YORK,NY 10032. RP BARSKY, AJ (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,WARREN 631,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH40487] NR 29 TC 70 Z9 70 U1 0 U2 5 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 1992 VL 180 IS 1 BP 20 EP 27 DI 10.1097/00005053-199201000-00006 PG 8 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HA104 UT WOS:A1992HA10400005 PM 1538202 ER PT J AU LINGGOOD, RM CHAPMAN, PH AF LINGGOOD, RM CHAPMAN, PH TI PINEAL TUMORS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE PINEAL TUMORS; SURGERY; RADIATION THERAPY; CHEMOTHERAPY ID ENDODERMAL SINUS TUMOR; SUPRASELLAR GERMINOMAS; STEREOTAXIC BIOPSY; REGION TUMORS; INFRATENTORIAL; METASTASES; HYDROCEPHALUS; MANAGEMENT; THERAPY AB From 1972-1985, 30 patients with pineal area tumor have been treated with combinations of surgery and irradiation, no patient receiving chemotherapy as a primary recommendation. Patients ranged between 3 and 69 years of age, 18 were male and 12 female. In 18 patients a tissue diagnosis was made initially, 14 patients required shunts before definitive management and in 8 of the 14 tissue diagnosis was made at the same time. Eight patients had no surgical intervention at any time. Patients who have received irradiation have had whole brain irradiation, local field irradiation, or craniospinal irradiation. Two elderly patients died rapidly of their malignant processes before definitive treatment could be given. Only one patient with a non neoplastic lesion was seen. This was a bleed from an AVM with no underlying tumor. One patient with a pineocytoma was not irradiated. Overall, two-thirds of our patients are alive 5 to 15 years after treatment. There has been no surgical mortality and minimal morbidity from biopsy. Late effects of treatment include one patient with mild hearing loss and three patients with endocrinopathies amenable to medical treatment. We believe that tissue diagnosis allows optimal field design and dose recommendations to be made by the radiotherapist in addition to defining prognosis. In our experience, endodermal sinus tumor and pineoblastoma are highly malignant, and in view of their poor prognosis with conventional management consideration of more radical treatment with a possible role for chemotherapy is suggested. RP LINGGOOD, RM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 35 TC 37 Z9 38 U1 0 U2 2 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JAN PY 1992 VL 12 IS 1 BP 85 EP 91 PG 7 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA GX450 UT WOS:A1992GX45000009 PM 1541982 ER PT J AU ROLAK, LA RUTECKI, P ASHIZAWA, T HARATI, Y AF ROLAK, LA RUTECKI, P ASHIZAWA, T HARATI, Y TI CLINICAL-FEATURES OF TODD POST-EPILEPTIC PARALYSIS SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Note ID FOCAL SEIZURES AB Two hundred and twenty nine patients with generalised tonic-clonic seizures were prospectively evaluated. Fourteen were identified who had transient focal neurological deficits thought to be Todd's post-epileptic paralysis (PEP). Eight of these 14 patients had underlying focal brain lesions associated with the postictal deficits. All patients with PEP were weak, but there was wide variation in the pattern (any combination of face, arm, leg), severity (plegia to mild), tone (spastic, flaccid, or normal), and reflexes (increased, decreased, or normal). Significant sensory loss occurred in only one patient. The only other signs of PEP were aphasia (in five patients all with underlying lesions) and gaze palsy (in four patients). Post-epileptic paralysis persisted from half an hour to 36 hours (mean of 15 hours). Post-epileptic paralysis may occur with the first seizure or after many years of seizures and does not appear after every seizure. The clinical features of PEP are thus heterogeneous. C1 HOUSTON VET AFFAIRS MED CTR,HOUSTON,TX. RP ROLAK, LA (reprint author), BAYLOR COLL MED,DEPT NEUROL,6501 FANNIN,NB302,HOUSTON,TX 77030, USA. NR 16 TC 60 Z9 62 U1 2 U2 2 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD JAN PY 1992 VL 55 IS 1 BP 63 EP 64 DI 10.1136/jnnp.55.1.63 PG 2 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA HA978 UT WOS:A1992HA97800018 PM 1548500 ER PT J AU HYMAN, BT TANZI, RE MARZLOFF, K BARBOUR, R SCHENK, D AF HYMAN, BT TANZI, RE MARZLOFF, K BARBOUR, R SCHENK, D TI KUNITZ PROTEASE INHIBITOR-CONTAINING AMYLOID-BETA PROTEIN-PRECURSOR IMMUNOREACTIVITY IN ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ALZHEIMERS DISEASE; AMYLOID-BETA PROTEIN PRECURSOR; IMMUNOHISTOCHEMISTRY; KUNITZ PROTEASE INHIBITOR; SENILE PLAQUES ID MESSENGER-RNA; SENILE PLAQUES; NEXIN-II; BRAIN; EXPRESSION; DOMAIN; GENE; CDNA; LOCALIZATION; DEPOSITION AB The amyloid beta-protein (beta/A4) that is deposited in senile plaques and in cerebral vessels in Alzheimer's disease (AD) is derived from a larger membrane-associated glycoprotein, the amyloid beta-protein precursor (APP). The gene encoding APP produces at least four major transcripts. Three of the four transcripts contain an alternatively-spliced exon encoding a Kunitz protease inhibitor domain (KPI). We now report the results of a series of experiments using novel immunohistochemical reagents to anatomically localize beta/A4, APP, and KPI-containing forms of APP (APP-KPI) in the hippocampal formation and temporal neocortex. A new monoclonal antibody against beta/A4 recognized senile plaques and vascular amyloid, but no cellular elements. Anti-APP and anti-KPI monoclonal antibodies stained neurons, including proximal axons and dendrites. The neuritic component of some plaques in patients with AD and in elderly control individuals were also immunoreactive for both APP and APP-KPI. Quantitative assessment of senile plaques in temporal neocortex showed that, on average, about one-third of beta/A4 immunoreactive plaques stained with either anti-APP or anti-KPI. Amyloid beta-protein precursor and APP-KPI immunoreactivity were also found in the white and grey matter vessels of both AD patients and control individuals. These results suggest that KPI-containing forms of APP are present in dystrophic neurites of senile plaques, and normally in neurons, neuronal processes, and in the vascular compartment in the brain. Thus, APP-KPI is in a position to be intimately associated with beta/A4 deposition in the neuropil, in plaques and in amyloid angiopathy. C1 ATHENA NEUROSCI,S SAN FRANCISCO,CA. RP HYMAN, BT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,EDWARDS RES ROOM 410,FRUIT ST,BOSTON,MA 02114, USA. FU NIA NIH HHS [P 50 AG05134, AG08487] NR 42 TC 149 Z9 149 U1 1 U2 4 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 JAN PY 1992 VL 51 IS 1 BP 76 EP 83 DI 10.1097/00005072-199201000-00009 PG 8 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA GZ914 UT WOS:A1992GZ91400008 PM 1740675 ER PT J AU HUANG, Q ZHOU, D DIFIGLIA, M AF HUANG, Q ZHOU, D DIFIGLIA, M TI NEUROBIOTIN-TM, A USEFUL NEUROANATOMICAL TRACER FOR INVIVO ANTEROGRADE, RETROGRADE AND TRANSNEURONAL TRACT-TRACING AND FOR INVITRO LABELING OF NEURONS SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE BIOTIN; AVIDIN; NEUROBIOTIN-TM; BASAL GANGLIA; CEREBRAL CORTEX; ANTEROGRADE TRACING; RETROGRADE TRACING; TRANSNEURONAL TRACING; CELL CULTURE ID CULTURES; BIOCYTIN; ORIGIN; RAT AB The biotin derivative, N-(2-aminoethyl) biotinamide hydrochloride, or Neurobiotin(TM) has been shown recently to be a useful marker for intracellular and anterograde tracing. The properties of Neurobiotin(TM) as a tracer were further examined in this study by making pressure injections into different regions of the cerebral cortex or the rostral neostriatum of rats or by incubating striatal cells in culture with the tracer. Results showed extensive anterograde transport of Neurobiotin(TM) in cortical axons and terminals within the neostriatum 2-70 h after single or multiple cortical injections of the tracer. Similarly, profuse axonal projections to the medial portion of the globus pallidus were seen after an injection of Neurobiotin(TM) into the rostral neostriatum. Transneuronal labeling of medium-size neostriatal neurons was observed following injections of Neurobiotin(TM) into the prefrontal cortex. At the ultrastructural level, anterogradely labeled cortical axon terminals and transneuronally labeled neurons were readily identified in the caudate-putamen by the presence of both fine particulate and large punctate reaction products. Retrograde fillings of neurons resembling a Golgi-impregnation were seen in the ventral posterior complex of the thalamus after injections in the sensorimotor cortex. Neurons in the medial globus pallidus were also retrogradely labeled following tracer injections in the rostral caudate-putamen. Finally, Neurobiotin(TM) was readily and selectively taken up by striatal neurons in culture, where it extensively labeled somata and neurites. These results show that Neurobiotin(TM) is a versatile new tracer, which can be potentially useful for the study of neuronal organization in vivo and in vitro. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NINDS NIH HHS [NS-16367] NR 11 TC 51 Z9 51 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 J9 J NEUROSCI METH JI J. Neurosci. Methods PD JAN PY 1992 VL 41 IS 1 BP 31 EP 43 DI 10.1016/0165-0270(92)90121-S PG 13 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HF733 UT WOS:A1992HF73300004 PM 1578900 ER PT J AU HERRIN, JT AF HERRIN, JT TI EFFECTS OF URETERAL FUNCTION ON ASSESSMENT OF HYDRONEPHROSIS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID URINARY-TRACT; HYDROURETERONEPHROSIS; OBSTRUCTION; RENOGRAPHY; CHILDREN RP HERRIN, JT (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 2 Z9 2 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 JAN PY 1992 VL 33 IS 1 BP 78 EP 80 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GY676 UT WOS:A1992GY67600022 PM 1731001 ER PT J AU PAK, KY NEDELMAN, MA KANKE, M KHAW, BA MATTIS, JA STRAUSS, HW DEAN, RT BERGER, HJ AF PAK, KY NEDELMAN, MA KANKE, M KHAW, BA MATTIS, JA STRAUSS, HW DEAN, RT BERGER, HJ TI AN INSTANT KIT METHOD FOR LABELING ANTIMYOSIN FAB' WITH TC-99M - EVALUATION IN AN EXPERIMENTAL MYOCARDIAL INFARCT MODEL SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID MONOCLONAL-ANTIBODY; CHELATING AGENT; TC-99M; FRAGMENTS AB An instant kit method for labeling antibody Fab' fragments was developed. The method utilizes a ligand exchange reaction between the intermediate complex Tc-99m-D-glucarate and the free sulfhydryl groups on the antibody Fab' fragment. Radiolabeling of the Fab' using generator eluate achieves quantitative Tc-99m incorporation in less than 30 min at room temperature. The radiolabel is stable in human plasma for at least 24 hr and stable to incubation with 10 mM diethylene-triaminepentaacetic acid (24 hr) and 1 mM diaminodithiol agent (up to 3 hr). Mouse biodistribution of Tc-99m-antimyosin shows faster blood clearance and lower uptake in the lungs, liver, and spleen in comparison to In-111-antimyosin. Technetium-99m-antimyosin and In-111-antimyosin showed equivalent ability to detect myocardial infarct in a canine model. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. UNIV PENN,SCH MED,DIV NUCL MED,PHILADELPHIA,PA 19104. RP PAK, KY (reprint author), CENTOCOR INC,DIV RES & DEV,244 GREAT VALLEY PKWY,MALVERN,PA 19355, USA. NR 32 TC 22 Z9 22 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 JAN PY 1992 VL 33 IS 1 BP 144 EP 149 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GY676 UT WOS:A1992GY67600034 PM 1730981 ER PT J AU NEER, RM AF NEER, RM TI THE UTILITY OF SINGLE-PHOTON ABSORPTIOMETRY AND DUAL-ENERGY X-RAY ABSORPTIOMETRY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID BONE; FRACTURE; WOMEN; MASS; AGE RP NEER, RM (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BULLFINCH 3,BOSTON,MA 02114, USA. NR 12 TC 5 Z9 5 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 JAN PY 1992 VL 33 IS 1 BP 170 EP 170 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GY676 UT WOS:A1992GY67600039 PM 1730986 ER PT J AU HARRIGAN, TP KAREH, JA OCONNOR, DO BURKE, DW HARRIS, WH AF HARRIGAN, TP KAREH, JA OCONNOR, DO BURKE, DW HARRIS, WH TI A FINITE-ELEMENT STUDY OF THE INITIATION OF FAILURE OF FIXATION IN CEMENTED FEMORAL TOTAL HIP COMPONENTS SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article DE TOTAL HIP; INTERFACE; CEMENT; FAILURE; STAIR CLIMBING; DEBONDING ID STEM DESIGN AB In order to study initial mechanisms of failure in cemented femoral total hip components, an anatomically accurate three-dimensional linear finite element model was constructed and verified against experimental strain measurements in the cement mantle. Good agreement was found between predicted and measured strains. The likelihood of failure initiation due to cement-prosthesis debonding and crack initiation at voids was studied for loading conditions simulating both one-legged stance and stair climbing. The "out of plane" forces involved in stair climbing appear to be the greatest threat to the fixation of total hip replacements. In stair climbing, cement-prosthesis debonding and pore crack initiation were probable in the proximal anteromedial region of the cement mantle, and near the distal tip of the implant. The proximal stresses in stair climbing were higher than the distal stresses in either stair climbing or one-legged stance. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 18 TC 83 Z9 83 U1 0 U2 1 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD JAN PY 1992 VL 10 IS 1 BP 134 EP 144 DI 10.1002/jor.1100100116 PG 11 WC Orthopedics SC Orthopedics GA GX482 UT WOS:A1992GX48200015 PM 1727933 ER PT J AU GREENBERG, DB SAWICKA, J EISENTHAL, S ROSS, D AF GREENBERG, DB SAWICKA, J EISENTHAL, S ROSS, D TI FATIGUE SYNDROME DUE TO LOCALIZED RADIATION SO JOURNAL OF PAIN AND SYMPTOM MANAGEMENT LA English DT Note DE FATIGUE; RADIATION; ASTHENIA; BREAST CANCER AB For cancer patients, fatigue is a disturbing symptom caused by many factors. Since fatigue is the most common side effect of localized radiation to the breast, this treatment provides a unique opportunity to follow patients prospectively as they develop one type of fatigue. We evaluated the effect of radiation treatment in 15 women with Stage I or II node-negative breast cancer who were otherwise healthy. Fatigue, contrary to our hypothesis, did not increase linearly with cumulative radiation dose over time. It dropped from the first to second week and rose in the third week. The cumulative effects reached a plateau in the fourth week (after an average of 17 fractions), which was maintained during the remaining weeks of treatment. Within 3 wk after treatment, fatigue had diminished. No patient had sustained depressive symptoms. Cardiopulmonary exercise capacity in 5 patients at 6 and 12 wk did not change from just before radiation. Other markers, including reverse triiodothyronine and pulse change with orthostatic stress, did not correlate with subjective fatigue nor cumulative radiation in 15 patients. The curve of the fatigue syndrome during treatment conforms to the adaptation of the organism to a continuing stress and begins to describe a mild fatigue syndrome associated with radiation. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,COX 2,100 BLOSSOM ST,BOSTON,MA 02114, USA. NR 0 TC 107 Z9 107 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0885-3924 J9 J PAIN SYMPTOM MANAG JI J. Pain Symptom Manage. PD JAN PY 1992 VL 7 IS 1 BP 38 EP 45 DI 10.1016/0885-3924(92)90106-R PG 8 WC Health Care Sciences & Services; Medicine, General & Internal; Clinical Neurology SC Health Care Sciences & Services; General & Internal Medicine; Neurosciences & Neurology GA HC250 UT WOS:A1992HC25000008 PM 1538180 ER PT J AU AUGUSTINE, GJ ADLER, EM CHARLTON, MP HANS, M SWANDULLA, D ZIPSER, K AF AUGUSTINE, GJ ADLER, EM CHARLTON, MP HANS, M SWANDULLA, D ZIPSER, K TI PRESYNAPTIC CALCIUM SIGNALS DURING NEUROTRANSMITTER RELEASE - DETECTION WITH FLUORESCENT INDICATORS AND OTHER CALCIUM CHELATORS SO JOURNAL OF PHYSIOLOGY-PARIS LA English DT Article DE CALCIUM; NEUROTRANSMITTER RELEASE; FLUORESCENT INDICATORS ID SQUID GIANT SYNAPSE; TRANSMITTER RELEASE; DIFFUSION; CHANNELS; SINGLE; CELLS AB Synthetic calcium buffers, including fluorescent calcium indicators, were microinjected into squid 'giant' presynaptic nerve terminals to investigate the calcium signal that triggers neurotransmitter secretion. Digital imaging methods, applied in conjunction with the fluorescent calcium indicator dye fura-2, reveal that transient rises in presynaptic calcium concentration are associated with action potentials. Transmitter release terminates within 1-2 ms after a train of action potentials, even though presynaptic calcium concentration remains at micromolar levels for many seconds longer. Microinjection of the calcium buffer, EGTA, into the presynaptic terminal has no effect on transmitter release evoked by single presynaptic action potentials. EGTA injection does, however, block the change in calcium concentration measured by fura-2. Therefore, the calcium signal measured by fura-2 is not responsible for triggering release. These results suggest that the rise in presynaptic calcium concentration that triggers release must be highly localized to escape detection with fura-2 imaging. Unlike EGTA, microinjection of BAPTA - a calcium buffer with an equilibrium affinity for calcium similar to that of EGTA - produces a potent, dose-dependent, and reversible block of action-potential evoked transmitter release. The superior ability of BAPTA to block transmitter release apparently is due to the more rapid calcium-binding kinetics of BAPTA compared to EGTA. Because EGTA should bind calcium within a few tens of microseconds under the conditions of our experiments, the inability of EGTA to block release indicates that transmitter release is triggered within a few tens of microseconds after the entry of calcium into the presynaptic terminal. Chemical analogs of BAPTA that have altered affinity for calcium, but presumed similar on rates for calcium binding, have varied abilities to block transmitter release. The differential effects of these buffers on release are consistent with the conclusion that the presynaptic calcium signal reaches levels of 100 muM or higher in the absence of exogenous calcium buffers. The above results suggest that the presynaptic calcium signal for transmitter release has dimensions that are unconventional: very rapid (microseconds), highly localized (nanometers) and exceedingly large (hundreds of micromolar). To detect this signal, the calcium receptor that triggers release must be positioned very close to presynaptic calcium channels and must bind calcium rapidly. Further, since presynaptic calcium levels in the order of 1 muM do not trigger release while levels of hundreds of micromolar are reached during an action potential, this receptor must have a low affinity for calcium. Similar spatially localized 'domains' of calcium action may occur in all cells that produce rapid calcium-dependent events. C1 MARINE BIOL LAB,WOODS HOLE,MA 02543. MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,CHARLESTON,MA. UNIV TORONTO,DEPT PHYSIOL,TORONTO M5S 1A1,ONTARIO,CANADA. MAX PLANCK INST BIOPHYS CHEM,W-3400 GOTTINGEN,GERMANY. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. RP AUGUSTINE, GJ (reprint author), DUKE UNIV,MED CTR,DEPT NEUROBIOL,POB 3209,DURHAM,NC 27710, USA. RI Augustine, George/J-9228-2013 NR 24 TC 17 Z9 17 U1 2 U2 6 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0928-4257 J9 J PHYSIOLOGY-PARIS JI J. Physiol.-Paris PY 1992 VL 86 IS 1-3 BP 129 EP 134 DI 10.1016/S0928-4257(05)80017-8 PG 6 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA KQ851 UT WOS:A1992KQ85100016 PM 1364192 ER PT J AU OTTO, MW POLLACK, MH SACHS, GS ONEIL, CA ROSENBAUM, JF AF OTTO, MW POLLACK, MH SACHS, GS ONEIL, CA ROSENBAUM, JF TI ALCOHOL DEPENDENCE IN PANIC DISORDER PATIENTS SO JOURNAL OF PSYCHIATRIC RESEARCH LA English DT Article ID MAJOR DEPRESSION; SOCIAL PHOBIA; ANXIETY; SYMPTOMS; ABUSE; AGORAPHOBICS; WITHDRAWAL; FAMILIES; PROBANDS AB The present study examined the prevalence of alcohol dependence among panic disorder patients. Twenty-four of 100 patients had a history of alcohol dependence according to DSM-III-R criteria; only one patient met criteria for current alcohol dependence. The lifetime prevalence obtained for this clinic sample exceeded that for the general population, and appeared to be due primarily to higher than expected rates among women. A childhood history of anxiety disorders and co-morbid diagnoses of social phobia and major depression were each associated with relatively higher rates of alcohol dependence. The clinical implications of these findings are discussed. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,BOSTON,MA 02114, USA. NR 38 TC 48 Z9 51 U1 3 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0022-3956 J9 J PSYCHIAT RES JI J. Psychiatr. Res. PD JAN PY 1992 VL 26 IS 1 BP 29 EP 38 DI 10.1016/0022-3956(92)90013-E PG 10 WC Psychiatry SC Psychiatry GA HF457 UT WOS:A1992HF45700003 PM 1560407 ER PT J AU KRANE, SM AF KRANE, SM TI PROCEEDINGS - 4TH DUNLOP,EDWARD INTERNATIONAL-SYMPOSIUM - RHEUMATOID-ARTHRITIS - CURRENT CONCEPTS AND FUTURE-DIRECTIONS - MONTREAL, CANADA, MAY 23-25, 1991 - CONCLUDING REMARKS SO JOURNAL OF RHEUMATOLOGY LA English DT Editorial Material RP KRANE, SM (reprint author), MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 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 JAN PY 1992 VL 19 SU 32 BP 104 EP 106 PG 3 WC Rheumatology SC Rheumatology GA HG407 UT WOS:A1992HG40700024 ER PT J AU GERTLER, JP ABBOTT, WM AF GERTLER, JP ABBOTT, WM TI PROTHROMBOTIC AND FIBRINOLYTIC FUNCTION OF NORMAL AND PERTURBED ENDOTHELIUM SO JOURNAL OF SURGICAL RESEARCH LA English DT Review ID ACTIVATED PROTEIN-C; HUMAN UMBILICAL VEIN; SURFACE ANTICOAGULANT ACTIVITY; TUMOR-NECROSIS-FACTOR; PLASMINOGEN-ACTIVATOR; FACTOR-XA; FACTOR-VA; HEMOSTATIC PROPERTIES; PROCOAGULANT ACTIVITY; CELL PROCOAGULANT C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV VASC SURG,CAMBRIDGE,MA 02138. RP GERTLER, JP (reprint author), SUNY,HLTH SCI CTR,DIV VASC SURG,BROOKLYN,NY 11203, USA. NR 65 TC 41 Z9 41 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JAN PY 1992 VL 52 IS 1 BP 89 EP 95 DI 10.1016/0022-4804(92)90284-7 PG 7 WC Surgery SC Surgery GA GX784 UT WOS:A1992GX78400015 PM 1312653 ER PT J AU BIEDERMAN, J AF BIEDERMAN, J TI NEW DEVELOPMENTS IN PEDIATRIC PSYCHOPHARMACOLOGY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Editorial Material RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114, USA. NR 4 TC 5 Z9 5 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1992 VL 31 IS 1 BP 14 EP 15 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GZ437 UT WOS:A1992GZ43700003 PM 1537766 ER PT J AU DEVEAUGHGEISS, J MOROZ, G BIEDERMAN, J CANTWELL, D FONTAINE, R GREIST, JH REICHLER, R KATZ, R LANDAU, P AF DEVEAUGHGEISS, J MOROZ, G BIEDERMAN, J CANTWELL, D FONTAINE, R GREIST, JH REICHLER, R KATZ, R LANDAU, P TI CLOMIPRAMINE HYDROCHLORIDE IN CHILDHOOD AND ADOLESCENT OBSESSIVE-COMPULSIVE DISORDER - A MULTICENTER TRIAL SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE OBSESSIVE-COMPULSIVE DISORDER; CLOMIPRAMINE; OBSESSION; COMPULSION; Y-BOCS ID UNITED-STATES; SCALE AB Children and adolescents with obsessive compulsive disorder were studied in an 8-week, multicenter, double-blind, parallel groups trial of clomipramine hydrochloride (CMI) versus placebo. Efficacy assessments included the child version of the Yale-Brown Obsessive Compulsive Scale and the National Institute of Mental Health Global rating scale. At the end of 8 weeks, CMI-treated patients showed a mean reduction in Yale-Brown Obsessive Compulsive Scale score of 37% compared to 8% in the placebo group. Side effects were typical of tricyclic antidepressants. In a 1-year open label treatment, CMI continued to be effective and well tolerated. C1 UNIV WASHINGTON, HARBORVIEW MED CTR, SEATTLE, WA 98104 USA. CIBA GEIGY AG, PHARMACEUT, CH-4002 BASEL, SWITZERLAND. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. UNIV CALIF LOS ANGELES, INST NEUROPSYCHIAT, LOS ANGELES, CA 90024 USA. LOUIS H LAFONTAINE HOSP, MONTREAL H1N 3M5, QUEBEC, CANADA. UNIV WISCONSIN, SCH MED, MADISON, WI 53706 USA. CIBA GEIGY CORP, PHARMACEUT, SUMMIT, NJ 07901 USA. RP DEVEAUGHGEISS, J (reprint author), GLAXO INC, 5 MOORE DR, RES TRIANGLE PK, NC 27709 USA. NR 12 TC 196 Z9 196 U1 2 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0890-8567 EI 1527-5418 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1992 VL 31 IS 1 BP 45 EP 49 DI 10.1097/00004583-199201000-00008 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GZ437 UT WOS:A1992GZ43700008 PM 1537780 ER PT J AU HIRSHFELD, DR ROSENBAUM, JF BIEDERMAN, J BOLDUC, EA FARAONE, SV SNIDMAN, N REZNICK, JS KAGAN, J AF HIRSHFELD, DR ROSENBAUM, JF BIEDERMAN, J BOLDUC, EA FARAONE, SV SNIDMAN, N REZNICK, JS KAGAN, J TI STABLE BEHAVIORAL-INHIBITION AND ITS ASSOCIATION WITH ANXIETY DISORDER SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE BEHAVIORAL INHIBITION; ANXIETY DISORDER; CHILDREN; SHYNESS; TEMPERAMENT ID SOCIAL-BEHAVIOR; YOUNG-CHILDREN; CHILDHOOD; UNFAMILIAR; INTERVIEW; ETIOLOGY; VALIDITY; PARENTS AB "Behavioral inhibition to the unfamiliar" is a temperamental construct reflecting the tendency to be shy, timid, and constrained in novel situations. Previous work has suggested that it may be associated with anxiety disorders in children. Psychopathology was assessed in children from a nonclinical sample originally identified as behaviorally inhibited or uninhibited at 21 months and followed through 7 1/2 years. Children who remained inhibited at 4, 5 1/2 and 7 1/2 years (Stable Inhibited) had higher rates of anxiety disorders than children who were not consistently inhibited. Their parents had higher rates of multiple childhood anxiety disorders and of continuing anxiety disorder. These results suggest that the association between behavioral inhibition and anxiety disorder is accounted for by children who have stable behavioral inhibition. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BEHAV THERAPY UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,CHILD PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,DEPT PSYCHOL & SOCIAL RELAT,CAMBRIDGE,MA 02138. BOSTON UNIV,DOCTORAL PROGRAM CLIN PSYCHOL,BOSTON,MA 02215. YALE UNIV,DEPT PSYCHOL,NEW HAVEN,CT 06520. BROCKTON W ROXBURY VET ADM MED CTR,BROCKTON,MA. HARVARD UNIV,SCH MED,MASSACHUSETTS MENTAL HLTH CTR,BOSTON,MA 02115. RP HIRSHFELD, DR (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 34 TC 310 Z9 312 U1 3 U2 19 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1992 VL 31 IS 1 BP 103 EP 111 DI 10.1097/00004583-199201000-00016 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GZ437 UT WOS:A1992GZ43700016 PM 1537760 ER PT J AU BIEDERMAN, J AF BIEDERMAN, J TI CLINICAL-EXPERIENCE VS SCIENTIFIC STUDIES - REPLY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter ID ATTENTION DEFICIT DISORDER; DESIPRAMINE; ADD RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, 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 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1992 VL 31 IS 1 BP 170 EP 170 DI 10.1097/00004583-199201000-00027 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GZ437 UT WOS:A1992GZ43700028 ER PT J AU WILENS, TE STEINGARD, R BIEDERMAN, J AF WILENS, TE STEINGARD, R BIEDERMAN, J TI CLOMIPRAMINE FOR COMORBID CONDITIONS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter ID OBSESSIVE-COMPULSIVE DISORDER RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL CLIN,BOSTON,MA 02114, USA. NR 6 TC 7 Z9 7 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 1992 VL 31 IS 1 BP 171 EP 171 DI 10.1097/00004583-199201000-00031 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA GZ437 UT WOS:A1992GZ43700031 PM 1537774 ER PT J AU DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC GRAHAM, GF JANSEN, GT KRULL, EA STEGMAN, SJ AF DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC GRAHAM, GF JANSEN, GT KRULL, EA STEGMAN, SJ TI GUIDELINES OF CARE FOR BASAL-CELL CARCINOMA SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID CONTROLLED EXCISION; SURGICAL-TREATMENT; CURETTAGE; RECURRENCE; RADIOTHERAPY; CRYOTHERAPY; EPITHELIOMA; SKIN; ELECTRODESICCATION; CHEMOSURGERY RP DRAKE, LA (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BARTLETT-4,BOSTON,MA 02114, USA. NR 36 TC 54 Z9 54 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD JAN PY 1992 VL 26 IS 1 BP 117 EP 120 PG 4 WC Dermatology SC Dermatology GA GY248 UT WOS:A1992GY24800019 PM 1732317 ER PT J AU OSHEA, JP ABASCAL, VM WILKINS, GT MARSHALL, JE BRANDI, S ACQUATELLA, H BLOCK, PC PALACIOS, IF WEYMAN, AE AF OSHEA, JP ABASCAL, VM WILKINS, GT MARSHALL, JE BRANDI, S ACQUATELLA, H BLOCK, PC PALACIOS, IF WEYMAN, AE TI UNUSUAL SEQUELAE AFTER PERCUTANEOUS MITRAL VALVULOPLASTY - A DOPPLER ECHOCARDIOGRAPHIC STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID BALLOON VALVULOPLASTY; FOLLOW-UP; STENOSIS; VALVOTOMY; VALVE; COMMISSUROTOMY; REGURGITATION; RESTENOSIS; ADULTS AB Percutaneous mitral valvuloplasty is a promising new technique for the treatment of mitral stenosis, with a relatively low complication rate reported to date. To assess the sequelae of this procedure, Doppler echocardiographic studies were prospectively performed before and after percutaneous mitral valvuloplasty in a series of 172 patients (mean age 53 +/- 17 years). After balloon dilation, mitral valve area increased from 0.9 +/- 0.3 to 2 +/- 0.8 cm2 (p < 0.0001), mean gradient decreased from 16 +/- 6 to 6 +/- 3 mm Hg (p < 0.0001) and mean left atrial pressure decreased from 24 +/- 7 to 14 +/- 6 mm Hg (p < 0.0001). Although most patients were symptomatically improved, six (4%) were identified who had unusual sequelae evident on Doppler echocardiographic examination immediately after percutaneous mitral valvuloplasty. These included rupture of a posterior mitral valve leaflet, producing a flail distal leaflet portion with severe mitral regurgitation detected on Doppler color flow mapping (n = 1); asymptomatic rupture of the chordae tendinease attached to the anterior mitral valve leaflet with systolic anterior motion of the ruptured chordae into the left ventricular outflow tract (n = 1); a double-orifice mitral valve (n = 1); and evidence of a tear in the anterior mitral valve leaflet (n = 3), producing on both pulsed Doppler ultrasound and color flow mapping a second discrete jet of mitral regurgitation in addition to regurgitation through the main mitral valve orifice. All six patients made a satisfactory recovery and none has required mitral valve replacement. In a small percent of cases, percutaneous mitral valvuloplasty may produce unusual disruption of the mitral valve and supporting apparatus that may be readily detected by Doppler echocardiographic studies. C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,CARDIAC NONINVAS LAB,PHILLIPS HOUSE,8TH FLOOR,BOSTON,MA 02114. HOSP UNIV CARACAS,DEPT MED,CARACAS,VENEZUELA. NATL HEART FDN AUSTRALIA,CANBERRA,ACT,AUSTRALIA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CENT UNIV VENEZUELA,CARACAS,VENEZUELA. OI Acquatella, Harry/0000-0002-5115-8495 NR 17 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 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JAN PY 1992 VL 19 IS 1 BP 186 EP 191 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GX836 UT WOS:A1992GX83600029 PM 1729331 ER PT J AU LAVIZZOMOUREY, RJ ZINN, J TAYLOR, L AF LAVIZZOMOUREY, RJ ZINN, J TAYLOR, L TI ABILITY OF SURROGATES TO REPRESENT SATISFACTION OF NURSING-HOME RESIDENTS WITH QUALITY OF CARE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID LONG-TERM CARE; PATIENT SATISFACTION; MEDICAL-CARE AB Objective: To measure the ability of surrogates to accurately represent nursing home residents' satisfaction with the nursing home care. Design: Comparison by correlation analysis of questionnaire answers by nursing-home residents and their designated surrogates. Setting: Four non-profit community nursing homes. Participants: One-hundred fifty-two resident-surrogate pairs were included, based on the following criteria: (1) the resident was able to respond to questions verbally and in English, had cognitive abilities sufficient to understand the questions, and had a responsible party who had a telephone number in the medical record; (2) both the resident and the surrogate agreed to be interviewed. Outcome Measures: A 26-item instrument (21 specific and 5 global items) was developed to measure surrogates' perceptions of residents' satisfaction with the quality of the physician services, nursing care, and the nursing home environment. The instrument was scored on a 4-point Likert scale in which higher scores indicated greater satisfaction and paralleled a similar instrument designed for nursing home residents. Correlation of residents' with surrogates' scores on the satisfaction instrument was examined. Results: The mean score for most items was greater than 3.0, indicating overall satisfaction with the care. Correlations between surrogates and residents on specific items ranged from 0.1 to 0.55. Correlations were highest for global items and items addressing satisfaction with the environment. Conclusion: We conclude that nursing home residents' surrogates cannot accurately express the residents' satisfaction with all areas of nursing home care and that their evaluations should not be taken in lieu of the residents' opinions. RP LAVIZZOMOUREY, RJ (reprint author), PHILADELPHIA VET AFFAIRS MED CTR,GEN INTERNAL MED SECT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIA NIH HHS [K08AG00363-04] NR 25 TC 32 Z9 32 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JAN PY 1992 VL 40 IS 1 BP 39 EP 47 PG 9 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GY171 UT WOS:A1992GY17100008 PM 1727846 ER PT J AU WHALEN, RK ALTHAUSEN, AF DANIELS, GH AF WHALEN, RK ALTHAUSEN, AF DANIELS, GH TI EXTRAADRENAL PHEOCHROMOCYTOMA SO JOURNAL OF UROLOGY LA English DT Review DE ADRENAL GLAND NEOPLASMS; PARAGANGLIOMA; PHEOCHROMOCYTOMA ID MALIGNANT PHEOCHROMOCYTOMA; FOLLOW-UP; EXTRAADRENAL PHEOCHROMOCYTOMA; SUSPECTED PHEOCHROMOCYTOMA; I-131-MIBG SCINTIGRAPHY; SURGICAL-MANAGEMENT; URINARY-BLADDER; COMPUTED-TOMOGRAPHY; DIAGNOSIS; PARAGANGLIOMAS C1 MASSACHUSETTS GEN HOSP,DEPT MED,THYROID UNIT,BOSTON,MA 02114. RP WHALEN, RK (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114, USA. NR 156 TC 208 Z9 233 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JAN PY 1992 VL 147 IS 1 BP 1 EP 10 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA GX782 UT WOS:A1992GX78200001 PM 1729490 ER PT J AU KANTOFF, PW KALISH, LA MCDOWELLBRYANT, P CANELLOS, GP GIBBS, R RICHIE, JP GARNICK, MB AF KANTOFF, PW KALISH, LA MCDOWELLBRYANT, P CANELLOS, GP GIBBS, R RICHIE, JP GARNICK, MB TI LONG-TERM FOLLOW-UP OF 150 PATIENTS WITH TESTICULAR CANCER TREATED AT A SINGLE INSTITUTION SO JOURNAL OF UROLOGY LA English DT Article DE CARCINOMA; TESTICULAR NEOPLASMS; CISPLATIN; VINBLASTINE; BLEOMYCIN ID GERM-CELL TUMORS; PROGNOSTIC FACTORS; COMBINATION CHEMOTHERAPY; VINBLASTINE; BLEOMYCIN; CISPLATIN; TABLES AB Between 1977 and 1988, 150 patients with disseminated primary testicular germ cell tumors were treated with cisplatin, vinblastine and bleomycin. Of the 150 patients 90 (60%) achieved a complete response to chemotherapy. An additional 33 patients achieved a complete response after removal of residual masses following chemotherapy. Thus, 123 of 150 patients (82%) achieved a disease-free status following chemotherapy with or without an operation. After a median followup of 49 months the estimated long-term probability of remaining without failure and of surviving is 77%. With this data base a multivariate analysis of prognostic factors determined the Indiana University staging system to be highly predictive. Other staging systems proved to be less useful. The subset of patients with minimal and moderate disease by Indiana staging containing mature teratoma in the orchiectomy specimen has a particularly excellent prognosis (99% actuarial survival) with chemotherapy. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV UROL,BOSTON,MA 02115. GENET INST,CAMBRIDGE,MA. RP KANTOFF, PW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-06516] NR 14 TC 3 Z9 3 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 JAN PY 1992 VL 147 IS 1 BP 82 EP 88 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA GX782 UT WOS:A1992GX78200018 PM 1370332 ER PT J AU CAMBRIA, RP BREWSTER, DC ABBOTT, WM LITALIEN, GJ MEGERMAN, JJ LAMURAGLIA, GM MONCURE, AC ZELT, DT EAGLE, K AF CAMBRIA, RP BREWSTER, DC ABBOTT, WM LITALIEN, GJ MEGERMAN, JJ LAMURAGLIA, GM MONCURE, AC ZELT, DT EAGLE, K TI THE IMPACT OF SELECTIVE USE OF DIPYRIDAMOLE-THALLIUM SCANS AND SURGICAL FACTORS ON THE CURRENT MORBIDITY OF AORTIC-SURGERY SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 39TH SCIENTIFIC MEETING OF THE NORTH AMERICAN CHAPTER OF THE INTERNATIONAL SOC FOR CARDIOVASCULAR SURGERY CY JUN 03-04, 1991 CL BOSTON, MA SP INT SOC CARDIOVASC SURG, N AMER CHAPTER ID CORONARY-ARTERY DISEASE; PERIPHERAL VASCULAR-SURGERY; CARDIAC RISK; MYOCARDIAL-INFARCTION; RECONSTRUCTION; MORTALITY; ANEURYSM; ISCHEMIA; BYPASS; MANAGEMENT AB Preoperative cardiac testing in patients undergoing vascular surgery remains controversial. We have advocated selective use of dipyridamole-thallium scans based on clinical markers of coronary artery disease before aortic surgery. The present study assessed both the efficacy of this policy and the role of surgical factors in the current morbidity of aortic reconstruction. Two hundred two elective aortic reconstructions (151 abdominal aortic aneurysms, 51 aortoiliac occlusive disease) performed in the period from January 1989 to June 1990 were reviewed. Preoperative dipyridamole-thallium scanning was performed in 29% of all patients, prompting coronary angiograms in 11% and coronary artery bypass grafting/percutaneous transluminal coronary angioplasty in 9% of patients before aortic reconstruction. The overall operative mortality rate was 2%, with one cardiac-related death. Major cardiac (nonfatal myocardial infarction, unstable angina) and pulmonary complications occurred in an additional 4% and 6%, respectively, of patients. Coronary artery disease clinical markers and surgical factors were analyzed with stepwise logistic regression for the prediction of operative mortality rates and major cardiopulmonary complications. Variables retaining significance in predicting postoperative death or cardiopulmonary complications included prolonged (more than 5-hour) operative time (p < 0.004), operation for aortoiliac occlusive disease (p < 0.010), and a history of ventricular ectopy (p < 0.002). Prolonged operative time (p < 0.006) and the detection of intraoperative myocardial ischemia (p < 0.030) were predictive of major cardiac complications after univariate analysis. Selective use of the dipyridamole-thallium scan based on certain clinical markers of coronary artery disease will identify the approximately 10% of patients undergoing aortic reconstruction in whom preoperative invasive treatment of coronary artery disease is appropriate. Thereafter, the overall morbidity of aortic reconstruction, albeit minimal, is dominated by surgical factors rather than the extent of antecedent coronary artery disease. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP CAMBRIA, RP (reprint author), MASSACHUSETTS GEN HOSP,VASC SURG UNIT,BOSTON,MA 02114, USA. NR 30 TC 65 Z9 65 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JAN PY 1992 VL 15 IS 1 BP 43 EP 51 PG 9 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA GY963 UT WOS:A1992GY96300006 PM 1728689 ER PT J AU WATSON, GR WRIGHT, V DEIAUNE, W AF WATSON, GR WRIGHT, V DEIAUNE, W TI THE EFFICACY OF COMPREHENSION TRAINING AND READING PRACTICE FOR PRINT READERS WITH MACULAR LOSS SO JOURNAL OF VISUAL IMPAIRMENT & BLINDNESS LA English DT Article ID LOW VISION; PSYCHOPHYSICS AB The objectives of the project reported here were to discover whether the rehabilitation of reading recognition allows comprehension of print for low vision individuals who were former readers and to develop and test training strategies for enhancing comprehension for those who do not achieve good comprehension. C1 PENN COLL OPTOMETRY,PHILADELPHIA,PA 19141. US DEPT VET AFFAIRS,CTR REHABIL RES & DEV,DECATUR,GA 30033. RP WATSON, GR (reprint author), PENN COLL OPTOMETRY,PHILADELPHIA,PA 19141, USA. NR 49 TC 22 Z9 23 U1 0 U2 0 PU AMER FOUNDATION BLIND PI NEW YORK PA J VISUAL IMPAIRMENT BLINDNESS 11 PENN PLAZA SUITE 300, NEW YORK, NY 10001 SN 0145-482X J9 J VISUAL IMPAIR BLIN JI J. Vis. Impair. Blind. PD JAN PY 1992 VL 86 IS 1 BP 37 EP 43 PG 7 WC Rehabilitation SC Rehabilitation GA HA111 UT WOS:A1992HA11100018 ER PT J AU SMITH, AJ DEIAUNE, W GERUSCHAT, DR AF SMITH, AJ DEIAUNE, W GERUSCHAT, DR TI LOW VISION MOBILITY PROBLEMS - PERCEPTIONS OF O-AND-M SPECIALISTS AND PERSONS WITH LOW VISION SO JOURNAL OF VISUAL IMPAIRMENT & BLINDNESS LA English DT Article AB Through national survey research. this study explored low vision mobility problems, including the effects of different lighting conditions and the relationship between the reported perceptions of mobility practitioners and persons with low vision. C1 US DEPT VET AFFAIRS,CTR REHABIL RES & DEV,DECATUR,GA 30033. MARYLAND SCH BLIND,RES,BALTIMORE,MD 21236. RP SMITH, AJ (reprint author), PENN COLL OPTOMETRY,1200 W GODFREY AVE,PHILADELPHIA,PA 19141, USA. NR 24 TC 17 Z9 17 U1 0 U2 1 PU AMER FOUNDATION BLIND PI NEW YORK PA J VISUAL IMPAIRMENT BLINDNESS 11 PENN PLAZA SUITE 300, NEW YORK, NY 10001 SN 0145-482X J9 J VISUAL IMPAIR BLIN JI J. Vis. Impair. Blind. PD JAN PY 1992 VL 86 IS 1 BP 58 EP 62 PG 5 WC Rehabilitation SC Rehabilitation GA HA111 UT WOS:A1992HA11100022 ER PT J AU RAY, WA TAYLOR, JA LICHTENSTEIN, MJ MEADOR, KG AF RAY, WA TAYLOR, JA LICHTENSTEIN, MJ MEADOR, KG TI THE NURSING-HOME BEHAVIOR PROBLEM SCALE SO JOURNALS OF GERONTOLOGY LA English DT Article ID ALZHEIMERS-DISEASE; RATING-SCALE; PSYCHOACTIVE MEDICATION; MENTAL IMPAIRMENT; DEMENTIA SCALE; SYMPTOMS; CARE; RELIABILITY; DISTURBANCE; INSTRUMENT AB Nursing home patients frequently have serious disturbances of behavior that can lead to use of chemical or physical restrains. To support research into better management of these problems, we developed the Nursing Home Behavior Problem Scale (NHBPS), a 29-item inventory of serious behavior problems designed to be completed by nurses and nursing assistants. NHBPS scores were obtained for two samples of nursing home residents: 431 in Tennessee and 122 in Texas. The interrater correlation was .754 in the Tennessee sample and .827 in the Texas sample. The NHBPS had a correlation of -.747 with the NOSIE scale and .911 with the CMAI. There was a pronounced association of increased NHBPS scores with mental impairment and use of sedative drugs or restrains. These data suggest the NHBPS is a useful research instrument for measuring serious behavior problems in nursing home residents. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT PSYCHIAT,NASHVILLE,TN 37232. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. RP RAY, WA (reprint author), VANDERBILT UNIV,MED CTR,SCH MED,DEPT PREVENT MED,NASHVILLE,TN 37232, USA. NR 52 TC 79 Z9 79 U1 0 U2 1 PU GERONTOLOGICAL SOCIETY AMER PI WASHINGTON PA 1275 K STREET NW SUITE 350, WASHINGTON, DC 20005-4006 SN 0022-1422 J9 J GERONTOL JI J. Gerontol. PD JAN PY 1992 VL 47 IS 1 BP M9 EP M16 PG 8 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA GY680 UT WOS:A1992GY68000012 PM 1730851 ER PT J AU BELL, D SCULLY, R AF BELL, D SCULLY, R TI CLINICOPATHOLOGICAL FEATURES OF LYMPH-NODE (LN) INVOLVEMENT WITH OVARIAN SEROUS BORDERLINE TUMORS (OSBT) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A61 EP A61 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600368 ER PT J AU BELL, D LAGE, J AF BELL, D LAGE, J TI CLINICOPATHOLOGICAL CORRELATES OF SERUM CA-125 LEVELS IN OVARIAN BORDERLINE TUMORS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20007. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A61 EP A61 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600367 ER PT J AU BROOKS, JJ HERGAN, R RYAN, L AF BROOKS, JJ HERGAN, R RYAN, L TI PROGNOSTIC-SIGNIFICANCE OF HLA-DR PARAFFIN IMMUNOREACTIVITY IN MALIGNANT FIBROUS HISTIOCYTOMA (MFH) SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A4 EP A4 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600027 ER PT J AU CENTENO, BA LOUIS, DN KUPSKY, WJ SOBEL, RA AF CENTENO, BA LOUIS, DN KUPSKY, WJ SOBEL, RA TI THE AGNOR TECHNIQUE IN THE EVALUATION OF CHOROID-PLEXUS TUMORS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A105 EP A105 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600632 ER PT J AU EICHHORN, JH YOUNG, RH SCULLY, RE AF EICHHORN, JH YOUNG, RH SCULLY, RE TI PRIMARY OVARIAN SMALL-CELL CARCINOMAS OF NON-HYPERCALCEMIC TYPE - A REPORT OF 8 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A63 EP A63 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600381 ER PT J AU EICHHORN, JH BELL, DA YOUNG, RH SWYMER, C FLOTTE, TJ PREFFER, F SCULLY, RE AF EICHHORN, JH BELL, DA YOUNG, RH SWYMER, C FLOTTE, TJ PREFFER, F SCULLY, RE TI DNA CONTENT AND PROLIFERATIVE ACTIVITY IN OVARIAN SMALL-CELL CARCINOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A63 EP A63 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600380 ER PT J AU FERRY, J WHITE, W GROVE, A HARRIS, N AF FERRY, J WHITE, W GROVE, A HARRIS, N TI MALIGNANT-LYMPHOMA OF OCULAR ADNEXA - A SPECTRUM OF B-CELL NEOPLASIA INCLUDING LOW-GRADE B-CELL LYMPHOMA OF MALT TYPE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A77 EP A77 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600463 ER PT J AU HIRAKAWA, T THOR, AD OSAWA, Y MASON, JI SCULLY, RE AF HIRAKAWA, T THOR, AD OSAWA, Y MASON, JI SCULLY, RE TI STROMAL HYPERTHECOSIS OF THE OVARY - IMMUNOHISTOCHEMICAL DISTRIBUTION OF STEROIDOGENIC ENZYMES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MED FDN BUFFALO INC,BUFFALO,NY 14203. UNIV TEXAS,SW MED CTR,DALLAS,TX 75230. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A65 EP A65 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600390 ER PT J AU JONES, EC CLEMENT, PB YOUNG, RH AF JONES, EC CLEMENT, PB YOUNG, RH TI INFLAMMATORY PSEUDOTUMOR OF THE URINARY-BLADDER - A STUDY OF 11 CASES SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 VANCOUVER GEN HOSP,VANCOUVER V5Z 1M9,BC,CANADA. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A54 EP A54 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600329 ER PT J AU KAPLAN, MA FERRY, JA HARRIS, NL JACOBSON, JO AF KAPLAN, MA FERRY, JA HARRIS, NL JACOBSON, JO TI CLONAL ANALYSIS OF THE EPSTEIN-BARR-VIRUS (EBV) GENOME AND IMMUNOGLOBULIN (IG) GENES IN LYMPHOMAS OF TRANSPLANT RECIPIENTS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A80 EP A80 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600481 ER PT J AU MATTIA, AR FERRY, JA KOERNER, FC HARRIS, NL AF MATTIA, AR FERRY, JA KOERNER, FC HARRIS, NL TI BREAST LYMPHOMA - A B-CELL SPECTRUM INCLUDING LOW GRAPE MALTOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A83 EP A83 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600498 ER PT J AU OCONNELL, JX OJEMANN, RG PALMER, W PLATA, MJ ROSENBERG, AE AF OCONNELL, JX OJEMANN, RG PALMER, W PLATA, MJ ROSENBERG, AE TI GIANT CYSTIC ARACHNOID GRANULATIONS - AN UNUSUAL CAUSE OF LYTIC SKULL DEFECTS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A10 EP A10 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600065 ER PT J AU OCONNELL, JX KATTAPURAM, SV ROSENBERG, AE AF OCONNELL, JX KATTAPURAM, SV ROSENBERG, AE TI EPITHELIOID HEMANGIOMAS OF BONE SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A10 EP A10 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600064 ER PT J AU ROBERTS, DJ HABER, D SKLAR, J CRUM, CP AF ROBERTS, DJ HABER, D SKLAR, J CRUM, CP TI A WILMS-TUMOR GENE IS EXPRESSED IN A DISTINCT SUBSET OF EXTRARENAL WILMS-TUMORS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV DIAGNOST PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A108 EP A108 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600652 ER PT J AU TAMURA, A MATSUBARA, O THAN, KW KASUGA, T MARK, EJ AF TAMURA, A MATSUBARA, O THAN, KW KASUGA, T MARK, EJ TI IMMUNOHISTOCHEMICAL STUDY ON THE STRUCTURAL-CHANGES OF THE ALVEOLAR BASEMENT-MEMBRANE IN DAD SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 TOKYO MED & DENT UNIV,TOKYO 113,JAPAN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A116 EP A116 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600701 ER PT J AU THOR, AD MOORE, DH EDGERTON, SM KAWASAKI, ES REIHSAUS, E LYNCH, HT MARCUS, JN SMITH, HS AF THOR, AD MOORE, DH EDGERTON, SM KAWASAKI, ES REIHSAUS, E LYNCH, HT MARCUS, JN SMITH, HS TI ACCUMULATION OF P53 TUMOR SUPPRESSOR GENE PROTEIN IS AN INDEPENDENT MARKER OF PROGNOSIS IN BREAST CANCERS SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV CALIF LAWRENCE LIVERMORE NATL LAB,LIVERMORE,CA 94550. CETUS CORP,EMERYVILLE,CA 94608. CREIGHTON UNIV,OMAHA,NE 68178. 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 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A18 EP A18 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600113 ER PT J AU TORNOS, C SILVA, EG MCCABE, KM ORDONEZ, NG GERSHENSON, DM SCULLY, RE AF TORNOS, C SILVA, EG MCCABE, KM ORDONEZ, NG GERSHENSON, DM SCULLY, RE TI THE SPINDLE CELL VARIANT OF ENDOMETRIOID CARCINOMA SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77025. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JAN PY 1992 VL 66 IS 1 BP A69 EP A69 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600419 ER PT J AU ZUKERBERG, L FERRY, J LEVY, M HARRIS, N AF ZUKERBERG, L FERRY, J LEVY, M HARRIS, N TI EXPRESSION OF B-CELL ANTIGENS BY REED-STERNBERG CELLS IN NS AND MCHD SO LABORATORY INVESTIGATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 3 Z9 3 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 JAN PY 1992 VL 66 IS 1 BP A90 EP A90 PG 1 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA HA276 UT WOS:A1992HA27600545 ER PT J AU SULLIVAN, PK FABIAN, R DRISCOLL, D AF SULLIVAN, PK FABIAN, R DRISCOLL, D TI MANDIBULAR OSTEOTOMIES FOR TUMOR EXTIRPATION - THE ADVANTAGES OF RIGID FIXATION SO LARYNGOSCOPE LA English DT Article AB Adequate exposure of intraoral tumors occupying the posterior oral cavity, base of tongue, tonsil, and superior hypopharynx for wide-field primary surgical resection is critical to precise tumor ablation. The exposure resulting from a mandibular osteotomy has greatly assisted the tumor ablation of these areas. This procedure has also been beneficial in providing exposure to the anterior skull base, pterygomaxillary, and infratemporal space, clivus, and nasopharynx. In evaluating various osteotomy sites and methods of fixation, we reviewed 26 patients treated for benign or malignant neoplasia of the head and neck requiring mandibulotomy. The osteotomy complication rate was 2 (29%) of 7 for wire osteosynthesis and 1 (5.3%) of 19 for plate osteosynthesis. All patients with osteotomy complications had received preoperative radiation therapy. The one complication in the plated group was associated with a lateral stairstep osteotomy and two screws on either side of the osteotomy. This study suggests advantages of absolute rigid internal fixation of mandibular osteotomies used for tumor ablation. It is also concluded that a midline osteotomy reapproximated with rigid internal fixation has the benefits of 1. primary bone healing by means of plating counteracting the balanced forces acting on the symphysis; 2. improved reapproximation with minimal bony loss, improving occlusion; 3. decreased incidence of osteoradionecrosis as the symphysis lies outside the usual radiation ports; 4. preservation of the neurovascular bundle; and 5. maintenance of osteotomy-site immobility in an infected field. This review helped identify surgical techniques that decrease the complications that are commonly associated with mandibular osteotomies for precise tumor ablation. C1 MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL HEAD & NECK SURG,BOSTON,MA 02114. BROWN UNIV,AFFILIATED HOSP,DIV PLAST SURG & OTOLARYNGOL HEAD & NECK SURG,PROVIDENCE,RI 02912. NR 12 TC 28 Z9 31 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD JAN PY 1992 VL 102 IS 1 BP 73 EP 80 PG 8 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA HA475 UT WOS:A1992HA47500015 PM 1731161 ER PT J AU HORVATH, KA TORCHIANA, DF DAGGETT, WM NISHIOKA, NS AF HORVATH, KA TORCHIANA, DF DAGGETT, WM NISHIOKA, NS TI MONITORING MYOCARDIAL REPERFUSION INJURY WITH NADH FLUOROMETRY SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE ENRICHED REPERFUSATE; METABOLISM; NADH FLUORESCENCE ID FLUORESCENCE PHOTOGRAPHY; ISCHEMIA; STATES; HEART AB Using NADH fluorometry to monitor myocardial metabolism, the mechanism of reperfusion injury was investigated after the delivery of an experimental reperfusate. Using an isolated working heart preparation, rat hearts underwent 15 min of global ischemia at 37-degrees-C. Following the ischemic insult, an oxygenated enriched reperfusion solution was given for 5 min. The hearts were then returned to a working state and aortic flow recorded to evaluate recovery. NADH levels were monitored throughout the experiment with a fluorometer and glycogen, AMP, ADP, and ATP were measured biochemically pre- and postischemia, after reperfusion and after recovery. In this study, reperfusion injury was best abated by an enriched reperfusate. Our results indicate the mechanism for this amelioration is not high-energy phosphate replenishment. Rather, as indicated by NADH fluorescence, the hearts attain an intermediate level of metabolism that permits glycogen to be restored and functional recovery to be improved. C1 WELLMAN LABS PHOTOMED,50 BLOSSOM ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT CARDIAC SURG,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 12777] NR 14 TC 14 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1992 VL 12 IS 1 BP 2 EP 6 DI 10.1002/lsm.1900120103 PG 5 WC Dermatology; Surgery SC Dermatology; Surgery GA HB780 UT WOS:A1992HB78000001 PM 1614262 ER PT J AU DECOSTE, SD FARINELLI, W FLOTTE, T ANDERSON, RR AF DECOSTE, SD FARINELLI, W FLOTTE, T ANDERSON, RR TI DYE-ENHANCED LASER-WELDING FOR SKIN CLOSURE SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE THERMAL; PHOTOTHERMAL; INDOCYANINE GREEN; PHOTOSENSITIZATION ID CARBON-DIOXIDE LASER; ARGON-LASER; RAT; SUTURE AB The use of a laser to weld tissue in combination with a topical photosensitizing dye permits selective delivery of energy to the target tissue. A combination of indocyanine green (IG), absorption peak 780 nm, and the near-infrared (IR) alexandrite laser was studied with albino guinea pig skin. IG was shown to bind to the outer 25-mu-m of guinea pig dermis and appeared to be bound to collagen. The optical transmittance of full-thickness guinea pig skin in the near IR was 40% indicating that the alexandrite laser should provide adequate tissue penetration. Laser "welding" of skin in vivo was achieved at various concentrations of IG from 0.03 to 3 mg/cc using the alexandrite at 780 nm, 250-mu-sec pulse duration, 8 Hz, and a 4-mm spot size. A spectrum of welds was obtained from 1- to 20-W/cm2 average irradiance. Weak welds occurred with no thermal damage obtained at lower irradiances: stronger welds with thermal damage confined to the weld site occurred at higher irradiances. At still higher irradiances, local vaporization occurred with failure to "weld." Thus, there was an optimal range of irradiances for "welding," which varied inversely with dye concentration. Histology confirmed the thermal damage results that were evident clinically. IG dye-enhanced laser welding is possible in skin and with further optimization may have practical application. C1 MASSACHUSETTS GEN HOSP,WELLMAN LAB,DEPT DERMATOL,BOSTON,MA 02114. NR 16 TC 69 Z9 69 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 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1992 VL 12 IS 1 BP 25 EP 32 DI 10.1002/lsm.1900120107 PG 8 WC Dermatology; Surgery SC Dermatology; Surgery GA HB780 UT WOS:A1992HB78000005 PM 1377319 ER PT J AU SCHOMACKER, KT FRISOLI, JK COMPTON, CC FLOTTE, TJ RICHTER, JM NISHIOKA, NS DEUTSCH, TF AF SCHOMACKER, KT FRISOLI, JK COMPTON, CC FLOTTE, TJ RICHTER, JM NISHIOKA, NS DEUTSCH, TF TI ULTRAVIOLET LASER-INDUCED FLUORESCENCE OF COLONIC TISSUE - BASIC BIOLOGY AND DIAGNOSTIC POTENTIAL SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE FLUORESCENCE; DIAGNOSTICS; ADENOMA; HYPERPLASIA; POLYPS; LASER ID COLORECTAL POLYPS; SPECTROSCOPY; BRAIN; ANGIOPLASTY; SPECTRA; INVIVO; AORTA AB Laser-induced fluorescence (LIF) of colonic tissue was examined both in vitro and in vivo to assess the ability of the technique to distinguish neoplastic from hyperplastic and normal tissue and to relate the LIF spectra to specific constituents of the colon. Spectra from 86 normal colonic sites, 35 hyperplastic polyps, 49 adenomatous polyps, and 7 adenocarcinomas were recorded both in vivo and in vitro. With 337-nm excitation, the fluorescence spectra all had peaks at 390 and 460 nm, believed to arise from collagen and NADH, and a minimum at 425 nm, consistent with absorption attributable to hemoglobin. The spectra of colonic tissue recorded both in vivo and in vitro are different, primarily in the NADH fluorescence component, which decays exponentially with time after resection. When normal colonic tissue is compared to hyperplastic or adenomatous polyps, the predominant changes in the fluorescence spectra are a decrease in collagen fluorescence and a slight increase in hemoglobin reabsorption. A multivariate linear regression (MVLR) analysis was used to distinguish neoplastic tissue from non-neoplastic tissue with a sensitivity, specificity, predictive value positive, and predictive value negative toward neoplastic tissue of 80%, 92%, 82%, and 91%, respectively. When the MVLR technique was used to distinguish neoplastic polyps from non-neoplastic polyps, values of 86%, 77%, 86%, and 77% respectively, were obtained. The data suggest that the LIF measurements sense changes in polyp morphology, rather than changes in fluorophores specific to polyps, and it is this change in morphology that leads indirectly to discrimination of polyps. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 34 TC 355 Z9 362 U1 1 U2 14 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1992 VL 12 IS 1 BP 63 EP 78 DI 10.1002/lsm.1900120111 PG 16 WC Dermatology; Surgery SC Dermatology; Surgery GA HB780 UT WOS:A1992HB78000009 PM 1614265 ER PT J AU REN, Q VENUGOPALAN, V SCHOMACKER, K DEUTSCH, TF FLOTTE, TJ PULIAFITO, CA BIRNGRUBER, R AF REN, Q VENUGOPALAN, V SCHOMACKER, K DEUTSCH, TF FLOTTE, TJ PULIAFITO, CA BIRNGRUBER, R TI MIDINFRARED LASER ABLATION OF THE CORNEA - A COMPARATIVE-STUDY SO LASERS IN SURGERY AND MEDICINE LA English DT Article DE PULSE DURATIONS; CORNEAL TREPHINATION; ABLATION THRESHOLDS ID EXCIMER LASER; THERMAL-DAMAGE; YAG LASER; PULSE DURATION; TISSUE-TYPE; SURGERY; KERATOPLASTY; INCISIONS AB The ablation thresholds and patterns of collateral damage in cornea produced by Er:YAG (2.94-mu-m) and Er:YSGG (2.79-mu-m) lasers were measured. Two different pulse durations, 200-mu-s (normal spiking mode) and 100 ns (Q-switched mode), were used at both wavelengths. In the normal spiking mode, damage zones of 16 +/-2-mu-m and 39 +/- 7-mu-m and ablation thresholds of 250 +/- 20 mJ/cm2 and 420 +/- 35 mJ/cm2 were measured at 2.94-mu-m and 2.79-mu-m, respectively. In the Q-switched mode, damage zones of 4 +/- 2-mu-m and ablation thresholds of 150 +/- 10 mJ/cm2 were found irrespective of the laser used. The similarity between the results using the Er:YAG and Er:YSGG lasers in the Q-switched mode suggest that either laser can be used with equal effectiveness for corneal trephination. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,LASER RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP REN, Q (reprint author), UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,CTR OPHTHALM BIOPHYS,1638 NW 10TH AVE,MIAMI,FL 33136, USA. RI Ren, Qiushi/D-1451-2012; Birngruber, Reginald/Q-2342-2016 NR 29 TC 53 Z9 54 U1 1 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0196-8092 J9 LASER SURG MED JI Lasers Surg. Med. PY 1992 VL 12 IS 3 BP 274 EP 281 DI 10.1002/lsm.1900120306 PG 8 WC Dermatology; Surgery SC Dermatology; Surgery GA HY299 UT WOS:A1992HY29900005 PM 1508021 ER PT J AU SESSIONS, C LAWRENCE, D CLINKINGBEARD, C SHENKER, Y AF SESSIONS, C LAWRENCE, D CLINKINGBEARD, C SHENKER, Y TI REGULATION OF ADRENAL ATRIAL NATRIURETIC HORMONE RECEPTOR SUBTYPES SO LIFE SCIENCES LA English DT Article ID SMOOTH-MUSCLE CELLS; ALDOSTERONE SECRETION; PHYSIOLOGICAL-ROLE; DECREASED DENSITY; ALPHA-HANP; PEPTIDE; RAT; INHIBITION; CGMP; STIMULATION AB Regulation of atrial natriuretic hormone (ANH) receptor binding and aldosterone suppression was studied in isolated adrenal glomerulosa cells from rats fed a high-salt (HS) or low-salt (LS) diet for 3 days. In plasma of HS rats, aldosterone levels were 5 times lower and immunoreactive ANH two times higher than in LS rats. Competitive binding studies showed the same affinity for human atrial natriuretic hormone (hANH) in both pools of cells, but receptor density was 50% higher on LS cells. A linear ANH analog that binds to non-guanylate-cyclase-coupled receptors did not show increased binding to LS cells. Cyclic GMP production in response to hANH was identical in both groups. The aldosterone-inhibitory effect of hANH on both groups of basal and angiotensin II-stimulated cells was also identical. Thus a short-term high-salt diet causes decreased density of ANH receptors in glomerulosa cells without changing biological activity of ANH. These results suggest that dietary salt content changes the number of ANH receptors and that non-guanylate-cyclase-coupled receptors contain at least two classes of receptors. C1 UNIV WISCONSIN,DEPT INTERNAL MED,ENDOCRINOL & METAB SECT,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NIDDK NIH HHS [R29-DK-39444] NR 36 TC 9 Z9 9 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PY 1992 VL 50 IS 15 BP 1087 EP 1095 DI 10.1016/0024-3205(92)90345-P PG 9 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA HG809 UT WOS:A1992HG80900003 PM 1313518 ER PT J AU RAMESH, V CHENG, SV KOZAK, CA HERRON, BJ SHIH, VE TAYLOR, BA GUSELLA, JF AF RAMESH, V CHENG, SV KOZAK, CA HERRON, BJ SHIH, VE TAYLOR, BA GUSELLA, JF TI MAPPING OF ORNITHINE AMINOTRANSFERASE GENE-SEQUENCES TO MOUSE CHROMOSOME-7, CHROMOSOME-X, AND CHROMOSOME-3 SO MAMMALIAN GENOME LA English DT Article ID GYRATE ATROPHY; STRUCTURAL GENE; OAT LOCUS; RETINA; LOCALIZATION; DISEASE; CLONING; MICE AB Ornithine aminotransferase (OAT), a mitochondrial matrix enzyme, is deficient in patients with gyrate atrophy of the choroid and retina. In human, the OAT structural gene maps to Chromosome (Chr) 10q26 and several OAT-related sequences, some of which are known to be processed pseudogenes, which map to Xp11.3-11.21. Here, we report chromosomal localization in the mouse of the OAT gene and related sequences. Genomic DNA blot analysis of a well-characterized panel of Chinese hamster x mouse somatic cell hybrids using a human OAT probe revealed two murine loci, one on mouse Chr 7 and the other on Chr X. In addition, segregation of restriction fragment length polymorphisms (RFLPs) detected by the OAT probe in recombinant inbred (RI) strains detected a third locus on Chr 3 and positioned the X locus near Cf-8 and Rsvp. Progeny of an intersubspecific back-cross were used to map the Chr 7 locus between Tyr and Int-2, near Cyp2e-1. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,NEUROL SERV,AMINO ACID DISORDER LAB,BOSTON,MA 02129. NIAID,MOLEC MICROBIOL LAB,BETHESDA,MD 20892. JACKSON LAB,BAR HARBOR,ME 04609. FU NEI NIH HHS [EY05633]; NHGRI NIH HHS [HG00169]; NINDS NIH HHS [NS05096] NR 32 TC 10 Z9 10 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1992 VL 3 IS 1 BP 17 EP 22 DI 10.1007/BF00355836 PG 6 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA JT426 UT WOS:A1992JT42600004 PM 1349842 ER PT J AU KOIZUMI, T MACDONALD, M BUCAN, M HOPWOOD, JJ MORRIS, CP SCOTT, HS GUSELLA, JF NADEAU, JH AF KOIZUMI, T MACDONALD, M BUCAN, M HOPWOOD, JJ MORRIS, CP SCOTT, HS GUSELLA, JF NADEAU, JH TI LINKAGE, BUT NOT GENE ORDER, OF HOMOLOGOUS LOCI, INCLUDING ALPHA-L-IDURONIDASE (IDUA), IS CONSERVED IN THE HUNTINGTON DISEASE REGION OF THE MOUSE AND HUMAN GENOMES SO MAMMALIAN GENOME LA English DT Article ID DNA MARKERS; MAPS; CHROMOSOME-17; SYNTENY; COMPLEX; 4P16.3; FAMILY AB Alpha-L-iduronidase (IDUA), which when deficient causes mucopolysaccharidosis type I, is located near the Huntington disease locus (HD) on human Chromosome (Chr) 4p16.3, approximately 10(6) base pairs (bp) from the telomere. As part of our continuing efforts to define a detailed comparative map for this chromosomal segment in mice and humans, we have used an interspecific backcross between C57BL/6J and an inbred strain derived from Mus spretus to map Idua, the mouse homolog of IDUA. We also mapped the mouse homolog of D4S115, an anonymous locus approximately 250 kb proximal to IDUA. As expected, both Idua and D4S115h are located on the proximal portion of mouse Chr 5 near homologs for other loci on human Chr 4p. Comparison of gene order in mice and humans demonstrates, however, that a chromosomal rearrangement within this conserved synteny has occurred since divergence of lineages leading to mice and humans. C1 KANAZAWA UNIV,SCH MED,INST EXPTL ANIM,KANAZAWA,ISHIKAWA 920,JAPAN. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV PENN,SCH MED,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. ADELAIDE CHILDRENS HOSP INC,DEPT CHEM PATHOL,LYSOSOMAL DIS RES UNIT,ADELAIDE,SA 5006,AUSTRALIA. JACKSON LAB,BAR HARBOR,ME 04609. RI Scott, Hamish/B-2122-2009 OI Scott, Hamish/0000-0002-5813-631X FU NHGRI NIH HHS [HG00169, HG00189]; NICHD NIH HHS [HD21355] NR 31 TC 11 Z9 11 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1992 VL 3 IS 1 BP 23 EP 27 DI 10.1007/BF00355837 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA JT426 UT WOS:A1992JT42600005 PM 1533802 ER PT J AU AMBROSE, C CHENG, S FONTAINE, B NADEAU, JH MACDONALD, M GUSELLA, JF AF AMBROSE, C CHENG, S FONTAINE, B NADEAU, JH MACDONALD, M GUSELLA, JF TI THE ALPHA-SUBUNIT OF THE SKELETAL-MUSCLE SODIUM-CHANNEL IS ENCODED PROXIMAL TO TK-1 ON MOUSE CHROMOSOME-11 SO MAMMALIAN GENOME LA English DT Article ID HYPERKALEMIC PERIODIC PARALYSIS; GROWTH-HORMONE GENE; THYMIDINE KINASE; PARAMYOTONIA-CONGENITA; MOLECULAR-CLONING; RAT-BRAIN; LINKAGE; LOCALIZATION; EXPRESSION; LOCUS AB Recent evidence suggests that the human neuromuscular disorders, hyperkalemic periodic paralysis and paramyotonia congenita, are both caused by genetic defects in the alpha-subunit of the adult skeletal muscle sodium channel, which maps near the growth hormone cluster (GH) on Chromosome (Chr) 17q. In view of the extensive homology between this human chromosome and mouse Chr 11, we typed an interspecies backcross to determine whether the murine homolog (Scn4a) of this sodium channel gene mapped within the conserved chromosomal segment. The cytosolic thymidine kinase gene, Tk-1, was also positioned on the genetic map of Chr 11. Both Scn4a and Tk-1 showed clear linkage to mouse Chr 11 loci previously typed in this backcross, yielding the map order: Tr(J)-(Re, Hox-2, Krt-1)-Scn4a-Tk-1. No mouse mutant that could be considered a model of either hyperkalemic periodic paralysis or paramyotonia congenita has been mapped to the appropriate region of mouse Chr 11. These data incorporate an additional locus into the already considerable degree of homology observed for these human and mouse chromosomes. These data are also consistent with the view that the conserved segment region may extend to the telomere on mouse Chr 11 and on human 17q. C1 HARVARD UNIV,DEPT GENET,BOSTON,MA 02129. JACKSON LAB,BAR HARBOR,ME 04609. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. FU NHGRI NIH HHS [HG00189, HG00169]; NINDS NIH HHS [NS22224] NR 45 TC 11 Z9 11 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1992 VL 3 IS 3 BP 151 EP 155 DI 10.1007/BF00352459 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA JT432 UT WOS:A1992JT43200003 PM 1352160 ER PT J AU WHITE, RA BIRKENMEIER, CS PETERS, LL BARKER, JE LUX, SE AF WHITE, RA BIRKENMEIER, CS PETERS, LL BARKER, JE LUX, SE TI MURINE ERYTHROCYTE ANKYRIN CDNA - HIGHLY CONSERVED REGIONS OF THE REGULATORY DOMAIN SO MAMMALIAN GENOME LA English DT Article ID HEREDITARY SPHEROCYTOSIS; MEMBRANE-SKELETON; BINDING-SITES; CYTOPLASMIC DOMAIN; FUNCTIONAL DOMAINS; STRUCTURAL BASIS; MESSENGER-RNAS; BRAIN ANKYRIN; SPECTRIN; PROTEIN AB Ankyrin is an essential link between cyto-skeletal proteins, such as spectrin, and membrane bound proteins, such as protein 3, the erythrocyte anion exchanger. Although the amino acid structure of human ankyrin is known, the functional regions have been only partially defined. Sequence comparisons between mouse and human ankyrin offer one mechanism of identifying highly conserved regions that probably have functional significance. We report the isolation and sequencing of a series of overlapping murine erythroid ankyrin (Ank-1) cDNAs from spleen and reticulocyte libraries (total span 6238 bp) and identify potentially important regions of murine-human reticulocyte ankyrin homology. Comparison of the predicted peptide sequences of mouse and human erythroid ankyrins shows that these ankyrins are highly conserved in both the N-terminal, protein 3 binding domain (96% amino acid identity) and in the central spectrin-binding domain (97% identity), but differ in the C-terminal regulatory domain (79% identity). However, the C-terminal regulatory domain contains two regions of peptide sequence that are perfectly conserved. We postulate these regions are important in the regulatory functions of this domain. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. JACKSON LAB,BAR HARBOR,ME 04609. FU NHLBI NIH HHS [HL15157, HL32262]; NIDDK NIH HHS [DK34083] NR 41 TC 21 Z9 22 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0938-8990 J9 MAMM GENOME JI Mamm. Genome PY 1992 VL 3 IS 5 BP 281 EP 285 DI 10.1007/BF00292156 PG 5 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA JT434 UT WOS:A1992JT43400006 PM 1386265 ER PT J AU DRIGAN, R SPIRITO, A GELBER, RD AF DRIGAN, R SPIRITO, A GELBER, RD TI BEHAVIORAL-EFFECTS OF CORTICOSTEROIDS IN CHILDREN WITH ACUTE LYMPHOBLASTIC-LEUKEMIA SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE STEROIDS; SYSTEMIC CHEMOTHERAPY; BEHAVIOR ID THERAPY AB We evaluated the behavior of 38 children with standard-risk and high-risk acute lymphoblastic leukemia who received corticosteroids as part of their antileukemia chemotherapy. Each patient was assessed on two occasions: 16 weeks following remission and 1 year thereafter. Parent reports on emotional lability, attention span/hyperactivity, sleep disturbance, listlessness, peer relations, and depressed mood were obtained for 4 consecutive weeks: week before, week during, and 2 weeks after treatment administration. At the 16 week evaluation, standard-risk (N = 17) and high-risk (N = 21) treatment differed by steroid dose and systemic chemotherapy, while at the 1 year testing, treatment differed only by steroid dose (prednisone 40 mg/m2 vs. 120 mg/m2). Statistically significant changes in all measures were observed during treatment as compared with before and after treatment for both risk groups and assessment times. High-risk patients exhibited greater behavioral effects than standard-risk patients only for emotional lability, listlessness, and depressed mood at the 16 week testing, when both steroid dose and chemotherapy differed. Girls had slightly greater behavioral effects than boys, while no influence of age was observed. At the doses tested, steroid dose per se does not appear to be the primary variable affecting behavioral changes. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RHODE ISL HOSP,BROWN MED SCH,PROVIDENCE,RI 02902. RP DRIGAN, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 14 TC 47 Z9 47 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 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1992 VL 20 IS 1 BP 13 EP 21 DI 10.1002/mpo.2950200104 PG 9 WC Oncology; Pediatrics SC Oncology; Pediatrics GA GV593 UT WOS:A1992GV59300003 PM 1727206 ER PT J AU PAVLIDIS, NA DROSOS, AA PAPADIMITRIOU, C TALAL, N MOUTSOPOULOS, HM AF PAVLIDIS, NA DROSOS, AA PAPADIMITRIOU, C TALAL, N MOUTSOPOULOS, HM TI LYMPHOMA IN SJOGRENS-SYNDROME SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE LYMPHOMA DEVELOPMENT; SPONTANEOUS REGRESSION; AUTOIMMUNE DISEASE ID MALIGNANT-LYMPHOMA AB Sjogren's syndrome is an autoimmune disease with a known predisposition for lymphoma development. Eight of 120 patients with primary Sjogren's syndrome followed at the University of loannina over the past 7 years developed non-Hodgkin's lymphoma diagnosed according to the Kiel classification. The lymphomas differed by location and grading. Six were called low grade (immunocytoma) and two intermediate grade non-Hodgkin's lymphomas. Five of the immunocytomas involved the minor salivary or lacrimal glands. Immunoperoxidase staining for light chains revealed monoclonal populations. Two patients showed spontaneous regression not previously reported in Sjogren's syndrome. Thus, in Sjogren's syndrome, low grade non-Hodgkin's lymphomas and especially immunocytomas are the most common lymphomas. These lymphomas tend to evolve very slowly and may regress spontaneously. Given these facts, a conservative approach to treatment is indicated in those patients with only localized disease. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. RP PAVLIDIS, NA (reprint author), UNIV IOANNINA,SCH MED,DEPT INTERNAL MED,GR-45110 IOANNINA,GREECE. NR 15 TC 39 Z9 41 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1992 VL 20 IS 4 BP 279 EP 283 DI 10.1002/mpo.2950200403 PG 5 WC Oncology; Pediatrics SC Oncology; Pediatrics GA HZ956 UT WOS:A1992HZ95600002 PM 1608349 ER PT J AU CASE, DC SANTARELLI, MT CAREY, RW ANDERSON, J GOTTLIEB, A AF CASE, DC SANTARELLI, MT CAREY, RW ANDERSON, J GOTTLIEB, A TI PHASE-II TRIAL OF IFOSFAMIDE MESNA AND MITOXANTRONE IN PREVIOUSLY TREATED PATIENTS WITH NON-HODGKINS-LYMPHOMA - CANCER AND LEUKEMIA GROUP-B STUDY 8753 SO MEDICAL AND PEDIATRIC ONCOLOGY LA English DT Article DE CHEMOTHERAPY; LYMPHOMA; IFOSFAMIDE ID ISOPHOSPHAMIDE NSC-109724; COMBINATION CHEMOTHERAPY; REGIMEN AB Ifosfamide (2.0 g/m2 intravenously/day x 3) with mesna (400 mg/m2 intravenously q 4 h daily x 3) was combined with mitoxantrone (14 mg/m2 intravenously x 1) and given on a 3 week schedule to patients with previously treated non-Hodkgin's lymphoma. In 45 eligible/evaluable patients, a 47% response rate (95% confidence interval: 32%, 62%) was achieved of which 25% were complete responses and 22% were partial responses. Median duration of remission was 10 months with 42% of patients in remission at 18 months. Hematologic toxicity (granulocytopenia) was the dose-limiting toxicity with severe or life-threatening granulocytopenia in 98% of patients at full protocol doses. Nausea/vomiting was seen in 73% of patients but was usually mild/moderate. Three patients had significant hematuria secondary to ifosfamide. Two patients had severe changes in the left ventricular ejection fraction (LVEF) secondary to mitoxantrone; and one patient had acute neurologic dysfunction secondary to ifosfamide. Ifosfamide/mesna can be safely combined with mitoxantrone at full doses in previously treated patients with non-Hodkgin's lymphoma. This combination should be considered for other trials in lymphoma. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. UNIV NEBRASKA,MED CTR,DEPT PREVENT & SOCIETAL MED,OMAHA,NE 68105. SUNY SYRACUSE,DEPT MED,HLTH SERV CTR,PORTLAND,ME 04102. MAINE MED CTR,DEPT MED,DIV ONCOL,PORTLAND,ME 04102. CANC & LEUKEMIA GRP B,LEBANON,NH. RP CASE, DC (reprint author), MAINE MED CTR,DEPT MED,DIV HEMATOL,PORTLAND,ME 04102, USA. FU NCI NIH HHS [CA 03927, CA 35190, CA 31946] NR 22 TC 7 Z9 7 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0098-1532 J9 MED PEDIATR ONCOL JI Med. Pediatr. Oncol. PY 1992 VL 20 IS 4 BP 325 EP 329 DI 10.1002/mpo.2950200411 PG 5 WC Oncology; Pediatrics SC Oncology; Pediatrics GA HZ956 UT WOS:A1992HZ95600010 PM 1608355 ER PT J AU SMITH, ME BAKER, CR BRANCH, LG WALLS, RC GRIMES, RM KARKLINS, JM KASHNER, M BURRAGE, R PARKS, A ROGERS, P SACZUK, A WAGSTERWEARE, M AF SMITH, ME BAKER, CR BRANCH, LG WALLS, RC GRIMES, RM KARKLINS, JM KASHNER, M BURRAGE, R PARKS, A ROGERS, P SACZUK, A WAGSTERWEARE, M TI CASE-MIX GROUPS FOR VA HOSPITAL-BASED HOME CARE SO MEDICAL CARE LA English DT Article DE HOSPITAL-BASED HOME CARE; LONG-TERM CARE REIMBURSEMENT; CASE MIX MODELS ID LONG-TERM CARE; RESOURCE UTILIZATION GROUPS; INSTITUTIONALIZATION; SERVICES; TRIAL AB The purpose of this study is to group hospital-based home care (HBHC) patients homogeneously by their characteristics with respect to cost of care to develop alternative case mix methods for management and reimbursement (allocation) purposes. Six Veterans Affairs (VA) HBHC programs in Fiscal Year (FY) 1986 that maximized patient, program, and regional variation were selected, all of which agreed to participate. All HBHC patients active in each program on October 1, 1987, in addition to all new admissions through September 30, 1988 (FY88), comprised the sample of 874 unique patients. Statistical methods include the use of classification and regression trees (CART software: Statistical Software; Lafayette, CA), analysis of variance, and multiple linear regression techniques. The resulting algorithm is a three-factor model that explains 20% of the cost variance (R2 = 20%, with a cross validation R2 of 12%). Similar classifications such as the RUG-II, which is utilized for VA nursing home and intermediate care, the VA outpatient resource allocation model, and the RUG-HHC, utilized in some states for reimbursing home health care in the private sector, explained less of the cost variance and, therefore, are less adequate for VA home care resource allocation. C1 VET HLTH ADM,MED CTR,SALT LAKE CITY,UT. VET HLTH ADM,MED CTR,MEMPHIS,TN. VET HLTH ADM,MED CTR,NEW ORLEANS,LA. US DEPT VET AFFAIRS,VET HLTH ADM,OFF GERIATR & EXTENDED CARE,WASHINGTON,DC. BOSTON UNIV,SCH MED,BOSTON,MA 02118. ABT ASSOCIATES INC,CAMBRIDGE,MA. UNIV TEXAS,HLTH SCI CTR,SCH PUBL HLTH,HOUSTON,TX 77225. VET HLTH ADM,MED CTR,BUFFALO,NY. VET HLTH ADM,MED CTR,BALTIMORE,MD. JOHN L MCCLELLAN MEM VET ADM MED CTR,US DEPT VET AFFAIRS,VET HLTH ADM,LITTLE ROCK,AR 72205. UNIV ARKANSAS MED SCI HOSP,COLL MED,LITTLE ROCK,AR 72205. NR 34 TC 13 Z9 13 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD JAN PY 1992 VL 30 IS 1 BP 1 EP 16 DI 10.1097/00005650-199201000-00001 PG 16 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA GZ535 UT WOS:A1992GZ53500001 PM 1309585 ER PT J AU VERHEY, LJ LYMAN, JT AF VERHEY, LJ LYMAN, JT TI SOME CONSIDERATIONS REGARDING W-VALUES FOR HEAVY CHARGED-PARTICLE RADIOTHERAPY SO MEDICAL PHYSICS LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. UNIV CALIF BERKELEY,LAWRENCE BERKELEY LAB,DIV RES MED & RADIAT BIOPHYS,BERKELEY,CA 94720. FU NCI NIH HHS [CA22286] NR 12 TC 13 Z9 13 U1 0 U2 1 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD JAN-FEB PY 1992 VL 19 IS 1 BP 151 EP 153 DI 10.1118/1.596888 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HE208 UT WOS:A1992HE20800017 PM 1620040 ER PT J AU BRASIER, AR RON, D AF BRASIER, AR RON, D TI LUCIFERASE REPORTER GENE ASSAY IN MAMMALIAN-CELLS SO METHODS IN ENZYMOLOGY LA English DT Review ID PHASE RESPONSE ELEMENT; FIREFLY LUCIFERASE; ANGIOTENSINOGEN GENE; BINDING-PROTEINS; TRANSCRIPTION; EXPRESSION; ENHANCERS C1 MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. RP BRASIER, AR (reprint author), UNIV TEXAS,MED BRANCH,DIV ENDOCRINOL & HYPERTENS,GALVESTON,TX 77555, USA. NR 20 TC 33 Z9 33 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0076-6879 J9 METHOD ENZYMOL JI Method Enzymol. PY 1992 VL 216 BP 386 EP 397 PG 12 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA KL577 UT WOS:A1992KL57700034 PM 1336098 ER PT B AU BRUCCOLERI, RE HABER, E NOVOTNY, J AF BRUCCOLERI, RE HABER, E NOVOTNY, J BE Ratner, VA Kolchanov, NA TI APPLICATION OF CONFORMATIONAL SEARCH TO ANTIBODY MODELING SO MODELLING AND COMPUTER METHODS IN MOLECULAR BIOLOGY AND GENETICS LA English DT Proceedings Paper CT 1st International Conference on Modelling and Computer Methods in Molecular Biology and Genetics CY AUG 28-SEP 01, 1990 CL NOVOSIBIRSK, RUSSIA SP USSR ACAD SCI, NOVOSIBIRSK SCI CTR SIBERIAN BRANCH C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NOVA SCIENCE PUBLISHERS PI COMMACK PA 6080 JERICHO TPKE #207, COMMACK, NY 11725-2808 BN 1-560-72077-8 PY 1992 BP 169 EP 190 PG 22 WC Biochemistry & Molecular Biology; Computer Science, Interdisciplinary Applications; Genetics & Heredity SC Biochemistry & Molecular Biology; Computer Science; Genetics & Heredity GA BZ45F UT WOS:A1992BZ45F00024 ER PT J AU FOLBERG, R JAKOBIEC, FA MCLEAN, IW ZIMMERMAN, LE AF FOLBERG, R JAKOBIEC, FA MCLEAN, IW ZIMMERMAN, LE TI IS PRIMARY ACQUIRED MELANOSIS OF THE CONJUNCTIVA EQUIVALENT TO MELANOMA INSITU SO MODERN PATHOLOGY LA English DT Article ID MALIGNANT-MELANOMA; MELANOCYTIC LESIONS; CLASSIFICATION; CRYOTHERAPY; EXPERIENCE C1 UNIV IOWA,MASSACHUSETTS EYE & EAR INFIRM,DEPT PATHOL,IOWA CITY,IA 52242. ARMED FORCES INST PATHOL,WASHINGTON,DC. RP FOLBERG, R (reprint author), UNIV IOWA,MASSACHUSETTES EYE & EAR INFIRM,DEPT OPHTHALMOL,ROOM 233 MRC,IOWA CITY,IA 52242, USA. FU NEI NIH HHS [EY07043] NR 25 TC 20 Z9 20 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JAN PY 1992 VL 5 IS 1 BP 2 EP 5 PG 4 WC Pathology SC Pathology GA HA713 UT WOS:A1992HA71300002 PM 1542634 ER PT J AU ANTONIADES, HN AF ANTONIADES, HN TI LINKING CELLULAR INJURY TO GENE-EXPRESSION AND HUMAN PROLIFERATIVE DISORDERS - EXAMPLES WITH THE PDGF GENES SO MOLECULAR CARCINOGENESIS LA English DT Article ID GROWTH-FACTOR PDGF; IDIOPATHIC PULMONARY FIBROSIS; PRIMARY HUMAN ASTROCYTOMAS; HUMAN GASTRIC CARCINOMAS; RECEPTOR GENES; BRAIN-TUMORS; MESSENGER-RNA; FACTOR-ALPHA; COEXPRESSION; FIBROBLASTS C1 CTR BLOOD RES,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. RP ANTONIADES, HN (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,677 HUNTINGTON,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 30101]; NHLBI NIH HHS [HL 29583] NR 26 TC 19 Z9 19 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1992 VL 6 IS 3 BP 175 EP 181 DI 10.1002/mc.2940060302 PG 7 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA KA057 UT WOS:A1992KA05700001 PM 1445619 ER PT J AU LI, CY YANDELL, DW LITTLE, JB AF LI, CY YANDELL, DW LITTLE, JB TI EVIDENCE FOR COINCIDENT MUTATIONS IN HUMAN LYMPHOBLAST CLONES SELECTED FOR FUNCTIONAL LOSS OF A THYMIDINE KINASE GENE SO MOLECULAR CARCINOGENESIS LA English DT Article DE GENOMIC INSTABILITY; GLOBAL MUTAGENESIS; CARCINOGENESIS ID DIPLOID HUMAN-LYMPHOBLASTS; C3H 10T1/2 CELLS; SACCHAROMYCES-CEREVISIAE; HUMAN DNA; X-RAYS; LOCUS; TRANSFORMATION; RECOMBINATION; SEQUENCE; YEAST AB A mitotic "recombination-competent state" inducible by x-irradiation is thought to exist in yeast. We sought evidence for such a process in mammalian cells by examining the occurrence of mutations at unlinked loci in clones derived from a human lymphoblast cell line. A total of 169 independent clones that arose spontaneously or after exposure to x-rays or ethyl methanesulfonate were selected for new somatic mutations at the thymidine kinase gene on chromosome 17q. They were subsequently screened for coincident mutations by use of variable-number-of-tandem-repeat probes located on different chromosomes. Three coincident mutations were positively identified by Southern analysis on chromosomes 7 and 14; they included one that produced a new allele and two that caused loss of allele heterozygosity. Densitometric analysis of the latter two indicated the presence of two copies of the remaining allele. Several possible coincident genetic events were also observed on chromosome 17. These findings revealed a coincident mutant fraction of about 10(-2)/cell, whereas the expected mutation fraction at these loci is less than 10(-4)/cell. These results may thus provide the first molecular evidence that a "global" mutational process capable of inducing genetic instability exists in mammalian cells. C1 HARVARD UNIV,SCH PUBL HLTH,RADIOBIOL LAB,665 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,HOWE LAB,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RI Li, Chuan-Yuan/H-4148-2013 FU NCI NIH HHS [CA-47542]; NIEHS NIH HHS [ES-00002] NR 35 TC 29 Z9 30 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 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PY 1992 VL 5 IS 4 BP 270 EP 277 DI 10.1002/mc.2940050407 PG 8 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA JB221 UT WOS:A1992JB22100005 PM 1497803 ER PT J AU BRACH, MA KHARBANDA, SM HERRMANN, F KUFE, DW AF BRACH, MA KHARBANDA, SM HERRMANN, F KUFE, DW TI ACTIVATION OF THE TRANSCRIPTION FACTOR-KAPPA-B IN HUMAN KG-1 MYELOID-LEUKEMIA CELLS TREATED WITH 1-BETA-D-ARABINOFURANOSYLCYTOSINE SO MOLECULAR PHARMACOLOGY LA English DT Article ID DNA-BINDING SUBUNIT; GENE-EXPRESSION; ARABINOFURANOSYLCYTOSINE; ELONGATION; TEMPLATE; PROTEINS; INVITRO; NUMBER; BETA; REL AB The present studies have examined the effects of 1-beta-D-arabinofuranosylcytosine (ara-C) on activation of the transcription factor kappa-B (NF-kappa-B). The results demonstrate that treatment of human KG-1 myeloid leukemia cells with ara-C is associated with induction of protein binding to the NF-kappa-B consensus sequence. NF-kappa-B binding was activated at 30 min and reached maximal levels of binding at 1-2 hr of ara-C treatment. The NF-kappa-B consensus sequence was ligated to the heterologous thymidine kinase (TK) promoter and the human growth hormone (GH) reporter gene to determine whether ara-C-induced NF-kappa-B activity includes an enhancer function. Ara-C treatment had little effect on transient expression of pTKGH in KG-1 cells but increased transcription of the p (NF-kappa-B) TKGH vector by 8-fold. The results also demonstrate that ara-C transiently increases NF-kappa-B mRNA levels. However, the finding that ara-C induced binding of NF-kappa-B to DNA occurs in the presence of cycloheximide indicates that this agent activates preexisting NF-kappa-B protein. These results suggest that ara-C induces a cytoplasmic pathway that transduces signals to the nucleus by activation of NF-kappa-B. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. UNIV FREIBURG,MED CTR,DEPT HEMATOL & ONCOL,W-7800 FREIBURG,GERMANY. FU NCI NIH HHS [CA29431, CA42802] NR 25 TC 37 Z9 38 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1992 VL 41 IS 1 BP 60 EP 63 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HL064 UT WOS:A1992HL06400009 PM 1732723 ER PT J AU DATTA, R KHARBANDA, S KUFE, DW AF DATTA, R KHARBANDA, S KUFE, DW TI TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL REGULATION OF H1 HISTONE GENE-EXPRESSION BY 1-BETA-D-ARABINOFURANOSYLCYTOSINE SO MOLECULAR PHARMACOLOGY LA English DT Article ID CELL-CYCLE REGULATION; MESSENGER-RNA DEGRADATION; MYELOID-LEUKEMIA CELLS; DNA-SYNTHESIS; PROTEIN-SYNTHESIS; MAMMALIAN-CELLS; PROMOTER REGION; HUMAN H-1; 3' END; REPLICATION AB Recent studies have demonstrated that 1-beta-D-arabinofuranosylcytosine (ara-C) activates the transcription of the jun/fos early response genes in human myeloid leukemia cells. The basis for ara-C-induced control of gene expression remains unclear. However, down-regulation of H-1 histone mRNA levels has been reported as one of the earliest changes in specific gene expression associated with ara-C treatment. In this report, we describe the mechanisms responsible for H-1 histone expression by this agent. Treatment of HL-60 cells with ara-C resulted in a decrease in H-1 histone mRNA levels that was detectable by 15 min. In contrast, this down-regulation by ara-C was completely blocked by treatment of the cells with cycloheximide. Nuclear run-on analyses demonstrated that ara-C treatment is associated with inhibition of H-1 histone gene transcription. The results also demonstrate that cycloheximide abrogates the transcriptional down-regulation by ara-C but alone has no detectable effect. We also show that ara-C treatment is associated with a decrease in stability of the H-1 histone transcript and that this effect is also reversed by inhibition of protein synthesis. Taken together, these findings demonstrate that ara-C regulates H-1 histone expression at both the transcriptional and posttranscriptional levels. The results also indicate that control of this gene by ara-C involves the activation of at least two signaling events that require de novo protein synthesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA29431] NR 40 TC 6 Z9 6 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JAN PY 1992 VL 41 IS 1 BP 64 EP 68 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HL064 UT WOS:A1992HL06400010 PM 1732724 ER PT S AU MAHIDA, YR CIACCI, C PODOLSKY, DK AF MAHIDA, YR CIACCI, C PODOLSKY, DK BE Stead, RH Perdue, MH Cooke, H Powell, DW Barrett, KE TI PEPTIDE GROWTH-FACTORS - ROLE IN EPITHELIAL-LAMINA PROPRIA CELL-INTERACTIONS SO NEURO-IMMUNO-PHYSIOLOGY OF THE GASTROINTESTINAL MUCOSA: IMPLICATIONS FOR INFLAMMATORY DISEASES SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON NEURO-IMMUNO-PHYSIOLOGY OF GASTROINTESTINAL MUCOSA : IMPLICATIONS FOR INFLAMMATORY DISEASES CY JAN 24-28, 1992 CL TUCSON, AZ SP NEW YORK ACAD SCI, ABBOTT LABS, AMER GASTROENTEROL ASSOC, ASTRA PHARMA, BURROUGHS WELLCOME, UNIV N CAROLINA CHAPEL HILL, CTR GASTROINTESTINAL BIOL & DIS, CROHNS & COLITIS FDN AMER, G D SEARLE & CO, GLAXO GRP RES, GLAXO PHARM RP PODOLSKY, DK (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. RI ciacci, carolina/A-2594-2012 OI ciacci, carolina/0000-0002-7426-1145 FU NIDDK NIH HHS [DK41557, P30 DK43351] NR 0 TC 3 Z9 3 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-757-3 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1992 VL 664 BP 148 EP 156 DI 10.1111/j.1749-6632.1992.tb39757.x PG 9 WC Gastroenterology & Hepatology; Immunology; Neurosciences; Physiology SC Gastroenterology & Hepatology; Immunology; Neurosciences & Neurology; Physiology GA BX07T UT WOS:A1992BX07T00015 PM 1456646 ER PT J AU CARNES, M BROWNFIELD, M LENT, SJ NICHOLS, K SCHULER, L AF CARNES, M BROWNFIELD, M LENT, SJ NICHOLS, K SCHULER, L TI PULSATILE ACTH AND CORTISOL IN GOATS - EFFECTS OF INSULIN-INDUCED HYPOGLYCEMIA AND DEXAMETHASONE SO NEUROENDOCRINOLOGY LA English DT Article DE ACTH, PULSATILE; ULTRADIAN RHYTHM; HYPOGLYCEMIA, GOAT ID CORTICOTROPIN-RELEASING FACTOR; ANTERIOR-PITUITARY CELLS; ADRENOCORTICOTROPIN SECRETION; CORTICOSTEROID RESPONSES; INTERMEDIATE PITUITARY; ARGININE VASOPRESSIN; PLASMA CORTICOTROPIN; ACTION-POTENTIALS; OVINE ANTERIOR; CONSCIOUS DOGS AB Insulin-induced hypoglycemia is a metabolic stress that stimulates secretion of adrenocorticotropic hormone (ACTH) and cortisol in a number of animal species. Dexamethasone is a potent synthetic glucocorticoid that suppresses the secretion of ACTH and cortisol. Both ACTH and cortisol exhibit complex secretory patterns demonstrating ultradian and circadian rhythms. This work investigated the pattern of ACTH and cortisol response to hypoglycemia in goats and the effect of dexamethasone on this response. Five goats were pretreated with dexamethasone (0.1 mg/kg) and 5 with saline. Blood samples were taken every 2 min for 60 min before and 60 min after administration of insulin (2.5 IU/kg, i.v.). Immunoreactive ACTH and cortisol were measured in all samples and glucose in selected samples. Data sets were analyzed for significant pulses with the Cluster Analysis program. Complete data sets were compared as well as those for each 30-min interval. Plasma glucose was lower than preinsulin levels at 10 min, declined rapidly between 10 and 30 min, and remained low 30-60 min after insulin injection in both treatment groups. Controls showed a rapid rise in ACTH and cortisol beginning 30 +/- 10 min postinsulin. The increase in mean plasma hormone levels during hypoglycemia was predominantly due to an increase in amplitude of secretory pulses for ACTH and cortisol compared with the 30 min before insulin. Dexamethasone significantly lowered mean ACTH and cortisol levels and prevented alteration in plasma ACTH and cortisol secretion during hypoglycemia but did not totally ablate pulsatile activity of either hormone. The amplitude of ACTH and cortisol pulses was significantly decreased by dexamethasone treatment. The frequency of cortisol but not ACTH pulses was also significantly decreased. The highest cross-correlation between plasma ACTH and cortisol occurred at a lag of 0 min in control goats. Cross-correlation was lower and no consistent lag was seen in dexamethasone-treated goats. In control goats, during the fall in plasma glucose, before the rapid rise in plasma ACTH and cortisol, secretion appeared to be relatively quiescent compared to the prior 30 min. Specifically, a slight reduction occurred in frequency, amplitude, and area of ACTH pulses, in amplitude and area of cortisol pulses, and in cortisol levels. While this unexpected observation may have been an artifact of the sampling protocol, it bears further investigation. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT COMPARAT BIOSCI,MADISON,WI 53706. FU NIDDK NIH HHS [IR01-DK40759-01] NR 43 TC 11 Z9 11 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0028-3835 J9 NEUROENDOCRINOLOGY JI Neuroendocrinology PD JAN PY 1992 VL 55 IS 1 BP 97 EP 104 DI 10.1159/000126102 PG 8 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA HB188 UT WOS:A1992HB18800014 PM 1319009 ER PT J AU KELLER, TL HALPERIN, JJ WHITMAN, M AF KELLER, TL HALPERIN, JJ WHITMAN, M TI PCR DETECTION OF BORRELIA-BURGDORFERI DNA IN CEREBROSPINAL-FLUID OF LYME NEUROBORRELIOSIS PATIENTS SO NEUROLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; CHRONIC NEUROLOGIC MANIFESTATIONS; AMYOTROPHIC LATERAL SCLEROSIS; HUMAN-IMMUNODEFICIENCY-VIRUS; NERVOUS-SYSTEM; SPIROCHETAL ETIOLOGY; MULTIPLE-SCLEROSIS; FALSE POSITIVES; DISEASE; ANTIBODIES AB We used the polymerase chain reaction (PCR), a method useful in the detection of Borrelia burgdorferi in vitro, to evaluate CSF in patients thought to have neuroborreliosis. Nested pairs of oligonucleotide primers were designed to recognize the C-terminal region of B burgdorferi OspA. CSF samples were obtained from (1) patients with immunologic evidence of systemic B burgdorferi infection and clinical manifestations suggestive of CNS dysfunction, (2) seronegative patients with clinical disorders consistent with Lyme borreliosis, and (3) patient and contamination controls; all were analyzed in a blinded fashion. PCR detected B burgdorferi OspA DNA in CSF of (1) 10 of 11 patients with Lyme encephalopathy, (2) 28 of 37 patients with inflammatory CNS disease, (3) seven of seven seronegative patients with Lyme-compatible disorders, and (4) zero of 23 patient controls. Zero of 83 additional contamination controls were PCR-positive. In eight patients from whom we obtained CSF before and after parenteral antimicrobial therapy, PCR results invariably predicted clinical outcome accurately. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INST CELL & MOLEC BIOL,BOSTON,MA 02115. SUNY STONY BROOK,DEPT NEUROL,STONY BROOK,NY 11794. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DEPT CELL & MOLEC PHYSIOL,BOSTON,MA 02115. NR 49 TC 103 Z9 104 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1992 VL 42 IS 1 BP 32 EP 42 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA HA895 UT WOS:A1992HA89500006 PM 1734321 ER PT J AU LOUIS, DN ARRIAGADA, PV HYMAN, BT HEDLEYWHYTE, ET AF LOUIS, DN ARRIAGADA, PV HYMAN, BT HEDLEYWHYTE, ET TI OLFACTORY DYSGENESIS OR HYPOPLASIA - A VARIANT IN THE ARRHINENCEPHALY SPECTRUM SO NEUROLOGY LA English DT Article ID BRAIN AB Postmortem examination of a 65-year-old anosmic woman revealed rudimentary olfactory bulbs, an imperforate cribriform plate, and sulcal abnormalities of the orbitofrontal surface of the brain. The remainder of the brain, skull, and body was normal. This abnormality most likely resulted from a local insult to the area of the cribriform plate during early fetal life, occurring after the induction of olfactory bulb differentiation, but before migration and complete differentiation of the olfactory bulbs. Such a lesion can be dated to approximately 11 to 12 weeks gestational age. The malformation may represent another variant in the arhinencephaly spectrum, but is termed "olfactory dysgenesis" or "olfactory hypoplasia" to separate it from true olfactory aplasia and arhinencephaly. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LOUIS, DN (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,WARREN 3,BOSTON,MA 02114, USA. NR 21 TC 5 Z9 5 U1 1 U2 4 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JAN PY 1992 VL 42 IS 1 BP 179 EP 182 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA HA895 UT WOS:A1992HA89500031 PM 1734299 ER PT J AU SHEPHERD, GMG COREY, DP AF SHEPHERD, GMG COREY, DP TI SENSATIONAL SCIENCE SO NEW BIOLOGIST LA English DT Article C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP SHEPHERD, GMG (reprint author), HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115, USA. RI Shepherd, Gordon/F-2679-2010 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 1043-4674 J9 NEW BIOL PD JAN PY 1992 VL 4 IS 1 BP 48 EP 52 PG 5 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA HC449 UT WOS:A1992HC44900008 PM 1346972 ER PT B AU KLEINMAN, RE AF KLEINMAN, RE BE CHANDRA, RK TI IMMUNE-RESPONSE TO DIETARY ANTIGENS AND THE DEVELOPMENT OF HYPOALLERGENIC FORMULAS, (REPRINTED FROM NUTRITION RESEARCH, JANUARY, 1992) SO NUTRITION AND IMMUNOLOGY LA English DT Proceedings Paper CT INTERNATIONAL CONF ON NUTRITION AND IMMUNOLOGY CY JUL 14-18, 1991 CL ST JOHNS, CANADA SP MEM UNIV NEWFOUNDLAND, MED RES COUNCIL CANADA, NUTR RES INST FDN, CANADIAN CANC SOC, NEWFOUNDLAND CANC TREATMENT & RES FDN, ROYAL COLL PHYSICIANS & SURGEONS CANADA, NUTRICIA RES, CARNATION NUTR PROD, MILUPA, SANDOZ NUTR RP KLEINMAN, RE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ARTS BIOMEDICAL PUBL & DISTRIBUTORS LTD PI ST JOHNS PA ST JOHNS BN 0-921554-02-8 PY 1992 BP 343 EP 352 PG 10 WC Immunology; Nutrition & Dietetics SC Immunology; Nutrition & Dietetics GA BW67T UT WOS:A1992BW67T00024 ER PT J AU KLEINMAN, RE AF KLEINMAN, RE TI IMMUNE-RESPONSE TO DIETARY ANTIGENS AND THE DEVELOPMENT OF HYPOALLERGENIC FORMULAS SO NUTRITION RESEARCH LA English DT Article DE HYPOALLERGENIC FORMULAS; FOOD PROTEINS; DIETARY ANTIGENS ID RAT SMALL-INTESTINE; EPITHELIAL-CELLS; INFANT FORMULAS; GUINEA-PIGS; PROTEIN; MILK; MOUSE AB In high risk infants who are breast-fed, special formulas which do not cause sensitization are a useful alternative. New formulas are likely to be developed based on biochemical and immunologic modifications of their proteins. Both in vitro and in vivo tests for evaluation of such formulas are discussed. RP KLEINMAN, RE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 34 TC 1 Z9 1 U1 2 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0271-5317 J9 NUTR RES JI Nutr. Res. PD JAN PY 1992 VL 12 IS 1 BP 151 EP 160 DI 10.1016/S0271-5317(05)80419-1 PG 10 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HL924 UT WOS:A1992HL92400015 ER PT J AU GOFF, BA ATANASOFF, P BROWN, E MUNTZ, HG BELL, DA RICE, LW AF GOFF, BA ATANASOFF, P BROWN, E MUNTZ, HG BELL, DA RICE, LW TI ENDOCERVICAL GLANDULAR ATYPIA IN PAPANICOLAOU SMEARS SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID INTRAEPITHELIAL NEOPLASIA; CERVICAL NEOPLASIA; DIAGNOSIS; CYTOLOGY AB The importance of endocervical glandular atypia in a cervicovaginal Papanicolaou smear has not been fully investigated. Between July 1988 and June 1989, 21,930 cervicovaginal smears were reviewed by the Massachusetts General Hospital Cytopathology Laboratory. One hundred smears with endocervical atypia were identified, an incidence of 0.46%. Follow-up was available on 63 cases: Seven had negative follow-up smears for at least 2 years, 15 had negative biopsies, seven had endocervical polyps, two had endometrial hyperplasia, eight had mild dysplasia, five had moderate dysplasia, six had severe dysplasia, six had squamous carcinoma in situ, five had adenocarcinoma in situ, and two had invasive adenocarcinoma. Twelve women's smears showed endocervical atypia with features suggestive of reactive atypia, three of these had dysplasia. Twenty-six (41%) of the Papanicolaou smears with endocervical atypia had coexisting squamous atypia or dysplasia. We condude that endocervical atypia may be associated with substantial cervical disease in as many as half of cases. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP GOFF, BA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT GYNECOL SERV,VINCENT 1,BOSTON,MA 02114, USA. NR 21 TC 104 Z9 105 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD JAN PY 1992 VL 79 IS 1 BP 101 EP 104 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA GX292 UT WOS:A1992GX29200021 PM 1727566 ER PT J AU SILVERMAN, PR WORDEN, JW AF SILVERMAN, PR WORDEN, JW TI CHILDRENS UNDERSTANDING OF FUNERAL RITUAL SO OMEGA-JOURNAL OF DEATH AND DYING LA English DT Article ID DEATH AB One hundred-twenty children who experienced the death of one of their parents were interviewed about their view of the funeral ritual. Ninety-five percent of them attended the funeral. Shortly after the death they recalled little about the funeral. Two years later, children reported that it was important to them that they had attended. Attendance helped them to acknowledge the death, provided an occasion for honoring their deceased parent, and made it possible for them to receive support and comfort. RP SILVERMAN, PR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114, USA. NR 26 TC 14 Z9 14 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0030-2228 J9 OMEGA-J DEATH DYING JI Omega-J. Death Dying PY 1992 VL 25 IS 4 BP 319 EP 331 PG 13 WC Psychology, Multidisciplinary; Social Sciences, Biomedical SC Psychology; Biomedical Social Sciences GA KC032 UT WOS:A1992KC03200007 ER PT J AU WEISMAN, AD AF WEISMAN, AD TI A TASK-BASED APPROACH TO COPING WITH DYING - COMMENTARY SO OMEGA-JOURNAL OF DEATH AND DYING LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WEISMAN, AD (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,W END HOUSE,BOSTON,MA 02114, USA. NR 3 TC 1 Z9 1 U1 0 U2 0 PU BAYWOOD PUBL CO INC PI AMITYVILLE PA 26 AUSTIN AVE, AMITYVILLE, NY 11701 SN 0030-2228 J9 OMEGA-J DEATH DYING JI Omega-J. Death Dying PY 1992 VL 24 IS 2 BP 95 EP 96 PG 2 WC Psychology, Multidisciplinary; Social Sciences, Biomedical SC Psychology; Biomedical Social Sciences GA HC645 UT WOS:A1992HC64500002 ER PT J AU MCGREW, BR NICHOLS, DW STANTON, VP CAI, H WHORF, RC PATEL, V COOPER, GM LAUDANO, AP AF MCGREW, BR NICHOLS, DW STANTON, VP CAI, H WHORF, RC PATEL, V COOPER, GM LAUDANO, AP TI PHOSPHORYLATION OCCURS IN THE AMINO TERMINUS OF THE RAF-1 PROTEIN SO ONCOGENE LA English DT Article ID GLYCOGEN-SYNTHASE KINASE-3; COMPLETE CODING SEQUENCE; RABBIT SKELETAL-MUSCLE; PDGF BETA-RECEPTOR; TYROSINE PHOSPHORYLATION; TRANSFORMING ACTIVITY; POLYACRYLAMIDE GELS; SIGNAL TRANSDUCTION; HUMAN C-RAF-1; V-RAF AB The ability of the Raf-1 protein to morphologically transform murine fibroblasts can be activated by amino-terminal deletions or substitutions. We have compared the phosphorylation states of full-length and representative transforming and non-transforming amino-terminal deletion mutants of the Raf-1 protein using phosphoamino acid analysis and tryptic phosphopeptide mapping. Several [P-32]orthophosphate-labeled tryptic phosphopeptides that were present in the full-length Raf-1 protein were absent from the highly transforming 22W Raf-1 mutant (lacking 305 amino-terminal residues). Peptide-specific antisera localized Raf-1 phosphorylation sites to several amino-terminal cyanogen bromide and tryptic peptides that are deleted from the 22W protein. A major phosphorylated tryptic peptide of the Raf-1 protein was immunoprecipitated by antiserum directed against amino acid residues 257-275, a highly conserved region of the raf family. This tryptic peptide is entirely deleted from the highly transforming 22W protein. Subtractive Edman degradation and electrophoretic analysis of the immunoprecipitated tryptic peptide indicated that phosphorylation of the Raf-1 protein occurs at serine 259. Multiple phosphorylated tryptic peptide forms were immunoprecipitated by antiserum directed against Raf-1 residues 283-309. The majority of this tryptic peptide is also deleted from the highly transforming Raf-1 mutant 22W. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP MCGREW, BR (reprint author), UNIV NEW HAMPSHIRE,DEPT BIOCHEM,SPAULDING LIFE SCI BLDG,DURHAM,NH 03824, USA. FU NCI NIH HHS [CA18689, K08 CA01052] NR 42 TC 14 Z9 14 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JAN PY 1992 VL 7 IS 1 BP 33 EP 42 PG 10 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HC227 UT WOS:A1992HC22700005 PM 1741164 ER PT J AU MAZZANTI, R CROOP, JM GATMAITAN, Z BUDDING, M STEIGLITZ, K ARCECI, R ARIAS, IM AF MAZZANTI, R CROOP, JM GATMAITAN, Z BUDDING, M STEIGLITZ, K ARCECI, R ARIAS, IM TI BENZOQUINAMIDE INHIBITS P-GLYCOPROTEIN MEDIATED DRUG EFFLUX AND POTENTIATES ANTICANCER AGENT CYTOTOXICITY IN MULTIDRUG RESISTANT CELLS SO ONCOLOGY RESEARCH LA English DT Article ID HAMSTER OVARY CELLS; CHINESE-HAMSTER; TUMOR-CELLS; CYTO-TOXICITY; DOXORUBICIN RESISTANCE; MEMBRANE GLYCOPROTEIN; CYCLOSPORINE-A; VERAPAMIL; REVERSAL; INVITRO AB We have previously shown that efflux of cytotoxic drugs from multidrug resistant (MDR) cell lines can be quantitated at the single cell level using a sensitive fluorescence microscopy technique. Based on the structure of compounds which inhibited the efflux of Rhodamine-123 (Rho-123) using this methodology, we hypothesized that the antiemetic, antihistaminic agent benzquinamide (BZQ) would interfere with P-glycoprotein (P-gp) mediated drug transport and potentiate the effects of anticancer agents in MDR cell lines. We show that-BZQ interferes with P-gp mediated drug efflux and increases drug accumulation in MDR cells using Rho-123 as a fluorescent probe. BZQ increases the cytotoxicity of chemotherapeutic agents to both human and hamster MDR cell lines in vitro. A slight increase in cytotoxicity to chemotherapeutic agents is also observed in the parental cell lines with BZQ. BZQ increases [H-3]daunorubicin accumulation and inhibits the binding of [I-125]iodoaryl azidoprazosin to the P-gp in MDR cells. BZQ is a new agent to increase the cytotoxic effects of anticancer agents in MDR cells and may ultimately prove useful as an adjunct in cancer chemotherapy. C1 TUFTS UNIV,DEPT PHYSIOL,BOSTON,MA 02111. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA-48162]; NIDDK NIH HHS [DK-34928, DK-35652] NR 39 TC 12 Z9 12 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0965-0407 J9 ONCOL RES JI Oncol. Res. PY 1992 VL 4 IS 8-9 BP 359 EP 365 PG 7 WC Oncology SC Oncology GA KK079 UT WOS:A1992KK07900006 PM 1362504 ER PT J AU OZMENT, RR LAIW, ZC LATINA, MA AF OZMENT, RR LAIW, ZC LATINA, MA TI THE USE OF TISSUE PLASMINOGEN-ACTIVATOR IN EXPERIMENTAL FILTRATION SURGERY SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID GLAUCOMA FILTERING SURGERY; BETA-AMINOPROPIONITRILE; D-PENICILLAMINE; RABBITS; FIBRIN; 5-FLUOROURACIL; BLEBS; MODEL AB Tissue plasminogen activator (tPA), a clot-specific fibrinolytic agent, was used as an adjunct to filtration surgery in Dutch belted rabbits to determine its effects on the outcome of filtration surgery. Thirty-eight animals that underwent a standardized posterior-lip sclerectomy in both eyes were divided into five postoperative protocol groups. In masked fashion, experimental eyes received 25-mu-g of tPA in 100-mu-L of diluent. Fellow eyes received 100-mu-L of diluent and served as controls. Group 1 received daily subconjunctival tPA. Group 2 received intracameral, followed by daily subconjunctival, tPA. Groups 3, 4, and 5 received intracameral tPA on postoperative days 1 and 2;2 and 3; and 3, 4, and 5, respectively. Intraocular pressure (IOP), quality of bleb, number of days to bleb failure, and incidence of intraocular bleeding were determined in each group. No significant tPA effect was seen in groups 1 or 2. In groups 3, 4, and 5, the tPA-treated eyes demonstrated marked reduction of IOP and improvement in the quality of the blebs lasting between 6 to 24 hours. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. EYE RES INST,BOSTON,MA. NR 27 TC 7 Z9 9 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD JAN PY 1992 VL 23 IS 1 BP 22 EP 30 PG 9 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA HA025 UT WOS:A1992HA02500006 PM 1574262 ER PT J AU SOUKIASIAN, SH FOSTER, CS NILES, JL RAIZMAN, MB AF SOUKIASIAN, SH FOSTER, CS NILES, JL RAIZMAN, MB TI DIAGNOSTIC-VALUE OF ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES IN SCLERITIS ASSOCIATED WITH WEGENERS GRANULOMATOSIS SO OPHTHALMOLOGY LA English DT Article ID ANTICYTOPLASMIC AUTOANTIBODIES; OCULAR MANIFESTATIONS; LIMITED FORMS; VASCULITIS; GLOMERULONEPHRITIS; MYELOPEROXIDASE; PSEUDOTUMOR; EXPERIENCE; DISEASE AB Serum antineutrophil cytoplasmic antibodies (ANCAs) are a sensitive and specific marker for generalized Wegener's granulomatosis. However, ANCA sensitivity and specificity in identifying patients in whom ophthalmic signs constitute the presenting or only definitive manifestation of Wegener's granulomatosis have not been tested. The authors report on 7 patients in whom scleritis was the initial manifestation leading to the diagnosis of Wegener's granulomatosis. Six had the limited form of Wegener's granulomatosis. Results of serum ANCA tests were positive in all these patients. In contrast, the serum ANCA was negative in 54 patients with ocular inflammation due to other disorders; 16 of these patients had scleritis. Serial ANCA titers reverted to normal in only two of the four patients with Wegener's granulomatosis who attained clinical remission. One of the patients who did not revert to normal experienced relapse 2 months after discontinuation of therapy. Antineutrophil cytoplasmic antibodies appear to be both sensitive and specific for Wegener's granulomatosis-associated scleritis, and testing is useful in the evaluation of patients with scleritis. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEPHROL & IMMUNOPATHOL,BOSTON,MA 02114. NR 46 TC 55 Z9 59 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JAN PY 1992 VL 99 IS 1 BP 125 EP 132 PG 8 WC Ophthalmology SC Ophthalmology GA GZ788 UT WOS:A1992GZ78800026 PM 1741124 ER PT J AU METSON, R RAUCH, SD AF METSON, R RAUCH, SD TI VIDEOLARYNGOSCOPY IN THE OFFICE - A CRITICAL-EVALUATION SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID LARYNGEAL EXAMINATION AB In view of the growing popularity of office videolaryngoscopy, surprisingly little objective data exist as to its influence on clinical practice. We reviewed 150 consecutive laryngeal recordings in an attempt to determine what effect videolaryngoscopy has had on our practice and the patient care provided. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02115. NR 3 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD JAN PY 1992 VL 106 IS 1 BP 56 EP 59 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA GZ508 UT WOS:A1992GZ50800023 PM 1734368 ER PT J AU KOZIEL, MJ WALKER, BD AF KOZIEL, MJ WALKER, BD TI VIRUSES, CHEMOTHERAPY AND IMMUNITY SO PARASITOLOGY LA English DT Article DE VIRAL DISEASES; IMMUNE RESPONSE; ANTIRETROVIRAL AGENTS; INTERFERONS ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; CHRONIC HEPATITIS-B; PHASE-I TRIAL; LYMPHOCYTES-T; 2',3'-DIDEOXYINOSINE DDI; REVERSE-TRANSCRIPTASE; CEREBROSPINAL-FLUID; AZIDOTHYMIDINE AZT AB An increasing number of antiviral agents are presently in various stages of development and testing, and an increasing number have recently been licensed for use in humans. These drugs have been used extensively to treat viral infections in immunocompromised individuals, and these studies indicate that for many antiviral agents the response to therapy is highly dependent on the integrity of the underlying host immune response. In particular, the response to zidovudine, acyclovir and ganciclovir in persons with HIV-1 infection is highly dependent upon CD4 number, which can be considered a surrogate marker for the state of host immune function in these subjects. Responses to interferons likewise can be shown to depend on the host immune response, with responses due to both direct antiviral effects of this agent as well as immunomodulatory effects mediated through interferon-induced upregulation of HLA molecule expression. The inter-dependence of host immunity with antiviral efficacy is underscored by the increased antiviral drug resistance in persons with advanced degrees of chronic immunosuppression, related to the higher level of viral replication and viraemia which occurs in the absence of an effective host immune response. Further definition of the precise mechanisms of these interactions should facilitate the rational design of antiviral agents and immunomodulatory therapies to improve treatment of viral infections. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KOZIEL, MJ (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 63 TC 4 Z9 4 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0031-1820 J9 PARASITOLOGY JI Parasitology PY 1992 VL 105 SU S BP S85 EP S92 PG 8 WC Parasitology SC Parasitology GA LU415 UT WOS:A1992LU41500009 PM 1285013 ER PT J AU LACK, EE YOUNG, RH SCULLY, RE AF LACK, EE YOUNG, RH SCULLY, RE TI PATHOLOGY OF OVARIAN NEOPLASMS IN CHILDHOOD AND ADOLESCENCE SO PATHOLOGY ANNUAL LA English DT Review ID GERM-CELL TUMORS; ENDODERMAL SINUS TUMOR; PEUTZ-JEGHERS SYNDROME; SEX CORD TUMOR; SCLEROSING STROMAL TUMORS; MALIGNANT STRUMA OVARII; MATURE CYSTIC TERATOMA; YOLK-SAC TUMOR; CLINICOPATHOLOGICAL ANALYSIS; ANNULAR TUBULES C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. RP LACK, EE (reprint author), GEORGETOWN UNIV,SCH MED,WASHINGTON,DC 20057, USA. NR 251 TC 26 Z9 27 U1 0 U2 1 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0079-0184 J9 PATHOL ANNU JI Pathol. Annu. PY 1992 VL 27 BP 281 EP 356 PN 2 PG 76 WC Pathology SC Pathology GA HW313 UT WOS:A1992HW31300010 PM 1316599 ER PT J AU DUCKETT, S SCHWARTZMAN, RJ OSTERHOLM, J RORKE, LB FRIEDMAN, D MCLELLAN, TL AF DUCKETT, S SCHWARTZMAN, RJ OSTERHOLM, J RORKE, LB FRIEDMAN, D MCLELLAN, TL TI BIOPSY DIAGNOSIS OF FAMILIAL ALEXANDERS DISEASE SO PEDIATRIC NEUROSURGERY LA English DT Article DE ROSENTHAL FIBERS; ASTROCYTOSIS ID ROSENTHAL FIBER FORMATION; ADULT; BRAIN AB A 26-year-old woman presented with headaches, incordination an a cerebellar mass (1982). The CT scan revealed dilated ventricles and a hypodense space-occupying lesion adjacent to the fourth ventricle. Neuronal loss, gliosis and masses of Rosenthal fibers were seen in biopsy. There was no evidence of neoplasm. A second biopsy 2 years later was similar to the original specimen. A diagnosis of Alexander's disease was suggested. Later that year the patient's 11-year-old brother manifested a clinical picture intially diagnosed as brain-stem glioma, but whose biopsy was characteristic of Alexander's disease. There has been a gradual deterioration of these siblings over the past 6 years (1986-1991). No evidence of neoplasm has appeared. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT NEUROL,BJ ALPERS NEUROPATHOL LAB,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT NEUROSURG,BJ ALPERS NEUROPATHOL LAB,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT RADIOL,BJ ALPERS NEUROPATHOL LAB,PHILADELPHIA,PA 19107. CHILDRENS HOSP,NEUROPATHOL LAB,PHILADELPHIA,PA 19104. RP DUCKETT, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,100 BLOSSOM ST,COX-5,BOSTON,MA 02114, USA. NR 23 TC 20 Z9 21 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PY 1992 VL 18 IS 3 BP 134 EP 138 DI 10.1159/000120652 PG 5 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA JX666 UT WOS:A1992JX66600003 PM 1457372 ER PT J AU FRIM, DM OGILVY, CS VONSATTAL, JP CHAPMAN, PH AF FRIM, DM OGILVY, CS VONSATTAL, JP CHAPMAN, PH TI IS INTRACEREBRAL SCHWANNOMA A DEVELOPMENTAL TUMOR OF CHILDREN AND YOUNG-ADULTS - CASE-REPORT AND REVIEW SO PEDIATRIC NEUROSURGERY LA English DT Article DE DEVELOPMENTAL TUMOR; INTRACEREBRAL SCHWANNOMA ID INTRASELLAR SCHWANNOMA; BRAIN-STEM AB A case of intracerebral schwannoma in an 11-year-old girl is presented. Of the small number of intracerebral schwannomas reported without association to a cranial nerve, the majority have occurred in children or young adults. Several possible etiologies for this tumor type are discussed. Based upon the distribution of ages at presentation and theories of the pathological origin of this tumor, the possibility that intracerebral schwannoma represents a developmental tumor is suggested. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,NEUROSURG SERV,GRAY 5,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROPATHOL SERV,BOSTON,MA 02114. NR 40 TC 33 Z9 34 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PY 1992 VL 18 IS 4 BP 190 EP 194 DI 10.1159/000120661 PG 5 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA KB567 UT WOS:A1992KB56700003 PM 1472431 ER PT J AU GUHA, A AF GUHA, A TI PLATELET-DERIVED GROWTH-FACTOR - A GENERAL-REVIEW WITH EMPHASIS ON ASTROCYTOMAS SO PEDIATRIC NEUROSURGERY LA English DT Article DE ASTROCYTOMAS; GROWTH FACTOR; PLATELET-DERIVED GROWTH FACTOR; ONCOGENES; BIOLOGICAL MODIFIERS ID HUMAN-MALIGNANT GLIOMA; SIMIAN SARCOMA-VIRUS; HUMAN-BRAIN-TUMORS; DIFFERENT DIMERIC FORMS; CENTRAL NERVOUS-SYSTEM; PDGF-RECEPTOR GENES; CELL-LINES; HUMAN GLIOBLASTOMA; C-SIS; MOLECULAR-BIOLOGY AB Growth factors acting in a paracrine or autocrine fashion are important in the development of normal cellular structures, and possibly in the development of neoplasia. For example, platelet-derived growth factor (PDGF) has been found in many normal tissues including the CNS, while minor changes in one of its forms (PDGF-B) converts it to the v-sis oncogene, capable of inducing sarcomas and astrocytomas in primates. PDGF is highly expressed in many human astrocytoma-derived cell lines, some of which also possess the PDGF-receptor(s), suggestive of an autocrine loop. Whether this finding is also present in the actual tumor, does it vary with tumor grade, what components of the tumor express PDGF and how does PDGF promote astrocytoma growth are some of the unanswered questions forming the basis of ongoing research efforts. This paper reviews the story of PDGF in a much oversimplified, however, hopefully understandable, fashion and presents the case of why this growth factor is of interest in understanding the biology of astrocytomas. C1 UNIV TORONTO,DEPT SURG,DIV NEUROSURG,TORONTO M5S 1A1,ONTARIO,CANADA. RP GUHA, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 76 TC 3 Z9 3 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-2291 J9 PEDIATR NEUROSURG JI Pediatr. Neurosurg. PY 1992 VL 17 IS 1 BP 14 EP 20 PG 7 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA HM581 UT WOS:A1992HM58100003 ER PT J AU KELLY, DH PATHAK, A MENY, R AF KELLY, DH PATHAK, A MENY, R TI ON GROWTH OF INFANTS WITH CHRONIC LUNG-DISEASE - REPLY SO PEDIATRIC PULMONOLOGY LA English DT Letter C1 UNIV MARYLAND HOSP,SIDS INST,BALTIMORE,MD 21201. RP KELLY, DH (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PULM UNIT,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD JAN PY 1992 VL 12 IS 1 BP 59 EP 60 DI 10.1002/ppul.1950120116 PG 2 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA HB231 UT WOS:A1992HB23100014 ER PT J AU JELLINEK, MS CATLIN, EA TODRES, ID CASSEM, EH AF JELLINEK, MS CATLIN, EA TODRES, ID CASSEM, EH TI FACING TRAGIC DECISIONS WITH PARENTS IN THE NEONATAL INTENSIVE-CARE UNIT - CLINICAL PERSPECTIVES SO PEDIATRICS LA English DT Article ID LIFE SUPPORT; DEATH; NURSERY; GRIEF; ILL C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NEONATAL & PEDIAT INTENS CARE,BOSTON,MA 02114. NR 24 TC 21 Z9 21 U1 0 U2 2 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JAN PY 1992 VL 89 IS 1 BP 119 EP 122 PG 4 WC Pediatrics SC Pediatrics GA GY514 UT WOS:A1992GY51400023 PM 1727994 ER PT S AU FALK, E AF FALK, E BE Brakman, P Kluft, C TI DYNAMICS IN THROMBUS FORMATION SO PLASMINOGEN ACTIVATION IN FIBRINOLYSIS, IN TISSUE REMODELING, AND IN DEVELOPMENT SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON PLASMINOGEN ACTIVATION IN FIBRINOLYSIS, IN TISSUE REMODELING, AND IN DEVELOPMENT CY OCT 22-25, 1991 CL LEIDEN, NETHERLANDS SP NEW YORK ACAD SCI, GAUBIUS INST, TNO HLTH RES RP FALK, E (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK SN 0077-8923 BN 0-89766-732-8 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1992 VL 667 BP 204 EP 223 DI 10.1111/j.1749-6632.1992.tb51618.x PG 20 WC Biochemistry & Molecular Biology; Pathology; Physiology SC Biochemistry & Molecular Biology; Pathology; Physiology GA BX33K UT WOS:A1992BX33K00029 PM 1309039 ER PT J AU GARRIDO, L ACKERMAN, JL VEVEA, JM MARK, JE WANG, SH AF GARRIDO, L ACKERMAN, JL VEVEA, JM MARK, JE WANG, SH TI POLYMER DISTRIBUTION IN SILICA AEROGELS IMPREGNATED WITH SILOXANES BY H-1 NUCLEAR-MAGNETIC-RESONANCE IMAGING SO POLYMER LA English DT Article DE AEROGELS; SILICA; SILOXANES; NUCLEAR MAGNETIC RESONANCE IMAGING; IMPREGNATION ID STRUCTURE PROPERTY BEHAVIOR; MOLECULAR-WEIGHT; TETRAETHOXYSILANE; NETWORKS AB Polymer-modified aerogel samples were prepared by vacuum impregnation of silica aerogels with dimethylsiloxane-vinylmethylsiloxane copolymers. The specimens were characterized by H-1 nuclear magnetic resonance (n.m.r.) relaxation measurements. The effects of the polymer molecular weight, irradiation and aerogel density upon the spin-lattice (T1) and spin-spin (T2) relaxation times were studied. Significant reduction was observed in the T2 values owing to increases in both aerogel and crosslink densities. H-1 n.m.r. images reveal a high degree of heterogeneity in the samples. Distribution maps of the polymer-silica interactions and crosslink density are obtained. C1 UNIV CINCINNATI,POLYMER RES CTR,CINCINNATI,OH 45221. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CINCINNATI,DEPT CHEM,CINCINNATI,OH 45221. RP GARRIDO, L (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,149 13TH ST,BOSTON,MA 02129, USA. RI Garrido, Leoncio/K-3092-2014; Ackerman, Jerome/E-2646-2015 OI Garrido, Leoncio/0000-0002-7587-1260; Ackerman, Jerome/0000-0001-5176-7496 NR 23 TC 13 Z9 13 U1 0 U2 4 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0032-3861 J9 POLYMER JI Polymer PY 1992 VL 33 IS 9 BP 1826 EP 1830 DI 10.1016/0032-3861(92)90479-G PG 5 WC Polymer Science SC Polymer Science GA HW190 UT WOS:A1992HW19000008 ER PT B AU KIRKPATRICK, R TUCKER, C RAMIREZ, J PARKER, SW GILLBODY, KM RILEY, PO KREBS, DE AF KIRKPATRICK, R TUCKER, C RAMIREZ, J PARKER, SW GILLBODY, KM RILEY, PO KREBS, DE BE Woollacott, M Horak, F TI CENTER OF GRAVITY CONTROL IN NORMAL AND VESTIBULOPATHIC GAIT SO POSTURE AND GAIT, CONTROL MECHANISMS 1992, VOL 1 AND 2 LA English DT Proceedings Paper CT 11th International Symposium of the Society for Postural and Gait Research - Posture and Gait: Control Mechanisms, 1992 CY MAY 24-27, 1992 CL PORTLAND, OR SP SOC POSTURAL & GAIT RES, UNIV OREGON, GOOD SAMARITAN HOSP, OREGON C1 MASSACHUSETTS GEN HOSP,BIOMOT LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV OREGONBOOKS PI EUGENE PA UNIV OREGON, UNIV OREGON PUBNS, 101 CHAPMAN HALL, EUGENE, OR 97403-1282 BN 0-87114-090-X PY 1992 BP A260 EP A263 PG 4 WC Neurosciences SC Neurosciences & Neurology GA BA19J UT WOS:A1992BA19J00066 ER PT B AU PARKER, SW KREBS, DE GILL, KM RILEY, PO AF PARKER, SW KREBS, DE GILL, KM RILEY, PO BE Woollacott, M Horak, F TI VARYING SWAY-REFERENCING GAIN TO QUANTIFY MEASUREMENT OF STANDING BALANCE IN PATIENTS WITH BILATERAL VESTIBULAR HYPOFUNCTION SO POSTURE AND GAIT, CONTROL MECHANISMS 1992, VOL 1 AND 2 LA English DT Proceedings Paper CT 11th International Symposium of the Society for Postural and Gait Research - Posture and Gait: Control Mechanisms, 1992 CY MAY 24-27, 1992 CL PORTLAND, OR SP SOC POSTURAL & GAIT RES, UNIV OREGON, GOOD SAMARITAN HOSP, OREGON C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV OREGONBOOKS PI EUGENE PA UNIV OREGON, UNIV OREGON PUBNS, 101 CHAPMAN HALL, EUGENE, OR 97403-1282 BN 0-87114-090-X PY 1992 BP A315 EP A318 PG 4 WC Neurosciences SC Neurosciences & Neurology GA BA19J UT WOS:A1992BA19J00080 ER PT J AU REISER, H FREEMAN, GJ RAZIWOLF, Z GIMMI, CD BENACERRAF, B NADLER, LM AF REISER, H FREEMAN, GJ RAZIWOLF, Z GIMMI, CD BENACERRAF, B NADLER, LM TI MURINE B7 ANTIGEN PROVIDES AN EFFICIENT COSTIMULATORY SIGNAL FOR ACTIVATION OF MURINE LYMPHOCYTES-T VIA THE T-CELL RECEPTOR CD3 COMPLEX SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MONOCLONAL-ANTIBODY; PROTEIN TAP; STIMULATION; LY-6; IDENTIFICATION; EXPRESSION; INDUCTION; MOLECULE; DISTINCT; VARIANT AB We demonstrate that the murine B7 (mB7) protein is a potent costimulatory molecule for the activation of resting murine CD4+ T cells through the T-cell receptor (TCR)/CD3 complex. Stable mB7-transfected Chinese hamster ovary cells, but not vector-transfected controls, synergize with anti-CD3 monoclonal antibody and Con A-induced T-cell activation, resulting ultimately in proliferation. mB7 exerted its effect by inducing production of interleukin 2 and expression of the interleukin 2 receptor. Thus, mB7 costimulates T-cell activation through the TCR/CD3 complex by positively modulating the normal pathway of T-cell expansion. In contrast to the pronounced effect of mB7 on the activation of T cells through the TCR/CD3 complex, the mB7-transfected CHO cell line costimulated T-cell activation via the glycosylphosphatidylinositol-anchored proteins Thy-1 and Ly-6A.2 only inefficiently. Finally, the combination of a calcium ionophore and mB7 is not sufficient to cause T-cell proliferation, while the combination of a calcium ionophore and phorbol 12-myristate 13-acetate (PMA) stimulates T cells efficiently. The signals that mB7 and PMA provide for murine T lymphocyte activation are therefore not interchangeable, although both costimulate activation through the TCR/CD3 complex. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP REISER, H (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-46967, CA-40216]; NIAID NIH HHS [AI-30169] NR 43 TC 163 Z9 164 U1 0 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 1 PY 1992 VL 89 IS 1 BP 271 EP 275 DI 10.1073/pnas.89.1.271 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GY047 UT WOS:A1992GY04700057 PM 1370349 ER PT J AU SHIOTA, G RHOADS, DB WANG, TC NAKAMURA, T SCHMIDT, EV AF SHIOTA, G RHOADS, DB WANG, TC NAKAMURA, T SCHMIDT, EV TI HEPATOCYTE GROWTH-FACTOR INHIBITS GROWTH OF HEPATOCELLULAR-CARCINOMA CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE AUTOCRINE GROWTH FACTOR; ALBUMIN EXPRESSION VECTOR ID MAMMALIAN-CELLS; SCATTER FACTOR; RAT PLATELETS; FACTOR-ALPHA; EXPRESSION; PURIFICATION; GENE; HYBRIDIZATION; INVITRO; PROTEIN AB Hepatocyte growth factor (HGF) is a potent mitogen for primary hepatocytes. Therefore, we examined HGF as a possible autocrine growth factor in hepatocellular carcinoma (HCC). We introduced an albumin-HGF expression vector into Fao HCC cells and transgenic mice. Expression of the albumin-HGF vector in Fao HCC cells inhibited their growth in vitro. In vivo, FaoHGF cells produced tumors that averaged 10% of the sizes of G418-resistant controls when transplanted into nude mice. In contrast, hepatocytes from transgenic mice expressing HGF grew more rapidly than did those from normal siblings. Further, growth of eight additional HCC cell lines was inhibited by the addition of recombinant HGF. Finally, of 35 tumor cell lines surveyed, only 6 cell lines expressed HGF mRNA, and no HCC cell line expressed HGF. Although HGF stimulates normal hepatocytes, it is a negative growth regulator for HCC cells. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. KYUSHU UNIV,FAC SCI,DEPT BIOL,FUKUOKA 812,JAPAN. FU NIDDK NIH HHS [DK01392, DK01937, P30 DK34928] NR 27 TC 293 Z9 298 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JAN 1 PY 1992 VL 89 IS 1 BP 373 EP 377 DI 10.1073/pnas.89.1.373 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GY047 UT WOS:A1992GY04700078 PM 1309612 ER PT J AU TYAN, ML AF TYAN, ML TI EFFECTS OF H-2 AND VITAMIN-A ON EYE DEFECTS IN CONGENIC MICE SO PROCEEDINGS OF THE SOCIETY FOR EXPERIMENTAL BIOLOGY AND MEDICINE LA English DT Article ID CRYSTALLIN; LOCUS; LENS AB Pregnant mice congenic with C57BL/10 (B10.A, B10.BR, B10.D2, B10.A(2R), B10.A(5R), B10.A(15R), B10.A(1R), B10.A(18R), and B10.OL) were fed Purina Mouse Chow or the same diet plus 200 IU of vitamin A daily. The pregnant dams were sacrificed on the 18th day of gestation and the fetuses were sexed and examined for defects in eye development. It was found that the frequency of microphthalmia and anophthalmia in the female progeny of mice fed Mouse Chow was 7.4-9.2% in B10.A and B10.BR, 4.0-5.5% in B10.A(18R), B10, B10.A(5R), B10.A(1R), B10.A(15R), and B10.A(2R), and 0.8% and 1.4% in B10.D2 and B10.OL mice, respectively. On average, the frequency of these defects in the female progeny was 6.2 times greater than that in males (P < 0.001). The right eye was 5.8 times more often affected than the left (P < 0.001). The addition of vitamin A to the diet increased the frequency of these eye abnormalities in all strains, suggesting that this effect is not mediated by loci associated with H-2, as is the case with vitamin A-enhanced cleft palate. The addition of vitamin A to the diet did not affect the ratios of affected males to females, affected right to left eye, or microphthalmia to anophthalmia. The results suggest that there are two loci on chromosome 17, one centromeric to E-beta and one telemeric to C4, that interact to determine to some degree the frequency of microphthalmia and anophthalmia. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP TYAN, ML (reprint author), W LOS ANGELES VET ADM MED CTR 111M,LOS ANGELES,CA 90073, USA. NR 9 TC 11 Z9 11 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0037-9727 J9 P SOC EXP BIOL MED JI Proc. Soc. Exp. Biol. Med. PD JAN PY 1992 VL 199 IS 1 BP 123 EP 127 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW106 UT WOS:A1992GW10600019 PM 1728030 ER PT J AU MARTIN, JB RISKIND, PN SWAAB, DF SAPER, CB RANCE, NF DEJONG, JMBV QUERIDO, A AF MARTIN, JB RISKIND, PN SWAAB, DF SAPER, CB RANCE, NF DEJONG, JMBV QUERIDO, A TI NEUROLOGIC MANIFESTATIONS OF HYPOTHALAMIC DISEASE SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID CEREBELLAR-ATAXIA; CORPUS-CALLOSUM; HYPOTHERMIA; HYPOGONADISM; EPILEPSY; AGENESIS C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. RP MARTIN, JB (reprint author), UNIV CALIF SAN FRANCISCO,SCH MED,DEPT NEUROL,ROOM S-224,513 PARNASSUS AVE,SAN FRANCISCO,CA 94143, USA. NR 38 TC 16 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1992 VL 93 BP 31 EP 42 PG 12 WC Neurosciences SC Neurosciences & Neurology GA KD672 UT WOS:A1992KD67200003 PM 1480755 ER PT J AU REPPERT, SM SWAAB, DF CORNER, MA REPASKE, DR MIRMIRAN, M AF REPPERT, SM SWAAB, DF CORNER, MA REPASKE, DR MIRMIRAN, M TI PRENATAL DEVELOPMENT OF A HYPOTHALAMIC BIOLOGICAL CLOCK SO PROGRESS IN BRAIN RESEARCH LA English DT Review ID PLASMA MELATONIN CONCENTRATIONS; RAT SUPRACHIASMATIC NUCLEUS; MATERNAL SCN LESIONS; CIRCADIAN-RHYTHMS; PINEALECTOMY ABOLISHES; CORTICOSTERONE RHYTHM; LATE GESTATION; PREGNANT EWE; FETAL SHEEP; VASOPRESSIN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP REPPERT, SM (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,32 FRUIT ST,BOSTON,MA 02114, USA. RI Repaske, David/E-3939-2011 NR 62 TC 34 Z9 35 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0079-6123 J9 PROG BRAIN RES JI Prog. Brain Res. PY 1992 VL 93 BP 119 EP 132 PG 14 WC Neurosciences SC Neurosciences & Neurology GA KD672 UT WOS:A1992KD67200010 PM 1480745 ER PT J AU KOHLER, SJ KOLODNY, NH AF KOHLER, SJ KOLODNY, NH TI SODIUM MAGNETIC-RESONANCE-IMAGING AND CHEMICAL-SHIFT IMAGING SO PROGRESS IN NUCLEAR MAGNETIC RESONANCE SPECTROSCOPY LA English DT Review ID DOUBLE-QUANTUM NMR; INTRACELLULAR SODIUM; DEXTRAN-MAGNETITE; HUMAN-BRAIN; HUMAN HEAD; HUMAN-BODY; 1.5 T; NA-23; INVIVO; RELAXATION C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. WELLESLEY COLL,DEPT CHEM,WELLESLEY,MA 02181. RP KOHLER, SJ (reprint author), GE,MED SYST,BOX 1292,CONCORD,MA 01742, USA. NR 74 TC 13 Z9 13 U1 2 U2 6 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0079-6565 J9 PROG NUCL MAG RES SP JI Prog. Nucl. Magn. Reson. Spectrosc. PY 1992 VL 24 BP 411 EP 433 DI 10.1016/0079-6565(92)80003-X PN 5 PG 23 WC Chemistry, Physical; Physics, Atomic, Molecular & Chemical; Spectroscopy SC Chemistry; Physics; Spectroscopy GA KG713 UT WOS:A1992KG71300002 ER PT J AU SMITH, RF SMITH, TF AF SMITH, RF SMITH, TF TI PATTERN-INDUCED MULTI-SEQUENCE ALIGNMENT (PIMA) ALGORITHM EMPLOYING SECONDARY STRUCTURE-DEPENDENT GAP PENALTIES FOR USE IN COMPARATIVE PROTEIN MODELING SO PROTEIN ENGINEERING LA English DT Article DE ALIGNMENTS; HOMOLOGY; MODELING; PROTEIN SEQUENCE; SECONDARY STRUCTURE ID DISTANTLY RELATED PROTEINS; AMINO-ACID-SEQUENCES; HOMOLOGOUS PROTEINS; GLOBULAR PROTEINS; PROFILE ANALYSIS; PREDICTION; IDENTIFICATION; TREES; SIMILARITIES; RECOGNITION AB A multiple sequence alignment algorithm is described that uses a dynamic programming-based pattern construction method to align a set of homologous sequences based on their common pattern of conserved sequence elements. This pattern-induced multi-sequence alignment (PIMA) algorithm can employ secondary-structure dependent gap penalties for use in comparative modelling of new sequences when the three-dimensional structure of one or more members of the same family is known. We show that the use of secondary structure information can significantly improve the accuracy of aligning structure boundaries in a set of homologous sequences even when the structure of only one member of the family is known. C1 HARVARD UNIV, DANA FARBER CANC INST, DEPT BIOSTAT, BOSTON, MA 02115 USA. RI sebastianovitsch, stepan/G-8507-2013 FU NCRR NIH HHS [RR02275] NR 56 TC 230 Z9 235 U1 0 U2 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0269-2139 J9 PROTEIN ENG JI Protein Eng. PD JAN PY 1992 VL 5 IS 1 BP 35 EP 41 DI 10.1093/protein/5.1.35 PG 7 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA HF802 UT WOS:A1992HF80200005 PM 1631044 ER PT J AU OTTO, MW POLLACK, MH MELTZERBRODY, S ROSENBAUM, JF AF OTTO, MW POLLACK, MH MELTZERBRODY, S ROSENBAUM, JF TI COGNITIVE-BEHAVIORAL THERAPY FOR BENZODIAZEPINE DISCONTINUATION IN PANIC DISORDER PATIENTS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article ID CARBAMAZEPINE TREATMENT; MULTICENTER TRIAL; DOUBLE-BLIND; ALPRAZOLAM; AGORAPHOBIA; WITHDRAWAL; DEPENDENCE; ANXIETY; CLONAZEPAM; IMIPRAMINE AB The discontinuation of benzodiazepine treatment in patients with panic disorder may be associated with emergent withdrawal and anxiety symptoms, relapse of panic, and the inability to complete benzodiazepine taper. Although some patients may respond to slow taper strategies or the use of pharmacologic adjuncts, many continue to experience significant difficulties during benzodiazepine discontinuation. This paper presents a cognitive-behavioral conceptualization of benzodiazepine discontinuation difficulties, emphasizing "fear of fear" cycles. From this perspective the discontinuation process is seen as exposing panic disorder patients to somatic sensations associated with panic at a time when there is both increased anxiety and concern about re-emergence or worsening of panic episodes. As a consequence, patients may re-enter a cycle of catastrophic interpretations of symptoms, increased vigilance and fear, and panic. Cognitive-behavioral interventions may ameliorate discontinuation-associated difficulties and prevent the return of the panic disorder. Preliminary data supporting the efficacy of these interventions are described. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNITS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 39 TC 34 Z9 36 U1 1 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1992 VL 28 IS 2 BP 123 EP 130 PG 8 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA JG201 UT WOS:A1992JG20100002 PM 1355299 ER PT J AU WIRSHING, WC MARDER, SR ECKMAN, T LIBERMAN, RP MINTZ, J AF WIRSHING, WC MARDER, SR ECKMAN, T LIBERMAN, RP MINTZ, J TI ACQUISITION AND RETENTION OF SKILLS TRAINING METHODS IN CHRONIC-SCHIZOPHRENIC OUTPATIENTS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 30TH ANNUAL MEETING OF THE AMERICAN COLLEGE OF NEUROPSYCHOPHARMACOLOGY CY DEC, 1991 CL SAN JUAN, PR SP AMER COLL NEUROPSYCHOPHARM ID DRUGS AB Forty-one DSM-III-R schizophrenic subjects on constant, low-dose maintenance neuroleptic drug therapy (5-10 mg of fluphenazine decanoate intramuscularly every 2 weeks) were randomly assigned to structured and modularized skills training or to supportive group psychotherapy. The skills training was designed by using cognitive and behavioral methods to compensate for the learning disabilities that plague many schizophrenic patients. Skill acquisition was assessed by using quantified performance on standardized role-play tests. Subjects who received skills training made significant gains In each of the areas taught, whereas those who participated in the control psychotherapy group did not. The knowledge and skills learned during training were retained without significant erosion over a 1-year followup period. These results suggest that the use of structured principles of learning and cognitive therapy can effectively train schizophrenics in skill areas pertinent to the self-management of their illness. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP WIRSHING, WC (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,B-151H,LOS ANGELES,CA 90073, USA. FU NIMH NIH HHS [MH-41573, MH-30911] NR 13 TC 19 Z9 20 U1 0 U2 0 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1992 VL 28 IS 3 BP 241 EP 245 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA JY721 UT WOS:A1992JY72100008 PM 1480726 ER PT J AU GANZINI, L CASEY, DE HOFFMAN, WF HEINTZ, RT AF GANZINI, L CASEY, DE HOFFMAN, WF HEINTZ, RT TI TARDIVE-DYSKINESIA AND DIABETES-MELLITUS SO PSYCHOPHARMACOLOGY BULLETIN LA English DT Article; Proceedings Paper CT 30TH ANNUAL MEETING OF THE AMERICAN COLLEGE OF NEUROPSYCHOPHARMACOLOGY CY DEC, 1991 CL SAN JUAN, PR SP AMER COLL NEUROPSYCHOPHARM ID RISK-FACTORS; RATS; DOPAMINE; LESIONS; BRAIN; PREVALENCE; METOCLOPRAMIDE; METABOLISM; INSULIN; BINDING AB Two studies examine the prevalence of tardive dyskinesia (TD) in neuroleptic-treated diabetic patients. Study 1 compared 38 diabetic patients with 38 nondiabetic patients treated for psychotic disorders with low to moderate doses of neuroleptics (mean chlorpromazine equivalents = 300 mg/day) for an average of 18 years. Study 2 compared 24 diabetic and 27 nondiabetic patients treated for an average of 2.6 years with a mean 31 mg/day of metoclopramide for gastrointestinal disease. Patients were examined for TD using standardized scales by raters blind to all treatment and illness variables. In both studies, there were no differences between the diabetic and nondiabetic groups in age, sex, type of psychiatric illness, and dose and duration of neuroleptic treatment or severity of parkinsonism. In both studies, the diabetic patients had significantly greater prevalence and severity of TD. No measures of diabetes severity were associated with TD in either study. Possible pathophysiologic mechanisms for the increased prevalence of TD in neuroleptic-treated patients with diabetes will be discussed. C1 DAMMASCH STATE HOSP,WILSONVILLE,OR. OREGON HLTH SCI UNIV,DEPT PSYCHIAT,PORTLAND,OR 97201. RP GANZINI, L (reprint author), PORTLAND VET AFFAIRS MED CTR,PSYCHIAT SERV 116AP,POB 1034,3710 SW VET HOSP PK RD,PORTLAND,OR 97207, USA. FU NIMH NIH HHS [MH-36657, MH-43586] NR 37 TC 23 Z9 23 U1 1 U2 1 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0048-5764 J9 PSYCHOPHARMACOL BULL JI Psychopharmacol. Bull. PY 1992 VL 28 IS 3 BP 281 EP 286 PG 6 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA JY721 UT WOS:A1992JY72100014 PM 1362276 ER PT J AU KOPANS, DB AF KOPANS, DB TI STANDARDIZED MAMMOGRAPHY REPORTING SO RADIOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID BREAST-CANCER; MORTALITY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 48 Z9 50 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0033-8389 J9 RADIOL CLIN N AM JI Radiol. Clin. N. Am. PD JAN PY 1992 VL 30 IS 1 BP 257 EP 264 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GZ798 UT WOS:A1992GZ79800016 PM 1732932 ER PT J AU GREENE, RE AF GREENE, RE TI MISSED LUNG NODULES - LOST OPPORTUNITIES FOR CANCER CURE SO RADIOLOGY LA English DT Editorial Material DE DIAGNOSTIC RADIOLOGY; EDITORIALS; LUNG NEOPLASMS, DIAGNOSIS; LUNG, NODULE ID CHEST RADIOGRAPHS RP GREENE, RE (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 11 TC 23 Z9 23 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1992 VL 182 IS 1 BP 8 EP 9 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GW054 UT WOS:A1992GW05400003 PM 1727314 ER PT J AU SAINI, S AF SAINI, S TI CONTRAST-ENHANCED MR IMAGING OF THE LIVER SO RADIOLOGY LA English DT Editorial Material DE CONTRAST MEDIA, EFFECTS; EDITORIALS; LIVER, MR; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT; MANGANESE ID SUPERPARAMAGNETIC IRON-OXIDE; ARTERIAL PORTOGRAPHY; DELAYED CT; AGENT; TOXICITY; CHELATE; TUMORS; CANCER; SPLEEN; DTPA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP SAINI, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 36 TC 26 Z9 26 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1992 VL 182 IS 1 BP 12 EP 14 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GW054 UT WOS:A1992GW05400005 PM 1727273 ER PT J AU PETEET, JR STOMPER, PC ROSS, DM COTTON, V TRUESDELL, P MOCZYNSKI, W AF PETEET, JR STOMPER, PC ROSS, DM COTTON, V TRUESDELL, P MOCZYNSKI, W TI EMOTIONAL SUPPORT FOR PATIENTS WITH CANCER WHO ARE UNDERGOING CT - SEMISTRUCTURED INTERVIEWS OF PATIENTS AT A CANCER INSTITUTE SO RADIOLOGY LA English DT Article DE NEOPLASMS, CT; SPECIAL REPORTS ID RADIOLOGY; ANXIETY AB To understand and improve the experience of cancer patients undergoing computed tomography (CT), 79 patients who underwent CT at a cancer institute participated in semistructured interviews about their experiences with CT. All patients had previously undergone CT; 75% (n = 59), three times or more. Anxiety about results was the most common concern during first and subsequent CT examinations. Technical aspects were a common concern during initial scanning, but not subsequently. Methods of relaxation most used by patients during CT were following instructions (56% [n = 44]), meditating and visualizing (44% [n = 35]), and praying (42% [n = 33]). Patients suggested several ways in which the radiology staff can support them during the evaluation of their malignancy. Fifty-five (70%) of the patients said they would like the radiologist to tell them the results of their scanning. Optimal care of patients with cancer who undergo CT goes beyond technical to emotional and spiritual support. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DIV PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT DIAGNOST RADIOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT NURSING,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT SOCIAL WORK,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,CHAPLAINCY SERV,BOSTON,MA 02115. NR 16 TC 16 Z9 16 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1992 VL 182 IS 1 BP 99 EP 102 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GW054 UT WOS:A1992GW05400021 PM 1727318 ER PT J AU REIMER, P SAINI, S HAHN, PF MUELLER, PR BRADY, TJ COHEN, MS AF REIMER, P SAINI, S HAHN, PF MUELLER, PR BRADY, TJ COHEN, MS TI TECHNIQUES FOR HIGH-RESOLUTION ECHO-PLANAR MR IMAGING OF THE PANCREAS SO RADIOLOGY LA English DT Article DE MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT; MAGNETIC RESONANCE (MR), ECHO PLANAR; MAGNETIC RESONANCE (MR), PULSE SEQUENCES; MAGNETIC RESONANCE (MR), TISSUE CHARACTERIZATION; PANCREAS, MR; PANCREAS, NEOPLASMS; PANCREATITIS ID MAGNETIC-RESONANCE; INSTANT IMAGES; BODY; ABDOMEN; LIVER AB Recent technical advances in echo-planar magnetic resonance (MR) imaging prompted an investigation of these new techniques in pancreatic MR imaging and evaluation of bowel lumen enhancement with an aqueous bowel contrast agent. In 42 subjects (36 healthy, six with pancreatic disease), various T1-weighted inversion-recovery and T2-weighted spin-echo fat-suppressed pulse sequences were assessed with an echo-planar technique implemented with a modified clinical MR imager. Single-excitation imaging (echo time, 26 msec) provided a higher (P < .05) signal-to-noise ratio than did conventional spin-echo and all other echo-planar techniques. In 13 (72%) of 18 healthy subjects who did not undergo administration of the contrast agent, the entire pancreas was distinguished from adjoining bowel. In all 18 subjects who underwent contrast-enhanced imaging, a significantly greater (P < .05) intraluminal signal intensity was apparent with all echo-planar pulse sequences and the entire pancreas was identified. In six patients with pancreatic disease, lesions could be identified by their difference in signal intensity. C1 MASSACHUSETTS GEN HOSP,CTR MGH NMR,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV GASTROINTESTINAL RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [CA PO1 48279] NR 22 TC 24 Z9 24 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JAN PY 1992 VL 182 IS 1 BP 175 EP 179 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GW054 UT WOS:A1992GW05400034 PM 1727278 ER PT J AU BUMP, EA ALSARRAF, R PIERCE, SM COLEMAN, CN AF BUMP, EA ALSARRAF, R PIERCE, SM COLEMAN, CN TI ELEVATION OF MOUSE KIDNEY THIOL CONTENT FOLLOWING ADMINISTRATION OF GLUTATHIONE SO RADIOTHERAPY AND ONCOLOGY LA English DT Article DE GLUTATHIONE; CYSTEINE; KIDNEY ID OXYGEN ENHANCEMENT RATIO; CYSTINE UPTAKE; TUMOR-CELLS; RADIOSENSITIZATION; TRANSPORT; RADIATION; BIOSYNTHESIS; INHIBITION; METABOLISM; MODULATION AB We have found that kidney glutathione and cysteine content in C3H mice can be increased by intraperitoneal administration of either glutathione (GSH) or glutathione disulfide (GSSG). Kidney thiol content is maximal 20-60 min after administration of 1000 mg/kg glutathione and returns to normal values by 2 h. The same time-course of thiol perturbation was observed when acivicin, an inhibitor of gamma-glutamyl transpeptidase, was administered 15 min prior to GSSG administration. The increase in kidney thiols after GSSG administration appears to saturate, with little additional increase as the administered dose is increased above 750 mg/kg. There was no significant change in liver GSH or cysteine after GSSG administration. We suggest that glutathione administration may provide a strategy for selective radioprotection or chemoprotection of specialized cells which can effectively utilize systemic GSH precursors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BUMP, EA (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA42391, CA46776] NR 25 TC 4 Z9 4 U1 0 U2 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD JAN PY 1992 VL 23 IS 1 BP 21 EP 25 DI 10.1016/0167-8140(92)90301-A PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA HD074 UT WOS:A1992HD07400004 PM 1736328 ER PT B AU SHIPLEY, WU KAUFMAN, DS GRIFFIN, P ALTHAUSEN, AF HENEY, NM PROUT, GR AF SHIPLEY, WU KAUFMAN, DS GRIFFIN, P ALTHAUSEN, AF HENEY, NM PROUT, GR BE MEYER, JL VAETH, JM TI RADIOCHEMOTHERAPY FOR INVASIVE-CARCINOMA OF THE BLADDER SO RADIOTHERAPY / CHEMOTHERAPY INTERACTIONS IN CANCER THERAPY: POTENTIAL BENEFITS AND HAZARDS IN THE CLINIC SE FRONTIERS OF RADIATION THERAPY AND ONCOLOGY LA English DT Proceedings Paper CT 26TH ANNUAL SAN FRANCISCO CANCER SYMP CY FEB 16-17, 1991 CL SAN FRANCISCO, CA SP FDN ST FRANCIS MEM HOSP RP SHIPLEY, WU (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5493-1 J9 FRONT RADIAT THER ON JI Front.Radiat.Ther.Oncol. PY 1992 VL 26 BP 142 EP 152 PG 11 WC Oncology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Pharmacology & Pharmacy; Radiology, Nuclear Medicine & Medical Imaging GA BW35T UT WOS:A1992BW35T00012 PM 1511915 ER PT J AU WADA, Y TAMURA, J MUSSELMAN, BD KASSEL, DB SAKURAI, T MATSUO, T AF WADA, Y TAMURA, J MUSSELMAN, BD KASSEL, DB SAKURAI, T MATSUO, T TI ELECTROSPRAY IONIZATION MASS-SPECTRA OF HEMOGLOBIN AND TRANSFERRIN BY A MAGNETIC-SECTOR MASS-SPECTROMETER - COMPARISON WITH THEORETICAL ISOTOPIC DISTRIBUTIONS SO RAPID COMMUNICATIONS IN MASS SPECTROMETRY LA English DT Article ID CARBOHYDRATE MOIETY; PERFORMANCE AB Electrospray ionization mass spectra of human hemoglobin chains and of transferrin were acquired on a magnetic sector mass spectrometer. The observed molecular ion for each hemoglobin chain was in good agreement with the theoretical isotopic distribution at a reasonable resolution of 2000. The clear separation of a variant beta-chain in admixture with the normal counterpart at mass 15 867 that differed from it by 14 Da (0.09%) ensured that a smaller mass difference could be detected. The molecular ions for human transferrin were too broad compared with the theoretical shape to determine the molecular mass accurately, probably due to the heterogeneity of the carbohydrate moiety. A decrease in mass by neuraminidase digestion, however, determined the average number of sialic acids in the molecule. C1 JEOL USA INC,PEABODY,MA 01960. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 01960. OSAKA UNIV,COLL GEN EDUC,INST PHYS,TOYONAKA,OSAKA 560,JAPAN. RP WADA, Y (reprint author), OSAKA MED CTR MATERNAL & CHILD HLTH,RES INST,DEPT MOLEC MED,840 MURODO CHO,IZUMI,OSAKA 59002,JAPAN. NR 22 TC 29 Z9 30 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0951-4198 J9 RAPID COMMUN MASS SP JI Rapid Commun. Mass Spectrom. PD JAN PY 1992 VL 6 IS 1 BP 9 EP 13 DI 10.1002/rcm.1290060104 PG 5 WC Chemistry, Analytical; Spectroscopy SC Chemistry; Spectroscopy GA GZ130 UT WOS:A1992GZ13000003 PM 1591399 ER PT B AU HARLOW HUNTER NASMYTH HUNT KIRSCHNER BEACH PINES REED YANAGIDA LEHNER AF HARLOW HUNTER NASMYTH HUNT KIRSCHNER BEACH PINES REED YANAGIDA LEHNER BE MARSH, J TI THE CYCLIN-DEPENDENT KINASE FAMILY SO REGULATION OF THE EUKARYOTIC CELL CYCLE SE CIBA FOUNDATION SYMPOSIA LA English DT Discussion CT SYMP ON REGULATION OF THE EUKARYOTIC CELL CYCLE CY JAN 21-23, 1992 CL CIBA FDN, LONDON, ENGLAND HO CIBA FDN RP HARLOW (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,CHARLESTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA CHICHESTER BN 0-471-93446-1 J9 CIBA F SYMP PY 1992 VL 170 BP 205 EP 208 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA BW54J UT WOS:A1992BW54J00013 ER PT J AU ARCECI, RJ PAMPFER, S POLLARD, JW AF ARCECI, RJ PAMPFER, S POLLARD, JW TI ROLE AND EXPRESSION OF COLONY-STIMULATING FACTOR-I AND STEEL FACTOR RECEPTORS AND THEIR LIGANDS DURING PREGNANCY IN THE MOUSE SO REPRODUCTION FERTILITY AND DEVELOPMENT LA English DT Article; Proceedings Paper CT SYMP ON OOCYTE DONATION CY NOV 22-24, 1991 CL MELBOURNE, AUSTRALIA SP SERONO ID TYROSINE KINASE RECEPTOR; FMS PROTO-ONCOGENE; CELL GROWTH-FACTOR; C-KIT RECEPTOR; FACTOR-I CSF-1; OP OP MOUSE; W-LOCUS; PLACENTAL DEVELOPMENT; SI-LOCUS; MUTANT MICE AB It is becoming apparent that the effects of female sex steroid hormones can be mediated by locally synthesized polypeptide growth factors in the uterus. In this paper we describe the patterns of expression of two such growth factors, steel factor and colony stimulating factor-1 (CSF-1), and their transmembrane tyrosine kinase receptors, the products of the c-kit and c-fms proto-oncogenes respectively. Both these uterine synthesized cytokines are directed to uterine hematopoietic cells, the preimplantation embryo and to the extra-embryonic tissues during the postimplantation period. Studies with the CSF-1-deficient osteopetrotic (op/op) mouse show that CSF-1 has important roles during embryonic development and in the regulation of uterine macrophages. These studies establish that CSF-1, whose sex steroid hormone-induced synthesis is restricted to the uterine epithelium, has a paracrine action on embryos as well as being a mediator of epithelial-mesenchymal interactions. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT DEV BIOL & CANC,1300 MORRIS PK AVE,BRONX,NY 10461. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NR 66 TC 13 Z9 13 U1 0 U2 0 PU C S I R O PUBLICATIONS PI COLLINGWOOD PA 150 OXFORD ST, PO BOX 1139, COLLINGWOOD VICTORIA 3066, AUSTRALIA SN 1031-3613 J9 REPROD FERT DEVELOP JI Reprod. Fertil. Dev. PY 1992 VL 4 IS 6 BP 619 EP 632 DI 10.1071/RD9920619 PG 14 WC Developmental Biology; Reproductive Biology; Zoology SC Developmental Biology; Reproductive Biology; Zoology GA LG811 UT WOS:A1992LG81100004 ER PT J AU WALKER, EM SMITH, AB GALE, GR JONES, MM AF WALKER, EM SMITH, AB GALE, GR JONES, MM TI ENHANCED MOBILIZATION OF HEPATIC CADMIUM IN MICE UPON COADMINISTRATION OF AN N,N-DISUBSTITUTED DITHIOCARBAMATE AND AN ALKYL MONOESTER OF DIMERCAPTOSUCCINATE SO RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY LA English DT Article ID ORGAN DISTRIBUTION; EXCRETION; DIETHYLDITHIOCARBAMATE; DIETHYLENETRIAMINEPENTAACETATE; DIHYDROXYETHYLDITHIOCARBAMATE; ANTAGONISTS AB Oral (po) administration of mono-iso-amyl(2,3-dimercapto) succinate (Mi-ADMS), 0.5 mmol/kg for three consecutive days, to mice previously injected with cadmium (Cd) chloride reduced the whole body Cd burden 34%. Intraperitoneal (ip) administration of N-iso-amyl-N-glucaminedithiocarbamate (i-AmGDTC) by the same regimen reduced total body Cd 41%. Coadministration of the two compounds reduced the whole body Cd burden 60% (p < 0.05). The liver Cd concentration was reduced 56% and 50%, respectively, by Mi-ADMS given po and i-AmGDTC given ip, each at 0.5 mmol/kg for three consecutive days. Coadministration of the two chelators reduced the liver Cd concentration 90% (p < 0.05). The kidney Cd concentration was reduced 10% by Mi-ADMS alone, and 60% by i-AmGDTC alone, but there was only a 47% reduction when the two chelators were coadministered, probably as a result of redistribution of mobilized hepatic Cd to the kidneys. As 50-50% of the administered Cd is sequestered in the liver in this mouse model, it is concluded that coadministration of the two chemical classes of Cd complexing agents may offer a therapeutic advantage over administration of either agent alone. C1 JOHN L MCCLELLAN MEM VET ADM MED CTR,LITTLE ROCK,AR 72205. UNIV ARKANSAS MED SCI HOSP,DEPT PATHOL,LITTLE ROCK,AR 72205. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29401. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC. VANDERBILT UNIV,DEPT CHEM,NASHVILLE,TN 37235. VANDERBILT UNIV,CTR MOLEC TOXICOL,NASHVILLE,TN 37235. FU NIEHS NIH HHS [ES-02638] NR 12 TC 0 Z9 0 U1 0 U2 0 PU P J D PUBLICATIONS LTD PI WESTBURY PA PO BOX 966, WESTBURY, NY 11590 SN 0034-5164 J9 RES COMMUN CHEM PATH PD JAN PY 1992 VL 75 IS 1 BP 121 EP 124 PG 4 WC Pathology; Pharmacology & Pharmacy SC Pathology; Pharmacology & Pharmacy GA HB581 UT WOS:A1992HB58100012 PM 1626122 ER PT J AU VONSATTEL, JPG MYERS, RH BIRD, ED GE, P RICHARDSON, EP AF VONSATTEL, JPG MYERS, RH BIRD, ED GE, P RICHARDSON, EP TI HUNTINGTONS-DISEASE - 7 CASES WITH RELATIVELY PRESERVED NEOSTRIATAL ISLETS SO REVUE NEUROLOGIQUE LA French DT Article ID BASAL GANGLIA; STRIATAL NEURONS; CHOREA; ACID; COMPARTMENTS; MODEL; ONSET; AGE AB Seven cases of Huntington's disease (HD) showing unusual neostriatal findings are reported. In these patients, the neostriatum contained scattered islets of relatively intact parenchyma. We attempted to determine whether these cases might represent a clinico-pathological entity, and also sought to acquire a better understanding of the neostriatal degenerative changes in HD. Cell counts showed that the number of neurons in the islets was the same as in the normal neostriatum, but there was an increased number of astrocytes. The nature of these islets is poorly understood. Analysis of their topography and of the morphometric data indicates that they probably do not represent preserved striosomes. In HD patients with preserved neostriatal islets, the symptoms appear earlier, and the course of the disease is more rapid than in HD patients with the usual neostriatal lesions. The exceptional neuropathological phenotype of our seven HD cases probably indicates a different genotype. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL NEUROPATHOL,BOSTON,MA 02115. MCLEAN HOSP,CTR BRAIN TISSUE RESOURCE,BELMONT,MA 02178. HARVARD UNIV,SCH MED,BELMONT,MA 02178. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. FU NIMH NIH HHS [MH/NS 31862]; NINDS NIH HHS [NS 16367] NR 46 TC 6 Z9 6 U1 0 U2 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0035-3787 J9 REV NEUROL JI Rev. Neurol. PY 1992 VL 148 IS 2 BP 107 EP 116 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA HF509 UT WOS:A1992HF50900002 PM 1534925 ER PT J AU GELBERMAN, RH SEILER, JG ROSENBERG, AE HEYMAN, P AMIEL, D AF GELBERMAN, RH SEILER, JG ROSENBERG, AE HEYMAN, P AMIEL, D TI INTERCALARY FLEXOR TENDON GRAFTS - A MORPHOLOGICAL-STUDY OF INTRASYNOVIAL AND EXTRASYNOVIAL DONOR TENDONS SO SCANDINAVIAN JOURNAL OF PLASTIC AND RECONSTRUCTIVE SURGERY AND HAND SURGERY LA English DT Article DE INTRASYNOVIAL; EXTRASYNOVIAL; TENDON GRAFT; PASSIVE MOTION ID AUTOGRAFT; RABBIT AB Intercalary intrasynovial and extrasynovial flexor tendon graft donors were placed within the synovial sheaths of the medial and lateral forepaw digits of 22 dogs and treated with early controlled passive mobilization. Specimens were studied by light and transmission electron microscopy at 10 and 21 days. Early repair in the extrasynovial tendons occurred by an ingrowth of connective tissue from the digital sheath. Adhesions obliterated the gliding surface and occupied the space between the tendon's gliding surface and surrounding tissues. There was no epitenon response noted in the extrasynovial tendon grafts. While there was considerable new collagen fibril formation within the repair site at the ultrastructural level, there was a lack of longitudinal remodeling. In contrast, the intrasynovial tendon grafts showed early healing, with minimal adhesion formation, by a proliferation and migration of cells from the epitenon. These cells showed greater cellular activity and collagen production at 10 and 21 days compared to cells in extrasynovial tendons at the same intervals. The findings of this study suggest that the use of intrasynovial autogenous tendon graft donors, coupled with early controlled motion, stimulates an intrinsic repair process in both the tendon stump and autogenous tendon graft. These findings differ significantly from the experimental findings in which extrasynovial, paratenon-covered grafts are used. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV CALIF SAN DIEGO,DEPT ORTHOPAED CONNECT TISSUE BIOCHEM,LA JOLLA,CA 92093. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5R01-AR22097] NR 46 TC 51 Z9 54 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0284-4311 J9 SCAND J PLAST RECONS JI Scand. J. Plast. Reconstr. Surg. Hand Surg. PY 1992 VL 26 IS 3 BP 257 EP 264 PG 8 WC Surgery SC Surgery GA KC784 UT WOS:A1992KC78400004 PM 1470872 ER PT J AU AMIN, F DAVIDSON, M DAVIS, KL AF AMIN, F DAVIDSON, M DAVIS, KL TI HOMOVANILLIC-ACID MEASUREMENT IN CLINICAL RESEARCH - A REVIEW OF METHODOLOGY SO SCHIZOPHRENIA BULLETIN LA English DT Review ID HUMAN CEREBROSPINAL-FLUID; URINARY CATECHOLAMINE METABOLITE; NORADRENERGIC NEURONAL-ACTIVITY; CSF MONOAMINE METABOLITES; BRAIN DOPAMINE METABOLISM; AMINE METABOLITES; SCHIZOPHRENIC-PATIENTS; RAT-BRAIN; 3,4-DIHYDROXYPHENYLACETIC ACID; PLASMA DOPAMINE AB Despite its serious limitations, measuring the concentrations of homovanillic acid (HVA) in body fluids is perhaps the most direct method currently available to assess the changing activity of central dopamine (DA) neurons in living humans. The concentrations of HVA in body fluids are determined not only by the activity of central DA neurons but also by a number of unrelated factors such as the other sources of HVA and the elimination of HVA from the body. This article reviews many factors that help to determine the concentrations of HVA in body fluids and therefore must be considered in studies employing HVA as a possible index of central DA neuronal activity. The need for further methodological work is indicated to improve the use of body fluid HVA measurements in clinical research. C1 BRONX VET AFFAIRS MED CTR,MT SINAI SCH MED,NEW YORK,NY. RP AMIN, F (reprint author), VET ADM MED CTR,PSYCHIAT SERV,RM 3-B 50,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 196 TC 117 Z9 117 U1 1 U2 7 PU US GOVERNMENT PRINTING OFFICE PI WASHINGTON PA SUPT OF DOCUMENTS, WASHINGTON, DC 20402-9325 SN 0586-7614 J9 SCHIZOPHRENIA BULL JI Schizophr. Bull. PY 1992 VL 18 IS 1 BP 123 EP 148 PG 26 WC Psychiatry SC Psychiatry GA HH615 UT WOS:A1992HH61500018 PM 1553492 ER PT J AU WIRSHING, WC MARDER, SR JOHNSTONCRONK, K LEBELL, M MACKENZIE, J MINTZ, J ECKMAN, T LIBERMAN, RP AF WIRSHING, WC MARDER, SR JOHNSTONCRONK, K LEBELL, M MACKENZIE, J MINTZ, J ECKMAN, T LIBERMAN, RP TI MANAGEMENT OF RISK OF RELAPSE IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Mintz, Jim/N-7385-2014 OI Mintz, Jim/0000-0002-8299-5851 NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 107 EP 108 DI 10.1016/0920-9964(92)90128-R PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800047 ER PT J AU STERN, RG KAHN, RS DAVIDSON, M HARVEY, PD AMIN, F APTER, SH DUMONT, K HIRSCHOWITZ, J DAVIS, KL AF STERN, RG KAHN, RS DAVIDSON, M HARVEY, PD AMIN, F APTER, SH DUMONT, K HIRSCHOWITZ, J DAVIS, KL TI SIGNIFICANT DECREASE IN PSYCHOPATHOLOGY WITHIN 3 DAYS OF HALOPERIDOL TREATMENT IN CHRONIC-SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,BRONX,NY 10468. MT SINAI MED SCH,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 109 EP 110 DI 10.1016/0920-9964(92)90134-Q PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800053 ER PT J AU AMES, D WIRSHING, WC LEE, MA CUMMINGS, JL VANPUTTEN, T MARDER, SR BARTZOKIS, G AF AMES, D WIRSHING, WC LEE, MA CUMMINGS, JL VANPUTTEN, T MARDER, SR BARTZOKIS, G TI SELEGILINE IN THE TREATMENT OF AKATHISIA, TARDIVE-DYSKINESIA, AND NEGATIVE SCHIZOPHRENIC SYMPTOMS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Bartzokis, George/K-2409-2013 NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 110 EP 111 DI 10.1016/0920-9964(92)90136-S PG 2 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800055 ER PT J AU KAHN, RS DAVIDSON, M KNOTT, P STERN, RG AMIN, F WEBSTER, L APTER, SA DAVIS, KL AF KAHN, RS DAVIDSON, M KNOTT, P STERN, RG AMIN, F WEBSTER, L APTER, SA DAVIS, KL TI EFFECT OF HALOPERIDOL ON CSF MONOAMINE METABOLITES IN SCHIZOPHRENIA - SYMPTOMATIC IMPROVEMENT IS RELATED TO ALTERED DOPAMINE-SEROTONIN INTERACTION SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 118 EP 118 DI 10.1016/0920-9964(92)90155-X PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800074 ER PT J AU KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL AF KAHN, RS DAVIDSON, M HIRSCHOWITZ, J STERN, RG DAVIS, BM GABRIEL, S MOORE, C DAVIS, KL TI NOCTURNAL GROWTH-HORMONE SECRETION IN SCHIZOPHRENIC-PATIENTS AND HEALTHY-SUBJECTS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 125 EP 125 DI 10.1016/0920-9964(92)90169-6 PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800088 ER PT J AU KAHN, RS SIEVER, L KNOTT, P STERN, RG AMIN, F DUMONT, K APTER, SA DAVIDSON, M AF KAHN, RS SIEVER, L KNOTT, P STERN, RG AMIN, F DUMONT, K APTER, SA DAVIDSON, M TI M-CHLOROPHENYLPIPERAZINE AS A PROBE OF SEROTONIN FUNCTION IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR,MT SINAI SCH MED,DEPT PSYCHIAT,BRONX,NY 10468. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JAN PY 1992 VL 6 IS 2 BP 138 EP 138 DI 10.1016/0920-9964(92)90199-F PG 1 WC Psychiatry SC Psychiatry GA HB658 UT WOS:A1992HB65800118 ER PT B AU HASELTINE, WA AF HASELTINE, WA BE ROSSI, GB DIANZANI, F BETHGIRALDO, E GIRALDO, G CHIECOBIANCHI, L VERANI, P TI MOLECULAR-BIOLOGY OF THE AIDS VIRUS - 10 YEARS OF DISCOVERY - HOPE FOR THE FUTURE SO SCIENCE CHALLENGING AIDS LA English DT Proceedings Paper CT 7TH INTERNATIONAL CONF ON AIDS CY JUN 16-21, 1991 CL FLORENCE, ITALY SP EUROPEAN ECON COMMUNITY, REG TOSCANA, ASSOC NAZL LOTTA CONTRO AIDS, ASSOC SALUTE DONNA, IST SUPER SANITA, ITALIAN MINIST HLTH, WHO, INT AIDS SOC, COMMUNE FIRENZE, FDN ITALIANA RIC CANC RP HASELTINE, WA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU KARGER PI BASEL PA BASEL BN 3-8055-5485-0 PY 1992 BP 71 EP 106 PG 36 WC Immunology; Medicine, Research & Experimental; Pathology; Virology SC Immunology; Research & Experimental Medicine; Pathology; Virology GA BU75U UT WOS:A1992BU75U00008 ER PT J AU WILLIAMS, ME AF WILLIAMS, ME TI INSULIN MANAGEMENT OF A DIABETIC PATIENT ON HEMODIALYSIS SO SEMINARS IN DIALYSIS LA English DT Article RP WILLIAMS, ME (reprint author), JOSLIN DIAB CTR,JOSLIN PL,BOSTON,MA 02215, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0894-0959 J9 SEMIN DIALYSIS JI Semin. Dial. PD JAN-MAR PY 1992 VL 5 IS 1 BP 69 EP 73 DI 10.1111/j.1525-139X.1992.tb00459.x PG 5 WC Urology & Nephrology SC Urology & Nephrology GA HD073 UT WOS:A1992HD07300016 ER PT B AU WALL, C HARRIS, LR LATHAN, CE AF WALL, C HARRIS, LR LATHAN, CE BE COHEN, B TOMKO, DL GUEDRY, F TI INTERACTIONS BETWEEN OTOLITHS AND VISION REVEALED BY THE RESPONSE TO Z-AXIS LINEAR MOVEMENTS SO SENSING AND CONTROLLING MOTION: VESTIBULAR AND SENSORIMOTOR FUNCTION SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Proceedings Paper CT CONF ON SENSING AND CONTROLLING MOTION : VESTIBULAR AND SENSORIMOTOR FUNCTION CY JUL 07-11, 1991 CL PALO ALTO, CA SP NEW YORK ACAD SCI, NASA, NIDOCD, USN, OFF NAVAL RES RP WALL, C (reprint author), MASSACHUSETTS EYE & EAR INFIRM,VESTIBULAR TESTING LAB,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA NEW YORK BN 0-89766-734-4 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PY 1992 VL 656 BP 898 EP 900 PG 3 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA BW41U UT WOS:A1992BW41U00093 PM 1599214 ER PT J AU MARTUZA, RL AF MARTUZA, RL TI MOLECULAR NEUROSURGERY FOR GLIAL AND NEURONAL DISORDERS SO STEREOTACTIC AND FUNCTIONAL NEUROSURGERY LA English DT Article; Proceedings Paper CT MEETING OF THE AMERICAN SOC FOR STEREOTACTIC AND FUNCTIONAL NEUROSURGERY CY JUN 16-19, 1991 CL PITTSBURGH, PA SP AMER SOC STEREOTACT & FUNCT NEUROSURG DE GENETICS; GLIOMA; GENES; VIRUS ID GLIOMA AB Molecular neurosurgery is the surgical use of molecules to destroy, sustain, or modulate or augment neurons, supporting cells or tumor cells within the nervous system. Molecules designed for surgical use may be engineered to be used in their molecular state or may be packaged as liposomes, viruses or genetically engineered cells. This article summarizes the current state of development of one aspect of molecular neurosurgery - the use of genetically engineered viruses to treat brain tumors. Both herpes virus and retrovirus strategies are discussed. Each virus has its own set of advantages and disadvantages that can be used in the design of an appropriate therapeutic strategy. Further application of this technology to intrinsic glial and neuronal disorders is discussed, and future perspectives are presented. C1 MASSACHUSETTS GEN HOSP,NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NINDS NIH HHS [NS24279] NR 8 TC 7 Z9 7 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1011-6125 J9 STEREOT FUNCT NEUROS JI Stereotact. Funct. Neurosurg. PY 1992 VL 59 IS 1-4 BP 92 EP 99 DI 10.1159/000098923 PG 8 WC Neurosciences; Neuroimaging; Surgery SC Neurosciences & Neurology; Surgery GA JQ015 UT WOS:A1992JQ01500014 PM 1338233 ER PT J AU LEVINE, RL JONES, JC BEE, N AF LEVINE, RL JONES, JC BEE, N TI STROKE AND PARKINSONS-DISEASE SO STROKE LA English DT Meeting Abstract C1 MIDDLETON VET ADM HOSP,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 136 EP 136 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600030 ER PT J AU YOKOTA, M PETERSON, J KAOUTZANIS, M KOWALL, N AF YOKOTA, M PETERSON, J KAOUTZANIS, M KOWALL, N TI THE DISTRIBUTION OF PROTEIN-KINASE-C ISOZYMES IS DIFFERENTIALLY ALTERED IN ISCHEMIC GERBIL HIPPOCAMPUS SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 151 EP 151 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600089 ER PT J AU NOZAKI, K MOSKOWITZ, MA MAYNARD, KI KOKETSU, N DAWSON, TM BREDT, DS SNYDER, SH AF NOZAKI, K MOSKOWITZ, MA MAYNARD, KI KOKETSU, N DAWSON, TM BREDT, DS SNYDER, SH TI ORIGIN AND DISTRIBUTION OF NITRIC-OXIDE SYNTHASE-IMMUNOREACTIVE NERVE-FIBERS IN RAT CEREBRAL-ARTERIES SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NR 0 TC 11 Z9 11 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 154 EP 154 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600101 ER PT J AU MOSKOWITZ, MA WEI, EP BOCCALINI, P KONTOS, HA AF MOSKOWITZ, MA WEI, EP BOCCALINI, P KONTOS, HA TI CALCITONIN GENE-RELATED PEPTIDE MEDIATES NITROVASODILATOR-INDUCED RELAXATION IN FELINE CEREBRAL ARTERIOLES SO STROKE LA English DT Meeting Abstract C1 VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 155 EP 155 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600103 ER PT J AU NOZAKI, K MOSKOWITZ, MA BOCCALINI, P AF NOZAKI, K MOSKOWITZ, MA BOCCALINI, P TI C-FOS PROTEIN EXPRESSION IN RAT BRAIN-STEM AFTER SUBARACHNOID HEMORRHAGE (SAH) SO STROKE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD JAN PY 1992 VL 23 IS 1 BP 155 EP 155 PG 1 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HA876 UT WOS:A1992HA87600104 ER PT J AU SAUNDERS, KD TOMPKINS, RK CATES, JA LONGMIRE, WP ROSLYN, JJ AF SAUNDERS, KD TOMPKINS, RK CATES, JA LONGMIRE, WP ROSLYN, JJ TI THE NATURAL-HISTORY OF CARCINOMA OF THE BILE-DUCT IN PATIENTS LESS THAN 45 YEARS OF AGE SO SURGERY GYNECOLOGY & OBSTETRICS LA English DT Article ID HILAR CHOLANGIOCARCINOMA; PROGNOSTIC FACTORS; BILIARY-TRACT; RADIOTHERAPY; RESECTION; CANCER AB Traditionally regarded as a disease of the elderly, the natural history Of carcinoma of the bile duct in young patients has not been well defined. Of 186 patients (mean age of C62 years) treated at UCLA (1954 to 1988) for carcinoma of the bile duct, 26 were less than 45 years old. Younger patients had symptoms for an average of 4.5 +/- 0.8 months prior to diagnosis, as compared with 2.3 +/- 0.2 months for patients more than 45 years old (p < 0.03). Of the younger patients, 96 per cent were managed surgically with either resection, surgical palliative bypass or laparotomy and tube drainage. Among the younger patients who underwent resections, 92 per cent were alive at one year, as compared with 60 per cent of patients who underwent palliative bypass procedures. Two patients who underwent tumor resections survived four years or longer. We conclude that carcinoma of the bile duct is not limited to the elderly and occurs in a significant number of young patients. In the younger population, carcinoma of the bile duct is characterized by delays in diagnosis. Early suspicion and aggressive management of young patients with obstructive jaundice are essential to ensure the best possible outcome for patients with this disease. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT SURG,DIV GEN SURG,10833 LE CONTE AVE,RM 72-215,CHS,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 20 TC 4 Z9 4 U1 0 U2 0 PU FRANKLIN H MARTIN FOUNDATION PI CHICAGO PA 55 E ERIE ST, CHICAGO, IL 60611 SN 0039-6087 J9 SURG GYNECOL OBSTET JI Surg. Gynecol. Obstet. PD JAN PY 1992 VL 174 IS 1 BP 1 EP 6 PG 6 WC Obstetrics & Gynecology; Surgery SC Obstetrics & Gynecology; Surgery GA GY399 UT WOS:A1992GY39900001 PM 1729742 ER PT J AU RITTENBERG, T EHRLICH, HP AF RITTENBERG, T EHRLICH, HP TI FREE FATTY-ACIDS AND DIALYZED SERUM ALTERATIONS OF FIBROBLAST POPULATED COLLAGEN LATTICE CONTRACTION SO TISSUE & CELL LA English DT Article DE FIBROBLASTS; COLLAGEN; WOUND HEALING; FREE FATTY ACIDS; SERUM; CELL CONTRACTION ID DERMAL FIBROBLASTS; WOUND CONTRACTION; CELL CONTRACTION; INVITRO; TISSUE AB Fibroblast populated collagen lattices (FPCL) have facilitated the in vitro study of wound contraction and scar contracture. Mixing fibroblasts, serum containing culture medium and soluble collagen, together and then incubating the mixture at 37-degrees-C produces a FPCL. The fibroblasts elongate and spread within the collagen matrix, and by forces associated with cell locomotion they reorganize the collagen fibers. The reorganization of the collagen produces a reduction in size of the FPCL, called lattice contraction. It was also found that dialyzed fetal bovine serum did not support lattice contraction. Supplementing dialyzed serum with fatty acids accelerated lattice contraction. The fatty acid composition of the fibroblast plasma membrane influences that membrane fluidity. These studies demonstrated that lattice contraction was enhanced by the additions of saturated fatty acids in the order of laurate (C-12), palmitic (C-16), and stereate (C-18). With unsaturated fatty acids additions, the order of enhanced lattice contraction was archidonate (4 C = C), linoleate (2 C = C) and oleate (1 C = C). The addition of dialyzed serum with or without fatty acids neither altered ATP-induced cell contraction activity nor cell proliferation. It was concluded that free fatty acid additions do not modulate FPCL contraction by enhancing microfilaments contraction or increasing cell numbers. The mechanism of action was proposed to be by altering cell membrane fluidity. This finding further supports the theory that the mechanism for lattice contraction is cell locomotion, rather than cell contraction. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT PATHOL & SURG,BOSTON,MA 02114. FU NIGMS NIH HHS [GM-32705] NR 15 TC 7 Z9 7 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0040-8166 J9 TISSUE CELL JI Tissue Cell PY 1992 VL 24 IS 2 BP 243 EP 251 DI 10.1016/0040-8166(92)90097-Q PG 9 WC Anatomy & Morphology; Cell Biology SC Anatomy & Morphology; Cell Biology GA HP297 UT WOS:A1992HP29700009 PM 1589872 ER PT J AU GRECO, RM EHRLICH, HP AF GRECO, RM EHRLICH, HP TI DIFFERENCES IN CELL-DIVISION AND THYMIDINE INCORPORATION WITH RAT AND PRIMATE FIBROBLASTS IN COLLAGEN LATTICES SO TISSUE & CELL LA English DT Article DE FIBROBLAST DIVISION; FLOW CYTOMETRY; CELL CYCLE; COLLAGEN LATTICE CONTRACTION ID HUMAN DERMAL FIBROBLASTS; NATIVE COLLAGEN; CONTRACTION; INVITRO; MATRIX; PROLIFERATION AB Human and gorilla dermal fibroblasts, primate cells, suspended in a collagen lattice, do not divide for the first 3 days. In contrast, rat fibroblasts divide within 24 hr. In this study, the proliferation of rat fibroblasts were compared to primate fibroblasts. Rat fibroblasts in monolayer culture increase from 100,000 to 355,000 in 2 days, and human cells increase from 100,000 to 436,000 in the same period. An initial seeding of 100,000 rat fibroblasts suspended in collagen increased to 163,000 cells in 2 days. An initial 100,000 human fibroblasts seeded in collagen decreased to 80,000 cells in 2 days. Retarded proliferation of human and gorilla fibroblasts in collagen is unrelated to a defect in DNA synthesis. By autoradiography human fibroblasts suspended in collagen incorporate labelled thymidine. By flow cytometry analysis, the DNA concentrations of human fibroblasts suspended in collagen exhibited 41% in a 4N chromosome state. compared to 14% in monolayer culture. Nuclei of gorilla fibroblasts from collagen displayed 42% in a 4N state, compared to 19% in monolayer culture. With nuclei of rat fibroblasts from collagen, 14% were in a 4N state, compared to 9% in monolayer culture. Primate fibroblasts show a three-fold increase in the number of nuclei in a 4N state compared to rat fibroblasts suspended in collagen. After replating fibroblasts released from collagen in monolayer culture in the presence of 1 mM hydroxyurea (an inhibitor of DNA synthesis) primate fibroblasts doubled in 24 hr. Under identical conditions, rat fibroblasts showed no cell division. Primate cells suspended in collagen have completed DNA synthesis but show a delay in cell division, indicating fibroblasts are arrested in G2 of the cell cycle. Polymerized collagen produces a physical constraint on primate fibroblasts which retards these cells from entering mitosis. In contrast rat fibroblasts show no constraint and readily enter mitosis upon completion of DNA synthesis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT PATHOL,WOUND HEALING LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT SURG,BOSTON,MA 02114. RP EHRLICH, HP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURNS INST,DEPT PATHOL,WOUND HEALING LAB,BOSTON,MA 02114, USA. NR 11 TC 11 Z9 11 U1 1 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 0040-8166 J9 TISSUE CELL JI Tissue Cell PY 1992 VL 24 IS 6 BP 843 EP 851 DI 10.1016/0040-8166(92)90020-8 PG 9 WC Anatomy & Morphology; Cell Biology SC Anatomy & Morphology; Cell Biology GA KC477 UT WOS:A1992KC47700006 PM 1485326 ER PT J AU ANDERSON, KC AF ANDERSON, KC TI WHO SHOULD RECEIVE LEUKODEPLETED BLOOD COMPONENTS SO TRANSFUSION SCIENCE LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL CONF ON THROMBOTIC THROMBOCYTOPENIC PURPURA RESEARCH CY JUN 15-16, 1990 CL ALLMO COLLEGIO BORROMEO, PAVIA, ITALY HO ALLMO COLLEGIO BORROMEO RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0955-3886 J9 TRANSFUS SCI JI Transfus. Sci. PD JAN PY 1992 VL 13 IS 1 BP 107 EP 109 DI 10.1016/0955-3886(92)90132-Z PG 3 WC Hematology SC Hematology GA HG388 UT WOS:A1992HG38800022 ER PT J AU HIBBERD, PL TOLKOFFRUBIN, NE COSIMI, AB SCHOOLEY, RT ISAACSON, D DORAN, M DELVECCHIO, A DELMONICO, FL AUCHINCLOSS, H RUBIN, RH AF HIBBERD, PL TOLKOFFRUBIN, NE COSIMI, AB SCHOOLEY, RT ISAACSON, D DORAN, M DELVECCHIO, A DELMONICO, FL AUCHINCLOSS, H RUBIN, RH TI SYMPTOMATIC CYTOMEGALOVIRUS DISEASE IN THE CYTOMEGALOVIRUS ANTIBODY SEROPOSITIVE RENAL-TRANSPLANT RECIPIENT TREATED WITH OKT3 SO TRANSPLANTATION LA English DT Article; Proceedings Paper CT 10TH ANNUAL MEETING OF THE AMERICAN SOC OF TRANSPLANT PHYSICIANS CY MAY 28-29, 1991 CL CHICAGO, IL SP AMER SOC TRANSPLANT PHYSICIANS ID VIRUS INFECTION; REACTIVATION AB A prospective study to investigate risk factors for CMV disease was conducted in 94 renal transplant recipients. CMV disease was defined as either unexplained fever for > 3 days with viremia or unexplained fever for > 3 days with isolation of CMV from the urine or throat wash and at least one of the following: leukopenia, elevated serum alanine aminotransferase, or biopsy-proved invasive tissue infection of the lung or gastrointestinal tract. Fifty-three patients received immunosuppressive regimens consisting of prednisone and cyclosporine, with or without azathioprine. The remaining 41 patients were treated with these agents plus OKT3 (21 received OKT3 to treat rejection, 20 received OKT3 prophylactically). Thirty-seven patients were at minimal risk of CMV disease (donor and recipient seronegative for CMV); 12 patients were at risk of primary disease (donor seropositive, recipient seronegative), and 45 were at risk of reactivation disease (recipient seropositive at the time of transplantation). The incidences of CMV disease in the 3 groups were 0%, 58%, and 36%, respectively. Although the incidence of CMV disease in patients at risk of primary disease was not influenced by the immunosuppressive regimen, immunosuppression had a profound effect on the occurrence of CMV disease in CMV-seropositive transplant recipients. The incidence of CMV disease in those receiving OKT3 was 59%; but only 21% in those who did not receive OKT3. OKT3 increased the risk of CMV disease five-fold (odds ratio 5.2 (95% confidence limits 1.4-17.5)). In the CMV-seropositive patient, OKT3 was also the most important predictor of CMV disease by multivariate analysis (P < 0.002). A pilot study of preemptive therapy with ganciclovir (2.5 mg/kg daily during OKT3 therapy) in 17 patients decreased the incidence of CMV disease without appreciable toxicity. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIALYSIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN INVEST PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL18646] NR 19 TC 211 Z9 213 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JAN PY 1992 VL 53 IS 1 BP 68 EP 72 DI 10.1097/00007890-199201000-00013 PG 5 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HA583 UT WOS:A1992HA58300013 PM 1310173 ER PT J AU MOSES, RD WINN, HJ AUCHINCLOSS, H AF MOSES, RD WINN, HJ AUCHINCLOSS, H TI EVIDENCE THAT MULTIPLE DEFECTS IN CELL-SURFACE MOLECULE INTERACTIONS ACROSS SPECIES-DIFFERENCES ARE RESPONSIBLE FOR DIMINISHED XENOGENEIC T-CELL RESPONSES SO TRANSPLANTATION LA English DT Article ID ANTIGEN-PRESENTING CELLS; HLA-CW3 TRANSGENIC MICE; LYMPHOCYTES-T; HISTOCOMPATIBILITY ANTIGENS; HLA-B7 ANTIGENS; ALPHA-3 DOMAIN; GENE-TRANSFER; HEAVY-CHAIN; RECOGNITION; MOUSE AB The purpose of the present study was to identify which of the several possible defects in cell-surface-molecule interactions are responsible for diminished mouse helper T cell responses to xenoantigens. We measured primary mouse anti-monkey, anti-pig, and anti-human proliferation in vitro in experimental systems in which potential defects were partially corrected by lymphokine supplementation and/or the use of transgenic or hybridoma cell populations. We found that the diminished mouse helper T cell responses to xenoantigens result from at least two defects in cell-surface-molecule interactions between T cells and xenogeneic APCs, specifically TCR and/or CD8 interactions with xenogeneic class I MHC molecules and accessory molecule interactions with their ligands (probably LFA-1 with ICAM-1/ICAM-2 and/or LFA-2 with LFA-3). Other investigators have identified additional defects, such as in lymphokine function across species differences. Thus, there appear to be multiple defects responsible for the diminished cellular immune response to xenoantigens. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,TRANSPLANTAT UNIT,55 FRUIT ST,BOSTON,MA 02114. FU NHLBI NIH HHS [HL36372, HL18646] NR 47 TC 97 Z9 98 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD JAN PY 1992 VL 53 IS 1 BP 203 EP 209 DI 10.1097/00007890-199201000-00039 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HA583 UT WOS:A1992HA58300039 PM 1346345 ER PT J AU WONG, TK HERSHMAN, JM AF WONG, TK HERSHMAN, JM TI CHANGES IN THYROID-FUNCTION IN NONTHYROID ILLNESS SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID FREE-THYROXINE; SERUM THYROTROPIN; TRIIODOTHYRONINE; HORMONE; ASSAY; ULTRAFILTRATION; SECRETION; DIALYSIS; BINDING; T4 AB Nonthyroid illness can cause changes in thyroid function that have been described as low triiodothyronine (T3) and low thyroxine (T4) states. Reduced peripheral conversion of T4 to T3 explains the low serum T3 concentration. The explanation for the low serum T4 level is multifactorial; whether free-thyroxine (FT4) level is normal or reduced remains controversial. Cytokines such as tumor necrosis factor alpha, which are produced by the immune system during severe illness, may inhibit thyroid function directly and be responsible for the changes in pituitary-thyroid function. RP WONG, TK (reprint author), UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90073, USA. NR 28 TC 27 Z9 27 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD JAN-FEB PY 1992 VL 3 IS 1 BP 8 EP 12 DI 10.1016/1043-2760(92)90085-F PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GX703 UT WOS:A1992GX70300002 PM 18407071 ER PT J AU LEES, S KLOPHOLZ, DZ AF LEES, S KLOPHOLZ, DZ TI SONIC VELOCITY AND ATTENUATION IN WET COMPACT COW FEMUR FOR THE FREQUENCY-RANGE 5 TO 100 MHZ SO ULTRASOUND IN MEDICINE AND BIOLOGY LA English DT Article DE ULTRASONIC VELOCITY; ULTRASONIC ATTENUATION; COW FEMUR ID BONE AB Ultrasonic studies on bone have not been done as intensively as other tissues, probably because there is less opportunity to examine bone in vivo by this modality. There is considerable interest in using ultrasonics to learn about the material properties of bone for which purpose the sonic spectrum may be useful. The longitudinal sonic velocity and attenuation have been found for several sections from one sample of wet cow femur for both the axial and radial directions over the frequency range of 5 to 100 MHz. The basic technique was solid-to-solid contact using a fused quartz buffer rod coupled to the bone specimen. There is clear evidence of velocity dispersion which Lakes et al. (1986) did not find over a frequency range up to 16 MHz. While there seems to be a peak in both velocity and attenuation at 70 MHz, it is necessary to obtain measurements at higher frequencies to make sure this is not an artifact. The axial sonic velocity varied from 4.29 km/s at 5 MHz to 4.447 km/s at 50 MHz, while the radial velocity was 3.45 km/s at 5 MHz and increased to 3.62 km/s at 50 MHz. The attenuation coefficient axially started at a mean value of 3.5 db/mm at 5 MHz and increased to a mean of 19 db/mm at 100 MHz. The corresponding radial attenuation coefficients are 5.2 and 26, respectively. C1 NORTHEASTERN UNIV,DEPT BIOMED ENGN,BOSTON,MA 02115. RP LEES, S (reprint author), FORSYTH DENT CTR,DEPT BIOENGN,140 FENWAY,BOSTON,MA 02115, USA. FU NIA NIH HHS [AG02325] NR 8 TC 30 Z9 30 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0301-5629 J9 ULTRASOUND MED BIOL JI Ultrasound Med. Biol. PY 1992 VL 18 IS 3 BP 303 EP 308 DI 10.1016/0301-5629(92)90099-V PG 6 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA HQ766 UT WOS:A1992HQ76600007 PM 1595136 ER PT J AU YODER, IC PAPANICOLAOU, N AF YODER, IC PAPANICOLAOU, N TI IMAGING THE URETHRA IN MEN AND WOMEN SO UROLOGIC RADIOLOGY LA English DT Article DE URETHRA; VOIDING CYSTOURETHROGRAPHY; RETROGRADE URETHROGRAPHY; URETHRAL VALVES; URETHRAL STRICTURES; URETHRAL DIVERTICULA AB This review describes and illustrates the radiologic techniques, normal anatomy, and common congenital and acquired lesions of the urethra in men and women. Voiding cystourethrography and retrograde urethrography are the most common imaging modalities employed in the diagnosis of anatomic lesions of the urethra. The appearance of the urethra may then dictate the need for further functional evaluation with urodynamic studies. Congenital lesions in men include posterior and anterior urethral valves and duplicated urethra. In women, ectopic insertion of the ureter into the urethra is the usual congenital lesion. Acquired urethral lesions include benign prostatic hypertrophy in men and strictures and diverticula in both men and women. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP YODER, IC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV GENITOURINARY RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 15 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-1091 J9 UROL RADIOL PY 1992 VL 14 IS 1 BP 24 EP 28 DI 10.1007/BF02926897 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging; Urology & Nephrology SC Radiology, Nuclear Medicine & Medical Imaging; Urology & Nephrology GA JA732 UT WOS:A1992JA73200006 PM 1615569 ER PT J AU PAPANICOLAOU, N YODER, IC LEE, MJ AF PAPANICOLAOU, N YODER, IC LEE, MJ TI PRIMARY RETROPERITONEAL NEOPLASMS - HOW CLOSE CAN WE COME IN MAKING THE CORRECT DIAGNOSIS SO UROLOGIC RADIOLOGY LA English DT Article DE RETROPERITONEUM; NEOPLASM; LYMPHADENOPATHY; IMAGING ID CT AB The primary retroperitoneal tumors form a rare and diverse group of neoplasms, the origin of which is independent of the various retroperitoneal organs and unrelated to systemic diseases, such as lymphomas, lymphadenopathy, or metastases. Radiologic investigation, mainly cross-sectional imaging and, to a lesser extent, angiography is essential in the diagnosis and management of these tumors. The radiologist often is challenged to identify the origin and specific tissue composition of the imaged neoplasms. When the radiologic findings are combined with patient information and clinical data, the correct diagnosis may be made in many cases. Imaging-guided percutaneous needle biopsy further enhances the diagnostic yield of the various imaging modalities by establishing the diagnosis without the need for exploration. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PAPANICOLAOU, N (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 10 Z9 12 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-1091 J9 UROL RADIOL PY 1992 VL 14 IS 3 BP 221 EP 228 DI 10.1007/BF02926936 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging; Urology & Nephrology SC Radiology, Nuclear Medicine & Medical Imaging; Urology & Nephrology GA KA568 UT WOS:A1992KA56800023 PM 1337801 ER PT J AU TOMPKINS, RG BURKE, JF AF TOMPKINS, RG BURKE, JF TI BURN WOUND CLOSURE USING PERMANENT SKIN REPLACEMENT MATERIALS SO WORLD JOURNAL OF SURGERY LA English DT Article ID HUMAN EPIDERMAL-KERATINOCYTES; CULTURED EPITHELIAL AUTOGRAFTS; ARTIFICIAL SKIN; CHONDROITIN-6-SULFATE SUBSTRATE; ALLOGENEIC EPIDERMIS; BIOLOGIC ATTACHMENT; GRAFTABLE COLLAGEN; ANCHORING FIBRILS; DERMAL ALLOGRAFTS; FULL-THICKNESS AB Over the past decade, very significant advances in the development of clinically useful, permanent skin replacement materials have taken place. The most prominent and successful approaches to the physiological closure of an open wound have been either by creating a totally artificial dermal matrix material, by using culture techniques to expand cell populations for autologous transplantation, or by using a combination of these methods. As a result of substantial early progress in this field, permanent skin replacement materials as a treatment modality promise significant contributions to improved wound management and increased survival rates for patients with devastating soft tissue destruction such as massive burn injuries. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON UNIT,BOSTON,MA. RP TOMPKINS, RG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,TRAUMA SERV,BIGELOW 1302,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM 07035, GM 21700] NR 38 TC 13 Z9 18 U1 1 U2 3 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 JAN-FEB PY 1992 VL 16 IS 1 BP 47 EP 52 PG 6 WC Surgery SC Surgery GA GZ119 UT WOS:A1992GZ11900009 PM 1290266 ER PT J AU TREDGET, EE YU, YM AF TREDGET, EE YU, YM TI THE METABOLIC EFFECTS OF THERMAL-INJURY SO WORLD JOURNAL OF SURGERY LA English DT Article ID TUMOR NECROSIS FACTOR; RAT SKELETAL-MUSCLE; CHAIN AMINO-ACIDS; RETICULOENDOTHELIAL SYSTEM FUNCTION; LYMPHOCYTE IMMUNE-RESPONSES; TOTAL PARENTERAL-NUTRITION; SEVERELY BURNED CHILDREN; PHASE GENE-EXPRESSION; HUMAN GROWTH-HORMONE; ALANYL-L-GLUTAMINE AB Major thermal injury is associated with extreme hypermetabolism and catabolism as the principal metabolic manifestations encountered following successful resuscitation from the shock phase of the burn injury. Substrate and hormonal measurements, indirect calorimetry, and nitrogen balance are biochemical metabolic parameters which are useful and more readily available biochemical parameters worthy of serial assessment for the metabolic management of burn patients. However, the application of stable isotopes with gas chromatography/mass spectroscopy and more recently, new immunoassays for growth factors and cytokines has increased our understanding of the metabolic manifestations of severe trauma. The metabolic response to injury in burn patients is biphasic wherein the initial ebb phase is followed by a hypermetabolic and catabolic flow phase of injury. The increased oxygen consumption/metabolic rate is in part fuelled by evaporative heat loss from wounds of trauma victims, but likely also by a direct central effect of inflammation upon the hypothalamus. Although carbohydrates in the form of glucose appear to be an important fuel source following injury, a maximum of 5-6 mg/kg/min only is beneficial. Burn patients have accelerated gluconeogenesis, glucose oxidation, and plasma clearance of glucose. Additionally, considerable futile cycling of carbohydrate intermediates occurs which includes anaerobic lactate metabolism and Cori cycle activity arising from wound metabolism of glucose and other substrates. Similarly, accelerated lipolysis and futile fatty acid cycling occurs following burn injury. However, recent evidence suggests that lipids in the diet of burned and other injured patients serve not only as an energy source, but also as an important immunomodulator of prostaglandin metabolism and other immune responses. Amino acid metabolism in burn patients is characterized by increased oxidation, urea synthesis, and protein breakdown which is prolonged and difficult to reduce with current nutritional therapy. However, the current goal of nutritional support is to optimize protein synthesis. Specific unique requirements may exist for supplemental glutamine and arginine following burn injury but further research is needed before enhanced branched chain amino acids supplements can be recommended for burn patients. Recent research investigations have revealed the importance of enteral feeding to enhance mucosal defense against gut bacteria and endotoxin. Similarly, research has demonstrated that many of the metabolic perturbations of burns and sepsis may be due, at least in part, to inflammatory cytokines. Investigation of their pathogenesis and mechanism of action both at a tissue and a cellular level offer important prospects for improved understanding and therapeutic control of the metabolic disorders of burn patients. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP TREDGET, EE (reprint author), UNIV ALBERTA HOSP,FIREFIGHTERS BURN TREATMENT UNIT,2D382 WALTER MACKENZIE CTR,EDMONTON T6G 2B7,ALBERTA,CANADA. NR 172 TC 72 Z9 75 U1 1 U2 8 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 JAN-FEB PY 1992 VL 16 IS 1 BP 68 EP 79 PG 12 WC Surgery SC Surgery GA GZ119 UT WOS:A1992GZ11900012 PM 1290269 ER PT J AU BAKER, DB CASE, B HILLERDAL, G KAZEMI, H DODSON, R KOHYAMA, N MILETTE, J SUZUKI, Y DAVIS, J KRONENBERG, D SELIKOFF, IJ AF BAKER, DB CASE, B HILLERDAL, G KAZEMI, H DODSON, R KOHYAMA, N MILETTE, J SUZUKI, Y DAVIS, J KRONENBERG, D SELIKOFF, IJ TI LIMITATIONS IN DRAWING ETIOLOGIC INFERENCES BASED ON MEASUREMENT OF ASBESTOS FIBERS FROM LUNG-TISSUE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ELECTRON-MICROSCOPY; MALIGNANT MESOTHELIOMA; CHRYSOTILE ASBESTOS; LIGHT-MICROSCOPY; MINERAL FIBERS; WORKERS; DIAGNOSIS; DISEASE; BODIES; CLEARANCE C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260. UNIV HOSP UPPSALA,UPPSALA,SWEDEN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NATL INST IND HLTH SCI,KAWASAKI,JAPAN. MCCRONE ENVIRONM SERV,ATLANTA,GA. INST OCCUPAT MED,EDINBURGH EH8 9SV,MIDLOTHIAN,SCOTLAND. UNIV TEXAS,TYLER,TX. RP BAKER, DB (reprint author), CUNY MT SINAI SCH MED,DIV ENVIRONM & OCCUPAT MED,NEW YORK,NY 10029, USA. NR 34 TC 19 Z9 19 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 61 EP 73 DI 10.1111/j.1749-6632.1991.tb24444.x PG 13 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800005 PM 1809175 ER PT J AU GREENE, R SCHAEFER, CM OLIVER, LC DEMENT, J LILIS, R FINKELSTEIN, M GAMSU, G MARKOVITZ, A CASE, B SELIKOFF, IJ KRONENBERG, R ERNST, P AF GREENE, R SCHAEFER, CM OLIVER, LC DEMENT, J LILIS, R FINKELSTEIN, M GAMSU, G MARKOVITZ, A CASE, B SELIKOFF, IJ KRONENBERG, R ERNST, P TI IMPROVED DETECTION OF ASBESTOS-RELATED PLEURAL PLAQUES WITH DIGITAL RADIOGRAPHY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. HANNOVER MED SCH,W-3000 HANNOVER 61,GERMANY. NIEHS,RES TRIANGLE PK,NC 27709. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. ONTARIO MINIST LABOR,TORONTO,ONTARIO,CANADA. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. UNIV PITTSBURGH,PITTSBURGH,PA 15260. UNIV TEXAS,CTR HLTH,TYLER,TX. MCGILL UNIV,MONTREAL H3A 2T5,QUEBEC,CANADA. RP GREENE, R (reprint author), MASSACHUSETTS GEN HOSP,DEPT OCCUPAT MED,BOSTON,MA 02114, USA. NR 6 TC 1 Z9 2 U1 0 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 90 EP 99 DI 10.1111/j.1749-6632.1991.tb24448.x PG 10 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800008 PM 1809179 ER PT J AU BLANC, P MERCHANT, J ABERLE, D GREENE, R SELIKOFF JACOBSEN, M ROCKOFF, SD MYINT, RT GAMSU, G AF BLANC, P MERCHANT, J ABERLE, D GREENE, R SELIKOFF JACOBSEN, M ROCKOFF, SD MYINT, RT GAMSU, G TI CIGARETTE-SMOKING, ASBESTOS, AND PARENCHYMAL OPACITIES REVISITED SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PULMONARY FIBROSIS; CHEST RADIOGRAPHS; WORKERS; EXPOSURE; DISEASE; PNEUMOCONIOSIS; COHORT; HEALTH C1 UNIV IOWA,IOWA CITY,IA 52242. UNIV CALIF LOS ANGELES,CTR HLTH SCI,LOS ANGELES,CA 90024. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. GEORGE WASHINGTON UNIV,WASHINGTON,DC 20052. RP BLANC, P (reprint author), UNIV CALIF SAN FRANCISCO,DIV OCCUPAT & ENVIRONM MED,SAN FRANCISCO,CA 94117, USA. NR 24 TC 5 Z9 5 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 133 EP 144 DI 10.1111/j.1749-6632.1991.tb24453.x PG 12 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800012 PM 1839704 ER PT J AU MARK, EJ YOKOI, T AF MARK, EJ YOKOI, T TI ABSENCE OF EVIDENCE FOR A SIGNIFICANT BACKGROUND INCIDENCE OF DIFFUSE MALIGNANT MESOTHELIOMA APART FROM ASBESTOS EXPOSURE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PLEURAL MESOTHELIOMA; WILMS TUMOR; DIAGNOSIS; LUNG; DIFFERENTIATION; ADENOCARCINOMA; CHILDHOOD C1 NAGOYA UNIV,SCH MED,DEPT PATHOL,NAGOYA,AICHI 466,JAPAN. RP MARK, EJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 67 TC 21 Z9 21 U1 1 U2 2 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 196 EP 204 DI 10.1111/j.1749-6632.1991.tb24463.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800019 PM 1809132 ER PT J AU SUZUKI, Y SOFFRITTI, M CASTLEMAN, B DUNNIGAN, J ROGGLI, V MARK, EJ SCHWARTZ, A POTT, F SELIKOFF, IJ SEBASTIEN, P MILLER, J GROTH, D DAVIS, J MARKOWITZ, S MILLETTE, J MCCAUGHEY, E GOLDSTEIN, D AF SUZUKI, Y SOFFRITTI, M CASTLEMAN, B DUNNIGAN, J ROGGLI, V MARK, EJ SCHWARTZ, A POTT, F SELIKOFF, IJ SEBASTIEN, P MILLER, J GROTH, D DAVIS, J MARKOWITZ, S MILLETTE, J MCCAUGHEY, E GOLDSTEIN, D TI COMPARABILITY OF MESOTHELIOMA IN HUMANS AND IN EXPERIMENTAL ANIMAL STUDIES SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MALIGNANT MESOTHELIOMA; FIBROUS GLASS; ASBESTOS; WORKERS; LUNG; MORTALITY C1 CANADIAN TUMOUR REGISTRY,OTTAWA,ONTARIO,CANADA. INST ONCOL,BOLOGNA,ITALY. UNIV SHERBROOKE,SHERBROOKE J1K 2R1,QUEBEC,CANADA. DUKE UNIV,DURHAM,NC 27706. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. UNIV DUSSELDORF,W-4000 DUSSELDORF 1,GERMANY. UNIV PARIS 12,F-94010 CRETEIL,FRANCE. INST OCCUPAT MED,EDINBURGH EH8 9SV,MIDLOTHIAN,SCOTLAND. MCCRONE ENVIRONM,NORCROSS,GA. RP SUZUKI, Y (reprint author), CUNY,MT SINAI SCH MED,DEPT COMMUNITY MED,DIV ENVIRONM & OCCUPAT MED,NEW YORK,NY 10029, USA. NR 20 TC 2 Z9 2 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 219 EP 227 DI 10.1111/j.1749-6632.1991.tb24465.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800021 PM 1809134 ER PT J AU FASY, TM DAVIS, JMG MYINT, T JAURAND, MC ESMEN, N SCHWARTZ, A ROM, WN KANE, A MARK, E AF FASY, TM DAVIS, JMG MYINT, T JAURAND, MC ESMEN, N SCHWARTZ, A ROM, WN KANE, A MARK, E TI ASBESTOS FIBERS ARE MUTAGENIC AFTER ALL - NEW SIGNS OF ORTHODOXY FOR A PARADOXICAL GROUP OF CARCINOGENS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PLEURAL MESOTHELIAL CELLS; PSV2GPT-TRANSFORMED CHO CELLS; SISTER-CHROMATID EXCHANGES; MAMMALIAN-CELLS; CROCIDOLITE ASBESTOS; TUMOR PROMOTION; AS52 CELLS; MOLECULAR ANALYSES; ICR-191-INDUCED MUTATION; CHRYSOTILE ASBESTOS C1 INST OCCUPAT MED,EDINBURGH EH8 9SV,MIDLOTHIAN,SCOTLAND. INSERM,CRETEIL,FRANCE. UNIV PITTSBURGH,PITTSBURGH,PA 15260. GEORGE WASHINGTON UNIV,MED CTR,WASHINGTON,DC 20037. NYU MED CTR,NEW YORK,NY 10016. BROWN UNIV,PROVIDENCE,RI 02912. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP FASY, TM (reprint author), CUNY MT SINAI SCH MED,DEPT PATHOL,NEW YORK,NY 10029, USA. NR 68 TC 9 Z9 9 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 271 EP 282 DI 10.1111/j.1749-6632.1991.tb24471.x PG 12 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800026 PM 1809140 ER PT J AU WOITOWITZ, HJ GORMAN, E MARK, E KEYES, D SELIKOFF, IJ MILLER, J MANCUSO, T OTTO, JF MALTONI, C LILIS, R KRONENBERG, R GIBBS, G RUTTNER, J ENGLUND, A AF WOITOWITZ, HJ GORMAN, E MARK, E KEYES, D SELIKOFF, IJ MILLER, J MANCUSO, T OTTO, JF MALTONI, C LILIS, R KRONENBERG, R GIBBS, G RUTTNER, J ENGLUND, A TI ASPECTS OF ASBESTOS EXPOSURE IN PLACE IN THE FEDERAL-REPUBLIC-OF-GERMANY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 IST ONCOL F ADDARII,BOLOGNA,ITALY. UNIV TEXAS,CTR HLTH,TYLER,TX. UNIV ZURICH,CH-8006 ZURICH,SWITZERLAND. CARPENTERS NATL HLTH & SAFETY FUND,WASHINGTON,DC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ENVIRONM SCI INC,TUCSON,AZ. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. UNIV PITTSBURGH,PITTSBURGH,PA 15260. RP WOITOWITZ, HJ (reprint author), UNIV GIESSEN,KLINIKUM,INST & POLIKLIN ARBEITS & SOZIALMED,AULWEG 129-111,W-6300 GIESSEN,GERMANY. NR 2 TC 2 Z9 2 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 407 EP 415 DI 10.1111/j.1749-6632.1991.tb24486.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800039 PM 1809153 ER PT J AU OLIVER, LC SPRINCE, NL GREENE, R AF OLIVER, LC SPRINCE, NL GREENE, R TI ASBESTOS-RELATED ABNORMALITIES IN SCHOOL MAINTENANCE PERSONNEL SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID POPULATION; PREVALENCE; VALUES C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. RP OLIVER, LC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 18 TC 4 Z9 4 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 521 EP 529 DI 10.1111/j.1749-6632.1991.tb24503.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800051 PM 1809165 ER PT J AU MARKOWITZ, SB GARIBALDI, K LILIS, R LANDRIGAN, PJ KILBURN, K SELIKOFF, IJ KIPEN, H LEVIN, SM MILLER, J OLIVER, LC STIGLIANO, J FITE, J GOLDSTEIN, D AF MARKOWITZ, SB GARIBALDI, K LILIS, R LANDRIGAN, PJ KILBURN, K SELIKOFF, IJ KIPEN, H LEVIN, SM MILLER, J OLIVER, LC STIGLIANO, J FITE, J GOLDSTEIN, D TI ASBESTOS EXPOSURE AND FIRE FIGHTING SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID FIGHTERS; MORTALITY; WORKERS; HEALTH; COHORT C1 UNIV SO CALIF,LOS ANGELES,CA 90089. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,PISCATAWAY,NJ 08854. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. INT UNION OPERATING ENGINEERS,NEW YORK,NY. WHITE LUNG ASSOC,BALTIMORE,MD. MED TOXICOL PARTNERSHIP,DENVER,CO. RP MARKOWITZ, SB (reprint author), CUNY MT SINAI SCH MED,DIV ENVIRONM & OCCUPAT MED,BOX 1057,1 GUSTAVE L LEVY PL,NEW YORK,NY 10029, USA. NR 19 TC 5 Z9 5 U1 1 U2 3 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 573 EP 581 DI 10.1111/j.1749-6632.1991.tb24507.x PG 9 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800055 PM 1809170 ER PT J AU IRWIG, HG OLIVER, LC PAGE, T WEGMAN, DH ELLENBECKER, MJ AF IRWIG, HG OLIVER, LC PAGE, T WEGMAN, DH ELLENBECKER, MJ TI ASBESTOS IN PLACE - A BUILDING MANAGEMENT PERSPECTIVE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PULM UNIT,BOSTON,MA 02114. BROWN UNIV,DEPT ECON,PROVIDENCE,RI 02912. UNIV LOWELL,DEPT WORK ENVIRONM,LOWELL,MA 01854. RP IRWIG, HG (reprint author), BEACON CONSTRUCT CO,PROGRAM MANAGEMENT GRP,3 CTR PLAZA,BOSTON,MA 02108, USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 31 PY 1991 VL 643 BP 589 EP 596 DI 10.1111/j.1749-6632.1991.tb24510.x PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM568 UT WOS:A1991JM56800057 PM 1809172 ER PT J AU MULLERWIELAND, D WHITE, MF BEHNKE, B GEBHARDT, A NEUMANN, S KRONE, W KAHN, CR AF MULLERWIELAND, D WHITE, MF BEHNKE, B GEBHARDT, A NEUMANN, S KRONE, W KAHN, CR TI PERTUSSIS TOXIN INHIBITS AUTOPHOSPHORYLATION AND ACTIVATION OF THE INSULIN-RECEPTOR KINASE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PHOSPHORYLATION; PROTEIN; CELLS; RIBOSYLATION C1 BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV COLOGNE,INNERE MED POLIKLIN,W-5000 COLOGNE 41,GERMANY. RP MULLERWIELAND, D (reprint author), UNIV COLOGNE,KLIN 2,W-5000 COLOGNE 41,GERMANY. FU NIADDK NIH HHS [AM31036, AM33201]; NIDDK NIH HHS [DK38712] NR 24 TC 25 Z9 25 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD DEC 31 PY 1991 VL 181 IS 3 BP 1479 EP 1485 DI 10.1016/0006-291X(91)92106-T PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA GX736 UT WOS:A1991GX73600082 PM 1722405 ER PT J AU WOLFSON, JS HOOPER, DC AF WOLFSON, JS HOOPER, DC TI OVERVIEW OF FLUOROQUINOLONE SAFETY SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID QUINOLONE ANTIBACTERIAL AGENTS; SKIN STRUCTURE INFECTIONS; PLASMA THEOPHYLLINE CONCENTRATIONS; ALLERGIC INTERSTITIAL NEPHRITIS; GYRASE-INHABITING ANTIBIOTICS; AMINOBUTYRIC ACID BINDING; URINARY-TRACT INFECTION; SINGLE-DOSE PEFLOXACIN; RAT-BRAIN MEMBRANES; ACUTE-RENAL-FAILURE AB The safety of the fluoroquinolone antimicrobial agents is reviewed, discussing documented and potential clinical and laboratory adverse effects and drug-drug interactions. In prospective, randomized, double-blind clinical trials comparing fluoroquinolones to nonquinolone drugs or placebo, the fluoroquinolones were not significantly different (22 studies) or were superior (5 studies) to comparison agents but were only rarely more toxic (2 studies). Adverse effects included mild gastrointestinal toxicities and less common but more problematic central nervous system toxicities. Clinically important interactions occurred with coadministration of antacids and all fluoroquinolones and with theophylline and enoxacin and to a lesser extent ciprofloxacin and pefloxacin but not other fluoroquinolones. Potential adverse effects such as cartilage damage, DNA damage, teratogenicity, and crystalluria, while of concern, have not as yet been shown to be of clinical importance. Therapy of bacterial infections in children and adolescents is relatively contraindicated, but growing clinical experience with treatment of these patients has not so far revealed serious bone or cartilage toxicity. The fluoroquinolones thus far have exhibited a favorable safety profile, but our clinical experience is still limited, and monitoring for as yet unappreciated toxicities is warranted. C1 MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,14 FRUIT ST,BOSTON,MA 02114. NR 188 TC 33 Z9 34 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 DEC 30 PY 1991 VL 91 SU 6A BP S153 EP S161 DI 10.1016/0002-9343(91)90330-Z PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HA400 UT WOS:A1991HA40000031 PM 1767803 ER PT J AU WIGZELL, H GRUNEWALD, J TEHRANI, M ESIN, S MELLSTEDT, H OSTERBORG, A DERSIMONIAN, H BRENNER, M AHLBERG, R LEFVERT, AK ORN, M EKLUND, A JANSON, CH AF WIGZELL, H GRUNEWALD, J TEHRANI, M ESIN, S MELLSTEDT, H OSTERBORG, A DERSIMONIAN, H BRENNER, M AHLBERG, R LEFVERT, AK ORN, M EKLUND, A JANSON, CH TI T-CELL V-GENE USAGE IN MAN IN SOME NORMAL AND ABNORMAL SITUATIONS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MONOCLONAL-ANTIBODIES; TUMOR-THERAPY; ENTEROTOXIN-B; BETA-CHAIN; RECEPTOR; LEUKEMIA; DETERMINANTS; IMMUNIZATION; POPULATIONS; ANERGY C1 KAROLINSKA INST,DEPT ONCOL,S-10401 STOCKHOLM 60,SWEDEN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. KAROLINSKA HOSP,DEPT MED,S-10401 STOCKHOLM 60,SWEDEN. KAROLINSKA HOSP,THORAX CLIN,S-10401 STOCKHOLM 60,SWEDEN. RP WIGZELL, H (reprint author), KAROLINSKA INST,DEPT IMMUNOL,S-10401 STOCKHOLM 60,SWEDEN. RI Esin, Semih/B-7566-2013 FU NIAMS NIH HHS [AR 39582] NR 26 TC 7 Z9 7 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 30 PY 1991 VL 636 BP 9 EP 19 DI 10.1111/j.1749-6632.1991.tb33433.x PG 11 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM207 UT WOS:A1991JM20700002 PM 1793233 ER PT J AU SLAYTER, HS WOLD, JK MIDTVEDT, T AF SLAYTER, HS WOLD, JK MIDTVEDT, T TI INTESTINAL MUCIN OF GERM-FREE RATS - BIOCHEMICAL AND ELECTRON-MICROSCOPIC CHARACTERIZATION SO CARBOHYDRATE RESEARCH LA English DT Article ID BRONCHIAL MUCUS GLYCOPROTEINS; MUCOUS GLYCOPROTEINS; GEL; SIZE AB Purified germ-free rat intestinal mucin was found by chemical analysis to contain 25% protein, enriched in serine, threonine, and proline. 75% carbohydrate, and no nucleic acid. IT was anaLYzed by darkfield electron microscopy and found to consist of long filamentous molecules with a maximum length of approximately 740 nm, a mean length of 456 nm, and a mean width of 7 nm. Given reasonable assumptions derived from earlier work on other well-characterized mucins, the molecular weight of the peptide, calculated by the length from electron microscopy, was 200 000, and, given the chemical composition, the molecular weight of the entire mucin molecule was calculated to be approximately 800000. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,STRUCT MOLEC BIOL LAB,BOSTON,MA 02115. UNIV OSLO,INST PHARM,N-0316 OSLO 3,NORWAY. KAROLINSKA INST,DEPT MED MICROBIAL ECOL,S-10401 STOCKHOLM 60,SWEDEN. RP SLAYTER, HS (reprint author), HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM 14237] NR 29 TC 14 Z9 14 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD DEC 30 PY 1991 VL 222 BP 1 EP 9 DI 10.1016/0008-6215(91)89001-V PG 9 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA GZ507 UT WOS:A1991GZ50700001 PM 1813101 ER PT J AU KVEDAR, JC DARYANANI, HA BADEN, HP AF KVEDAR, JC DARYANANI, HA BADEN, HP TI A COMPARISON OF THE CROSS-LINKED COMPONENTS OF STRATUM-CORNEUM OF EPIDERMIS AND THE CUTICLE OF THE CORTEX OF HAIR SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID CORNIFIED ENVELOPE; MAMMALIAN EPIDERMIS; KERATINOCYTES; PRECURSORS; PROTEINS C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 13 TC 4 Z9 5 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 26 PY 1991 VL 642 BP 44 EP 50 PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM212 UT WOS:A1991JM21200005 PM 1809099 ER PT J AU BADEN, HP AF BADEN, HP TI WHERE WE HAVE BEEN AND WHERE WE SHOULD BE - CLINICAL RELEVANCE OF THE MOLECULAR AND STRUCTURAL BIOLOGY OF HAIR SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Editorial Material RP BADEN, HP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD DEC 26 PY 1991 VL 642 BP 435 EP 435 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM212 UT WOS:A1991JM21200034 ER PT J AU WINTER, HS BLICKMAN, JG KHAW, KT MARK, EJ KLEINMAN, RE COMPTON, CC AF WINTER, HS BLICKMAN, JG KHAW, KT MARK, EJ KLEINMAN, RE COMPTON, CC TI AN 8-YEAR-OLD GIRL WITH RECURRENT ABDOMINAL DISTENSION AFTER SURGICAL-CORRECTION OF HIRSCHSPRUNGS-DISEASE - INTESTINAL NEURONAL DYSPLASIA ASSOCIATED WITH LONG-SEGMENT HIRSCHSPRUNGS-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID HOLLOW VISCERAL MYOPATHY; DOUBLE ZONAL AGANGLIONOSIS; PSEUDO-OBSTRUCTION; HYPOPERISTALSIS SYNDROME; COLON; PSEUDOOBSTRUCTION; FAMILY C1 CHILDRENS HOSP MED CTR,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BOSTON UNIV,SCH MED,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP WINTER, HS (reprint author), BOSTON CITY HOSP,BOSTON,MA 02118, USA. NR 20 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 26 PY 1991 VL 325 IS 26 BP 1865 EP 1874 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA GW528 UT WOS:A1991GW52800008 ER PT J AU SHULL, S HEINTZ, NH PERIASAMY, M MANOHAR, M JANSSEN, YMW MARSH, JP MOSSMAN, BT AF SHULL, S HEINTZ, NH PERIASAMY, M MANOHAR, M JANSSEN, YMW MARSH, JP MOSSMAN, BT TI DIFFERENTIAL REGULATION OF ANTIOXIDANT ENZYMES IN RESPONSE TO OXIDANTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR NECROSIS FACTOR; CONTAINING SUPEROXIDE-DISMUTASE; TRACHEAL EPITHELIAL-CELLS; XANTHINE-OXIDASE; INTERLEUKIN-1; EXPRESSION; INDUCTION; TOXICITY; CDNA; RNA AB We have demonstrated the selective induction of manganese superoxide dismutase (MnSOD) or catalase mRNA after exposure of tracheobronchial epithelial cells in vitro to different oxidant stresses. Addition of H2O2 caused a dose-dependent increase in catalase mRNA in both exponentially growing and confluent cells. A 3-fold induction of catalase mRNA was seen at a nontoxic dose of 250-mu-M H2O2. Increase in the steady-state mRNA levels of glutathione peroxidase (GPX) and MnSOD were less striking. Expression of catalase, MnSOD, and GPX mRNA was highest in confluent cells. In contrast, constitutive expression of copper and zinc SOD (CuZnSOD) mRNA was greatest in dividing cells and was unaffected by H2O2 in both exponentially growing and confluent cells. MnSOD mRNA was selectively induced in confluent epithelial cells exposed to the reactive oxygen species-generating system, xanthine/xanthine oxidase, while steady-state levels of GPX, catalase, and CuZnSOD mRNA remained unchanged. The 3-fold induction of MnSOD mRNA was dose-dependent, reaching a peak at 0.2 unit/ml xanthine oxidase. MnSOD mRNA increases were seen as early as 2 h and reached maximal induction at 24 h. Immunoreactive MnSOD protein was produced in a corresponding dose- and time-dependent manner. Induction of MnSOD gene expression was prevented by addition of actinomycin D and cycloheximide. These data indicate that epithelial cells of the respiratory tract respond to different oxidant insults by selective induction of certain antioxidant enzymes. Hence, gene expression of antioxidant enzymes does not appear to be coordinately regulated in these cell types. C1 UNIV VERMONT,SCH MED,DEPT PATHOL,BURLINGTON,VT 05405. UNIV VERMONT,SCH MED,DEPT PHYSIOL & BIOPHYS,BURLINGTON,VT 05405. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. RP SHULL, S (reprint author), UNIV VERMONT,SCH MED,DEPT BIOCHEM,BURLINGTON,VT 05405, USA. FU NHLBI NIH HHS [HL-39469] NR 30 TC 334 Z9 338 U1 1 U2 13 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 25 PY 1991 VL 266 IS 36 BP 24398 EP 24403 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GW845 UT WOS:A1991GW84500027 PM 1761541 ER PT J AU DRUKER, BJ ROBERTS, TM AF DRUKER, BJ ROBERTS, TM TI GENERATION OF A LARGE LIBRARY OF POINT MUTATIONS IN POLYOMA MIDDLE-T ANTIGEN SO NUCLEIC ACIDS RESEARCH LA English DT Article ID PHOSPHATIDYLINOSITOL KINASE-ACTIVITY; GRADIENT GEL-ELECTROPHORESIS; RECOMBINANT RETROVIRUSES; ONCOGENIC TRANSFORMATION; CELL-TRANSFORMATION; MURINE RETROVIRUS; DNA FRAGMENTS; VIRUS GENOME; PROTEIN; MUTANTS AB Polyoma middle T antigen (MTAg) transforms cells by associating with and activating a variety of intracellular proteins, including src family members and a phosphatidylinositol-3 kinase. In order to assist in the study of the relative importance of the various associated biochemical activities for transformation by polyomavirus MTAg, a library of MTAg mutants was constructed. Chemically mutagenized MTAg DNA was purified from wild-type DNA by separation on denaturing gradient gels and placed into a recombinant retrovirus vector. Utilizing the resultant library of MTAg-expressing retroviruses, fibroblast cell lines expressing individual MTAg mutants were generated and screened for a non-transformed morphology. Of the first seven non-transformed clones tested, all express the MTAg protein. We estimate that approximately 24% of the G418-resistant colonies contain a transformation-defective MTAg mutant. A more thorough evaluation of one such clone revealed four single base-pair changes as compared to wild-type. Further genetic dissection of this mutant reveals that substituting leucine for proline at amino acid 248 results in a completely transformation defective MTAg. The utility of this mutagenesis and screening procedure as well as the description of several new MTAg mutants is described. This library of mutations should be of general interest for studying the transforming ability of MTAg. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DRUKER, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA3002] NR 46 TC 13 Z9 13 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD DEC 25 PY 1991 VL 19 IS 24 BP 6855 EP 6861 DI 10.1093/nar/19.24.6855 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GX701 UT WOS:A1991GX70100025 PM 1662365 ER PT J AU RIVKEES, SA REPPERT, SM AF RIVKEES, SA REPPERT, SM TI APPEARANCE OF MELATONIN RECEPTORS DURING EMBRYONIC LIFE IN SIBERIAN HAMSTERS (PHODOPUS-SUNGORUS) SO BRAIN RESEARCH LA English DT Note DE MELATONIN; MELATONIN RECEPTOR; FETUS; RATHKES POUCH; THYROID ID LATE GESTATION; MESSENGER-RNA; RHYTHMS; FETAL; SIGNAL; BRAIN; AUTORADIOGRAPHY; TRANSDUCTION; LOCALIZATION; INHIBITION AB Maternal melatonin readily crosses the placenta to provide the fetus with time-of-day and day length information. To determine if melatonin could have a broader role during development than is currently recognized, melatonin receptor expression was examined in somatic sites during Siberian hamster embryogenesis. Using I-125-labeled-2-iodomelatonin ([I-125]MEL), melatonin receptor expression was examined in whole fetuses by in vitro autoradiography. [I-125]MEL binding sites were first apparent at gestational day (GD) 10 over the primitive oral pharynx. From GD 12 to 14, binding was present over the nasal pharynx, Rathke's pouch, caudal arteries, and over the thyroid gland during its migration along the thyroglossal duct. By GD 16, Rathke's pouch had differentiated into the pituitary gland, which continued to express specific [I-125]MEL binding until birth. From GD 16 until birth, binding was no longer detectable over the thyroid gland, but persisted over the nasal epithelium. At all ages, binding sites exhibited high affinity for [I-125]MEL and appeared to be coupled with guanosine nucleotide-binding proteins. These data suggest that melatonin receptors are expressed in several somatic sites, including Rathke's pouch and the thyroid gland, during fetal development. C1 MASSACHUSETTS GEN HOSP,PEDIAT ENDOCRINE UNIT,BOSTON,MA 02114. RP RIVKEES, SA (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD-14427, HD-00924]; NIDDK NIH HHS [DK-42125] NR 29 TC 34 Z9 34 U1 1 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 DEC 24 PY 1991 VL 568 IS 1-2 BP 345 EP 349 DI 10.1016/0006-8993(91)91424-Y PG 5 WC Neurosciences SC Neurosciences & Neurology GA GX850 UT WOS:A1991GX85000052 PM 1667620 ER PT J AU FAUSTMAN, D LI, XP LIN, HY FU, YE EISENBARTH, G AVRUCH, J GUO, J AF FAUSTMAN, D LI, XP LIN, HY FU, YE EISENBARTH, G AVRUCH, J GUO, J TI LINKAGE OF FAULTY MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I TO AUTOIMMUNE DIABETES SO SCIENCE LA English DT Article ID ISLET-CELL ANTIBODIES; INSULIN-DEPENDENT DIABETICS; VIRAL PEPTIDES; PROTEIN-A; T-CELLS; MELLITUS; GENE; SUSCEPTIBILITY; ASSAY; MICE AB Pancreatic islet cells are the targets of an autoimmune response in type I diabetes. In the nonobese diabetic (NOD) mouse model of autoimmune diabetes, expression of major histocompatibility complex (MHC) class I proteins was inversely correlated with diabetes; in this mouse a mutation in the MHC class II-linked gene for the putative MHC class I peptide transporter was also present. Mice deficient in MHC class I expression because they do not produce beta-2-microglobulin also developed late onset autoimmune diabetes. In cells from humans with type I diabetes expression of MHC class I was decreased; subsets of prediabetics categorized as most likely to become hyperglycemic also had low MHC class I. T cell responses to self antigens are faulty in diabetics. In sets of genetically identical twins that are discordant for diabetes, the defect appeared to reside with the antigen presenting cell. Thus, a lack of surface MHC class I protein is associated with autoimmune diabetes; the concomitant defect in antigen presentation may impair the development of self tolerance, which could result in autoimmune disease. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DIABET UNIT,IMMUNOBIOL LAB,BOSTON,MA 02129. JOSLIN DIABET CTR,BOSTON,MA 02115. MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02139. RP FAUSTMAN, D (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 37 TC 185 Z9 185 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD DEC 20 PY 1991 VL 254 IS 5039 BP 1756 EP 1761 DI 10.1126/science.1763324 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GW316 UT WOS:A1991GW31600033 PM 1763324 ER PT J AU ROSENZWEIG, A WATKINS, H HWANG, DS MIRI, M MCKENNA, W TRAILL, TA SEIDMAN, JG SEIDMAN, CE AF ROSENZWEIG, A WATKINS, H HWANG, DS MIRI, M MCKENNA, W TRAILL, TA SEIDMAN, JG SEIDMAN, CE TI PRECLINICAL DIAGNOSIS OF FAMILIAL HYPERTROPHIC CARDIOMYOPATHY BY GENETIC-ANALYSIS OF BLOOD-LYMPHOCYTES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID MYOSIN HEAVY-CHAIN; LEFT-VENTRICULAR HYPERTROPHY; AMINO-ACID-SEQUENCE; MOLECULAR-BASIS; SUDDEN-DEATH; CLINICAL MANIFESTATIONS; PATHO-PHYSIOLOGY; SKELETAL-MUSCLE; DNA-SEQUENCE; ALPHA AB Background. The clinical diagnosis of familial hypertrophic cardiomyopathy is usually made on the basis of the physical examination, electrocardiogram, and echocardiogram. Making an accurate diagnosis can be particularly difficult in children, who may not have cardiac hypertrophy until adulthood. Recently, we demonstrated that mutations in the cardiac myosin heavy-chain genes cause familial hypertrophic cardiomyopathy in some families. We report a diagnostic test for familial hypertrophic cardiomyopathy that relies on the detection of mutations in the beta-myosin heavy-chain gene in circulating lymphocytes that we used to evaluate three generations of a family, including the children. Methods and Results. Using the polymerase chain reaction, we found that normal and mutant beta-cardiac myosin heavy-chain genes are transcribed in circulating lymphocytes. This allowed us to examine beta-cardiac myosin heavy-chain messenger RNA from blood lymphocytes, even though ordinary expression of the gene is virtually restricted to the heart. Base sequences amplified from this messenger RNA were analyzed with a ribonuclease protection assay to identify small deletions, abnormal splicing, or missense mutations. Using this technique we identified a novel missense mutation in a patient with familial hypertrophic cardiomyopathy. We evaluated 15 of the patient' s adult relatives and found perfect agreement with the clinical diagnosis (8 affected and 7 not affected). Clinical analysis of 14 of the children (age, 1 to 20 years) of these affected family members revealed 1 child with echocardiographic findings diagnostic of familial hypertrophic cardiomyopathy. However, genetic analyses showed that six other children had also inherited the missense mutation and might later manifest the disease. Conclusions. Transcripts of beta-cardiac myosin heavy-chain gene can be detected in blood lymphocytes and used to screen for mutations that cause familial hypertrophic cardiomyopathy. This approach makes practical the identification of mutations responsible for this disorder and may be applicable to other diseases in which direct analysis is difficult because the mutated gene is expressed only in certain tissues. Preclinical or prenatal screening in an affected family will make it possible to study the disease longitudinally and to develop preventive interventions. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DIV CARDIOL,BOSTON,MA 02115. ST GEORGE HOSP,SCH MED,DEPT CARDIOL SCI,LONDON,ENGLAND. TAICHUNG VET GEN HOSP,DIV CARDIOL,TAICHUNG,TAIWAN. JOHNS HOPKINS UNIV HOSP,DIV CARDIOL,BALTIMORE,MD 21205. HOWARD HUGHES MED INST,BOSTON,MA. RP ROSENZWEIG, A (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,25 SHATTUCK ST,BOSTON,MA 02115, USA. RI McKenna, William/C-3243-2008 OI McKenna, William/0000-0001-7994-2460 FU NHLBI NIH HHS [HL02228, HL35877, HL46320] NR 54 TC 139 Z9 140 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 19 PY 1991 VL 325 IS 25 BP 1753 EP 1760 DI 10.1056/NEJM199112193252501 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA GV739 UT WOS:A1991GV73900001 PM 1944483 ER PT J AU SCHAPIRO, BL NEWBURGER, PE KLEMPNER, MS DINAUER, MC AF SCHAPIRO, BL NEWBURGER, PE KLEMPNER, MS DINAUER, MC TI CHRONIC GRANULOMATOUS-DISEASE PRESENTING IN A 69-YEAR-OLD MAN SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID NEUTROPHIL CYTOCHROME-B; RESPIRATORY BURST OXIDASE; 2 CYTOSOLIC COMPONENTS; INTERFERON-GAMMA; PLASMA-MEMBRANE; CHAIN; ACTIVATION; ABSENCE; DEFICIENCIES; DIAGNOSIS C1 TUFTS UNIV,SCH MED,BOSTON,MA 02111. UNIV MASSACHUSETTS,SCH MED,DEPT PEDIAT,WORCESTER,MA 01605. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP SCHAPIRO, BL (reprint author), TUFTS UNIV NEW ENGLAND MED CTR,DIV GEOG MED & INFECT DIS,750 WASHINGTON ST,BOX 067,BOSTON,MA 02111, USA. OI Newburger, Peter/0000-0002-8615-673X FU NCI NIH HHS [CA-38325]; NHLBI NIH HHS [HL45635, HL02253] NR 42 TC 82 Z9 84 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 19 PY 1991 VL 325 IS 25 BP 1786 EP 1790 DI 10.1056/NEJM199112193252506 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA GV739 UT WOS:A1991GV73900006 PM 1719419 ER PT J AU BECK, WS FERRY, JA HAHN, PF FERRY, JA DEMIRJIAN, ZN MARK, EJ AF BECK, WS FERRY, JA HAHN, PF FERRY, JA DEMIRJIAN, ZN MARK, EJ TI A 68-YEAR-OLD MAN WITH RECURRENT FEVER AND DIARRHEA AFTER TREATMENT FOR LYMPHOMA - MEGALOBLASTIC-ANEMIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID MILIARY TUBERCULOSIS; HEMATOLOGIC ABNORMALITIES; PERNICIOUS-ANEMIA; METHOTREXATE; DEFICIENCY; DIAGNOSIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BECK, WS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 29 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 19 PY 1991 VL 325 IS 25 BP 1791 EP 1800 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA GV739 UT WOS:A1991GV73900007 ER PT J AU BARTON, NW BRADY, RO MURRAY, GJ ARGOFF, CE GREWAL, RP YU, KT DAMBROSIA, JM DIBISCEGLIE, AM HILL, SC PARKER, RI DOPPELT, SH MANKIN, HJ AF BARTON, NW BRADY, RO MURRAY, GJ ARGOFF, CE GREWAL, RP YU, KT DAMBROSIA, JM DIBISCEGLIE, AM HILL, SC PARKER, RI DOPPELT, SH MANKIN, HJ TI ENZYME-REPLACEMENT THERAPY FOR GAUCHERS-DISEASE - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID GLUCOCEREBROSIDASE C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP BARTON, NW (reprint author), NIH,BETHESDA,MD 20892, USA. NR 3 TC 18 Z9 18 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 19 PY 1991 VL 325 IS 25 BP 1811 EP 1811 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA GV739 UT WOS:A1991GV73900022 ER PT J AU METZ, S HOLMES, D ROBERTSON, RP LEITNER, W DRAZNIN, B AF METZ, S HOLMES, D ROBERTSON, RP LEITNER, W DRAZNIN, B TI GENE-EXPRESSION OF TYPE-I PHOSPHOLIPASE-A2 IN PANCREATIC BETA-CELLS - REGULATION OF MESSENGER-RNA LEVELS BY STARVATION OR GLUCOSE EXCESS SO FEBS LETTERS LA English DT Article DE INSULIN; PANCREATIC ISLET; PHOSPHOLIPASE; GLUCOSE; BETA-CELL; FASTING ID MEMBRANE-ASSOCIATED PHOSPHOLIPASE-A2; INSULIN-SECRETION; RAT ISLETS; CDNA CLONING; HYPERGLYCEMIA; ACCUMULATION; SEQUENCE; CALCIUM AB Messenger RNA from intact rat pancreatic islets, or from transformed hamster beta (HIT) cells, hybridized with the cDNA probe for type I (but not type II) phospholipase A2. The levels of phospholipase A2 mRNA increased in islets from fasted rats; they decreased in islets cultured in a high glucose concentration (control values at 5.5 mM glucose = 150 +/- 6% of those at 22 mM) which impaired subsequent insulin secretion (reduction in second-phase release = 70 +/- 11%). These studies uniquely demonstrate that type I phospholipase A2 is expressed specifically in beta cells and that nutrient availability modulates transcript levels, an effect which could contribute to the detrimental influence of prolonged hyperglycemia on islet function. C1 VET ADM MED CTR,DENVER,CO 80220. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DIV ENDOCRINOL,MADISON,WI. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DIV ENDOCRINOL,MADISON,WI 53706. FU NIDDK NIH HHS [DK38325, DK37312] NR 26 TC 30 Z9 30 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD DEC 16 PY 1991 VL 295 IS 1-3 BP 110 EP 112 DI 10.1016/0014-5793(91)81397-Q PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA GZ363 UT WOS:A1991GZ36300029 PM 1662640 ER PT J AU TRAVIN, MI FLORES, AR BOUCHER, CA NEWELL, JB LARAIA, PJ AF TRAVIN, MI FLORES, AR BOUCHER, CA NEWELL, JB LARAIA, PJ TI SILENT VERSUS SYMPTOMATIC ISCHEMIA DURING A TL-201 EXERCISE TEST SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; ACUTE MYOCARDIAL-INFARCTION; PROGNOSTIC-SIGNIFICANCE; UNSTABLE ANGINA; STRESS TEST; CHEST PAIN; FOLLOW-UP; TREADMILL; SCINTIGRAPHY; SENSITIVITY AB One hundred thirty-four patients with redistribution on a thallium-201 exercise test who did not experience angina (group 1) were compared with 134 patients also having redistribution who had angina during the test (group 2). The groups were matched by age, sex, and peak exercise heart rate. Although patients in both groups achieved an equivalent exercise level, patients in group 1 had less frequent (53 vs 71%, p < 0.005) and less severe (0.15 +/- 0.13 vs 0.20 +/ 0.13 mV, p < 0.005) ischemic ST-segment depression. Group 1 also had less ischemic thallium-201 images in terms of the number of redistributing defects, the severity of the worst redistributing defect, and an ischemic index composite of both extent and severity. Patients in group 1 were less likely to undergo early revascularization (12 vs 29%, p < 0.005), but in the remaining patients the occurrence of adverse cardiac events was similar (21% vs 29%, P = not significant). By multivariate analysis, only the ischemic index correlated with early revascularization in group 1 (p = 0.0017), whereas the percent maximal predicted heart rate correlated best in group 2 (p = 0.0003). In group 1 the ratio of lung/heart thallium-201 uptake correlated best with an outcome of nonfatal myocardial infarction or cardiac death (p = 0.0024); in group 2 the presence of fixed left ventricular dilatation did (p = 0.0022). Thus, patients with exercise-induced thallium-201 redistribution without angina have less ischemia than experiencing angina. They are also less likely to undergo early revascularization, but their prognosis is otherwise similar to patients with angina during the test. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. SPAULDING REHABIL HOSP,DIV CARDIOL,BOSTON,MA 02114. RP TRAVIN, MI (reprint author), ROGER WILLIAMS GEN HOSP,DIV CARDIOL,825 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. NR 29 TC 19 Z9 19 U1 0 U2 0 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 DEC 15 PY 1991 VL 68 IS 17 BP 1600 EP 1608 DI 10.1016/0002-9149(91)90316-D PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GU998 UT WOS:A1991GU99800010 PM 1746460 ER PT J AU MCDONALD, JA POTTER, NU AF MCDONALD, JA POTTER, NU TI A METHOD FOR ESTIMATING YEAR OF BIRTH USING SOCIAL-SECURITY NUMBER SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. NR 1 TC 2 Z9 2 U1 1 U2 2 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 DEC 15 PY 1991 VL 134 IS 12 BP 1475 EP 1475 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HC444 UT WOS:A1991HC44400019 PM 1776625 ER PT J AU GRIBBEN, JG FREEDMAN, AS WOO, SD BLAKE, K SHU, RS FREEMAN, G LONGTINE, JA PINKUS, GS NADLER, LM AF GRIBBEN, JG FREEDMAN, AS WOO, SD BLAKE, K SHU, RS FREEMAN, G LONGTINE, JA PINKUS, GS NADLER, LM TI ALL ADVANCED STAGE NON-HODGKINS-LYMPHOMAS WITH A POLYMERASE CHAIN-REACTION AMPLIFIABLE BREAKPOINT OF BCL-2 HAVE RESIDUAL CELLS CONTAINING THE BCL-2 REARRANGEMENT AT EVALUATION AND AFTER TREATMENT SO BLOOD LA English DT Article ID T(14-18) CHROMOSOMAL TRANSLOCATION; FOLLICULAR LYMPHOMAS; BONE-MARROW; CLUSTER REGION; B-CELLS; DNA; GENE; AMPLIFICATION; SURVIVAL; DISEASE C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU FIC NIH HHS [TWO4496]; NCI NIH HHS [CA40216, 5KO8 CA0115] NR 24 TC 319 Z9 321 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 DEC 15 PY 1991 VL 78 IS 12 BP 3275 EP 3280 PG 6 WC Hematology SC Hematology GA GV584 UT WOS:A1991GV58400024 PM 1742487 ER PT J AU RAGO, R MITCHEN, J CHENG, AL OBERLEY, T WILDING, G AF RAGO, R MITCHEN, J CHENG, AL OBERLEY, T WILDING, G TI DISRUPTION OF CELLULAR-ENERGY BALANCE BY SURAMIN IN INTACT HUMAN PROSTATIC-CARCINOMA CELLS, A LIKELY ANTIPROLIFERATIVE MECHANISM SO CANCER RESEARCH LA English DT Article ID TRANSFORMING GROWTH-FACTOR; FACTOR RECEPTOR-BINDING; LIVING CELLS; FACTOR-ALPHA; INHIBITION; ASSAY; DRUG; DIFFERENTIATION; PROLIFERATION; MITOCHONDRIA AB The antiparasitic drug, suramin, has antiproliferative effects in human carcinoma cells. It has been suggested that this occurs through blockade of growth factor-receptor interactions. Three types of evidence that suramin rapidly inhibits cellular respiration or disrupts cellular energy balance in intact cells of the human prostate carcinoma cell line, DU145, are presented. Beginning at approximately 10(-4) M, suramin rapidly causes dose-dependent inhibition of tetrazolium conversion by mitochondrial dehydrogenases in intact cells, demonstrating an inhibition of respiration. This effect is reversed by exchange with suramin-free media but not by pretreatment with serum, epidermal growth factor, insulin-like growth factor I, acidic and basic fibroblast growth factors, or calcium. Rhodamine 123 (10-mu-g/ml) uptake by mitochondria in intact DU145 cells is inhibited in the presence of 10(-3) M suramin. Treatment with 10(-4)-10(-3)M suramin causes the loss of rhodamine 123 from cells with mitochondria prestained with rhodamine 123, indicating that suramin is acting as an ionophore or respiratory poison. Also shown by electron microscopy are progressive toxic changes in mitochondria of DU145 cells within 1 h after treatment with 10(-4) M suramin. These data indicate that in intact DU145 cells 10(-4) M suramin rapidly disrupts cellular energy balance or respiration as seen by three studies of mitochondrial state. Disruption of energy balance or respiration represents a likely antiproliferative mechanism, as is thought to be a primary mechanism for the action of suramin in parasitic diseases. This proposed mechanism of action for suramin can explain the most prominent observed clinical toxicities of nephrotoxicity, adrenal toxicity, coagulopathy, and demyelinating neuropathy. C1 UNIV WISCONSIN,CTR CLIN CANC,DEPT HUMAN ONCOL,K4-666 CSC,600 HIGHLAND AVE,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI 53705. OI Cheng, Ann-Lii/0000-0002-9152-6512 FU NCI NIH HHS [CA50590, T32 CA09614] NR 52 TC 42 Z9 43 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 15 PY 1991 VL 51 IS 24 BP 6629 EP 6635 PG 7 WC Oncology SC Oncology GA GU416 UT WOS:A1991GU41600022 PM 1742736 ER PT J AU KHARBANDA, S RUBIN, E GUNJI, H HINZ, H GIOVANELLA, B PANTAZIS, P KUFE, D AF KHARBANDA, S RUBIN, E GUNJI, H HINZ, H GIOVANELLA, B PANTAZIS, P KUFE, D TI CAMPTOTHECIN AND ITS DERIVATIVES INDUCE EXPRESSION OF THE C-JUN PROTOONCOGENE IN HUMAN MYELOID-LEUKEMIA CELLS SO CANCER RESEARCH LA English DT Article ID DNA TOPOISOMERASE-I; MAMMALIAN-CELLS; PROTO-ONCOGENE; TRANSCRIPTIONAL REGULATION; ANTITUMOR-ACTIVITY; GROWTH-FACTORS; PHASE-II; GENE; SEQUENCE; CYCLE AB We have recently demonstrated that certain camptothecin derivatives are effective agents in the treatment of human tumor xenografts in nude mice. While camptothecin and its derivatives are recognized as inhibitors of topoisomerase I, little is known about the effects of these agents on specific gene expression, particularly genes involved in growth control. The c-jun early response gene codes for a leucine zipper transcription factor. The present studies demonstrate that 20(S)-camptothecin, 9-amino-20(S)-camptothecin, and 9-nitro-20(S)-camptothecin inhibit the growth of human U-937 myeloid leukemia cells and induce expression of the c-jun gene. c-jun transcripts were increased at 3 h and reached a maximum at 6 h of drug exposure. We also demonstrate that the induction of c-jun gene expression by these agents occurs at the transcriptional level. H7, a nonselective inhibitor of protein kinase C, completely blocked c-jun expression in 20(S)-camptothecin-treated cells, while another protein kinase inhibitor, HA1004, had no detectable effect. Similar findings were obtained for other leucine zipper encoding genes, including jun-B. These results suggest that 20(S)-camptothecin, 9-amino-20(S)-camptothecin, and 9-nitro-20(S)-camptothecin activate a cellular response involving the induction of early response genes. Finally, we demonstrate that induction of c-jun expression occurs in association with internucleosomal DNA fragmentation, a characteristic of programmed cell death. C1 ST JOSEPH HOSP,STEHLIN FDN CANC RES,CANC RES LAB,HOUSTON,TX 77002. RP KHARBANDA, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01CA50529, CA42802] NR 55 TC 80 Z9 80 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 15 PY 1991 VL 51 IS 24 BP 6636 EP 6642 PG 7 WC Oncology SC Oncology GA GU416 UT WOS:A1991GU41600023 PM 1742737 ER PT J AU KISHIMOTO, E HAY, DI GIBBONS, RJ AF KISHIMOTO, E HAY, DI GIBBONS, RJ TI INHIBITION OF ADHESION-PROMOTING ACTIVITY OF A HUMAN SALIVARY PROTEIN WHICH PROMOTES ADHESION OF STREPTOCOCCUS-MUTANS JBP TO HYDROXYAPATITE SO FEMS MICROBIOLOGY LETTERS LA English DT Article DE ADHESION-PROMOTING PROTEIN; AMINE; BACTERIAL ADHESION; INHIBITION; PELLICLE; SUBMANDIBULAR-SUBLINGUAL SALIVA; STREPTOCOCCUS-MUTANS JBP ID SEROTYPE-C STRAINS; ADSORPTION AB The adhesion-promoting proteins (APP) (molecular mass approx. 300 kDa), which promote adhesion of Streptococcus mutans JBP (serotype c) to hydroxyapatite, were isolated from human submandibular-sublingual (SMSL) saliva by gel filtration on a Trisacryl GP2000 M column. The effects of hexoses, pentoses, methyl-pentoses, hexosamines, N-acetylhexosamines, a basic amino acid, polyamines and ammonium chloride on the bacterial adhesion-promoting activity of the APP were examined. Galactosamine, mannosamine, L-lysine, spermine, putrescine, and ammonium chloride inhibited the adhesion-promoting activities of the APP. The other sugars, including the N-acetylhexosamines, were without effect. Thus, compounds containing a primary amino-group appear to have a specific inhibitory effect on adhesion of S. mutans JBP to APP adsorbed onto hydroxyapatite, an activity which is lost if the amino-group is acetylated. C1 FORSYTH DENT CTR,DEPT BIOCHEM,BOSTON,MA 02115. FORSYTH DENT CTR,DEPT MICROBIOL,BOSTON,MA 02115. RP KISHIMOTO, E (reprint author), OKAYAMA UNIV,SCH DENT,DEPT PREVENT DENT,2-5-1 SHIKATA CHO,OKAYAMA 700,JAPAN. NR 11 TC 10 Z9 10 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1097 J9 FEMS MICROBIOL LETT JI FEMS Microbiol. Lett. PD DEC 15 PY 1991 VL 90 IS 1 BP 19 EP 22 DI 10.1016/0378-1097(91)90639-R PG 4 WC Microbiology SC Microbiology GA GX351 UT WOS:A1991GX35100004 ER PT J AU RUBIN, D LAPOSATA, M AF RUBIN, D LAPOSATA, M TI REGULATION OF AGONIST-INDUCED PROSTAGLANDIN-E1 VERSUS PROSTAGLANDIN-E2 PRODUCTION - A MASS ANALYSIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GAMMA-LINOLENIC ACID; UNSATURATED FATTY-ACIDS; RAT-LIVER MICROSOMES; CANINE KIDNEY-CELLS; ARACHIDONIC-ACID; HUMAN-PLATELETS; PROLONGED SURVIVAL; ENDOTHELIAL-CELLS; MAMMALIAN-CELLS; COA SYNTHETASE AB Prostaglandin E1 (PGE1) and prostaglandin E2 (PGE2), derived by enzymatic oxidation of cellular dihomogammalinolenic acid (DHLA) and arachidonic acid (AA), respectively, have diverse and, at times, distinct biological actions. It has been suggested that PGE, specifically inhibits a variety of inflammatory processes, and, in light of the potential therapeutic benefit of PGE1 and its fatty acid precursor in inflammatory disorders, there is growing interest in the biochemical mechanisms which determine the balance between PGE1 and PGE2 synthesis. Metabolic studies in this area have been hampered by the difficulties in measuring the extremely small masses of these prostaglandins which are generated in cell culture systems. We studied the regulation of PGE1 versus PGE2 synthesis using an essential fatty acid-deficient, PGE-producing, mouse fibrosarcoma cell line, EFD-1. Because EFD-1 cells contain no endogenous AA or DHLA, we were able to replete the cells with AA and DHLA of known specific activities; thus, the mass of both cellular AA and DHLA, and synthesized PGE1 and PGE2, could be accurately determined. The major finding of this study is that production of PGE2 was highly favored over production of PGE1 due to preferential incorporation of AA versus DHLA into, and release from, the total cellular phospholipid pool. Further, we correlated the selective release of AA versus DHLA from total cellular phospholipids with the selective incorporation of AA versus DHLA into specific phospholipid pools. In addition, we showed that conversion of DHLA to AA by DELTA-5 desaturase was enhanced by increasing the cellular mass of n - 6 fatty acids and by increasing the cell proliferative activity. Together, these results indicate that the relative abundance of PGE2 versus PGE1 in vivo is not merely a function of the relative abundance of AA versus DHLA in tissues, but also relates to markedly different cellular metabolism of these two fatty acids. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RUBIN, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 43159] NR 57 TC 16 Z9 16 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 15 PY 1991 VL 266 IS 35 BP 23618 EP 23623 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GV319 UT WOS:A1991GV31900018 PM 1748640 ER PT J AU KANSAS, GS TEDDER, TF AF KANSAS, GS TEDDER, TF TI TRANSMEMBRANE SIGNALS GENERATED THROUGH MHC CLASS-II, CD19, CD20, CD39, AND CD40 ANTIGENS INDUCE LFA-1-DEPENDENT AND INDEPENDENT ADHESION IN HUMAN B-CELLS THROUGH A TYROSINE KINASE-DEPENDENT PATHWAY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ROUS-SARCOMA VIRUS; HUMAN LYMPHOCYTE-B; PROTEIN-KINASE; MONOCLONAL-ANTIBODIES; SURFACE-ANTIGEN; HOMOTYPIC ADHESION; REGULATORY ROLE; HUMAN-PLATELETS; T-CELLS; AGGREGATION AB Transmembrane signals generated following mAb binding to CD19, CD20, CD39, CD40, CD43, Leu-13 Ag, and HLA-D region gene products induced rapid and strong homotypic adhesion in a panel of human B cell lines. Lower levels of adhesion were also observed after engagement of CD21, CD22, and CD23. Adhesion induced by mAb binding to these Ag was identical with respect to the kinetics of adhesion and the morphology of the resulting cellular aggregates, and was distinct from PMA-induced adhesion in both of these properties. Adhesion was not observed in response to mAb binding to MHC class I, CD24, CD38, CD44, CD45RA, or CD72. In contrast to B cell lines, homotypic adhesion was not induced in two pre-B cell lines, in spite of their high level expression of CD19 and HLA-D. Adhesion induced by suboptimal stimulation through these surface Ag or by PMA was mediated primarily through LFA-1 and ICAM-1. However, optimal stimulation through CD19, CD20, CD39, CD40, and HLA-D induced strong homotypic adhesion that was not blocked by anti-LFA-1 mAb. This alternate pathway of adhesion was also observed in LFA-1-deficient cell lines and in the presence of EDTA, suggesting that adhesion was not mediated by integrins. Adhesion in response to engagement of cell-surface Ag was unaffected by H7 or genestein, but was significantly inhibited by staurosporine, and was completely ablated by sphingosine and herbimycin. These studies indicate that engagement of multiple B cell-surface molecules initiates a signal transduction cascade that involves tyrosine kinases but not protein kinase C, and which leads to homotypic adhesion. Furthermore, adhesion was mediated by at least two distinct cell-surface adhesion receptors: LFA-1/ICAM-1 and a heretofore unknown adhesion receptor. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP KANSAS, GS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-26872] NR 54 TC 228 Z9 228 U1 0 U2 4 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD DEC 15 PY 1991 VL 147 IS 12 BP 4094 EP 4102 PG 9 WC Immunology SC Immunology GA GW031 UT WOS:A1991GW03100008 PM 1721639 ER PT J AU AKSENTIJEVICH, I SACHS, DH SYKES, M AF AKSENTIJEVICH, I SACHS, DH SYKES, M TI NATURAL ANTIBODIES CAN INHIBIT BONE-MARROW ENGRAFTMENT IN THE RAT-]MOUSE SPECIES COMBINATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NONLETHAL PREPARATIVE REGIMEN; T-CELL DEPLETION; MONOCLONAL-ANTIBODIES; IMMUNE-DEFICIENCY; RAT LYMPHOCYTES; GRAFT-REJECTION; MICE; TOLERANCE; CHIMERISM; SKIN AB Specific tolerance can be induced in animals by transplanting hemopoietic cells across concordant species barriers. Despite the fact that the rat-mouse species combination is considered concordant, we have recently demonstrated that normal murine serum contains natural antibodies (nAb), predominantly of the IgM and IgG3 subclasses, with markedly greater binding to rat bone marrow cells (BMC) than to rat splenocytes or thymocytes. Since much greater numbers of rat BMC than of allogeneic murine BMC are required to achieve engraftment in mice, we considered the possibility that these nAbs might be responsible, and that the increased numbers of BMC might be required to absorb these nAb. To evaluate the effect of these nAb on engraftment of rat BMC in mice, we have now performed adoptive transfer studies using T and B cell-deficient severe combined immunodeficiency disease (SCID) mice as recipients. Administration of as few as 5 x 10(5) T cell-depleted rat BMC led to induction of stable xenochimerism in SCID mice conditioned with 4-Gy whole body irradiation. Rat T cells developed after a delay of several weeks, and conferred the ability to reject non-donor-type rat skin grafts, whereas donor-type grafts were accepted. Adoptive transfer of 4 ml of normal BALB/c serum led to a marked reduction in the level of rat chimerism in SCID recipients of 2 x 10(6) F344 BMC. The ability of sera to inhibit engraftment of rat BMC correlated with their cytotoxic nAb content, and the inhibitory effect of highly cytotoxic sera could be overcome by administration of large numbers of rat BMC. Thus, normal mouse serum has a limited ability to hinder engraftment of rat BMC, and this degree of resistance can be overcome by adsorption when large numbers of BMC are administered. Eliminating nAb from serum may be more difficult in discordant species combinations in recipients with functional B cells, but may likewise permit the use of BMT as a means of inducing transplantation tolerance. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. NR 42 TC 36 Z9 36 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD DEC 15 PY 1991 VL 147 IS 12 BP 4140 EP 4146 PG 7 WC Immunology SC Immunology GA GW031 UT WOS:A1991GW03100014 PM 1753089 ER PT J AU VIVIER, E ROCHET, N KOCHAN, JP PRESKY, DH SCHLOSSMAN, SF ANDERSON, P AF VIVIER, E ROCHET, N KOCHAN, JP PRESKY, DH SCHLOSSMAN, SF ANDERSON, P TI STRUCTURAL SIMILARITY BETWEEN FC-RECEPTORS AND T-CELL RECEPTORS - EXPRESSION OF THE GAMMA-SUBUNIT OF FC-EPSILON-RI IN HUMAN T-CELLS, NATURAL-KILLER-CELLS AND THYMOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID AFFINITY IGE RECEPTOR; ZETA-CHAIN; ANTIGEN RECEPTOR; TYROSINE PHOSPHORYLATION; MOLECULAR-CLONING; LYMPHOCYTES-T; ACTIVATION; COMPLEX; CD16; ANTIBODY AB The TCR complex is composed of a clonotypic heterodimer (Ti-alpha:beta or gamma:delta) noncovalently associated with the CD3 complex (gamma, delta, and epsilon), and with one or more disulfide-linked dimers whose components are designated-zeta and eta. Zeta and eta are alternative transcripts of a common gene and are structurally related to the gamma-subunit of the FcR for IgE expressed on mast cells and basophils (Fc-epsilon-RI). Recent evidence suggests that gamma can also be expressed in natural killer cells and in a murine cytotoxic T cell line, CTLL. Because zeta, eta, and gamma have the potential to join together to form disulfide linked homo- and heterodimers, it has been postulated that alternative dimeric forms composed of these zeta-related subunits might subserve unique signal transducing functions in hematopoietic cells. We have used mAb reactive with zeta and gamma to systematically examine the expression of these zeta-related dimers in human T cells, NK cells, and thymocytes. Our results show that each cell type expresses characteristic combinations of zeta-related homo- and hetero-dimers, and are therefore consistent with the possibility that these subunits contribute to the functional heterogeneity of lymphocyte subsets. C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL, 44 BINNEY ST, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT RHEUMATOL & IMMUNOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. HOFFMANN LA ROCHE INC, ROCHE RES CTR, NUTLEY, NJ 07110 USA. NR 48 TC 80 Z9 80 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 EI 1550-6606 J9 J IMMUNOL JI J. Immunol. PD DEC 15 PY 1991 VL 147 IS 12 BP 4263 EP 4270 PG 8 WC Immunology SC Immunology GA GW031 UT WOS:A1991GW03100032 PM 1836482 ER PT J AU BLUM, HE AF BLUM, HE TI LIVER-BIOPSY SO DEUTSCHE MEDIZINISCHE WOCHENSCHRIFT LA German DT Letter RP BLUM, HE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,149 13TH ST,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0012-0472 J9 DEUT MED WOCHENSCHR JI Dtsch. Med. Wochenschr. PD DEC 13 PY 1991 VL 116 IS 50 BP 1933 EP 1933 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HJ039 UT WOS:A1991HJ03900008 PM 1748073 ER PT J AU KAJIWARA, K HAHN, LB MUKAI, S TRAVIS, GH BERSON, EL DRYJA, TP AF KAJIWARA, K HAHN, LB MUKAI, S TRAVIS, GH BERSON, EL DRYJA, TP TI MUTATIONS IN THE HUMAN RETINAL DEGENERATION SLOW GENE IN AUTOSOMAL DOMINANT RETINITIS-PIGMENTOSA SO NATURE LA English DT Article ID RHODOPSIN GENE; RDS; MICE AB THE murine retinal degeneration slow (rds) gene is a semidominant mutation with a phenotype having rod and cone photoreceptors that develop abnormally and then slowly degenerate 1-3. The phenotype is a possible model for retinitis pigmentosa, one of the scores of hereditary human retinal degenerations, which is also characterized by photoreceptor degeneration. We report here three mutations of the human homologue of the rds gene (RDS) that cosegregate with autosomal dominant retinitis pigmentosa in separate families. Our results indicate that some cases of autosomal dominant retinitis pigmentosa are due to mutations at the RDS locus. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. UNIV TEXAS,SW MED CTR,DEPT PSYCHIAT,DALLAS,TX 75237. RP DRYJA, TP (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 19 TC 354 Z9 361 U1 1 U2 6 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD DEC 12 PY 1991 VL 354 IS 6353 BP 480 EP 483 DI 10.1038/354480a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GV078 UT WOS:A1991GV07800061 PM 1684223 ER PT J AU LEIFER, D SOBEL, RA SHAHANI, B FERRUCCI, JT PLATIKA, D AF LEIFER, D SOBEL, RA SHAHANI, B FERRUCCI, JT PLATIKA, D TI A 71-YEAR-OLD WOMAN WITH A SENSORIMOTOR NEUROPATHY AND RADIOGRAPHICALLY DEMONSTRABLE ABNORMALITIES - MIXED INFLAMMATORY DEMYELINATING AND AXONAL SENSORIMOTOR PERIPHERAL NEUROPATHY (QUESTIONABLE PARANEOPLASTIC, QUESTIONABLE MULTIFACTORIAL) - NEUROGENIC ATROPHY OF SKELETAL-MUSCLE, SEVERE - RENAL-CELL CARCINOMA, CLEAR-CELL TYPE - (DIABETES-MELLITUS, TYPE-II) (HYPOTHYROIDISM) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID IDIOPATHIC HYPEREOSINOPHILIC SYNDROME; SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTINUCLEAR ANTIBODIES; THERAPEUTIC CONSIDERATIONS; VASCULITIS; DISEASE; POLYNEUROPATHY; EOSINOPHILIA; PATIENT; NERVE C1 MASSACHUSETTS GEN HOSP,NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEIFER, D (reprint author), CHILDRENS HOSP MED CTR,NEUROL,BOSTON,MA 02115, USA. NR 108 TC 7 Z9 7 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 DEC 12 PY 1991 VL 325 IS 24 BP 1723 EP 1735 PG 13 WC Medicine, General & Internal SC General & Internal Medicine GA GU418 UT WOS:A1991GU41800008 ER PT J AU RIGOTTI, NA PASHOS, CL AF RIGOTTI, NA PASHOS, CL TI NO-SMOKING LAWS IN THE UNITED-STATES - AN ANALYSIS OF STATE AND CITY ACTIONS TO LIMIT SMOKING IN PUBLIC PLACES AND WORKPLACES SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID NONSMOKERS AB Objective. - To assess the prevalence, content, and growth of state and city laws restricting smoking in public places and workplaces in the United States and to identify factors associated with their passage. Design. - A mailed survey of city clerks in US cities with a population of 25 000 or greater (N = 980) and review of existing data sources confirmed the status of smoking restrictions in 902 (92%) of the cities in the sample. State laws were identified by contacting each state's Legislative Reference Bureau (100% response). Content of laws was coded using previously developed categories. Main Outcome Measures. - Prevalence, comprehensiveness, and cumulative incidence of no-smoking laws in states and in cities with a population of 25 000 or greater. Results. - By July 1989, 44 states and 500 (51%) of the cities in our sample had adopted some smoking restriction, but content varied widely. While 42% of cities limited smoking in government buildings, 27% in public places, 24% in restaurants, and 18% in private workplaces, only 17% of cities and 20% of states had comprehensive laws restricting smoking in all four of these sites. The number of city no-smoking laws increased tenfold from 1980 to 1989. City no-smoking laws were independently associated with population size, geography, state tobacco production, and adult smoking prevalence. Laws were more common in larger cities, Western cities, and states with fewer adult smokers. Laws were less common in tobacco-producing states and in the South. Conclusions. - No-smoking laws are more widespread than previously appreciated, especially at the local level, reflecting a rapid pace of city government action in the 1980s. Nonetheless, comprehensive laws, which are most likely to provide meaningful protection from environmental tobacco smoke exposure, remain uncommon and represent a major gap in smoking control policy. Laws are most needed in smaller and non-Western cities and in states that produce tobacco and have a higher proportion of smokers. C1 HARVARD UNIV,JOHN F KENNEDY SCH GOVT,INST STUDY SMOKING BEHAV & POLICY,CAMBRIDGE,MA 02138. RP RIGOTTI, NA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN INTERNAL MED UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [1-RO3-CA48386-01] NR 22 TC 41 Z9 41 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD DEC 11 PY 1991 VL 266 IS 22 BP 3162 EP 3167 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GT654 UT WOS:A1991GT65400026 PM 1956105 ER PT J AU BAXENDALE, S BATES, GP MACDONALD, ME GUSELLA, JF LEHRACH, H AF BAXENDALE, S BATES, GP MACDONALD, ME GUSELLA, JF LEHRACH, H TI THE DIRECT SCREENING OF COSMID LIBRARIES WITH YAC CLONES SO NUCLEIC ACIDS RESEARCH LA English DT Note ID DNA SEGMENT C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. RP BAXENDALE, S (reprint author), IMPERIAL CANC RES FUND,GENOME ANAL LAB,POB 123,LINCOLNS INN FIELDS,LONDON WC2A 3PX,ENGLAND. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 NR 7 TC 48 Z9 48 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD DEC 11 PY 1991 VL 19 IS 23 BP 6651 EP 6651 DI 10.1093/nar/19.23.6651 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GV816 UT WOS:A1991GV81600053 PM 1754409 ER PT J AU AYASH, L KORBUT, T HERMAN, TS TEICHER, BA AF AYASH, L KORBUT, T HERMAN, TS TEICHER, BA TI COMBINATION OF THE MINOR GROOVE-BINDER U73-975 OR THE INTERCALATOR MITOXANTRONE WITH ANTITUMOR ALKYLATING-AGENTS IN MCF-7 OR MCF-7/CP CELLS SO CANCER LETTERS LA English DT Article DE U73-975; MINOR GROOVE BINDERS; COMBINATION CHEMOTHERAPY AND MODULATION; ALKYLATING AGENT ID CLINICAL CORRELATION; CARCINOMA-CELLS; TUMOR-CELL; RESISTANT; CC-1065; DNA; RHODAMINE-123; TOXICITY; BINDING; INVITRO AB In an effort to improve the cytotoxicity of clinically used anticancer alkylating agents, the topoisomerase II inhibitory drugs U73-975 or mitoxantrone were added to cell cultures exposed to CDDP, carboplatin, BCNU, melphalan or thiotepa. In the MCF-7 human breast cancer cell line and in the MCF-7/CP (CDDP resistant) subline, U73-975 and mitoxantrone were both potent cytotoxic agents (IC50 0.002-mu-M and 0.006-mu-M for U73-975, respectively and 0.8-mu-M and 0.1-mu-M for mitoxantrone, respectively). As evaluated by isobologram analysis, the addition of either U73-975 or mitoxantrone to 1 h exposure to CDDP resulted in greater-than-additive killing in the MCF-7 parent cells. While U73-975 was also greater-than-additive in cytotoxicity with CDDP in the MCF-7/CP line, mitoxantrone and CDDP were only additive in cytotoxicity in these cells. In the case of carboplatin, the addition of U73-975 or mitoxantrone to treatment with the drug resulted in greater-than-additive cell killing in the MCF-7 parental cell line but in the MCF-7/CP cell line these combinations were only additive in cell killing. Addition of U73-975 to treatment with BCNU resulted in only additive cytotoxicity in both cell lines; however, the combination of mitoxantrone with BCNU resulted in greater-than-additive cell killing in both the parental and CDDP resistant cell lines. When either U73-975 or mitoxantrone was added to treatment with melphalan greater-than-additive cytotoxicity resulted in both cell lines except at low melphalan concentrations in the MCF-7/CP cell line. Finally, the addition of either modulator to treatment with thiotepa in the MCF-7 cell line produced variable interactions depending on thiotepa concentration, but in the MCF-7/CP cell line either modulator in combination with thiotepa caused greater-than-additive cell killing. These results indicate that the addition of topoisomerase II inhibitory drugs may substantially increase the cytotoxicity of some alkylating agents. In vivo experiments are necessary, however, to ascertain whether a therapeutic gain is achievable. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. FU NCI NIH HHS [P01-CA38493] NR 28 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD DEC 9 PY 1991 VL 61 IS 1 BP 7 EP 14 DI 10.1016/0304-3835(91)90070-X PG 8 WC Oncology SC Oncology GA GZ750 UT WOS:A1991GZ75000002 PM 1764699 ER PT J AU THOMAS, LJ DEGASPERI, R SUGIYAMA, E CHANG, HM BECK, PJ ORLEAN, P URAKAZE, M KAMITANI, T SAMBROOK, JF WARREN, CD YEH, ETH AF THOMAS, LJ DEGASPERI, R SUGIYAMA, E CHANG, HM BECK, PJ ORLEAN, P URAKAZE, M KAMITANI, T SAMBROOK, JF WARREN, CD YEH, ETH TI FUNCTIONAL-ANALYSIS OF T-CELL MUTANTS DEFECTIVE IN THE BIOSYNTHESIS OF GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR - RELATIVE IMPORTANCE OF GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR VERSUS N-LINKED GLYCOSYLATION IN T-CELL ACTIVATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOUSE LYMPHOMA-CELLS; HAMSTER OVARY CELLS; ANTIGEN RECEPTOR; PHOSPHATIDYLINOSITOL ANCHOR; GLUCOSE STARVATION; LYMPHOCYTES-T; GROWTH-FACTOR; OLIGOSACCHARIDES; PROTEINS; COMPLEX AB The glycosylphosphatidylinositol (GPI) anchor, potentially capable of generating a number of second messengers, such as diacylglycerol, phosphatidic acid, and inositol phosphate glycan, has been postulated to be involved in signal transduction in various cell types, including T-cells. We have identified a panel of T-cell hybridoma mutants that are defective at various steps of GPI anchor biosynthesis. Since they were derived from a functional T-T hybridoma, we were able to determine the precise role of the GPI anchor in T-cell activation. Two mutants were chosen for this analysis. The first mutant is defective at the first step of GPI anchor biosynthesis, i.e. in the transfer of N-acetylglucosamine to a phosphatidylinositol acceptor. Thus, it cannot form any GPI precursors or GPI-like compounds. Interestingly, this mutant can be activated by antigen, superantigen, and concanavalin A in a manner comparable to the wild-type hybridoma. These data strongly suggest that the GPI anchor, its precursor, or its potential cleavage product, inositol phosphate glycan, is not required for the early phase of T-cell activation. The second mutant is able to synthesize the first two GPI precursors, but is not able to add mannose residues to them due to a deficiency in dolichol-phosphate-mannose (Dol-P-Man) biosynthesis. Unexpectedly, all of the Dol-P-Man mutants are defective in activation by antigen, superantigen, and concanavalin A despite normal T-cell receptor expression. Here, we show that the activation defect was due to a pleiotropic glycosylation abnormality because Dol-P-Man is required for both GPI anchor and N-linked oligosaccharide biosynthesis. When the yeast Dol-P-Man synthase gene was stably transfected into the mutants, full expression of surface GPI-anchored proteins was restored. However, N-linked glycosylation was either partially or completely corrected in different transfectants. Reconstitution of activation defects correlates well with the status of N-linked glycosylation, but not with the expression of GPI-anchored proteins. These results thus reveal an unexpected role of N-linked glycosylation in T-cell activation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,PAIN CONTROL UNIT,BOSTON,MA 02114. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. UNIV ILLINOIS,DEPT BIOCHEM,URBANA,IL 61801. FU NHLBI NIH HHS [HL-45851]; NIAMS NIH HHS [AR-03564]; NICHD NIH HHS [HD-21087] NR 60 TC 29 Z9 29 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 5 PY 1991 VL 266 IS 34 BP 23175 EP 23184 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GT483 UT WOS:A1991GT48300063 PM 1835975 ER PT J AU OLIVER, FJ DELARUBIA, G FEENER, EP LEE, ME LOEKEN, MR SHIBA, T QUERTERMOUS, T KING, GL AF OLIVER, FJ DELARUBIA, G FEENER, EP LEE, ME LOEKEN, MR SHIBA, T QUERTERMOUS, T KING, GL TI STIMULATION OF ENDOTHELIN-1 GENE-EXPRESSION BY INSULIN IN ENDOTHELIAL-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE GENE; PROTEIN-KINASE-C; MESSENGER-RNA; SEQUENCE; BINDING; PROMOTER; TRANSCRIPTION; RECEPTORS AB The present study characterized the regulation of the genetic expression of the vasoactive peptide endothelin-1 (ET-1) by insulin in bovine aortic endothelial cells. By RNA blot analysis, insulin (1.67 x 10(-8) M) increased ET-1 mRNA levels by 2.3-fold over the basal within 10 min and attained a maximum (5.3-fold increase) in 2 h. Dose-response studies showed that a maximum effect of insulin was reached at 1.67 x 10(-8) M although a significant increase can be observed at 1.66 x 10(-9) M. Radioligand receptor studies indicated that the affinity constant for insulin receptors on endothelial cells correlated closely with the dose response observed for ET-1 mRNA. The ET-1 mRNA half-life was estimated with actinomycin D studies to be 20 min in control cells and was not affected by insulin treatment. Moreover, the effects of phorbol 12-myristate 13-acetate (PMA) and insulin were additive in the induction of ET-1 gene expression. When protein kinase C in the bovine aortic endothelial cells was down-regulated by preincubation with 8 x 10(-7) M PMA for 24 or 48 h, insulin was still able to increase ET-1 mRNA levels whereas PMA was ineffective. Using a chloramphenicol acetyltransferase (CAT) fusion plasmid containing the CAT gene and the 5'-flanking region of the ET-1 gene (Lee, M. E., Bloch, K. D., Clifford, J. A., and Quertermous, T. (1990) J. Biol. Chem. 265, 10446-10450), we observed that 1.67 x 10(-8) M insulin increased CAT enzyme activity and mRNA levels. The insulin dose-response curve observed for CAT activity correlated with that observed for ET-1 mRNA levels. These results suggest that insulin stimulates expression of the ET-1 gene at the transcriptional level via its own receptors. This effect is mediated mostly through a protein kinase C-independent pathway, suggesting the existence of an insulin-responsive element in the ET-1 gene 5'-flanking sequence. C1 JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. FU NEI NIH HHS [EY0-5110]; NIDDK NIH HHS [DK36836, P30 DK036836] NR 36 TC 193 Z9 196 U1 0 U2 2 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 5 PY 1991 VL 266 IS 34 BP 23251 EP 23256 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GT483 UT WOS:A1991GT48300072 PM 1744120 ER PT J AU SPRINGER, TA AF SPRINGER, TA TI THE NEXT CLUSTER OF DIFFERENTIATION (CD) WORKSHOP SO NATURE LA English DT Article RP SPRINGER, TA (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 6 TC 0 Z9 1 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD DEC 5 PY 1991 VL 354 IS 6352 BP 415 EP 416 DI 10.1038/354415a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA GT761 UT WOS:A1991GT76100058 PM 1956408 ER PT J AU WANG, CC AF WANG, CC TI TREATMENT OF ADVANCED LARYNGEAL CARCINOMA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP WANG, CC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD DEC 5 PY 1991 VL 325 IS 23 BP 1656 EP 1657 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA GR770 UT WOS:A1991GR77000026 ER PT J AU HYMAN, BT ARRIAGADA, PV VANHOESEN, GW AF HYMAN, BT ARRIAGADA, PV VANHOESEN, GW TI PATHOLOGICAL-CHANGES IN THE OLFACTORY SYSTEM IN AGING AND ALZHEIMERS-DISEASE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID TOPOGRAPHIC DISTRIBUTION; NEUROFIBRILLARY TANGLES; RAT; CORTEX; BULB; IDENTIFICATION; PROJECTIONS; DEMENTIA; NEURONS; NOSE C1 MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. UNIV IOWA, DEPT ANAT, IOWA CITY, IA 52242 USA. RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. NR 28 TC 6 Z9 6 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD DEC 3 PY 1991 VL 640 BP 14 EP 19 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM812 UT WOS:A1991JM81200003 ER PT J AU CRONINGOLOMB, A RIZZO, JF CORKIN, S GROWDON, JH AF CRONINGOLOMB, A RIZZO, JF CORKIN, S GROWDON, JH TI VISUAL FUNCTION IN ALZHEIMERS-DISEASE AND NORMAL AGING SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID DEGENERATION C1 MASSACHUSETTS EYE & EAR INFIRM, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. MIT, CTR CLIN RES, CAMBRIDGE, MA 02139 USA. MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. RP CRONINGOLOMB, A (reprint author), BOSTON UNIV, DEPT PSYCHOL, BOSTON, MA 02115 USA. NR 13 TC 1 Z9 1 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD DEC 3 PY 1991 VL 640 BP 28 EP 35 PG 8 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM812 UT WOS:A1991JM81200005 ER PT J AU NITSCH, R PITTAS, A BLUSZTAJN, JK SLACK, BE GROWDON, JH WURTMAN, RJ AF NITSCH, R PITTAS, A BLUSZTAJN, JK SLACK, BE GROWDON, JH WURTMAN, RJ TI ALTERATIONS OF PHOSPHOLIPID METABOLITES IN POSTMORTEM BRAIN FROM PATIENTS WITH ALZHEIMERS-DISEASE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID ACETYLCHOLINE C1 MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. BOSTON UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02118 USA. RP NITSCH, R (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT NEUROL, BOSTON, MA 02114 USA. NR 10 TC 5 Z9 5 U1 0 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD DEC 3 PY 1991 VL 640 BP 110 EP 113 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM812 UT WOS:A1991JM81200019 ER PT J AU TANZI, RE HYMAN, BT AF TANZI, RE HYMAN, BT TI STUDIES OF AMYLOID BETA-PROTEIN PRECURSOR EXPRESSION IN ALZHEIMERS-DISEASE SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MESSENGER-RNA; HUMAN-BRAIN; DIFFERENTIAL EXPRESSION; NEXIN-II; GENE; LOCALIZATION; DOMAIN; CDNA C1 MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02114 USA. RP TANZI, RE (reprint author), MASSACHUSETTS GEN HOSP, EXPTL NEUROPATHOL LAB, BOSTON, MA 02114 USA. NR 31 TC 0 Z9 0 U1 1 U2 1 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD DEC 3 PY 1991 VL 640 BP 149 EP 154 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM812 UT WOS:A1991JM81200026 ER PT J AU BERNSTEIN, SH KHARBANDA, SM SHERMAN, ML STONE, RM KUFE, DW AF BERNSTEIN, SH KHARBANDA, SM SHERMAN, ML STONE, RM KUFE, DW TI INHIBITION OF PROTEIN-KINASE-C IS ASSOCIATED WITH A DECREASE IN C-MYC EXPRESSION IN HUMAN MYELOID-LEUKEMIA CELLS SO FEBS LETTERS LA English DT Article DE PROTEIN KINASE-C; C-MYC ID MURINE ERYTHROLEUKEMIA-CELLS; MONOCYTIC DIFFERENTIATION; POTENT INHIBITOR; GROWTH-FACTOR; INDUCTION; ONCOGENE; HL-60; GENE; SANGIVAMYCIN; JUN AB Treatment of human myeloid leukemic cells with phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with activation and then partial down-regulation of protein kinase C activity. Previous work has suggested that the activation of protein kinase C by TPA contributes to the decrease in c-myc expression during differentiation of these cells. The present studies demonstrate that the decline in c-myc mRNA levels following exposure of HL-60 cells to TPA is preceded by an increase in expression of this gene. In contrast, exposure of HL-60 cells to inhibitors of protein kinase C activity is associated with down-modulation of c-myc expression. Similar findings have been obtained in U-937 myeloid leukemia cells. Taken together, these findings suggest that phorbol esters have a biphasic effect on c-myc expression. Whereas the activation of protein kinase C by phorbol esters may be associated with an increase in c-myc gene expression, the subsequent partial down-regulation of kinase activity may initiate a cascade of events resulting in the down-modulation of c-myc expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA42802, K08CA01092] NR 28 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD DEC 2 PY 1991 VL 294 IS 1-2 BP 73 EP 76 DI 10.1016/0014-5793(91)81346-A PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA GV806 UT WOS:A1991GV80600018 PM 1743296 ER PT J AU MEHTA, MC KATSUMI, O SHIH, VE HIROSE, T AF MEHTA, MC KATSUMI, O SHIH, VE HIROSE, T TI GYRATE ATROPHY OF THE CHOROID AND RETINA IN A 5-YEAR-OLD GIRL SO ACTA OPHTHALMOLOGICA LA English DT Article DE COBBLESTONE LESIONS; ELECTROPHYSIOLOGY; GYRATE ATROPHY; ORNITHINE; VITAMIN-B6 ID PLASMA-ORNITHINE; VITAMIN-B6; TRIAL AB A 5-year-old Asian-Indian female presented with bilateral cobblestone-like peripheral lesions, a single area of chorioretinal atrophy, infero-nasal to the disc, in her right eye and a non-recordable single flash ERG. Serum ornithine level was assayed at 841-mu-mol/l, ten times normal levels, and a diagnosis of gyrate atrophy, due to ornithine aminotransferase deficiency was made. The patient was refractory to any form of therapy and her clinical lesions spread rapidly in both eyes, showing both centrifugal and centripetal spread in her right eye. A rapid deterioration in her psychophysical tests was also seen over the 28 months follow-up. The presence of cobblestone-like peripheral lesions in a child should alert the clinician to the possibility of gyrate atrophy, and the rapid spread of the chorioretinal lesions coupled with non-recordable single flash ERGs, in a young patient may suggest a much poorer prognosis. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,EYE RES INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,RETINA ASSOCIATES INC,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,AMINO ACID DISORDER LAB,BOSTON,MA 02114. FU NINDS NIH HHS [NS 05096] NR 7 TC 1 Z9 1 U1 0 U2 0 PU ARHUS UNIV HOSPITAL PI AARHUS PA DEPT OHPTHALMOLOGY, DK-8000 AARHUS, DENMARK SN 0001-639X J9 ACTA OPHTHALMOL PD DEC PY 1991 VL 69 IS 6 BP 810 EP 814 PG 5 WC Ophthalmology SC Ophthalmology GA GW119 UT WOS:A1991GW11900023 PM 1789102 ER PT J AU HANNA, EZ AF HANNA, EZ TI ATTITUDES TOWARD PROBLEM DRINKERS, REVISITED - PATIENT-THERAPIST FACTORS CONTRIBUTING TO THE DIFFERENTIAL TREATMENT OF PATIENTS WITH ALCOHOL-PROBLEMS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE PROBLEM DRINKER; STEREOTYPE; ATTITUDES; TREATMENT ID RESIDENTS; DIAGNOSIS AB Although there are many treatment alternatives open to people with drinking problems, health professionals still exhibit negative attitudes towards alcoholics. In a previous study, the author demonstrated that those patients who were self-labelled alcoholics were treated in a less preferential manner than those who did not identify as such. This study used both overt and unobtrusive measures to determine whether negative attitudes of intake interviewers towards problem drinkers were elicited by the patient's self-label as an alcoholic or by other variables related to perceived treatment outcome. Pre- and postinterview data on patient likability, doctor's eagerness to work with the patient, interview content, treatment disposition, and patient compliance were collected from first-time patients, and from their interviewers, in the walk-in psychiatry and alcohol treatment units of a large, urban teaching hospital. The results elucidate how stereotypes interact with patient characteristics to influence both professional behavior and patient compliance. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP HANNA, EZ (reprint author), NIAAA,DIV BIOMETRY & EPIDEMIOL,5600 FISHERS LANE,ROOM 14C-26,ROCKVILLE,MD 20857, USA. NR 17 TC 11 Z9 11 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD DEC PY 1991 VL 15 IS 6 BP 927 EP 931 DI 10.1111/j.1530-0277.1991.tb05190.x PG 5 WC Substance Abuse SC Substance Abuse GA GV648 UT WOS:A1991GV64800005 PM 1665015 ER PT J AU VANDERKOLK, BA VANDERHART, O AF VANDERKOLK, BA VANDERHART, O TI THE INTRUSIVE PAST - THE FLEXIBILITY OF MEMORY AND THE ENGRAVING OF TRAUMA SO AMERICAN IMAGO LA English DT Article C1 INST PSYCHOTRAUMA, UTRECHT, NETHERLANDS. RP VANDERKOLK, BA (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA 02114 USA. NR 82 TC 129 Z9 129 U1 4 U2 11 PU JOHNS HOPKINS UNIV PRESS PI BALTIMORE PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD 21218-4319 SN 0065-860X J9 AM IMAGO JI Am. Imago PD WIN PY 1991 VL 48 IS 4 BP 425 EP 454 PG 30 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA GY779 UT WOS:A1991GY77900002 ER PT J AU BRAVERMAN, AC THOMAS, JD LEE, RT AF BRAVERMAN, AC THOMAS, JD LEE, RT TI DOPPLER ECHOCARDIOGRAPHIC ESTIMATION OF MITRAL-VALVE AREA DURING CHANGING HEMODYNAMIC CONDITIONS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID PRESSURE HALF-TIME; VENTRICULAR COMPLIANCE; AORTIC-INSUFFICIENCY; CONTINUITY EQUATION; STENOSIS; REGURGITATION; GRADIENT; QUANTIFICATION; VALIDATION; SEVERITY AB Patients with mitral stenosis often present during periods of hemodynamic stress such as pregnancy or infections. The Doppler pressure half-time method of mitral valve area (MVA) determination is dependent on the net atrioventricular compliance as well as the peak transmitral gradient. The continuity equation method of MVA determination is based on conservation of mass and may be less sensitive to changes in the hemodynamic state. To test this hypothesis, 17 patients admitted for catheterization with symptomatic mitral stenosis and no more than mild regurgitation underwent Doppler echocardiography at rest and during supine bicycle exercise targeted to an increase in heart rate by 20 to 30 beats/minute. Net atrioventricular compliance was also estimated noninvasively. Cardiac output and transmitral gradient increased significantly during exercise (p < 0.001), while net atrioventricular compliance decreased (p < 0.001). MVA by the pressure half-time method increased significantly during exercise from 1.0 +/- 0.2 to 1.4 +/- 0.4 cm2 (p < 0.001). There was no significant difference in MVA estimation using the continuity equation comparing rest to exercise, with the mean area remaining constant at 0.8 +/- 0.3 cm2 (p = 0.83). Thus, during conditions of changing hemodynamics, the continuity equation method for estimating MVA may be preferable to the pressure half-time method. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,75 FRANCIS ST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-01835] NR 26 TC 47 Z9 47 U1 0 U2 0 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 DEC 1 PY 1991 VL 68 IS 15 BP 1485 EP 1490 DI 10.1016/0002-9149(91)90283-Q PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA GT331 UT WOS:A1991GT33100013 PM 1746431 ER PT J AU CUNNINGHAM, JJ AF CUNNINGHAM, JJ TI BODY-COMPOSITION AS A DETERMINANT OF ENERGY-EXPENDITURE - A SYNTHETIC REVIEW AND A PROPOSED GENERAL PREDICTION EQUATION SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE RESTING ENERGY EXPENDITURE; TOTAL ENERGY EXPENDITURE; BODY COMPOSITION; FAT-FREE MASS; FAT MASS ID RESTING METABOLIC-RATE; FAT-FREE MASS; WEIGHT-LOSS; OBESE PATIENTS; CALORIC REQUIREMENTS; COMPUTED-TOMOGRAPHY; MODERATELY OBESE; ADIPOSE-TISSUE; HEALTHY WOMEN; MEN AB Differences in body composition have often been examined in conjunction with measurements of energy expenditure in men and women. Numerous studies during the past decade examined the relationship between resting energy expenditure (REE) and the components of a two-compartment model of composition, namely the fat-free mass (FFM) and the fat mass (FM). A synthetic review of these studies confirms a primary correlation between REE and FFM in adults over a broad range of body weights. A generalized prediction equation is proposed as REE = 370 + 21.6 X FFM. This equation explains 65-90% of the variation in REE. Several studies suggest, further, that FFM predicts total daily energy expenditure (TDEE) equally well. An independent contribution by FM to the prediction of either REE or TDEE is not supported for the general population, perhaps reflecting the relative constancy of the absolute FM in nonobese individuals. In the subset of obese women, FM may be a significant predictor. C1 SHRINERS BURN INST,SURG SERV,BOSTON,MA. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP CUNNINGHAM, JJ (reprint author), UNIV MASSACHUSETTS,DEPT NUTR,210 CHENOWETH,AMHERST,MA 01003, USA. NR 58 TC 262 Z9 265 U1 3 U2 15 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD DEC PY 1991 VL 54 IS 6 BP 963 EP 969 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA GT073 UT WOS:A1991GT07300002 PM 1957828 ER PT J AU LIEBER, CS AF LIEBER, CS TI PERSPECTIVES - DO ALCOHOL CALORIES COUNT SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE ETHANOL; ENERGY; DIETARY FAT; MICROSOMAL ETHANOL OXIDIZING SYSTEM; OXIDATIVE PHOSPHORYLATION ID CHRONIC ETHANOL-CONSUMPTION; UNITED-STATES ADULTS; MICROSOMAL-ENZYMES; OXIDIZING SYSTEM; ENERGY WASTAGE; BODY-WEIGHT; DIETARY-FAT; RAT-LIVER; ACETALDEHYDE; PHOSPHORYLATION AB Chronic consumption of substantial amounts of alcohol is not associated with the expected effect on body weight. Isocaloric substitution of carbohydrates by ethanol results in weight loss, and addition of ethanol to an otherwise normal diet does not produce the expected weight gain. This energy deficit cannot be explained by maldigestion or malabsorption but has been attributed to induction of the microsomal ethanol oxidizing system (a metabolic pathway that oxidizes ethanol without associated chemical energy production), increased sympathetic tone and associated thermogenesis, and/or enhanced ATP breakdown (with increased purine catabolism) secondary to the acetate produced from ethanol. All these hypotheses do not fully explain the lack of weight deficit when alcohol is consumed with a very-low-fat diet, which suggests that an alteration in the energy utilization derived from fat plays a major role, possibly through uncoupling of oxidation with phosphorylation in mitochondria damaged by chronic ethanol consumption. C1 BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 64 TC 118 Z9 123 U1 0 U2 3 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD DEC PY 1991 VL 54 IS 6 BP 976 EP 982 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA GT073 UT WOS:A1991GT07300004 PM 1957830 ER PT J AU OKUNIEFF, P AF OKUNIEFF, P TI INTERACTIONS BETWEEN ASCORBIC-ACID AND THE RADIATION OF BONE-MARROW, SKIN, AND TUMOR SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT CONF ON ASCORBIC ACID : BIOLOGIC FUNCTIONS AND RELATION TO CANCER CY SEP 10-12, 1990 CL NIH, BETHESDA, MD SP NCI, NIDDKD HO NIH DE ASCORBIC ACID; RADIATION THERAPY; RADIATION EFFECTS; RADIATION-PROTECTIVE AGENTS ID CORYNEBACTERIUM-PARVUM; MAMMALIAN-CELLS; RADIOSENSITIZATION; RADIOPROTECTION; RADIOTHERAPY; ENHANCEMENT; METABOLISM; TISSUE; INVIVO AB In studies of isotransplants of a murine fibrosarcoma, FSaII, ascorbic acid administered 50 min before wholebody radiation significantly increased the dose of radiation required to cause a fatal radiation syndrome and the dose of radiation required to obtain skin desquamation. A single intraperitoneal dose of 4.5 g/kg body wt was not cytotoxic and did not affect the radiation dose required to control 50% of tumors or to achieve remissions. The mechanism of this differential radiomodification of normal tissue sensitivity and tumor tissue response is unclear. The data suggest that after high-dose ascorbic acid the radiation dose given to cancer patients could be in without increasing acute complications but with an expected increase in tumor-control probability. However, only acute radiation reaction endpoints have been studied. Application of these findings to humans must therefore await further studies confirming that late reacting tissues are similarly protected by ascorbic acid. RP OKUNIEFF, P (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 17 TC 11 Z9 11 U1 0 U2 0 PU AMER SOC CLIN NUTRITION INC PI BETHESDA PA 9650 ROCKVILLE PIKE SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD DEC PY 1991 VL 54 IS 6 SU S BP S1281 EP S1283 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA GU397 UT WOS:A1991GU39700033 ER PT J AU PERRIN, JM AF PERRIN, JM TI ADOLESCENTS WITH CHRONIC ILLNESS SO AMERICAN JOURNAL OF DISEASES OF CHILDREN LA English DT Editorial Material ID PREVALENCE; CHILDHOOD; SEVERITY RP PERRIN, JM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0002-922X J9 AM J DIS CHILD JI Am. J. Dis. Child. PD DEC PY 1991 VL 145 IS 12 BP 1361 EP 1362 PG 2 WC Pediatrics SC Pediatrics GA GZ350 UT WOS:A1991GZ35000008 PM 1669660 ER PT J AU LINDGRENFURMAGA, EM SCHUNA, AA AF LINDGRENFURMAGA, EM SCHUNA, AA TI SWITCHING FROM ENALAPRIL TO LISINOPRIL SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Letter C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PHARM SERV,MADISON,WI 53705. RP LINDGRENFURMAGA, EM (reprint author), UNIV ILLINOIS,COLL PHARM,DEPT PHARM PRACTICE,833 S WOOD ST,CHICAGO,IL 60680, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD DEC PY 1991 VL 48 IS 12 BP 2605 EP 2605 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GR456 UT WOS:A1991GR45600008 ER PT J AU ALTHERR, MR BENGTSSON, U ELDER, FFB LEDBETTER, DH WASMUTH, JJ MCDONALD, ME GUSELLA, JF GREENBERG, F AF ALTHERR, MR BENGTSSON, U ELDER, FFB LEDBETTER, DH WASMUTH, JJ MCDONALD, ME GUSELLA, JF GREENBERG, F TI MOLECULAR CONFIRMATION OF WOLF-HIRSCHHORN SYNDROME WITH A SUBTLE TRANSLOCATION OF CHROMOSOME-4 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID HUNTINGTONS-DISEASE GENE; DNA MARKERS; SHORT ARM; LOCUS; D4S10 AB Wolf-Hirschhorn syndrome is a clinically recognizable, multiple congenital anomaly syndrome usually associated with terminal deletion of the short arm of chromosome 4. A girl with clinical features of Wolf-Hirschhorn syndrome did not show an obvious deletion of chromosome 4, and a molecular defect was suspected. RFLPs of genomic DNA from the proband and her parents were studied using DNA probes from the distal region of chromosome 4p. Fluorescence in situ hybridization using a cosmid p847.351 containing the fragment 847 E-C was performed to investigate the possibility of a subtle translocation. Cytogenetic analyses done on the child and on both parents did not conclusively reveal abnormalities of chromosome 4. Molecular studies using two probes mapped to distal 4p showed the absence of the maternal haplotype in the child. These findings are thus consistent with a molecular deletion of 4p and confirm the diagnosis of Wolf-Hirschhorn syndrome. Cytogenetic experiments involving fluorescence in situ hybridization showed that the mother carried a subtle translocation between chromosomes 4 and 19, 46,XX,t(4,19)(p16.3; p13.3), which resulted in an unbalanced form in the child. Chorionic villus sampling for prenatal diagnosis in a subsequent pregnancy showed the fetus to be unaffected. This provides the first evidence, in chromosome 4p, of a molecular deletion due to a subtle, inherited translocation leading to the Wolf-Hirschhorn phenotype. Such subtle translocations may become an important mechanism for some recurrent genetic defects. C1 BAYLOR COLL MED,INST MOLEC GENET,1 BAYLOR PLAZA,ROOM S903,HOUSTON,TX 77030. UNIV CALIF IRVINE,COLL MED,DEPT BIOL CHEM,IRVINE,CA 92717. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP GREENBERG, F (reprint author), BAYLOR COLL MED,INST MOLEC GENET,1 BAYLOR PLAZA,ROOM S903,HOUSTON,TX 77030, USA. FU NINDS NIH HHS [NS25631-02] NR 24 TC 84 Z9 84 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD DEC PY 1991 VL 49 IS 6 BP 1235 EP 1242 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA GU672 UT WOS:A1991GU67200010 PM 1746553 ER PT J AU BOELAERT, JR FENVES, AZ COBURN, JW AF BOELAERT, JR FENVES, AZ COBURN, JW TI DEFEROXAMINE THERAPY AND MUCORMYCOSIS IN DIALYSIS PATIENTS - REPORT OF AN INTERNATIONAL REGISTRY SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE DIALYSIS; DEFEROXAMINE; FEROXAMINE; MUCORMYCOSIS; RHIZOPUS; IRON OVERLOAD ID AMBULATORY PERITONEAL-DIALYSIS; HEMODIALYSIS-PATIENTS; RECEIVING DEFEROXAMINE; CHELATED ALUMINUM; IRON OVERLOAD; DESFERRIOXAMINE; PHYCOMYCOSIS; ZYGOMYCOSIS; RISK; ASSOCIATION C1 BAYLOR UNIV,MED CTR,NEPHROL SECT,WACO,TX 76798. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,WADSWORTH DIV MED SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,WADSWORTH DIV,RES SERV,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RP BOELAERT, JR (reprint author), ALGEMEEN ZIEKENHUIS ST JAN,RENAL & INFECT DIS UNIT,B-8000 BRUGES,BELGIUM. NR 53 TC 108 Z9 111 U1 1 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD DEC PY 1991 VL 18 IS 6 BP 660 EP 667 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA GT961 UT WOS:A1991GT96100006 PM 1962650 ER PT J AU SUNDERLAND, MC ROODMAN, GD AF SUNDERLAND, MC ROODMAN, GD TI INTERLEUKIN-3 - ITS BIOLOGY AND POTENTIAL USES IN PEDIATRIC HEMATOLOGY ONCOLOGY SO AMERICAN JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; RECOMBINANT HUMAN INTERLEUKIN-3; HUMAN GRANULOCYTE-MACROPHAGE; HEMATOPOIETIC GROWTH-FACTORS; MYELOBLASTIC-LEUKEMIA CELLS; HUMAN GM-CSF; PROGENITOR CELLS; BONE-MARROW; HUMAN IL-3; MYELODYSPLASTIC SYNDROMES AB The hematopoietic growth factor interleukin (IL)-3 is a potent regulator of blood cell proliferation. It promotes the survival, proliferation, and development of hematopoietic stem cells and committed progenitor cells of the granulocyte-macrophage, erythrocyte, eosinophil, basophil, megakaryocyte, mast cell, and lymphocyte lineages. In addition, IL-3 enhances mature myeloid cell functions such as phagocytosis and activation of basophils and eosinophils, as well as monocyte cytotoxicity. The first phase of clinical trials suggested that IL-3 may augment myelopoiesis in a number of clinical conditions. It may be efficacious for treatment of primary marrow disorders, including myelodysplastic syndromes and aplastic anemia. However, replacement therapy with IL-3 alone is probably not sufficient to obtain maximal stimulation of myelopoiesis. Preclinical and clinical studies published to date suggest that sequential use or combinations of growth factors will be needed to obtain optimal hematopoietic responses. C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET ADM MED CTR,7400 MERTON MINTON BLVD,SAN ANTONIO,TX 78284. NR 87 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-8562 J9 AM J PEDIAT HEMATOL PD WIN PY 1991 VL 13 IS 4 BP 414 EP 425 PG 12 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA GR302 UT WOS:A1991GR30200005 PM 1785668 ER PT J AU SAFIRSTEIN, R MEGYESI, J SAGGI, SJ PRICE, PM POON, M ROLLINS, BJ TAUBMAN, MB AF SAFIRSTEIN, R MEGYESI, J SAGGI, SJ PRICE, PM POON, M ROLLINS, BJ TAUBMAN, MB TI EXPRESSION OF CYTOKINE-LIKE GENES JE AND KC IS INCREASED DURING RENAL ISCHEMIA SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ISCHEMIC RENAL FAILURE; IMMEDIATE EARLY GENES JE AND KC; TAMM-HORSFALL; CYTOKINES AND REGENERATION ID GROWTH-FACTOR; MESSENGER-RNA; MONOCYTE CHEMOATTRACTANT; SECRETORY PROTEIN; PRODUCT; ENCODES; ACID; GLYCOPROTEIN; FIBROBLASTS; MACROPHAGES AB Both mitogenic and inflammatory phenomena accompany the renal response to ischemic injury. Previous studies have shown that several nuclear-binding members of the immediate early genes are prominently expressed after renal ischemia and may underlie the mitogenic response to such injury. We now report on the expression of JE and KC, other growth-factor-responsive genes that code for small secreted glycoproteins with cytokine-like properties, which may play a role in inflammation. The expression of the immediate early genes JE and KC was determined in rat kidney tissue at varying time points after release of a 50-min period of bilateral renal hilar clamping. Relative levels of mRNA for JE and KC were analyzed by Northern blot analysis of cortical and outer stripe mRNA. KC mRNA rose rapidly to peak values at 1 h and returned toward low baseline levels by 24 h after release of the hilar clamp. By contrast, JE mRNA reached peak levels later and remained elevated for at least 96 h after ischemia. JE antigen was localized immunocytochemically to the apical regions of the cortical and medullary thick ascending limbs as well as in the lumen of the distal nephron in ischemic kidneys. Cells of the glomerulus and proximal tubules were negative for JE antigen. In contrast to the increase in JE and KC mRNA, steady-state levels of uromodulin (Tamm Horsfall) mRNA, a cytokine binding protein also made by the thick ascending limb, declined to virtually undetectable levels by 24 h after ischemia. Thus the increases in JE and KC are not generalized phenomena. These studies demonstrate that the kidney rapidly expresses genes encoding leukocyte chemoattractants in response to ischemia. JE and KC may serve the renal regenerative response either by promoting the movement of cells along the basement membrane of injured tubules or by attracting leukocytes into the ischemic kidney. The decline of the cytokine binding Tamm-Horsfall protein may also increase the activity of locally generated or filtered cytokines within the kidney. C1 CUNY MT SINAI SCH MED, DEPT MED, DIV CARDIOL, NEW YORK, NY 10029 USA. CUNY MT SINAI SCH MED, DEPT MED, DIV MOLEC MED, NEW YORK, NY 10029 USA. CUNY MT SINAI SCH MED, DEPT BIOCHEM, NEW YORK, NY 10029 USA. CUNY MT SINAI SCH MED, BROOKDALE CTR MOLEC BIOL, NEW YORK, NY 10029 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV MED, BOSTON, MA 02115 USA. RP SAFIRSTEIN, R (reprint author), CUNY MT SINAI SCH MED, DEPT MED, DIV RENAL, 1 GUSTAVE L LEVY PL, NEW YORK, NY 10029 USA. NR 33 TC 129 Z9 130 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD DEC PY 1991 VL 261 IS 6 BP F1095 EP F1101 PN 2 PG 7 WC Physiology SC Physiology GA GX687 UT WOS:A1991GX68700118 ER PT J AU VANDERKOLK, BA PERRY, JC HERMAN, JL AF VANDERKOLK, BA PERRY, JC HERMAN, JL TI CHILDHOOD ORIGINS OF SELF-DESTRUCTIVE BEHAVIOR SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BORDERLINE PERSONALITY-DISORDER; POSTTRAUMATIC-STRESS-DISORDER; MUTILATION; CHILDREN; TRAUMA; DISSOCIATION; SEPARATION; ATTACHMENT; VIOLENCE AB Objective: Clinical reports suggest that many adults who engage in self-destructive behavior have childhood histories of trauma and disrupted parental care. This study explored the relations between childhood trauma, disrupted attachment, and self-destruction, using both historical and prospective data. Method: Seventy-four subjects with personality disorders or bipolar II disorder were followed for an average of 4 years and monitored for self-destructive behavior such as suicide attempts, self-injury, and eating disorders. These behaviors were then correlated with independently obtained self-reports of childhood trauma, disruptions of parental care, and dissociative phenomena. Results: Histories of childhood sexual and physical abuse were highly significant predictors of self-cutting and suicide attempts. During followup, the subjects with the most severe histories of separation and neglect and those with past sexual abuse continued being self-destructive. The nature of the trauma and the subjects' age at the time of the trauma affected the character and the severity of the self-destructive behavior. Cutting was also specifically related to dissociation. Conclusions: Childhood trauma contributes to the initiation of self-destructive behavior, but lack of secure attachments helps maintain it. Patients who repetitively attempt suicide or engage in chronic self-cutting are prone to react to current stresses as a return of childhood trauma, neglect, and abandonment. Experiences related to interpersonal safety, anger, and emotional needs may precipitate dissociative episodes and self-destructive behavior. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. CAMBRIDGE HOSP,CAMBRIDGE,MA 02139. FU NIMH NIH HHS [MH-34123] NR 45 TC 442 Z9 447 U1 13 U2 61 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 DEC PY 1991 VL 148 IS 12 BP 1665 EP 1671 PG 7 WC Psychiatry SC Psychiatry GA GR842 UT WOS:A1991GR84200005 PM 1957928 ER PT J AU QUINN, DA HONEYMAN, TW JOSEPH, PM THOMPSON, BT HALES, CA SCHEID, CR AF QUINN, DA HONEYMAN, TW JOSEPH, PM THOMPSON, BT HALES, CA SCHEID, CR TI CONTRIBUTION OF NA+/H+ EXCHANGE TO PH REGULATION IN PULMONARY-ARTERY SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID GLOMERULAR MESANGIAL CELLS; INTRACELLULAR PH; ENDOTHELIAL-CELLS; ANGIOTENSIN-II; PROLIFERATION; VASOPRESSIN; ACTIVATION; ANTIPORTER; TRANSPORT; PATHWAYS AB In blood vessels in the systemic circulation, the plasmalemmal Na+/H+ exchanger has been implicated in a variety of cellular functions, including the regulation of intracellular pH (pH(i)) and cell volume, and the response to smooth muscle mitogens. The role of this transport system in pulmonary vascular smooth muscle has not been explored. The present study examined the characteristics of Na+/H+ exchange in cultured guinea pig pulmonary artery smooth muscle cells. These cells were subjected to an acid load, and the recovery from acid loading was monitored using the fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). In the absence of HCO3-, pH(i) recovery from acid loading was dependent on external Na+ and was inhibited by the Na+/H+ exchange inhibitor dimethylamiloride (DMA) (recovery rate was reduced from 54.4 +/- 5.5 to 12.8 +/- 2.0 mmol H+/liter.min). This exchanger was also active in the presence of HCO3-; DMA reduced resting pH(i) and slowed the rate of recovery from acid loading in HCO3- buffers. However, in the presence of HCO3-, other transport systems, presumably HCO3-/Cl- exchange, also contribute to the regulation of pH(i). In HCO3- buffers, the rate of recovery from acid load averaged 40.8 +/- 1.8 mmol H+/liter.min. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of HCO3-/Cl- exchange, slowed this recovery to 25.5 +/- 1.6 mmol H+/liter.min. A combination of DIDS and DMA further slowed the recovery to 19.7 +/- 1.5 mmol H+/liter.min. These findings indicate that the Na+/H+ exchanger plays a significant role in the regulation of pH(i) in pulmonary artery smooth muscle cells, even in HCO3--containing buffers. C1 UNIV MASSACHUSETTS,SCH MED,MED CTR,DEPT PHYSIOL,55 LAKE AVE N,WORCESTER,MA 01655. HARVARD UNIV,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. RP SCHEID, CR (reprint author), UNIV MASSACHUSETTS,SCH MED,MED CTR,DEPT PHYSIOL,55 LAKE AVE N,WORCESTER,MA 01655, USA. FU NHLBI NIH HHS [HL-39150, HL-41188, HL-07354] NR 28 TC 32 Z9 34 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD DEC PY 1991 VL 5 IS 6 BP 586 EP 591 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA GV119 UT WOS:A1991GV11900013 PM 1659836 ER PT J AU LEE, MJ MUELLER, PR SAINI, S HAHN, PF DAWSON, SL AF LEE, MJ MUELLER, PR SAINI, S HAHN, PF DAWSON, SL TI PERCUTANEOUS DILATATION OF BENIGN BILIARY STRICTURES - SINGLE-SESSION THERAPY WITH GENERAL-ANESTHESIA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID BALLOON DILATATION; MANAGEMENT; DILATION AB Percutaneous biliary stricture dilatation (PBSD) is an uncomfortable procedure for patients that presently requires multiple dilatation sessions spread over many days. We evaluated the use of general anesthesia to enable PBSD to be performed in a single sitting in 14 patients with benign biliary strictures (11 anastomotic and three iatrogenic strictures). Four patients had multiple strictures, and the other 10 had a single stricture. Strictures were documented by transhepatic cholangiography (11 patients) or T-tube cholangiography (three); quantitative biliary perfusion studies were additionally performed in seven cases. Dilatation was performed transhepatically in 11 patients and via a T-tube track in three. Balloons ranged from 8 to 12 mm in diameter and were manually inflated for 3 min with an average of five inflations per stricture. Stenting catheters were left across the strictured areas in all patients for 6-21 days (mean, 10 days) before removal. The mean duration of hospital stay for all patients was 5.7 days, which could further be divided into means of 3.6 days (range, 1-6 days) for 11 patients without complications and 13.7 days (range, 13-14 days) for three patients who had complications. Complications included cholangitis; liver hematoma (which resolved with conservative therapy in both cases); and pseudoaneurysm of the hepatic artery, which necessitated angiographic embolization. PBSD achieved long-term patency in 13 (93%) of 14 patients with a follow-up period of 2.0 to 5.5 years (mean, 3.2 years). A stricture recurred in one patient 1.5 years after dilatation. We conclude that PBSD with the patient under general anesthesia can be performed in a single visit to the radiology department with excellent long-term patency rates, a shorter hospital stay, and a pain-free procedure for the patient. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 15 TC 29 Z9 30 U1 0 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD DEC PY 1991 VL 157 IS 6 BP 1263 EP 1266 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ619 UT WOS:A1991GQ61900023 PM 1950878 ER PT J AU PRINCE, MR CHEW, FS AF PRINCE, MR CHEW, FS TI EPENDYMOMA OF THE 4TH VENTRICLE SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Prince, Martin/S-6850-2016 NR 4 TC 4 Z9 5 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD DEC PY 1991 VL 157 IS 6 BP 1278 EP 1278 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ619 UT WOS:A1991GQ61900028 PM 1950882 ER PT J AU CHEW, FS AF CHEW, FS TI FATE OF MANUSCRIPTS REJECTED FOR PUBLICATION IN THE AJR - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP CHEW, FS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD DEC PY 1991 VL 157 IS 6 BP 1352 EP 1353 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GQ619 UT WOS:A1991GQ61900043 ER PT J AU OISHI, SN PAGE, CP SCHWESINGER, WH AF OISHI, SN PAGE, CP SCHWESINGER, WH TI COMPLICATED PRESENTATIONS OF GROIN HERNIAS SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL MEETING OF THE SOUTHWESTERN SURGICAL CONGRESS CY APR 21-24, 1991 CL LAS VEGAS, NV SP SW SURG CONGRESS ID REPAIR AB Elective repair of simple (uncomplicated) inguinal and femoral hernias avoids incarceration and bowel obstruction (complicated presentations). To identify factors that perturb this strategy, we analyzed the records of 1,859 consecutive nonpediatric patients with groin hernias. Incarceration or bowel obstruction prompted operation in 22 of 77 (29%) women and in 15 of 34 (44%) patients with femoral hernia. Patients presenting with bowel obstruction were significantly older than those with incarceration only and/or uncomplicated presentation, and 13 of 25 (52%) required resection of necrotic bowel. Mortality was limited to five patients of advanced age with groin hernia and bowel obstruction. Four of the five patients had undergone resection of necrotic bowel. Complicated presentations of groin hernias are associated with a higher proportion of women and patients with femoral hernias. Gangrenous bowel was encountered only in those patients with groin hernia and bowel obstruction. Early diagnosis and elective repair of uncomplicated hernias should remain our strategy in patients of all ages. C1 UNIV TEXAS,HLTH SCI CTR,DEPT SURG,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 8 TC 37 Z9 37 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD DEC PY 1991 VL 162 IS 6 BP 568 EP 571 DI 10.1016/0002-9610(91)90110-Y PG 4 WC Surgery SC Surgery GA GX232 UT WOS:A1991GX23200011 PM 1670226 ER PT J AU JONES, MA YOUNG, RH SCULLY, RE AF JONES, MA YOUNG, RH SCULLY, RE TI DIFFUSE LAMINAR ENDOCERVICAL GLANDULAR HYPERPLASIA - A BENIGN LESION OFTEN CONFUSED WITH ADENOMA-MALIGNUM (MINIMAL DEVIATION ADENOCARCINOMA) SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE LAMINAR ENDOCERVICAL HYPERPLASIA; ENDOCERVICAL GLANDS; PSEUDONEOPLASTIC GLANDULAR LESION; CERVIX ID UTERINE CERVIX; MICROGLANDULAR HYPERPLASIA AB We report seven examples of a hitherto undescribed pseudoneoplastic glandular lesion of the uterine cervix that we have designated "diffuse laminar endocervical glandular hyperplasia." The patients ranged in age from 22 to 48 (mean 37) years. Only one of them had a history of hormone intake. All the lesions were incidental findings in hysterectomy specimens performed for dysfunctional uterine bleeding (five cases) or symptomatic leiomyomas (two cases). Microscopic examination revealed a proliferation of moderate-sized, evenly spaced, differentiated endocervical glands within the inner one-third of the cervical wall, sharply demarcated from the underlying cervical stroma. Reactive atypia was seen in some cases but significant cytologic atypia was absent. A marked inflammatory response was present in five of the seven cases. The main consideration in differential diagnosis was adenoma malignum (minimal deviation adenocarcinoma). Major features that helped in this distinction were a lack of irregular stromal infiltration and a desmoplastic stromal response, and an absence of focal malignant cytologic features. Follow-up for an average of 6.5 years in five of the seven cases was uneventful. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP JONES, MA (reprint author), MAINE MED CTR,DEPT PATHOL,PORTLAND,ME 04102, USA. NR 17 TC 29 Z9 30 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD DEC PY 1991 VL 15 IS 12 BP 1123 EP 1129 DI 10.1097/00000478-199112000-00002 PG 7 WC Pathology; Surgery SC Pathology; Surgery GA GV116 UT WOS:A1991GV11600002 PM 1746679 ER PT J AU JONES, EC CLEMENT, PB YOUNG, RH AF JONES, EC CLEMENT, PB YOUNG, RH TI SCLEROSING ADENOSIS OF THE PROSTATE-GLAND - A CLINICOPATHOLOGICAL AND IMMUNOHISTOCHEMICAL STUDY OF 11 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE PROSTATE GLAND; SCLEROSING ADENOSIS; ADENOSIS; ATYPICAL ADENOMATOUS HYPERPLASIA; BASAL CELL ID BASAL-CELL HYPERPLASIA; CYSTIC CARCINOMA; TUMOR; ADENOCARCINOMA AB Eleven cases of sclerosing adenosis of the prostate gland, a recently reported uncommon pseudoneoplastic lesion with characteristic histological, histochemical, and immunohistochemical features, are described. The well-circumscribed cellular lesions were composed of variably sized and shaped, often compressed, glands and small clusters of epithelial cells embedded in a cellular, often myxoid stroma. Mild cytologic atypia was occasionally present, and one case had moderate cytologic atypia. A distinct basement membrane often surrounded the glands and clusters. Luminal acid mucin was typically present. Keratin-positive basal cells were present in the glands and as spindle cells in the stroma. The basal cells were also immunoreactive for S-100 and muscle-specific actin, suggesting myoepithelial differentiation. Clinical follow-up has shown no evidence of prostatic carcinoma. The available evidence suggests that sclerosing adenosis of the prostate gland is a benign lesion with distinctive features that should enable it to be distinguished from prostatic adenocarcinoma. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP JONES, EC (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,855 W 12TH AVE,VANCOUVER V5Z 1M9,BC,CANADA. NR 21 TC 37 Z9 39 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD DEC PY 1991 VL 15 IS 12 BP 1171 EP 1180 DI 10.1097/00000478-199112000-00008 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA GV116 UT WOS:A1991GV11600008 PM 1720930 ER PT J AU JENKINSON, SG DUNCAN, CA BRYAN, CL LAWRENCE, RA AF JENKINSON, SG DUNCAN, CA BRYAN, CL LAWRENCE, RA TI EFFECTS OF AGE ON RAT GLUTATHIONE METABOLISM SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Article DE GLUTATHIONE; GLUTATHIONE PEROXIDASE; AGING RATS; GAMMA-GLUTAMYL TRANSPEPTIDASE ID GAMMA-GLUTAMYL-TRANSPEPTIDASE; PEROXIDASE-ACTIVITY; SUPEROXIDE-DISMUTASE; SELENIUM DEFICIENCY; LIPID-PEROXIDATION; S-TRANSFERASES; LIVER; ERYTHROCYTE; SENSITIVITY; INHIBITION AB The authors hypothesized that rat plasma or tissue glutathione metabolism could change with age due to possible decreases in glutathione-related enzyme activities. To test this hypothesis, the authors measured plasma and tissue concentrations of glutathione and glutathione-related enzymes. Animals were 3 months, 12 months, or 24 months old at the time of experiments. Plasma glutathione was found to be significantly increased in both the 12-month-old and 24-month-old groups compared to the 3-month-old rats. Tissue enzyme measurements showed no significant differences between the groups in lung or liver glutathione peroxidase or glutathione S-transferase. gamma-Glutamyl transpeptidase activity was significantly decreased in kidney and lung with aging. Decreases in tissue gamma-glutamyl transpeptidase activity occur with age; this may contribute to increases in plasma glutathione concentrations. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU PHS HHS [H-30556] NR 39 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD DEC PY 1991 VL 302 IS 6 BP 347 EP 352 DI 10.1097/00000441-199112000-00004 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA GU876 UT WOS:A1991GU87600004 PM 1685307 ER PT J AU WEINSTEIN, MJ BERG, J KUSUZAKI, K SPRINGFIELD, DS GEBHARDT, MC MANKIN, HJ AF WEINSTEIN, MJ BERG, J KUSUZAKI, K SPRINGFIELD, DS GEBHARDT, MC MANKIN, HJ TI INVITRO ASSAY OF NUCLEAR UPTAKE OF DOXORUBICIN HYDROCHLORIDE IN OSTEOSARCOMA CELLS OF DOGS SO AMERICAN JOURNAL OF VETERINARY RESEARCH LA English DT Article ID FLOW CYTOMETRIC ANALYSIS; PRIMARY TUMOR; CHEMOTHERAPY; RESISTANT; ADRIAMYCIN; SARCOMA; CANCER; GROWTH AB A rapid, simple chemosensitivity assay, assessing tumor cell nuclear uptake of doxorubicin hydrochloride, was evaluated in 16 dogs with appendicular osteosarcoma. Doxorubicin was administered to dogs in 5 biweekly treatments, and surgical resection was performed after the second or third treatment. The chemosensitivity assay was performed on biopsy specimens from all dogs before chemotherapy. It was repeated on tissue from resected tumors, and tumors were evaluated histologically to determine the degree of necrosis resulting from chemotherapy. Disease-free and total survival time correlated significantly (P < 0.05 in both cases) with the degree of postchemotherapy necrosis of the primary tumors. Significant correlation was not apparent between the percentage of tumor cells with nuclear uptake of doxorubicin (in either biopsy or resection samples) and disease-free or total survival time. The percentage of cells with nuclear uptake of doxorubicin in surgically resected tumors correlated significantly (P < 0.05) with percentage of necrosis. C1 TUFTS UNIV,FOSTER HOSP SMALL ANIM,SCH VET MED,DEPT SURG,N GRAFTON,MA 01536. MASSACHUSETTS GEN HOSP,ORTHOPAED ONCOL UNIT,BOSTON,MA 02114. NR 23 TC 9 Z9 9 U1 0 U2 1 PU AMER VETERINARY MEDICAL ASSOC PI SCHAUMBURG PA 1931 N MEACHAM RD SUITE 100, SCHAUMBURG, IL 60173-4360 SN 0002-9645 J9 AM J VET RES JI Am. J. Vet. Res. PD DEC PY 1991 VL 52 IS 12 BP 1951 EP 1955 PG 5 WC Veterinary Sciences SC Veterinary Sciences GA GT513 UT WOS:A1991GT51300005 PM 1789508 ER PT J AU DEFAVERI, J GRAYBILL, JR AF DEFAVERI, J GRAYBILL, JR TI IMMUNOHISTOPATHOLOGY OF MURINE PULMONARY HISTOPLASMOSIS DURING NORMAL AND HYPERSENSITIVE CONDITIONS SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID PNEUMONITIS; MICE; CAPSULATUM; ANTIGENS; LYMPHOCYTES; DEFENSE; CELLS AB Pulmonary histoplasmosis was induced in nonimmunized and immunized Balb-C nu/+ mice. The lung tissue burden of H. capsulatum, histopathology, the size of the inflammatory area, and the numbers of total T lymphocytes and subtypes in situ were evaluated serially after challenge. Over 3 days previously immunized mice developed a large lymphocyte/macrophage inflammatory response. This rapidly decreased in the next 2 wk. In contrast, the nonimmunized control mice developed a predominantly polymorphonuclear infiltrate that evolved more slowly over the first week of infection. This initial response was nonspecific but, after the first week, shifted to lymphocytes and granuloma formation. The lymphocyte infiltration in both immunized and nonimmunized mice was predominantly CD4. Previously immunized mice had a rapid decrease in tissue counts of H. capsulatum after Day 3, but nonimmunized mice continued to have increased counts through Day 7 after infection. These studies reproduce in the mouse model a host response similar to acute reinfection histoplasmosis in the human. In this condition an intense cell-mediated inflammatory response is thought to be elicited by fungal antigens and to represent host reaction rather than fungal replication. Our experimental model added new information relevant to the understanding of the pathogenesis of this process. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV ESTADO SAO PAULO,BOTUCATU MED SCH,DEPT PATHOL,SAO PAULO,BRAZIL. RP GRAYBILL, JR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED & RES,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 27 TC 4 Z9 4 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD DEC PY 1991 VL 144 IS 6 BP 1366 EP 1372 PG 7 WC Respiratory System SC Respiratory System GA GU988 UT WOS:A1991GU98800026 PM 1741551 ER PT J AU ROLF, N COTE, CJ AF ROLF, N COTE, CJ TI PERSISTENT CARDIAC-ARRHYTHMIAS IN PEDIATRIC-PATIENTS - EFFECTS OF AGE, EXPIRED CARBON-DIOXIDE VALUES, DEPTH OF ANESTHESIA, AND AIRWAY MANAGEMENT SO ANESTHESIA AND ANALGESIA LA English DT Article ID HALOTHANE; EPINEPHRINE; CHILDREN AB The presence of persistent arrhythmias was correlated with hypercarbia (end-tidal CO2 greater-than-or-equal-to 55 mm Hg for greater-than-or-equal-to 60 s). A continuous strip chart recording of oxygen saturation, a capnogram, and an electrocardiogram were obtained from 402 children. No episodes of arrhythmia occurred in 153 patients younger than 2 yr compared with 24 patients 2 yr of age or older (P = 0.0001). Older patients whose airways were managed via a mask had a higher incidence (13.2% [21 of 159 patients]) than tracheally intubated patients (3.3% [3 of 90 patients]) (P = 0.01). In older patients whose tracheas were intubated, hypercarbia was associated with arrhythmia in 1 of 20 hypercarbia episodes. Seven of 16 patients with hypercarbia, whose airways were managed via a mask, had an arrhythmia (P = 0.0014); in eight, arrhythmias were associated with light anesthesia; in seven, arrhythmias were not associated with either hypercarbia or light anesthesia. Arrhythmias developed in 13 of 55 patients 2 yr old or older whose airways were managed via a mask and who were undergoing orchiopexy or herniorrhaphy as compared with 1 of 30 tracheally intubated patients (P = 0.016). There was a higher incidence of arrhythmias during halothane anesthesia compared with that during all other techniques (P = 0.035). The authors conclude that the incidence of arrhythmias is extremely low in infants younger than 2 yr. Hypercarbia is associated with arrhythmias in pediatric patients whose airways are managed via a mask but not in patients whose tracheas are intubated. Light anesthesia, as evidenced by movement, increased arterial blood pressure, and heart rate, may be an equally important cause of arrhythmia particularly during procedures with wide variations in the strength of the surgical stimulus. Capnographic monitoring was not associated with a change in the incidence of arrhythmias. RP COTE, CJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 23 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD DEC PY 1991 VL 73 IS 6 BP 720 EP 724 PG 5 WC Anesthesiology SC Anesthesiology GA GR648 UT WOS:A1991GR64800008 PM 1952172 ER PT J AU FRATACCI, MD FROSTELL, CG CHEN, TY WAIN, JC ROBINSON, DR ZAPOL, WM AF FRATACCI, MD FROSTELL, CG CHEN, TY WAIN, JC ROBINSON, DR ZAPOL, WM TI INHALED NITRIC-OXIDE - A SELECTIVE PULMONARY VASODILATOR OF HEPARIN PROTAMINE VASOCONSTRICTION IN SHEEP SO ANESTHESIOLOGY LA English DT Article DE BLOOD, COAGULATION, HEPARIN-PROTAMINE; HEART, VASCULAR PRESSURES; HORMONES, THROMBOXANE-A2; LUNG, VASCULAR RESISTANCE; MUSCLE, SMOOTH, ENDOTHELIUM-DERIVED RELAXING FACTOR; NITRIC OXIDE ID ARTERIAL SMOOTH-MUSCLE; RELAXING FACTOR; AWAKE SHEEP; NITROPRUSSIDE; RELAXATION; REVERSAL; RELEASE; HYPERTENSION; ACTIVATION; LUNGS AB Nitric oxide (NO) has recently been discovered to bc an important endothelium-derived relaxing factor and produces profound relaxation of vascular smooth muscle. To learn if NO could be a potent and selective pulmonary vasodilator. NO was inhaled by 16 awake lambs in an attempt to reduce the increase in pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) induced by either the infusion of an exogenous pulmonary vasoconstrictor (the thromboxane analog U46619) or the endogenous release of thromboxane that occurs during the neutralization of heparin anticoagulation by protamine sulfate. Inhaling greater-than-or-equal-to 40 ppm of NO during a continuous U46619 infusion returned the PAP to a normal value, without affecting systemic blood pressure or vascular resistance. Pretreatment with the cyclooxygenase inhibitor indomethacin before infusing U46619 did not reduce the pulmonary vasodilatory effect of inhaled NO, and we conclude that the dilatory effect of NO on the lung's circulation is independent of cyclooxygenase products such as prostacyclin. Continuously inhaling NO at 180 ppm did not significantly reduce the mean peak thromboxane B2 concentration at 1 min after protamine injection; however, the mean values of pulmonary hypertension and vasoconstriction at 1 min were markedly reduced below the levels in untreated heparin-protamine reactions. Breathing NO at lower concentrations (40-80 ppm) did not decrease the mean peak PAP and PVR at 1 min after protamine but decreased the PAP and PVR values at 2, 3. and 5 min below those of control heparin-protamine reactions. Intravenous infusion of nitroprusside completely prevented the transient increase of PAP and PVR during the heparin-protamine reaction; however, marked concomitant systemic vasodilation occurred. Inhaled NO is a selective pulmonary vasodilator that can prevent thromboxane-induced pulmonary hypertension during the heparin-protamine reaction in lambs and can do so without causing systemic vasodilation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. RP ZAPOL, WM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 42397]; NIAMS NIH HHS [AR 79427] NR 36 TC 239 Z9 241 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD DEC PY 1991 VL 75 IS 6 BP 990 EP 999 DI 10.1097/00000542-199112000-00011 PG 10 WC Anesthesiology SC Anesthesiology GA GV115 UT WOS:A1991GV11500011 PM 1741521 ER PT J AU KATKOV, WN FRIEDMAN, LS CODY, H EVANS, A KUO, G CHOO, QL HOUGHTON, M DIENSTAG, JL AF KATKOV, WN FRIEDMAN, LS CODY, H EVANS, A KUO, G CHOO, QL HOUGHTON, M DIENSTAG, JL TI ELEVATED SERUM ALANINE AMINOTRANSFERASE LEVELS IN BLOOD-DONORS - THE CONTRIBUTION OF HEPATITIS-C VIRUS SO ANNALS OF INTERNAL MEDICINE LA English DT Note DE BLOOD DONORS; HEPATITIS, VIRAL, NON-A, NON-B; HEPATITIS-C VIRUS; ALANINE AMINOTRANSFERASE; HEPATITIS ANTIBODIES ID NON-B-HEPATITIS; TRANSFUSION-TRANSMITTED VIRUSES; NON-A; RECIPIENTS; ANTIBODY; RISK AB In 1983, anticipating the introduction of alanine aminotransferase (ALT) screening to limit the frequency of transfusion-associated non-A, non-B hepatitis, we evaluated 100 consecutive blood donors with elevated ALT levels. To assess the role of hepatitis C virus (HCV) in blood donors with ALT elevations, we tested donor sera for antibody to HCV (anti-HCV). Antibody was detected and "confirmed" by a second-generation recombinant immunoblot assay (RIBA-2) in 17% of donors. Aminotransferase levels were higher in donors with anti-HCV. Antibody to HCV was more frequent in donors with persistent ALT elevations and in those who used intravenous drugs; anti-HCV was less frequent in donors who were overweight, who drank alcohol regularly, and who had no alternative explanation for an elevated ALT level. We conclude that asymptomatic ALT elevations are infrequently associated with HCV infection, unless the elevation is substantial, persistent, or associated with intravenous drug use. Hepatitis C virus infection is an unlikely cause of asymptomatic ALT elevations in persons who drink alcohol regularly or who are obese; however, HCV infection is a more likely cause of ALT elevations in thin persons who do not drink alcohol regularly. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. CHIRON CORP,EMERYVILLE,CA. FU NIDDK NIH HHS [T32-DK07191] NR 10 TC 36 Z9 36 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 1991 VL 115 IS 11 BP 882 EP 884 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA GR171 UT WOS:A1991GR17100009 PM 1952477 ER PT J AU WARSHAW, AL AF WARSHAW, AL TI IMPLICATIONS OF MALIGNANT-CELL DNA CONTENT FOR TREATMENT OF PATIENTS WITH PANCREATIC-CANCER SO ANNALS OF SURGERY LA English DT Editorial Material ID CARCINOMA; MORTALITY; PANCREATODUODENECTOMY; MORBIDITY; SURVIVAL; BYPASS; BIOPSY RP WARSHAW, AL (reprint author), MASSACHUSETTS GEN HOSP,ACC-336,BOSTON,MA 02114, USA. NR 23 TC 8 Z9 8 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD DEC PY 1991 VL 214 IS 6 BP 645 EP 647 PG 3 WC Surgery SC Surgery GA GU525 UT WOS:A1991GU52500001 PM 1683766 ER PT J AU SAVAGE, AP MALT, RA AF SAVAGE, AP MALT, RA TI ELECTIVE AND EMERGENCY HEPATIC RESECTION - DETERMINANTS OF OPERATIVE MORTALITY AND MORBIDITY SO ANNALS OF SURGERY LA English DT Article ID PRIMARY HEPATOCELLULAR-CARCINOMA; METASTATIC COLORECTAL-CARCINOMA; PRIMARY LIVER-CANCER; SURGICAL-MANAGEMENT; MULTIVARIATE-ANALYSIS; CIRRHOTIC-PATIENTS; EXPERIENCE; SURGERY; SURVIVAL; TRAUMA AB To determine the reasons for improved mortality and morbidity rates after major hepatic resection, five variables were analyzed retrospectively in 300 patients operated on over a 27-year period: (1) the indication for surgery, (2) the surgical approach, (3) the urgency with which surgery was performed, (4) the nature of the surgical procedure, and (5) the experience of the surgeon. The operative mortality rate decreased from 19% between 1962 and 1979 to 9.7% between 1980 and 1988 (p < 0.05). The operative mortality rates for patients undergoing resection for benign hepatic neoplasms was 3.4%; for metastatic tumors, 6.3%; for primary hepatic malignancies, 19%; and for trauma, 33%. Fifty-seven percent of operations before 1980 were performed through a thoracoabdominal exposure as compared with 19% after 1980. Overall a thoracoabdominal exposure of the liver was associated with a 20% mortality rate as compared with 8.6% for operations with abdominal exposure of the liver (p < 0.02). Elective operations accounted for 65% of hepatic resections before 1980, as compared with 90% after 1980, and were associated with an 8.8% mortality rate as compared with 30.7% for urgent and emergency operations (p < 0.001). Segmental and wedge resections were associated with a 5.3% mortality rate as compared with 14.7% for major hepatic resections (p < 0.05), but this difference did not affect overall operative mortality rates because there was no change in the proportion of major hepatic resections after 1980. Surgical experience was not a determinant of operative mortality or morbidity rates in elective operations. Although there was no reduction in the complication rate after 1980, there was a reduction in postoperative stay from 26 days before 1980 to 16 days after 1980 (p < 0.001). A reduction in the incidence of postoperative sepsis and a change in its management was associated with improved operative mortality rates. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP MALT, RA (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114, USA. NR 67 TC 63 Z9 63 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD DEC PY 1991 VL 214 IS 6 BP 689 EP 695 DI 10.1097/00000658-199112000-00008 PG 7 WC Surgery SC Surgery GA GU525 UT WOS:A1991GU52500008 PM 1741648 ER PT J AU NEWTON, JR GRILLO, HC MATHISEN, DJ AF NEWTON, JR GRILLO, HC MATHISEN, DJ TI MAIN BRONCHIAL SLEEVE RESECTION WITH PULMONARY CONSERVATION SO ANNALS OF THORACIC SURGERY LA English DT Article; Proceedings Paper CT 27TH ANNUAL MEETING OF THE SOC OF THORACIC SURGEONS CY FEB 18-20, 1991 CL SAN FRANCISCO, CA SP SOC THORAC SURGEONS ID BRONCHOPLASTIC PROCEDURES; CARCINOMA; ADENOMA; TUMORS AB Twenty-seven main bronchial resections (19 left, 8 right) were performed without pulmonary resection between 1975 and 1991. The patients were 17 men and 9 women with an average age of 35 years (range, 20 to 65 years). Tumors comprised 55% of the lesions, including 9 carcinoid tumors (33%), 2 mucoepidermoid tumors, 2 fibrous histiocytomas, 1 hemangiopericytoma, and 1 large cell carcinoma. Scarring and stenosis secondary to multiple causes occurred in 10 patients (37%). Two patients had miscellaneous lesions. Presenting symptoms included dyspnea (52%), wheezing or stridor (44%), cough (41%), hemoptysis (37%), and pneumonia (18%). Preoperative chest roentgenogram was abnormal in 60% of patients, whereas tomograms delineated the lesion in 94%. All patients had bronchoscopy for lesion evaluation. Anesthesia was accomplished through a long single-lumen endotracheal tube in 19 cases and a double-lumen tube in 8 cases. Mobilization and exposure techniques to create a tension-free anastomosis were critical for left main bronchial resections and included pretracheal mobilization (100%), neck flexion (100%), tracheal and main bronchial retraction (85%), aortic and pulmonary artery retraction (44%), and intrapericardial hilar release (33%). All resections were for cure; there was no operative mortality. Morbidity in 4 patients (15%) included an anastomotic stenosis (successfully reresected), prolonged air leak and pneumonia, transient recurrent nerve palsy, and atelectasis. Median 5-year follow-up revealed 92% of patients alive, with only one of two late deaths being disease-related. Main bronchial resection is an ideal technique for selected benign and malignant lesions, allowing complete pulmonary parenchymal preservation. C1 MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 25 TC 30 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD DEC PY 1991 VL 52 IS 6 BP 1272 EP 1280 PG 9 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA GY251 UT WOS:A1991GY25100012 PM 1755680 ER PT J AU BEKKEN, K AF BEKKEN, K TI THE MANY FACES OF IMITATION IN LANGUAGE-LEARNING - SPEIDEL,GE, NELSON,KE SO APPLIED PSYCHOLINGUISTICS LA English DT Book Review RP BEKKEN, K (reprint author), MASSACHUSETTS GEN HOSP,NEUROLINGUIST LAB,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 2 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD DEC PY 1991 VL 12 IS 4 BP 507 EP 511 DI 10.1017/S0142716400005907 PG 5 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA HG908 UT WOS:A1991HG90800007 ER PT J AU HODGSON, J AF HODGSON, J TI UNFULFILLED EXPECTATIONS - HOME AND SCHOOL INFLUENCES ON LITERACY - SNOW,CE, BARNES,WS, CHANDLER,J, GOODMAN,IF, HEMPHILL,L SO APPLIED PSYCHOLINGUISTICS LA English DT Book Review RP HODGSON, J (reprint author), MASSACHUSETTS GEN HOSP,CTR READING & WRITING RES,BOSTON,MA 02114, USA. NR 7 TC 0 Z9 0 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD DEC PY 1991 VL 12 IS 4 BP 515 EP 522 DI 10.1017/S0142716400005920 PG 8 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA HG908 UT WOS:A1991HG90800009 ER PT J AU HRUZA, GJ DOVER, JS FLOTTE, TJ GOETSCHKES, M WATANABE, S ANDERSON, RR AF HRUZA, GJ DOVER, JS FLOTTE, TJ GOETSCHKES, M WATANABE, S ANDERSON, RR TI Q-SWITCHED RUBY-LASER IRRADIATION OF NORMAL HUMAN SKIN - HISTOLOGIC AND ULTRASTRUCTURAL FINDINGS SO ARCHIVES OF DERMATOLOGY LA English DT Article ID GUINEA-PIG SKIN; SELECTIVE PHOTOTHERMOLYSIS; TATTOOS; PULSES AB The Q-switched ruby laser is used for treatment of tattoos. The effects of Q-switched ruby laser pulses on sun-exposed and sun-protected human skin, as well as senile lentigines, were investigated with clinical observation, light microscopy, and transmission electron microscopy. A pinpricklike sensation occurred at radiant exposures as low as 0.2 J/cm2. Immediate erythema, delayed edema, and immediate whitening occurred with increasing radiant exposure. The threshold for immediate whitening varied inversely with skin pigmentation, ranging from a mean of 1.4 J/cm2 in lentigines to 3.1 J/cm2 in sun-protected skin. Transmission electron microscopy showed immediate alteration of mature melanosomes and nuclei within keratinocytes and melanocytes, but stage I and II melanosomes were unaffected. Histologically, immediate injury was confined to the epidermis. There was minimal inflammatory response 1 day after exposure. After 1 week, subthreshold exposures induced hyperpigmentation, with epidermal hyperplasia and increased melanin staining noted histologically. At higher radiant exposures, hypopigmentation occurred with desquamation of a pigmented scale/crust. All sites returned to normal skin color and texture without scarring within 3 to 6 months. These observations suggest that the human skin response to selective photothermolysis of pigmented cells is similar to that reported in animal models, including low radiant exposure stimulation of melanogenesis and high radiant exposure lethal injury to pigmented epidermal cells. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LAB,DEPT DERMATOL,BOSTON,MA 02114. NR 20 TC 76 Z9 77 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD DEC PY 1991 VL 127 IS 12 BP 1799 EP 1805 DI 10.1001/archderm.127.12.1799 PG 7 WC Dermatology SC Dermatology GA HB975 UT WOS:A1991HB97500005 PM 1845279 ER PT J AU SUPPES, T BALDESSARINI, RJ FAEDDA, GL TOHEN, M AF SUPPES, T BALDESSARINI, RJ FAEDDA, GL TOHEN, M TI RISK OF RECURRENCE FOLLOWING DISCONTINUATION OF LITHIUM TREATMENT IN BIPOLAR DISORDER SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID MANIC-DEPRESSIVE PATIENTS; PROPHYLACTIC LITHIUM; AFFECTIVE-ILLNESS; DOUBLE-BLIND; CALCIUM-ANTAGONISTS; RAPID RECURRENCE; WITHDRAWAL; CARBONATE; TRIAL AB Episode recurrence in bipolar disorder following discontinuation of stable maintenance treatment with lithium salts was analyzed from 14 studies involving 257 patients with bipolar I disorder. More than 50% of new episodes of illness occurred within 10 weeks of stopping an average of 30 months of treatment. By survival analysis of 124 cases in which the time to a new episode was known, the computed time to 50% failure of remission was 5.0 months after stopping therapy; the time to 25% recurrence of mania was 5.2 times earlier than for depression (2.7 vs 14 months). In 16 patients with a mean cycle length before treatment of 11.6 months, the time to a new episode when off lithium therapy was only 1.7 months. Risk of early recurrence of bipolar illness, especially of mania, evidently is increased following discontinuation of lithium use and may exceed that predicted by the course of the untreated disorder. The basis and management of risks associated with discontinuing effective long-term mood-stabilizing treatment require further study. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHIAT RES LABS,BELMONT,MA. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHOT DISORDERS PROGRAM,BELMONT,MA. RI Faedda, Gianni/E-6379-2012 OI Faedda, Gianni/0000-0001-6197-0543 FU NIMH NIH HHS [MH-47370, MH-31154, MH-36224] NR 49 TC 295 Z9 298 U1 2 U2 7 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 DEC PY 1991 VL 48 IS 12 BP 1082 EP 1088 PG 7 WC Psychiatry SC Psychiatry GA GW653 UT WOS:A1991GW65300006 PM 1845226 ER PT J AU SANTIAGO, S TOBIAS, J WILLIAMS, AJ AF SANTIAGO, S TOBIAS, J WILLIAMS, AJ TI A REAPPRAISAL OF THE CAUSES OF HEMOPTYSIS SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID FIBEROPTIC BRONCHOSCOPY AB We reviewed the records of 264 patients who underwent fiberoptic bronchoscopy for unexplained hemoptysis to determine the various causes of hemoptysis. Bronchogenic carcinoma (29%), bronchitis (23%), and idiopathic hemoptysis (22%) accounted for the majority of causes of hemoptysis. In contrast to older studies, the incidence of hemoptysis secondary to tuberculosis and bronchiectasis has decreased. Although our patient population is predominantly male and elderly, our data may well be representative of more recent epidemiologic trends in causes of hemoptysis. C1 UNIV CALIF LOS ANGELES,SCH MED,PULM DIS SECT,LOS ANGELES,CA 90024. RP SANTIAGO, S (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,LOS ANGELES,CA 90073, USA. NR 10 TC 61 Z9 65 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD DEC PY 1991 VL 151 IS 12 BP 2449 EP 2451 DI 10.1001/archinte.151.12.2449 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA HF433 UT WOS:A1991HF43300015 PM 1747002 ER PT J AU LEIFER, D HOCHBERG, FH AF LEIFER, D HOCHBERG, FH TI POSTTRAUMATIC PONTINE TRUNCAL SENSORY LEVEL SO ARCHIVES OF NEUROLOGY LA English DT Letter ID BRAIN-STEM LESIONS RP LEIFER, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD DEC PY 1991 VL 48 IS 12 BP 1216 EP 1216 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA GZ420 UT WOS:A1991GZ42000005 PM 1845022 ER PT J AU GREWAL, RP DOPPELT, SH THOMPSON, MA KATZ, D BRADY, RO BARTON, NW AF GREWAL, RP DOPPELT, SH THOMPSON, MA KATZ, D BRADY, RO BARTON, NW TI NEUROLOGIC COMPLICATIONS OF NONNEURONOPATHIC GAUCHERS-DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Article ID SPINAL-CORD COMPRESSION AB We describe eight patients with type 1 Gaucher's disease who developed neurologic complications that were secondary to systemic features of the illness. Four patients experienced neurologic difficulties because of coagulopathy, and the other four patients had involvement of the nervous system secondary to skeletal disease. Early recognition of these complications in patients with type 1 Gaucher's disease may lead to improved neurologic outcome. C1 NINCDS,OFF CLIN DIRECTOR,BETHESDA,MD 20892. NCI,PATHOL LAB,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. RP GREWAL, RP (reprint author), NINCDS,DEV & METAB NEUROL BRANCH,BLDG 10,ROOM 3D03,BETHESDA,MD 20892, USA. NR 8 TC 21 Z9 21 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD DEC PY 1991 VL 48 IS 12 BP 1271 EP 1272 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA GZ420 UT WOS:A1991GZ42000020 PM 1845033 ER PT J AU ANTONIADES, HN AF ANTONIADES, HN TI PDGF - A MULTIFUNCTIONAL GROWTH-FACTOR SO BAILLIERES CLINICAL ENDOCRINOLOGY AND METABOLISM LA English DT Article ID SMOOTH-MUSCLE CELLS; SIMIAN SARCOMA-VIRUS; CULTURED ENDOTHELIAL-CELLS; FACTOR-A-CHAIN; IDIOPATHIC PULMONARY FIBROSIS; DIFFERENT DIMERIC FORMS; FACTOR-LIKE PROTEIN; SIS MESSENGER-RNA; C-SIS; HUMAN-FIBROBLASTS C1 HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. RP ANTONIADES, HN (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,655 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA30101]; NHLBI NIH HHS [HL29583] NR 117 TC 57 Z9 57 U1 0 U2 0 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0950-351X J9 BAILLIERE CLIN ENDOC JI Baillieres Clin. Endocrinol. Metab. PD DEC PY 1991 VL 5 IS 4 BP 595 EP 613 PG 19 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GP499 UT WOS:A1991GP49900005 PM 1661577 ER PT J AU DEMETRI, GD GRIFFIN, JD AF DEMETRI, GD GRIFFIN, JD TI GRANULOCYTE COLONY-STIMULATING FACTOR AND ITS RECEPTOR SO BLOOD LA English DT Review ID RECOMBINANT HUMAN GRANULOCYTE; FACTOR G-CSF; HEMATOPOIETIC PROGENITOR CELLS; ACUTE MYELOBLASTIC-LEUKEMIA; ACUTE PROMYELOCYTIC LEUKEMIA; HUMAN GRANULOPOIESIS INVITRO; CHROMOSOMAL GENE STRUCTURE; GROWTH-FACTOR RECEPTORS; HUMAN-ENDOTHELIAL CELLS; FACTOR RG-CSF RP DEMETRI, GD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 170 TC 792 Z9 810 U1 1 U2 14 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 DEC 1 PY 1991 VL 78 IS 11 BP 2791 EP 2808 PG 18 WC Hematology SC Hematology GA GR781 UT WOS:A1991GR78100001 PM 1720034 ER PT J AU KURIU, A IKEDA, H KANAKURA, Y GRIFFIN, JD DRUKER, B YAGURA, H KITAYAMA, H ISHIKAWA, J NISHIURA, T KANAYAMA, Y YONEZAWA, T TARUI, S AF KURIU, A IKEDA, H KANAKURA, Y GRIFFIN, JD DRUKER, B YAGURA, H KITAYAMA, H ISHIKAWA, J NISHIURA, T KANAYAMA, Y YONEZAWA, T TARUI, S TI PROLIFERATION OF HUMAN MYELOID-LEUKEMIA CELL-LINE ASSOCIATED WITH THE TYROSINE-PHOSPHORYLATION AND ACTIVATION OF THE PROTOONCOGENE C-KIT PRODUCT SO BLOOD LA English DT Article ID HEMATOPOIETIC GROWTH-FACTOR; COLONY-STIMULATING FACTOR; KINASE RECEPTOR; W-LOCUS; STEEL LOCUS; MAST-CELLS; SI-LOCUS; LIGAND; MOUSE; EXPRESSION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP KURIU, A (reprint author), OSAKA UNIV,SCH MED,DEPT INTERNAL MED 2,FUKUSHIMA 1-1-50,FUKUSHIMA KU,OSAKA 553,JAPAN. NR 27 TC 95 Z9 96 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 DEC 1 PY 1991 VL 78 IS 11 BP 2834 EP 2840 PG 7 WC Hematology SC Hematology GA GR781 UT WOS:A1991GR78100005 PM 1720036 ER PT J AU IKEDA, H KANAKURA, Y TAMAKI, T KURIU, A KITAYAMA, H ISHIKAWA, J KANAYAMA, Y YONEZAWA, T TARUI, S GRIFFIN, JD AF IKEDA, H KANAKURA, Y TAMAKI, T KURIU, A KITAYAMA, H ISHIKAWA, J KANAYAMA, Y YONEZAWA, T TARUI, S GRIFFIN, JD TI EXPRESSION AND FUNCTIONAL-ROLE OF THE PROTOONCOGENE C-KIT IN ACUTE MYELOBLASTIC-LEUKEMIA CELLS SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; TYROSINE KINASE RECEPTOR; GROWTH-FACTOR; MAST-CELLS; MUTANT MICE; W-LOCUS; SIGNAL TRANSDUCTION; INVITRO DUPLICATION; STEEL LOCUS; SI-LOCUS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP IKEDA, H (reprint author), OSAKA UNIV,SCH MED,DEPT INTERNAL MED 2,1-1-50 FUKUSHIMA,FUKUSHIMA KU,OSAKA 553,JAPAN. NR 41 TC 233 Z9 234 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 DEC 1 PY 1991 VL 78 IS 11 BP 2962 EP 2968 PG 7 WC Hematology SC Hematology GA GR781 UT WOS:A1991GR78100022 PM 1720040 ER PT J AU SCHNEIDER, LC ANTIN, JH WEINSTEIN, H ABRAMS, JS PEARCE, MK GEHA, RS VERCELLI, D AF SCHNEIDER, LC ANTIN, JH WEINSTEIN, H ABRAMS, JS PEARCE, MK GEHA, RS VERCELLI, D TI LYMPHOKINE PROFILE IN BONE-MARROW TRANSPLANT RECIPIENTS SO BLOOD LA English DT Article ID HUMAN PERIPHERAL-BLOOD; T-CELLS; MESSENGER-RNA; INTERFERON-GAMMA; HOST-DISEASE; INSITU HYBRIDIZATION; IGE SYNTHESIS; ACUTE GRAFT; INTERLEUKIN-4; LYMPHOCYTES C1 BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. DNAX RES INST CELLULAR & MOLEC BIOL,PALO ALTO,CA. RP SCHNEIDER, LC (reprint author), CHILDRENS HOSP MED CTR,DIV IMMUNOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 28 TC 32 Z9 33 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 DEC 1 PY 1991 VL 78 IS 11 BP 3076 EP 3080 PG 5 WC Hematology SC Hematology GA GR781 UT WOS:A1991GR78100038 PM 1954393 ER PT J AU PARIS, JM CALLAHAN, PM LEE, JM CUNNINGHAM, KA AF PARIS, JM CALLAHAN, PM LEE, JM CUNNINGHAM, KA TI BEHAVIORAL SENSITIZATION TO COCAINE IS NOT ASSOCIATED WITH CHANGES IN SEROTONIN (5-HT) FIBER IMMUNOREACTIVITY IN RAT FOREBRAIN SO BRAIN RESEARCH BULLETIN LA English DT Note DE COCAINE; BEHAVIORAL SENSITIZATION; SEROTONIN; NEUROTOXICITY; 5-HT IMMUNOREACTIVITY; RAT ID DORSAL; BRAIN; NEURONS; MDMA; METHAMPHETAMINE; PROJECTIONS; AMPHETAMINE; NEUROTOXIN; TERMINALS; NUCLEUS AB We investigated whether cocaine-induced behavioral sensitization is associated with changes in serotonin (5-HT) immunoreactivity. Male Sprague-Dawley rats were injected with either cocaine (15 mg/kg, IP) or saline twice daily for seven days. Their behavior was observed and rated for locomotor activation and stereotypy. One day after the final injection, the brains were processed for 5-HT immunohistochemistry. The intensity of 5-HT immunoreactive staining of 5-HT axons and terminal varicosities was blindly rated in cocaine-sensitized rats and found not to differ from saline-treated rats. The results support the hypothesis that unlike some amphetamine derivatives, repeated cocaine administration which results in behavioral sensitization is not neurotoxic to 5-HT axons and terminals in the forebrain. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP PARIS, JM (reprint author), UNIV TEXAS,MED BRANCH,DEPT PHARMACOL & TOXICOL J-31,GALVESTON,TX 77550, USA. RI Cunningham, Kathryn/O-2718-2013 FU NIDA NIH HHS [DA05708, DA05381] NR 36 TC 8 Z9 8 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0361-9230 J9 BRAIN RES BULL JI Brain Res. Bull. PD DEC PY 1991 VL 27 IS 6 BP 843 EP 847 DI 10.1016/0361-9230(91)90220-E PG 5 WC Neurosciences SC Neurosciences & Neurology GA GV701 UT WOS:A1991GV70100013 PM 1786564 ER PT J AU ELIAS, AD MAZANET, R WHEELER, C ANDERSON, K AYASH, L SCHWARTZ, G TEPLER, I PAP, S PELAEZ, J HUNT, M SCHNIPPER, L GRIFFIN, J FREI, E ANTMAN, K AF ELIAS, AD MAZANET, R WHEELER, C ANDERSON, K AYASH, L SCHWARTZ, G TEPLER, I PAP, S PELAEZ, J HUNT, M SCHNIPPER, L GRIFFIN, J FREI, E ANTMAN, K TI GM-CSF POTENTIATED PERIPHERAL-BLOOD PROGENITOR-CELL (PBPC) COLLECTION WITH OR WITHOUT BONE-MARROW AS HEMATOLOGIC SUPPORT OF HIGH-DOSE CHEMOTHERAPY - 2 PROTOCOLS SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Article DE PROGENITOR CELLS; ABMT; GM-CSF; STEM CELLS; PERIPHERAL BLOOD; SOLID TUMOR ID COLONY-STIMULATING FACTOR; NON-HODGKINS-LYMPHOMA; HEMATOPOIETIC STEM-CELLS; BREAST-CANCER; TRANSPLANTATION; DISEASE AB High-dose chemotherapy with autologous bone marrow support (ABMS) achieves prolonged relapse-free survival in relapsed lymphomas and leukemias and has provided durable complete responses in certain solid tumors. The principal morbidity and mortality result from the infectious and bleeding complications during the 3-4 week aplasia until the bone marrow autograft can recover. Hematopoietic growth factors, alone or used after chemotherapy, increase the number of circulating progenitor cells in the peripheral blood compartment. In one trial, 12 patients with solid tumors were treated with high-dose chemotherapy and supported with both bone marrow and peripheral blood progenitor cells (PBPC) collected after GM-CSF administration. Reconstitution of bone marrow function occurred quickly (ANC > 500/mu-l by day 17; platelet-transfusion independence by day 16), resulting in short hospital stays (median, 28 days). In a second study, 12 patients with metastatic breast cancer responding to induction chemotherapy (doxorubicin, 5-fluorouracil, and methotrexate) were given GM-CSF during induction to collect PBPCs during leukocyte recovery. These PBPCs were used as the sole hematopoietic support during high-dose chemotherapy with cyclophosphamide, thiotepa, and carboplatin. Granulocyte and platelet reconstitution were extremely rapid (median, 14 and 12 days, respectively). When compared with 29 patients undergoing the same intensification therapy using ABMT as sole support, time to hematopoietic recovery, transfusion requirements, and duration of hospital stay were all significantly improved for the patients receiving PBPC. PBPC with or without marrow may enhance the safety, tolerance, and cost of high-dose therapy. Moreover, PBPC may render multiple course combination, high-dose therapy feasible. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. RP ELIAS, AD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 25 TC 17 Z9 17 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD DEC PY 1991 VL 20 SU S BP S25 EP S29 DI 10.1007/BF01908241 PG 5 WC Oncology SC Oncology GA HD348 UT WOS:A1991HD34800005 PM 1687204 ER PT J AU MEYER, GS AF MEYER, GS TI CRIMINAL PUNISHMENT FOR THE TRANSMISSION OF SEXUALLY-TRANSMITTED DISEASES - LESSONS FROM SYPHILIS SO BULLETIN OF THE HISTORY OF MEDICINE LA English DT Article ID AIDS RP MEYER, GS (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,FAC DEV GEN INTERNAL MED PROGRAM,BOSTON,MA 02115, USA. NR 36 TC 6 Z9 6 U1 0 U2 1 PU JOHNS HOPKINS UNIV PRESS PI BALTIMORE PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD 21218-4319 SN 0007-5140 J9 B HIST MED JI Bull. Hist. Med. PD WIN PY 1991 VL 65 IS 4 BP 549 EP 564 PG 16 WC Health Care Sciences & Services; History & Philosophy Of Science SC Health Care Sciences & Services; History & Philosophy of Science GA GW963 UT WOS:A1991GW96300005 PM 1802318 ER PT J AU METTLIN, C BONFIGLIO, J BERG, RL NELSON, G NEWELL, GR PATTERSON, WB RICHARDSON, J RIMER, B SORENSON, A WARNECKE, R AF METTLIN, C BONFIGLIO, J BERG, RL NELSON, G NEWELL, GR PATTERSON, WB RICHARDSON, J RIMER, B SORENSON, A WARNECKE, R TI PREVENTION AND DETECTION IN OLDER PERSONS SO CANCER LA English DT Article; Proceedings Paper CT NATIONAL WORKSHOP OF THE AMERICAN CANCER SOC : CANCER CONTROL AND THE OLDER PERSON CY MAR 14-16, 1991 CL ATLANTA, GA SP AMER CANC SOC AB Older persons are appropriate targets for a range of prevention and early detection interventions, however, greater emphasis should be given to structuring the delivery of prevention and detection services to the special needs of this population. This may require research and program development to reach older persons in the most effective and cost-effective manner. The American Cancer Society and other program efforts must accommodate the heterogeneity and special needs of segments of the older population. Racial and cultural minorities, impoverished persons, the cognitively impaired, and the physically impaired are four groups requiring special attention. Early detection guidelines specific to older persons should be developed. C1 AMER CANC SOC,DEPT DETECT & TREATMENT,ATLANTA,GA. UNIV ROCHESTER,SCH MED,DEPT COMMUNITY & PREVENT MED,ROCHESTER,NY 14627. CTR DIS CONTROL,CTR CHRON DIS PREVENT & HLTH PROMOT,ATLANTA,GA 30333. UNIV TEXAS,MD ANDERSON CANCER CTR,DEPT CANC PREVENT & CONTROL,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA 02115. UNIV SO CALIF,SCH MED,NORRIS COMPREHENS CANC CTR,DEPT PREVENT MED,LOS ANGELES,CA 90033. FOX CHASE CANC INST,DEPT POPULAT SCI BEHAV RES,CHELTENHAM,PA. NIA,BIOL AGING PROGRAM,NUTR PROGRAM,BETHESDA,MD 20892. SURVEY RES LAB,CHICAGO,IL. RP METTLIN, C (reprint author), NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,666 ELM ST,BUFFALO,NY 14263, USA. NR 0 TC 5 Z9 5 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 0008-543X J9 CANCER JI Cancer PD DEC 1 PY 1991 VL 68 IS 11 SU S BP 2530 EP 2533 DI 10.1002/1097-0142(19911201)68:11+<2530::AID-CNCR2820681510>3.0.CO;2-3 PG 4 WC Oncology SC Oncology GA GQ294 UT WOS:A1991GQ29400009 PM 1933798 ER PT J AU BERKMAN, B STEVENSON, E CRAVEDI, KG DAVIS, A LAWRENCE, W MOR, V OSTRANDER, V RUBENSTEIN, LJ SPEERS, M WILSON, K AF BERKMAN, B STEVENSON, E CRAVEDI, KG DAVIS, A LAWRENCE, W MOR, V OSTRANDER, V RUBENSTEIN, LJ SPEERS, M WILSON, K TI ADVOCACY - NECESSARY TO ACHIEVE CANCER CONTROL GOALS SO CANCER LA English DT Article; Proceedings Paper CT NATIONAL WORKSHOP OF THE AMERICAN CANCER SOC : CANCER CONTROL AND THE OLDER PERSON CY MAR 14-16, 1991 CL ATLANTA, GA SP AMER CANC SOC AB As resources become increasingly scarce, oncology professionals and consumers of oncology services are increasingly engaging in advocacy efforts to achieve goals in cancer control. Effective advocacy includes both legislative and direct educational efforts. C1 HARVARD UNIV,SCH MED,CTR GERIATR EDUC,DIV AGING,BOSTON,MA 02115. AMER CANC SOC,DEPT NURSING & PATIENT SERV,ATLANTA,GA. US HOUSE REPRESENTAT,HOUSE AGING COMM,SUBCOMM HLTH & LONG TERM CARE,WASHINGTON,DC 20515. AMER CANC SOC,DEPT PUBL ISSUES,WASHINGTON,DC. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,MASSEY CANC CTR,RICHMOND,VA 23298. BROWN UNIV,CTR GERONTOL & HLTH CARE RES,PROVIDENCE,RI 02912. AMER ASSOC RETIRED PERSONS,GEORGIA COUNCIL AGING,ATLANTA,GA. AMER ASSOC RETIRED PERSONS,HLTH ADVOCACY SERV,WASHINGTON,DC. CTR DIS CONTROL,CTR CHRON DIS PREVENT & HLTH PROMOT,ATLANTA,GA 30333. RP BERKMAN, B (reprint author), MASSACHUSETTS GEN HOSP,DEPT SOCIAL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD DEC 1 PY 1991 VL 68 IS 11 SU S BP 2540 EP 2542 DI 10.1002/1097-0142(19911201)68:11+<2540::AID-CNCR2820681512>3.0.CO;2-X PG 3 WC Oncology SC Oncology GA GQ294 UT WOS:A1991GQ29400011 PM 1933800 ER PT J AU SEIZINGER, BR AF SEIZINGER, BR TI GENES ASSOCIATED WITH TUMOR SUPPRESSION AND GROWTH-CONTROL IN THE HUMAN NERVOUS-SYSTEM SO CANCER AND METASTASIS REVIEWS LA English DT Review DE TUMOR SUPPRESSOR GENES; ANTIONCOGENES; BRAIN; NERVOUS SYSTEM; GROWTH REGULATION; HEREDITARY TUMOR SYNDROMES ID RETINOBLASTOMA SUSCEPTIBILITY GENE; NEUROFIBROMATOSIS TYPE-1 GENE; ENDOCRINE NEOPLASIA; CELL-CYCLE; P53 GENE; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; PRODUCT; CANCER; MUTATIONS; IDENTIFICATION AB Cancer, the uncontrolled proliferation of a population of somatic cells, is fundamentally a genetic disorder. Although the specific array of genetic changes causing individual tumor types remains largely obscure, the past two decades have witnessed a tremendous increase in our understanding of the specific genes regulating cell differentiation, proliferation, and senescence. There appear to be two distinct fundamental genetic mechanisms of tumorigenesis. One mechanism is associated with the activation of growth-promoting factors such as proto-oncogenes. Alternatively, tumor formation may be induced as the result of the loss or inactivation of genes which normally regulate or suppress cell growth. These genes have been termed 'tumor suppressor' genes or 'anti-oncogenes'. This review focuses on the role of 'tumor suppressor' genes in tumor formation and growth control of the human nervous system. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP SEIZINGER, BR (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA49455-03] NR 58 TC 2 Z9 2 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-7659 J9 CANCER METAST REV JI Cancer Metastasis Rev. PD DEC PY 1991 VL 10 IS 4 BP 281 EP 287 DI 10.1007/BF00554790 PG 7 WC Oncology SC Oncology GA HF670 UT WOS:A1991HF67000002 PM 1786629 ER PT J AU ROLLINS, BJ AF ROLLINS, BJ TI JE/MCP-1 - AN EARLY-RESPONSE GENE ENCODES A MONOCYTE-SPECIFIC CYTOKINE SO CANCER CELLS-A MONTHLY REVIEW LA English DT Review ID ACTIVATING FACTOR MCAF; MACROPHAGE INFLAMMATORY PROTEIN-1; HUMAN MONONUCLEAR PHAGOCYTES; GROWTH STIMULATORY ACTIVITY; HUMAN ENDOTHELIAL-CELLS; TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE CELLS; DOUBLE-STRANDED-RNA; CHEMOATTRACTANT PROTEIN-1; CHEMOTACTIC FACTOR AB The JE gene was one of the first growth-factor-inducible early-response genes to be identified. Sequence and expression analysis have revealed that JE encodes the monocyte-specific cytokine MCP-1 (also known as MCAF, TDCF, and SMC-CF). JE/MCP-1 specifically attracts monocytes in vitro and in vivo, but has no detectable effects on neutrophils or lymphocytes. In addition, JE/MCP-1 can suppress tumor formation in animal models by attracting and activating monocytes. These discoveries have drawn together the investigations of those who study the molecular basis of cell proliferation and those who work on the molecular basis of the inflammatory response. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROLLINS, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115, USA. NR 94 TC 105 Z9 107 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 1042-2196 J9 CANCER CELL-MON REV PD DEC PY 1991 VL 3 IS 12 BP 517 EP 524 PG 8 WC Oncology; Medicine, Research & Experimental SC Oncology; Research & Experimental Medicine GA HC628 UT WOS:A1991HC62800008 PM 1820095 ER PT J AU LAMBERT, JM GOLDMACHER, VS COLLINSON, AR NADLER, LM BLATTLER, WA AF LAMBERT, JM GOLDMACHER, VS COLLINSON, AR NADLER, LM BLATTLER, WA TI AN IMMUNOTOXIN PREPARED WITH BLOCKED RICIN - A NATURAL PLANT TOXIN ADAPTED FOR THERAPEUTIC USE SO CANCER RESEARCH LA English DT Article ID RIBOSOME-INACTIVATING PROTEINS; SACCHARIDE-BINDING SITE; A-CHAIN IMMUNOTOXINS; HUMAN B-CELLS; MONOCLONAL-ANTIBODIES; CYTO-TOXICITY; EUKARYOTIC RIBOSOMES; DIPHTHERIA-TOXIN; LYMPHOID-CELLS; TUMOR-CELLS AB Ricin, the cytotoxic protein isolated from castor beans, is composed of two subunits, A-chain and B-chain. Ricin intoxicates cells by binding through its B-chain to galactose-terminated oligosaccharides found on the surface of all eukaryotic cells and then transferring its A-chain to the cytosol where it disrupts protein synthesis by inactivating ribosomes. In addition to binding, the B-chain plays an important, but not yet understood, role in the translocation of the A-chain through a cellular membrane to the cytosol. Blocking the two galactose-binding sites of native ricin by chemical modification with affinity ligands created an altered toxin, called blocked ricin, that has at least a 3500-fold lower binding affinity and is more than 1000-fold less cytotoxic than native ricin for Namalwa cells (a Burkitt's lymphoma line) but that has maintained the translocation function of the B-chain and the catalytic activity of the A-chain. Conjugation of blocked ricin to monoclonal antibodies that bind to cell surface antigens creates new cytotoxins that approach the potency of native ricin. These cytotoxins incorporate the three essential functions of natural toxins, i.e., binding to cells, transport through a membrane, and catalytic inactivation of an essential cellular process; but in addition they possess a defined cellular target specificity. Such potent immunotoxins may play an important therapeutic role in cancer treatment. Clinical trials with an anti-CD19-blocked ricin and an anti-CD33-blocked ricin conjugate against B-cell cancers and acute myeloblastic leukemia have begun. C1 IMMUNOGEN INC,148 SIDNEY ST,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 56 TC 117 Z9 119 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD DEC 1 PY 1991 VL 51 IS 23 BP 6236 EP 6242 PG 7 WC Oncology SC Oncology GA GR475 UT WOS:A1991GR47500005 PM 1718599 ER PT J AU RUCKDESCHEL, JC MOORES, D LEE, JY EINHORN, LH MANDELBAUM, I KOELLER, J WEISS, GR LOSADA, M KELLER, JH AF RUCKDESCHEL, JC MOORES, D LEE, JY EINHORN, LH MANDELBAUM, I KOELLER, J WEISS, GR LOSADA, M KELLER, JH TI INTRAPLEURAL THERAPY FOR MALIGNANT PLEURAL EFFUSIONS - A RANDOMIZED COMPARISON OF BLEOMYCIN AND TETRACYCLINE SO CHEST LA English DT Article ID INTRACAVITARY BLEOMYCIN; MANAGEMENT; PLEURODESIS AB Between December 1985 and August 1988, there were 115 patients at 13 centers who were entered on a randomized comparison of tetracycline and bleomycin for treatment of malignant pleural effusions. Fifteen patients were not treated, primarily due to rapid progression of systemic cancer. Fifteen patients entered on a high-dose regimen of bleomycin (120 units) were excluded from this analysis (following early closure of that arm), leaving 85 patients randomized to low-dose bleomycin (60 units; 44 patients) or tetracycline (1 g; 41 patients). Patients were required to have a cytologically positive pleural effusion, good performance status (0, 1, or 2), lung reexpansion following tube thoracostomy with drainage rates of 100 ml/24 or less, no prior intrapleural therapy, no prior systemic bleomycin therapy, no chest irradiation, and no recent (four weeks) change in systemic therapy. A total of 11 patients (five with bleomycin and six with tetracycline) were not evaluable due to technical problems with tube drainage (one), loss to follow-up (two), sudden death due to pulmonary embolus (one), and rapid progression of systemic disease (seven). There were no clinically significant differences in demographic factors, primary site, performance status, or presence of metastases other than pleural effusion. Overall survival did not differ between the two groups. Median time to recurrence or progression of the effusion was 32 days for tetracycline-treated patients and at least 46 days for bleomycin-treated patients (p = 0.037). The recurrence rate within 30 days of instillation was 36 percent (10/28) with bleomycin and 67 percent (18/27) with tetracycline (p = 0.023) (not all patients were restudied in the first 30 days). By 90 days the corresponding recurrence rates were 30 Percent (11/37) for bleomycin and 53 percent (19/36) for tetracycline (p = 0.047). Toxicity was similar between groups. C1 UNIV ALABAMA,DIV BIOSTAT,BIRMINGHAM,AL 35294. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. INDIANA UNIV,INDIANAPOLIS,IN 46204. BRISTOL MYERS US,PHARMACEUT GRP,EVANSVILLE,IN. RP RUCKDESCHEL, JC (reprint author), UNION UNIV,ALBANY,NY 12208, USA. NR 30 TC 108 Z9 111 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1528 EP 1535 DI 10.1378/chest.100.6.1528 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100013 PM 1720370 ER PT J AU KOMADINA, KH SCHENK, DA LAVEAU, P DUNCAN, CA CHAMBERS, SL AF KOMADINA, KH SCHENK, DA LAVEAU, P DUNCAN, CA CHAMBERS, SL TI INTEROBSERVER VARIABILITY IN THE INTERPRETATION OF PULMONARY-ARTERY CATHETER PRESSURE TRACINGS SO CHEST LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; CRITICALLY ILL PATIENTS; WEDGE PRESSURE; HEMODYNAMIC STATUS; HEART; EXPERIENCE; FREQUENCY; BLOOD AB Study objective: We evaluated the ability of three independent reviewers (R1, R2, R3) using waveform analysis to accurately identify confirmed valid PCWP tracings, and their ability to consistently report the PCWP numerical value. Design: Sixty PA and PCWP tracings were prospectively obtained and blindly reviewed by three independent critical care physicians. Setting: The medical ICU of Wilford Hall USAF Medical Center. Patients or participants: Twenty mechanically ventilated patients with PA catheters inserted for hemodynamic assessment. Interventions: Sixty PA and PCWP tracings were reviewed blindly and independently for acceptability using waveform criteria by three critical care physicians. While recording all 60 tracings, blood was aspirated from the distal port of the PA catheter with the balloon "wedged" and blood gas analysis was done. Each reviewer analyzed the PCWP tracings for validity using waveform criteria, and reported a numerical PCWP reading for those tracings judged valid by waveform criteria. Reviewer sensitivity, specificity and accuracy in performing waveform analysis were assessed by comparing their predictions with those tracings that were confirmed valid by the aspiration of pulmonary capillary blood. Inter-reviewer agreement upon which validity of PCWP tracings was based and reviewer agreement on the numerical PCWP reading were also assessed. All tracings were blindly reviewed by each physician, first without and then with an AP tracing to define end-expiration. Measurements and results: Thirty-eight of 60 PCWP tracings were confirmed valid by the aspiration of pulmonary capillary blood. In the remaining 22 tracings, mixed venous blood was aspirated with the balloon wedged, and tracing validity was unconfirmed. Reviewer accuracy in identifying confirmed valid PCWP tracings, using waveform analysis, was 50 percent for R1, 65 percent for R2 and 57 percent for R3. No reviewer's accuracy was significantly different from a random guess which would yield an accuracy of 50 percent. Agreement by all three reviewers in identifying valid PCWP tracings using waveform analysis varied from 37 percent in the absence of an AP tracing to 66 percent when an AP tracing was available to identify end-expiration (p < 0.003). Agreement by all three reviewers on the PCWP numerical reading (within 4 mm Hg) was 79 percent without an AP tracing and 96 percent with an AP tracing (p = NS). The numerical reading reported by the ICU nurses and house staff correlated closely with the reviewers' readings. Agreement with the reported PCWP reading was improved only for R2 by the addition of an AP tracing. Conclusion: We conclude that the validation of PCWP tracings by waveform analysis is subject to interobserver variability, and reviewer accuracy in identifying confirmed valid tracings was no better than a random guess. Agreement on the numerical PCWP reading was high among the reviewers as was agreement by each individual reviewer with the reported PCWP. Finally, the presence of an AP tracing, to define end-expiration, adds little to the interpretation of the PCWP numerical reading by experienced physicians. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,PULM CRIT CARE SECT,SAN ANTONIO,TX 78284. WILFORD HALL USAF MED CTR,CARDIOL SECT,LACKLAND AFB,TX 78236. WILFORD HALL USAF MED CTR,PULM CRIT CARE SECT,LACKLAND AFB,TX 78236. RP KOMADINA, KH (reprint author), PARK NICOLLET MED CTR,5000 W 39TH ST,MINNEAPOLIS,MN 55416, USA. NR 19 TC 37 Z9 42 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1647 EP 1654 DI 10.1378/chest.100.6.1647 PG 8 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100033 PM 1959409 ER PT J AU BRYAN, CL COHEN, DJ DEW, JA TRINKLE, JK JENKINSON, SG AF BRYAN, CL COHEN, DJ DEW, JA TRINKLE, JK JENKINSON, SG TI GLUTATHIONE DECREASES THE PULMONARY REIMPLANTATION RESPONSE IN CANINE LUNG AUTOTRANSPLANTS SO CHEST LA English DT Article ID OXIDATIVE STRESS; RAT LUNG; TRANSPLANTATION; HEART; PRESERVATION; REPERFUSION; DISULFIDE; ISCHEMIA; STORAGE; DAMAGE AB The pulmonary reimplantation response (PRR) is a form of membrane permeability pulmonary edema occurring in lung transplants. The severity of the PRR reflects the quality and duration of lung graft preservation. Free radicals formed during ischemia with reperfusion in the autotransplanted dog lung may play a role in producing PRR. We hypothesized that the addition of reduced glutathione (GSH) to the preservative solution could decrease PRR if hydroperoxides are being formed. Six dogs underwent left lung autotransplantation after the lung was flushed with Euro-Collins solution (EC). These dogs demonstrated radiographic and histopathologic evidence of bilateral pulmonary edema, greatest in the transplanted left lung. They also had increases in lung wet to dry weight (W/D) ratios in both lungs (left, 12.0 +/- 0.9; right, 10.1 +/- 0.8) as compared with a group of five unmanipulated control animals (left, 6.0 +/- 0.5; right, 7.0 +/- 0.4). Malondialdehyde (MDA) concentrations were significantly increased in the transplanted left lungs (14 +/- 4) from this group as compared with the controls (5 +/- 7). Five additional dogs underwent left lung autotransplantation with GSH added to the EC cryopreservation fluid. These animals did not develop histologic or radiographic evidence of pulmonary edema, and W/D ratios as well as MDA concentrations were not different from those in controls. To evaluate the effect of ischemia alone on changes in lung GSH concentrations, ten additional dogs underwent left pneumonectomy. Left lungs were cryopreserved in EC + GSH. In five of the animals, the right lung was removed and preserved in EC alone. In the other five animals, the right lung remained in vivo for 3 h and was then removed. Lung GSH concentrations were doubled after 3 h of ischemia when incubated in EC + GSH compared to in vivo controls and to EC-treated lungs. These data suggest that GSH added to the preservation fluid prevents PRR following transplantation and that lung GSH concentrations actually increase during preservation prior to reimplantation and reperfusion if the lung graft is exposed to GSH in the preservation fluid. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. UNIV TEXAS,HLTH SCI CTR,DEPT MED,LUNG METAB UNIT,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG CARDIOTHORAC SURG,SAN ANTONIO,TX 78284. RP BRYAN, CL (reprint author), DIV PULM DIS,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 40 TC 18 Z9 19 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD DEC PY 1991 VL 100 IS 6 BP 1694 EP 1702 DI 10.1378/chest.100.6.1694 PG 9 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA GU051 UT WOS:A1991GU05100040 PM 1959416 ER PT J AU WANG, LN KOWALL, NW RICHARDSON, EP AF WANG, LN KOWALL, NW RICHARDSON, EP TI PHOSPHORYLATED NEUROFILAMENT EPITOPES IN THE ACHROMASIC NEURONS OF CORTICONIGRAL DEGENERATION SO CHINESE MEDICAL JOURNAL LA English DT Article ID MONOCLONAL-ANTIBODIES; NERVOUS-SYSTEM; PICKS DISEASE; EXPRESSION; PROTEINS AB By employing monoclonal phosphorylated neurofilaments antibody, we studied the abnormally pale-staining neurons in 3 cases of corticonigral degeneration by the avidin-biotin immunoperoxidase method. For comparison, the central chromatolysis in anterior horn cells secondary to cervical spine fracture and "ballooned" neurons in a case of Pick's disease and a case of Alzheimer's disease were studied with similar procedure. Achromasic neurons in the case of corticonigral degeneration and ballooned neurons in Pick's disease and Alzheimer's disease showed positive immunostaining, while neurons with central chromatolysis secondary to axonal injury did not. Our observations show that the achromasic neurons in corticonigral degeneration contain phosphorylated neurofilaments which share common antigenic characteristics with ballooned neurons in Pick's disease and Alzheimer's disease. The absence of positive immunostaining in reactive central chromatolysis suggests that despite the similarities in appearance with the usual histopathologic stains this cytoplasmic change is pathogenetically different from that in the other neuronal disorders mentioned above. C1 MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. RP WANG, LN (reprint author), CHINESE PEOPLES LIBERAT ARMY GEN HOSP,NEUROPATHOL LAB,BEIJING 100853,PEOPLES R CHINA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 16 TC 11 Z9 11 U1 0 U2 0 PU CHINESE MEDICAL ASSOCIATION PI BEIJING PA 42 DONGSI XIDAJIE, BEIJING 100710, PEOPLES R CHINA SN 0366-6999 J9 CHINESE MED J-PEKING JI Chin. Med. J. PD DEC PY 1991 VL 104 IS 12 BP 1011 EP 1017 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA GT606 UT WOS:A1991GT60600009 PM 1782810 ER PT J AU FORCE, T MILANI, R HIBBERD, P LORENZ, R UEDELHOVEN, W LEAF, A WEBER, P AF FORCE, T MILANI, R HIBBERD, P LORENZ, R UEDELHOVEN, W LEAF, A WEBER, P TI ASPIRIN-INDUCED DECLINE IN PROSTACYCLIN PRODUCTION IN PATIENTS WITH CORONARY-ARTERY DISEASE IS DUE TO DECREASED ENDOPEROXIDE SHIFT - ANALYSIS OF THE EFFECTS OF A COMBINATION OF ASPIRIN AND N-3 FATTY-ACIDS ON THE EICOSANOID PROFILE SO CIRCULATION LA English DT Article DE ARACHIDONIC ACID; EICOSAPENTAENOIC ACID; CYCLOOXYGENASE; THROMBOXANE ID LOW-DOSE ASPIRIN; DIETARY EICOSAPENTAENOIC ACID; VEIN-GRAFT PATENCY; THROMBOXANE BIOSYNTHESIS; DIFFERENTIAL INHIBITION; VASCULAR PROSTACYCLIN; PLATELET-AGGREGATION; ENDOTHELIAL-CELLS; UNSTABLE ANGINA; BLOOD-FLOW AB Background. It was the purpose of this study to determine the effects of the combination of aspirin (ASA) and fish oil, which is rich in n-3 polyunsaturated fatty acids, on the eicosanoid profile of patients with coronary artery disease. Specifically, we wanted to determine whether the ASA-induced reduction in prostacyclin production is due to inhibition of endothelial cell cyclooxygenase or to reduced endoperoxide shift from platelets and whether ASA negates the potentially beneficial effects of fish oil on the eicosanoid profile. Methods and Results. Fourteen patients with clinically stable but advanced coronary artery disease received 12 g (n = 8) or 16 g (n = 6) of fish oil concentrate containing 6 or 8 g of n-3 fatty acids for 6 weeks. In addition to the fish oil, patients received increasing daily doses of ASA (50 mg, 100 mg, 325 mg, and 1,300 mg; the latter in four divided doses). Each dose was taken for 2 weeks. With fish oil supplementation, red blood cell phospholipid fatty acid content of arachidonic acid (AA) decreased and of eicosapentaenoic acid (EPA) increased so that EPA as a percent of AA increased from 2% to 26%. Serum thromboxane B2, which represents the production of TXA2 by maximally stimulated platelets, was suppressed by 38% on fish oil alone and by 97% or greater on all doses of ASA. Excretion of PGI2-M, the main urinary metabolite of PGI2 (derived from AA), fell from 50 +/- 4 ng/g of creatinine to 42 +/- 2 ng/g on fish oil alone (p = 0.02). On 50 mg of ASA per day, PGI2-M excretion was 26 +/- 2 ng/g of creatinine (p < 0.001 versus fish oil alone). On 100 mg and 325 mg of ASA per day, PGI2-M was 24 +/- 3 ng/g and 27 +/- 3 ng/g, respectively (p = NS versus value on 50 mg per day). PGI3-M, the main urinary metabolite of PGI3 (derived from EPA), increased from 0.2 +/- 0.1 ng/g of creatinine to 4.9 +/- 0.7 ng/g on fish oil alone (p < 0.001). In contrast with the marked ASA-induced decline in PGI2-M, PGI3-M excretion was not affected by the addition of ASA, even at the higher doses (4.6 +/- 0.7 ng/g and 4.9 +/- 0.5 ng/g on 325 mg per day and 325 mg four times daily, respectively). Conclusions. Moderate-dose (325 mg per day or less) ASA taken once daily has no effect on PGI3 production despite significantly reducing PGI2 production. This suggests that endothelial cell cyclooxygenase is minimally inhibited by such doses of ASA and that a large percent of the PGI2 produced in patients with advanced coronary artery disease derives from the transfer of prostaglandin endoperoxides from activated platelets to endothelial cells. The loss of these substrates accounts for the decrease in PGI2 with moderate-dose ASA. Thus, the ASA-induced decrease in PGI2 may in large part be an unavoidable consequence of ASA-induced platelet cyclooxygenase inhibition. ASA does not negate the potentially beneficial effects of n-3 fatty acids on the eicosanoid profile. C1 HARVARD UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV MUNICH,KREISLAUFKRANKHEITEN,INST PROPHYLAXE & EPIDEMIOL,W-8000 MUNICH 2,GERMANY. RP FORCE, T (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,BIGELOW 840,BOSTON,MA 02114, USA. RI Milani, Richard/A-6045-2011; OI Force, Thomas/0000-0002-0450-8659 NR 47 TC 40 Z9 40 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD DEC PY 1991 VL 84 IS 6 BP 2286 EP 2293 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA GT612 UT WOS:A1991GT61200004 PM 1959184 ER PT J AU BENTIVEGNA, LA ABLIN, LW KIHARA, Y MORGAN, JP AF BENTIVEGNA, LA ABLIN, LW KIHARA, Y MORGAN, JP TI ALTERED CALCIUM HANDLING IN LEFT-VENTRICULAR PRESSURE OVERLOAD HYPERTROPHY AS DETECTED WITH AEQUORIN IN THE ISOLATED, PERFUSED FERRET HEART SO CIRCULATION RESEARCH LA English DT Article DE CALCIUM; AEQUORIN; HYPERTROPHY; DIASTOLIC DYSFUNCTION; PRESSURE OVERLOAD ID INTRACELLULAR CALCIUM; CARDIAC-HYPERTROPHY; MYOCARDIUM; MUSCLE; FAILURE; TRANSIENTS AB The purpose of this study was to test the hypothesis that systolic and diastolic dysfunction in left ventricular pressure-overload hypertrophy is caused by abnormal intracellular calcium handling. Experiments were performed with intact, buffer-perfused, isovolumic ferret hearts (n = 9 hypertrophied, n = 9 control) that were loaded with the bioluminescent indicator aequorin to monitor changes in cytoplasmic calcium. In each experiment, left ventricular pressure and intracellular calcium transients were simultaneously recorded. Compared with their age-matched controls, significant hypertrophy of the left ventricle developed 4 weeks after postvalvular aortic banding; at the time the animals were killed, the left ventricular weight/body weight ratio was increased in the banded animals (5.3 X 10(-3) versus 3.6 x 10(-3), p < 0.001). As indicated by the diastolic pressure-volume relation, left ventricular distensibility was significantly diminished in the hypertrophied hearts. In comparison to the controls, the hypertrophied hearts demonstrated a prolonged duration of isovolumic contraction (time to 90% decline from peak: 278 +/- 5.4 versus 247 +/- 10.2 msec, p < 0.05), but a marked decrease in peak systolic midwall stress (22.4 +/- 5.0 versus 38.6 +/- 5.7 g/cm2, p < 0.05). The increased duration of isovolumic contraction correlated with a similar prolongation of the calcium transient (time to 90% decline from peak: 245 +/- 19.5 versus 127 +/- 13.2 msec, p < 0.05), indicating that the rate of sequestration and perhaps release of calcium by the sarcoplasmic reticulum is decreased in hypertrophy. In contrast, control and hypertrophied hearts had similar peak systolic calcium levels (pCa: 6.4 +/- 0.2 versus 6.6 +/- 0.1, p = NS), indicating that the diminution in peak left ventricular midwall stress developed by the hypertrophied hearts was not due to decreased availability of activator calcium. We conclude that the prolonged time course of left ventricular pressure development, but not the diminished peak isovolumic midwall stress or decreased diastolic distensibility, may be related to alterations in intracellular calcium handling. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,HARVARD THORNDIKE LAB,BOSTON,MA 02215. FU NHLBI NIH HHS [HL-01611, HL-31117] NR 29 TC 49 Z9 50 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD DEC PY 1991 VL 69 IS 6 BP 1538 EP 1545 PG 8 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA GR971 UT WOS:A1991GR97100011 PM 1835431 ER PT J AU PUOPOLO, PR VOLPICELLI, SA JOHNSON, DM FLOOD, JG AF PUOPOLO, PR VOLPICELLI, SA JOHNSON, DM FLOOD, JG TI EMERGENCY TOXICOLOGY TESTING (DETECTION, CONFIRMATION, AND QUANTIFICATION) OF BASIC DRUGS IN SERUM BY LIQUID-CHROMATOGRAPHY WITH PHOTODIODE ARRAY DETECTION SO CLINICAL CHEMISTRY LA English DT Note DE SCREENING; CHROMATOGRAPHY; REVERSED-PHASE; GC MS CONFIRMATION METHOD ID TRICYCLIC ANTI-DEPRESSANTS; ULTRAVIOLET-SPECTRA; ANTIDEPRESSANTS; IDENTIFICATION; MULTICHANNEL; QUANTITATION; EXTRACTION; COLUMN AB We investigated the applicability of liquid chromatography with photodiode array detection as a serum drug screening technique in an emergency toxicology setting. Basic compounds are extracted from alkalinized serum with hexane and chromatographed on a cyanopropyl reversed-phase column. The photodiode array detector records the ultraviolet spectrum of each eluting peak for identification and quantification. More than 30 drugs/metabolites including antidepressants, antihistamines, phenothiazines, and analgesics are detected at their therapeutic concentrations or less. Quantitative run-to-run precision (CV) for antidepressant drugs at low therapeutic concentrations is < 6%. We evaluated the potential for interference of > 140 compounds of clinical interest. In a split-sample study, 151 of 154 positive drug findings by the method were confirmed by alternative techniques (gas chromatography/mass spectrometry and liquid chromatography with either normal-phase or reversed-phase columns). In the three unconfirmed findings, this method detected drugs at concentrations below the limit of identification of the comparison method. Also, 275 samples judged negative by this procedure were negative by a different liquid-chromatographic method. C1 MASSACHUSETTS GEN HOSP,CHEM LAB,GRAY 5,BOSTON,MA 02114. METPATH LABS,CAMBRIDGE,MA. NR 17 TC 34 Z9 34 U1 0 U2 2 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 DEC PY 1991 VL 37 IS 12 BP 2124 EP 2130 PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA GX357 UT WOS:A1991GX35700018 PM 1764789 ER PT J AU TRUHAN, AP AF TRUHAN, AP TI SUN PROTECTION IN CHILDHOOD SO CLINICAL PEDIATRICS LA English DT Article ID SKIN-CANCER; CUTANEOUS MELANOMA; MALIGNANT-MELANOMA; EXPOSURE HABITS; SUNSCREEN USE; SUNLIGHT; CHILDREN; AGE AB There is compelling evidence that childhood is a particularly vulnerable time for the photocarcinogenic effects of sun exposure on the skin. Studies indicate that excessive sun exposure during the first 10-20 years of life greatly increases the risk of skin cancer. Nonmelanoma skin cancer (basal cell and squamous cell carcinoma) has been associated with cumulative sun exposure, whereas melanoma has been associated with short, intense sun exposure or blistering sunburn. Under normal circumstances, children receive three times the annual sun exposure of adults; most of one's lifetime sun exposure occurs in childhood. Depletion of the earth's protective ozone layer adds to the photodamage problem. It is clear that sun protection is most vital in the early years. Those with fair skin are at highest risk. Photoprotective measures including sunscreen, clothing, and sun avoidance in childhood may significantly reduce the occurrence of melanoma and other skin cancer in later life. Regular use of sunscreen with a sun protection factor of 15 during the first 18 years of life could reduce the lifetime incidence of nonmelanoma skin cancer by 78%. Pediatricians can play a major role in educating parents and children. RP TRUHAN, AP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,ACC 715,BOSTON,MA 02114, USA. NR 27 TC 49 Z9 50 U1 0 U2 1 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD DEC PY 1991 VL 30 IS 12 BP 676 EP 681 DI 10.1177/000992289103001205 PG 6 WC Pediatrics SC Pediatrics GA GY709 UT WOS:A1991GY70900005 PM 1764876 ER PT J AU BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G AF BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G TI A RANDOMIZED TRIAL OF AMBULATORY CARE IN THE 3RD YEAR CLERKSHIP SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A883 EP A883 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200468 ER PT J AU BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG AF BUKOWSKI, DM DENEKE, SM LAWRENCE, RA JENKINSON, SG TI CYSTINE TRANSPORT IS NOT INDUCED IN ALVEOLAR TYPE-II CELLS STRESSED BY ARSENITE OR DIETHYLMALEATE (DEM) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,AUDIE L MURPHY VET ADM HOSP,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78285. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A813 EP A813 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200095 ER PT J AU CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C AF CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C TI OBSERVER VARIABILITY AND ENVIRONMENTAL NOISE IN SCREENING FOR HEARING-LOSS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A884 EP A884 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200473 ER PT J AU GERETY, MB KADRI, AA CROW, S CHIODO, LK KANTEN, DN MULROW, CD AF GERETY, MB KADRI, AA CROW, S CHIODO, LK KANTEN, DN MULROW, CD TI SCREENING TOOLS FOR DEPRESSION IN NURSING-HOME RESIDENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A884 EP A884 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200475 ER PT J AU GREENE, KE BRYAN, CL UTSET, OM ROODMAN, D JENKINSON, SG AF GREENE, KE BRYAN, CL UTSET, OM ROODMAN, D JENKINSON, SG TI LUNG INFLAMMATION AND FIBROSIS IN MICE CHRONICALLY EXPOSED TO TNF-ALPHA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A846 EP A846 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200277 ER PT J AU LAWRENCE, VA HILSENBECK, SG PAGE, CP TULEY, MR AF LAWRENCE, VA HILSENBECK, SG PAGE, CP TULEY, MR TI PREDICTING OPERATIVE PULMONARY RISK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A885 EP A885 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200483 ER PT J AU LEVINE, SM ANZUETO, A BRYAN, CL PETERS, JI ZAMORA, CA CALHOON, JH TRINKLE, JK JENKINSON, SG AF LEVINE, SM ANZUETO, A BRYAN, CL PETERS, JI ZAMORA, CA CALHOON, JH TRINKLE, JK JENKINSON, SG TI SINGLE LUNG TRANSPLANTATION IN PATIENTS WITH SYSTEMIC-DISEASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A867 EP A867 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200390 ER PT J AU LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA TULEY, MR AF LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA TULEY, MR TI FACTORS ASSOCIATED WITH IN-HOSPITAL HIP-FRACTURES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GERIATR RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. VANDERBILT UNIV,DEPT PREVENT MED,NASHVILLE,TN 37240. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A886 EP A886 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200484 ER PT J AU MORALES, C ANDRADE, F ANZUETO, A LEVINE, S MAXWELL, L JENKINSON, S AF MORALES, C ANDRADE, F ANZUETO, A LEVINE, S MAXWELL, L JENKINSON, S TI DIETHYLMALATE IMPAIRS DIAPHRAGMATIC FUNCTION DURING INSPIRATORY RESISTIVE BREATHING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A868 EP A868 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200393 ER PT J AU ROSSRUCKER, J BRYAN, C CALHOON, J JENKINSON, S AF ROSSRUCKER, J BRYAN, C CALHOON, J JENKINSON, S TI GLUTATHIONE DIMINISHES THE PULMONARY REIMPLANTATION RESPONSE IN CANINE LUNG AUTOTRANSPLANTATION AFTER 24 HOURS OF ISCHEMIC CRYOPRESERVATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A868 EP A868 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200394 ER PT J AU TILLIS, W BRYAN, C CHAMBERS, S DENEKE, S LAWRENCE, R JENKINSON, S AF TILLIS, W BRYAN, C CHAMBERS, S DENEKE, S LAWRENCE, R JENKINSON, S TI CATALASE ACTIVITY IN MESOTHELIAL CELLS, FIBROBLASTS, AND TYPE-II CELLS IS ASSOCIATED WITH VARIABLE RESISTANCE TO OXIDANT STRESS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. USAF,WILFORD HALL MED CTR,LACKLAND AFB,TX 78236. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0009-9279 J9 CLIN RES JI Clin. Res. PD DEC PY 1991 VL 39 IS 4 BP A812 EP A812 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GW912 UT WOS:A1991GW91200092 ER PT J AU YASUDA, T GOLD, HK YAOTIA, H GUERRERO, JL HOLT, RE FALLON, JT LEINBACH, RC COLLEN, D AF YASUDA, T GOLD, HK YAOTIA, H GUERRERO, JL HOLT, RE FALLON, JT LEINBACH, RC COLLEN, D TI ANTITHROMBOTIC EFFECTS OF RIDOGREL, A COMBINED THROMBOXANE-A2 SYNTHASE INHIBITOR AND PROSTAGLANDIN ENDOPEROXIDE-RECEPTOR ANTAGONIST, IN A PLATELET-MEDIATED CORONARY-ARTERY OCCLUSION PREPARATION IN THE DOG SO CORONARY ARTERY DISEASE LA English DT Article DE CORONARY THROMBOSIS; THROMBOXANE SYNTHASE; PROSTAGLANDIN ENDOPEROXIDE RECEPTOR; FIBRINOLYTIC AGENTS ID TISSUE PLASMINOGEN-ACTIVATOR; ACUTE MYOCARDIAL-INFARCTION; SYNTHETASE INHIBITION; THROMBIN INHIBITION; UNSTABLE ANGINA; CANINE MODEL; ONE MOLECULE; THROMBOLYSIS; BLOCKADE; ANGIOPLASTY AB The comparative antithrombotic effects of aspirin and ridogrel, a combined thromboxane A2 synthase inhibitor and prostaglandin endoperoxide-receptor antagonist, were studied in a heparinized canine preparation consisting of an everted (inside-out) circumflex coronary artery segment that is highly thrombogenic and spontaneously occludes with platelet-rich thrombus. In five control dogs coronary artery occlusion occurred within 2 minutes (range, 1 to 4 minutes) and persisted during a 60-minute observation period. Aspirin, 17 mg/kg given orally 2 hours before the experiment, in seven dogs abolished arachidonic acid-induced platelet aggregation, prolonged the template bleeding time marginally to 4.6 +/- 1.4 minutes, and resulted in cyclic occlusion and reflow in all dogs (P = 0.001 vs control by Fisher's exact test). Ridogrel, at a dose of 0.3 mg/kg intravenously over 10 minutes in six dogs, prolonged the template bleeding time from 3.8 +/- 1.2 minutes to 17 +/- 1 0 minutes and caused persistent patency in three dogs and cyclic occlusion and reflow in three dogs (P = 0.002 vs control and P = 0.07 vs aspirin). Ridogrel at a dose of 2.5 mg/kg over 10 minutes in five dogs prolonged the bleeding time from 3.3 +/- 1.7 minutes to 24 +/- 9.4 minutes, and was associated with persistent occlusion in one dog, reflow then reocclusion in one dog, and persistent patency in three dogs (P = 0.05 vs control); ridogrel, 5 mg/kg, prolonged the bleeding time from 3 +/- 1 minutes to 28 +/- 4.5 minutes in five dogs and was associated with persistent patency in two dogs (P = 0.008 vs control). The difference in patency between the combined high-dose ridogrel (2.5 or 5 mg/kg) and aspirin groups was also significant (P = 0.03 by Fisher's exact test). It is concluded that, in this highly thrombogenic animal model, ridogrel is more potent for the prevention of platelet-mediated thrombosis than aspirin. Effective antithrombotic intervention is, however, associated with marked prolongation of the bleeding time. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 4,ROOM 480,15 PARKMAN ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,B-3000 LOUVAIN,BELGIUM. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 34 TC 9 Z9 9 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD DEC PY 1991 VL 2 IS 10 BP 1103 EP 1110 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HA823 UT WOS:A1991HA82300008 ER PT J AU DEMONACO, HJ AF DEMONACO, HJ TI PHARMACOKINETICS - THE EMPERORS NEW CLOTHES SO CRITICAL CARE MEDICINE LA English DT Editorial Material DE PHARMACOKINETICS; AMINOGLYCOSIDES; SEVERITY OF ILLNESS INDEX; MORTALITY; TOXICITY ID AMINOGLYCOSIDE RP DEMONACO, HJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD DEC PY 1991 VL 19 IS 12 BP 1462 EP 1463 PG 2 WC Critical Care Medicine SC General & Internal Medicine GA GV376 UT WOS:A1991GV37600003 PM 1959363 ER PT J AU HEDLEYWHYTE, ET AF HEDLEYWHYTE, ET TI DYNAMIC NEUROPATHOLOGY SO CURRENT OPINION IN NEUROLOGY AND NEUROSURGERY LA English DT Editorial Material RP HEDLEYWHYTE, ET (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE LTD PI LONDON PA 34-42 CLEVELAND STREET, LONDON, ENGLAND W1P 6LB SN 0951-7383 J9 CURR OPIN NEUROL NEU PD DEC PY 1991 VL 4 IS 6 BP 867 EP 868 PG 2 WC Neurosciences SC Neurosciences & Neurology GA GT473 UT WOS:A1991GT47300009 ER PT J AU DUKER, JS TOLENTINO, FI AF DUKER, JS TOLENTINO, FI TI RETINOPATHY OF PREMATURITY AND PEDIATRIC RETINA AND VITREOUS DISORDERS SO CURRENT OPINION IN OPHTHALMOLOGY LA English DT Article AB This article reviews 19 of the past year's important papers dealing with vitreoretinal disorders in pediatric patients. As expected, retinopathy of prematurity received the bulk of investigators' attention, accounting for over half of the papers reviewed. Topics such as leukocoria, pediatric eye trauma, and retinal dystrophies, eg, fundus flavimaculatus and fenestrated sheen macular dystrophy, were the focus of other recent studies. RP DUKER, JS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,SO STANIFORD ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CURRENT SCIENCE PI PHILADELPHIA PA 400 MARKET STREET,SUITE 750 ATTN:SARAH WHEALEN/SUB MGR, PHILADELPHIA, PA 19106 SN 1040-8738 J9 CURR OPIN OPHTHALMOL PD DEC PY 1991 VL 2 IS 6 BP 690 EP 695 DI 10.1097/00055735-199112000-00006 PG 6 WC Ophthalmology SC Ophthalmology GA GV984 UT WOS:A1991GV98400006 ER PT J AU HARE, JW AF HARE, JW TI GESTATIONAL DIABETES-MELLITUS - LEVELS OF GLYCEMIA AS MANAGEMENT GOALS SO DIABETES LA English DT Article; Proceedings Paper CT 3RD INTERNATIONAL WORKSHOP-CONF ON GESTATIONAL DIABETES MELLITUS CY NOV 08-10, 1990 CL CHICAGO, IL SP AMER DIABETES ASSOC ID GLUCOSE-TOLERANCE; NONDIABETIC WOMEN; PREGNANCY; COMPLICATIONS; MORBIDITY; TIGHT AB In the United States, glucose tolerance test criteria for the diagnosis of gestational diabetes mellitus are, in plasma glucose after a 100-g challenge, as follows: fasting, > 5.8 mM; 1 h, > 10.6 mM; 2 h, > 9.2 mM; and 3 h, > 8.1 mM; any two values must be elevated. The Second International Workshop-Conference on Gestational Diabetes Mellitus recommended in 1985 that, once diagnosed, women should receive dietary therapy. If fasting or 2-h postprandial hyperglycemia later occurs (fasting, > 5.8 mM; 2-h, > 6.7 mM), insulin therapy should begin. Data from others have suggested both that the criteria for diagnosis may be too liberal and that the thresholds for instituting insulin therapy may be too high. We address these two issues by reviewing several papers with conflicting conclusions. There is controversy over whether women with gestational diabetes diagnosed by glucose tolerance testing, but who have fasting plasma glucose levels < 5.8 mM and 2-h postprandial values < 6.7 mM, should also be insulin treated. Finally, the usual clinical criteria for making therapeutic decisions all rely on glycemia. Other fuels (amino acids, lipids, and ketones) are regulated by circulating insulin and have deleterious effects on fetal development. Further study is required to make more sound clinical decisions based not just on glycemia but on the entire metabolic millieu. C1 BRIGHAM & WOMENS HOSP,CTR JOSLIN DIABET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 9 Z9 9 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0012-1797 J9 DIABETES JI Diabetes PD DEC PY 1991 VL 40 SU 2 BP 193 EP 196 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GV977 UT WOS:A1991GV97700043 PM 1748258 ER PT J AU BROWN, FM WATTS, M RABINOWE, SL AF BROWN, FM WATTS, M RABINOWE, SL TI AGGREGATION OF SUBCLINICAL AUTONOMIC NERVOUS-SYSTEM DYSFUNCTION AND AUTOANTIBODIES IN FAMILIES WITH TYPE-I DIABETES SO DIABETES LA English DT Article ID ANTI-ADRENAL MEDULLARY; MARIE-TOOTH NEUROPATHY; HEREDITARY MOTOR; SENSORY NEUROPATHY; DEVELOPING IDDM; HLA ANTIGENS; DUFFY LOCUS; HIGH-RISK; ANTIBODIES; CHROMOSOME-17 AB The purpose of our study was to evaluate the occurrence of autonomic nervous system autoantibodies (ANS) in the nondiabetic family members of insulin-dependent (type I) diabetic subjects. We studied 24 families, including 45 nondiabetic parents and 53 nondiabetic siblings of a type I diabetic proband. One hundred one nondiabetic population control subjects were also studied. Stored sera from nondiabetic family members and control subjects were evaluated for the presence of complement-fixing (CF) adrenal medullary antibodies (CF-ADM), sympathetic ganglia antibodies (CF-SG), and vagus nerve antibodies (CF-V) by indirect immunofluorescence. HLA-DR3 and -DR4 typing was performed on 42 nondiabetic family members and 104 diabetic subjects. One or more CF-ANS were in 45 of 93 (40%) nondiabetic family members compared to 2 of 70 (2.8%) control subjects. CF-SG were in 28 of 92 (30%) family members compared to 0 of 101 control subjects (P = 0.0001). CF-V were in 25 of 95 (26%) family members compared to 0 of 76 control subjects (P = 0.0001). CF-ADM were in 10 of 83 (12%) family members compared to 2 of 70 (2.8%) control subjects (P = 0.056). There was no HLA-DR3 or HLA-DR4 association with ANS. Subclinical autonomic dysfunction was demonstrated in 3 of 4 family members with autoantibodies compared to 0 of 4 family members without autoantibodies. C1 JOSLIN DIABET CTR,IMMUNOL & IMMUNOGENET SECT,NEUROENDOCRINE IMMUNOL LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV DIABET & METAB,BOSTON,MA 02115. RP RABINOWE, SL (reprint author), JOSLIN DIABET CTR,IMMUNOL & IMMUNOGENET SECT,NEUROENDOCRINE IMMUNOL LAB,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NCRR NIH HHS [MO1-RR-02635-06]; NIAID NIH HHS [1-RO1-AI-3097-01] NR 20 TC 11 Z9 11 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD DEC PY 1991 VL 40 IS 12 BP 1611 EP 1614 DI 10.2337/diabetes.40.12.1611 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GU710 UT WOS:A1991GU71000007 PM 1756901 ER PT J AU WARRAM, JH MARTIN, BC KROLEWSKI, AS AF WARRAM, JH MARTIN, BC KROLEWSKI, AS TI RISK OF IDDM IN CHILDREN OF DIABETIC MOTHERS DECREASES WITH INCREASING MATERNAL AGE AT PREGNANCY SO DIABETES LA English DT Article ID MELLITUS; FATHERS; COMPLEX AB Offspring of women with insulin-dependent diabetes mellitus (IDDM) have a significantly lower risk of IDDM than the offspring of men with IDDM. Furthermore, a negative association of the risk of IDDM in the offspring with maternal age at delivery has been reported (4). This study tested the association with maternal age in an independent set of families (n = 103) in which the mother had at least one pregnancy before and after the onset of IDDM. In the 304 offspring, the mean +/- SE risk of IDDM by age 20 was 6.0 +/- 2.4% for those born at maternal ages < 25 yr, whereas, the risk was significantly lower (0.7 +/- 0.7%) for those born at older maternal ages (P = 0.03). These 304 offspring were combined with a sample of 1391 offspring previously reported for a multivariate analysis of other factors related to pregnancy (4). In the combined analysis, the risk of IDDM in offspring born at maternal ages > 25 yr was one-fifth that for offspring born to younger mothers. The risk of IDDM in the offspring was not significantly related to birth order, mother's age at first pregnancy, or the interval between pregnancies for subsequent ones. The risk for the children born before the mother's onset of diabetes was higher than that for those exposed in utero to her diabetes, but the difference did not reach statistical significance. In conclusion, although genetic factors are important determinants of susceptibility to IDDM, exposure to maternal diabetes protects offspring from IDDM during the first 2 decades of life. Moreover, a child born to an IDDM mother > 25 yr old has an even lower risk than a child born to that mother at a younger age. The combined result is that a child born to a > 25-yr-old woman with IDDM has a very low risk of developing IDDM, almost as low as the children of nondiabetic parents. This has immediate practical implications for women with IDDM who are considering pregnancy and important implications for hypotheses regarding the mechanism that underlies the protective effect of exposure to maternal diabetes. RP WARRAM, JH (reprint author), JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 22 TC 33 Z9 33 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD DEC PY 1991 VL 40 IS 12 BP 1679 EP 1684 DI 10.2337/diabetes.40.12.1679 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GU710 UT WOS:A1991GU71000017 PM 1756908 ER PT J AU MOSS, JT KADMON, D AF MOSS, JT KADMON, D TI BCG AND THE TREATMENT OF SUPERFICIAL BLADDER-CANCER SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Review ID BACILLUS-CALMETTE-GUERIN; TRANSITIONAL CELL-CARCINOMA; LIVING MYCOBACTERIUM-BOVIS; TRANS-URETHRAL RESECTION; INTRAVESICAL MITOMYCIN-C; LYMPH-NODE METASTASES; DISEASE-FREE INTERVAL; TUMOR NECROSIS FACTOR; MALIGNANT-MELANOMA; RANDOMIZED TRIAL AB In this report, we review the evolution of bacillus Calmette-Guerin (BCG) immunotherapy as a legitimate form of treatment in superficial, nonmuscle-invasive bladder cancer. In the US, an estimated 45 000 new cases of bladder cancer are diagnosed each year and the annual death rate approaches 11 000. Approximately 70 percent of these cancers are superficial at the time of initial presentation. The treatment of superficial bladder cancer has three objectives: (1) eradication of existing disease, (2) prophylaxis against tumor recurrence, and (3) prevention of tumor progression (either muscular invasion, metastatic spread, or both). Cystectomy generally is reserved for muscle-invasive disease. Transurethral resection of the bladder tumor is the preferred initial therapy. Intravesical instillations of various chemotherapeutic agents following transurethral resection have been extensively investigated. Some of the common agents used include thiotepa, mitomycin, and doxorubicin. Despite such treatment efforts, however, over 40 percent of patients with superficial bladder cancer experience a recurrence of their tumor within three years. Approximately half of these recurrences either present as less-well-differentiated tumors or have already penetrated into the bladder musculature, metastasized, or both. Since Morales et al. first introduced intravesical BCG vaccine for prophylaxis as well as for treatment of superficial bladder tumors in 1976, support has grown rapidly for its use as an alternative to chemotherapy. When used with prophylactic intent following transurethral resection, recurrence rates are lower than those achieved with other agents. In addition, BCG is emerging as the consensus drug of choice for treating carcinoma in situ of the bladder. The mechanisms by which BCG exerts its antitumor activity remain largely unknown. BCG is thought to stimulate a localized, nonspecific inflammatory response that leads to subsequent shedding of tumor cells. A large body of clinical and experimental data suggest an association between the development of an immunologic response to BCG and successful antitumor activity. No universally accepted therapeutic regimen has been agreed upon. One regimen commonly used consists of an ampul of BCG mixed with 50 mL of NaCl 0.9%, instilled once a week for six weeks and retained for two hours prior to voiding. Maintenance therapy generally consists of intravesical doses given at three-month cycles for at least two years of recurrence-free follow-up. Because BCG is a biologic agent, the commercially available products may differ in weight, colony-forming units per vial, and antigenicity. How these product characteristics affect clinical responsiveness to different strains of BCG remains unanswered. C1 BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. BAYLOR COLL MED,SCOTT DEPT UROL,HOUSTON,TX 77030. RP MOSS, JT (reprint author), DEPT VET AFFAIRS MED CTR,PHARM SERV 119,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 183 TC 5 Z9 5 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD DEC PY 1991 VL 25 IS 12 BP 1355 EP 1367 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GV254 UT WOS:A1991GV25400017 PM 1815434 ER PT J AU CROWE, DL HU, L GUDAS, LJ RHEINWALD, JG AF CROWE, DL HU, L GUDAS, LJ RHEINWALD, JG TI VARIABLE EXPRESSION OF RETINOIC ACID RECEPTOR (RAR-BETA) MESSENGER-RNA IN HUMAN ORAL AND EPIDERMAL-KERATINOCYTES - RELATION TO KERATIN-19 EXPRESSION AND KERATINIZATION POTENTIAL SO DIFFERENTIATION LA English DT Article ID SQUAMOUS-CELL CARCINOMAS; VITAMIN-A; TERMINAL DIFFERENTIATION; RESPONSIVE ELEMENT; EPITHELIAL-CELLS; TERATOCARCINOMA CELLS; NUCLEAR RECEPTORS; GENE-EXPRESSION; IDENTIFICATION; CULTURE AB Previous studies have revealed that the cells that form the different regions of the oral and epidermal stratified squamous epithelia represent a number of intrinsically distinct keratinocyte subtypes, each of which is developmentally programmed to preferentially express a particular pattern of keratins and type of suprabasal histology. Retinoic acid (RA) is known to modulate stratified squamous epithelial differentiation, including expression of the basal cell keratin K19 and the suprabasal keratins K1/K10 and K4/K13. We have found that all keratinocyte subtypes are similar in their steady state levels of RAR-alpha and RAR-gamma mRNAs in culture and that these levels are only minimally affected by RA. In contrast, RAR-beta mRNA expression varies greatly among keratinocyte subtypes and, in eight of ten cell strains examined, directly correlated with their levels of K19 mRNA. Exposure to 10(-6) M RA increases the levels of RAR-beta and K19 mRNA; conversely, complete removal of RA from the medium results in reduced levels of these messages. RA does not coordinately induce RAR-beta and K19 messages in nonkeratinocyte cell types: fibroblasts cultured in the presence of 10(-6) M RA express very high levels of RAR-beta mRNA but do not express detectable K19, and mesothelial cells decrease their levels of RAR-beta and K19 mRNA in response to 10(-6) M RA. The correlation between RAR-beta and K19 mRNA levels in most keratinocyte subtypes suggests a role for RAR-beta in specifying patterns of keratin expression and suprabasal differentiation in stratified squamous epithelia. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT ORAL MED & ORAL PATHOL,CAMBRIDGE,MA 02138. FU NCI NIH HHS [R01 CA26656]; NIDCR NIH HHS [DEO7117] NR 69 TC 66 Z9 67 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD DEC PY 1991 VL 48 IS 3 BP 199 EP 208 DI 10.1111/j.1432-0436.1991.tb00258.x PG 10 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA HD273 UT WOS:A1991HD27300007 PM 1725165 ER PT J AU CABALLERIA, J BARAONA, E DEULOFEU, R HERNANDEZMUNOZ, R RODES, J LIEBER, CS AF CABALLERIA, J BARAONA, E DEULOFEU, R HERNANDEZMUNOZ, R RODES, J LIEBER, CS TI EFFECTS OF H-2-RECEPTOR ANTAGONISTS ON GASTRIC ALCOHOL-DEHYDROGENASE ACTIVITY SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE H-2-RECEPTOR ANTAGONISTS; CIMETIDINE; RANITIDINE; NIZATIDINE, FAMOTIDIN; ETHANOL; STOMACH; ALCOHOL DEHYDROGENASE ID HUMAN GASTROINTESTINAL-TRACT; H2-RECEPTOR ANTAGONISTS; LIVER ALCOHOL; ETHANOL; CIMETIDINE; RAT; FAMOTIDINE; METABOLISM; HISTAMINE; LOCALIZATION AB Inhibition of gastric alcohol dehydrogenase (ADH) activity by cimetidine results in elevated blood levels of ethanol after moderate consumption. To search for alternative H2-blockers lacking such an effect, we compared cimetidine, ranitidine, nizatidine, and famotidine. They inhibited rat gastric ADH noncompetitively, with a K(i) for ethanol oxidation of 0.68 mM for cimetidine, 0.5 mM for ranitidine, 1 mM for nizatidine, and 4.5 mM for famotidine. These concentrations are higher than therapeutic plasma levels, but intracellular concentrations in the gastric mucosa (assessed with [H-3]cimetidine and [C-14]famotidine) were at least 10- and 2-fold greater than in the blood, respectively. These results suggests that, given at therapeutic doses in vivo, the degree of inhibition by cimetidine and ranitidine should be significant and comparable, that by nizatidine should be smaller, and that by famotidine should be negligible. These drugs also exerted either mixed or competitive inhibition of rat hepatic ADH, but the effects of cimetidine and famotidine were observed at concentrations unlikely to occur in vivo. Thus, in alcoholics and in social drinkers who require treatment with H2-receptor antagonists, famotidine might be preferable to the other H-2 blockers tested. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,NEW YORK,NY 10468. CUNY,MT SINAI SCH MED,NEW YORK,NY 10468. HOSP CLIN BARCELONA,LIVER UNIT,BARCELONA 36,SPAIN. HOSP CLIN BARCELONA,BIOCHEM LAB,BARCELONA 36,SPAIN. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,NEW YORK,NY 10468, USA. FU NIAAA NIH HHS [AA 03508] NR 28 TC 58 Z9 58 U1 0 U2 3 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0163-2116 J9 DIGEST DIS SCI JI Dig. Dis. Sci. PD DEC PY 1991 VL 36 IS 12 BP 1673 EP 1679 DI 10.1007/BF01296608 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GV255 UT WOS:A1991GV25500003 PM 1684149 ER PT J AU LEES, JA BUCHKOVICH, KJ MARSHAK, DR ANDERSON, CW HARLOW, E AF LEES, JA BUCHKOVICH, KJ MARSHAK, DR ANDERSON, CW HARLOW, E TI THE RETINOBLASTOMA PROTEIN IS PHOSPHORYLATED ON MULTIPLE SITES BY HUMAN CDC2 SO EMBO JOURNAL LA English DT Article DE CDC2; PHOSPHORYLATION; RETINOBLASTOMA ID LARGE T-ANTIGEN; MATURATION-PROMOTING FACTOR; ADENOVIRUS E1A PROTEINS; H-1 HISTONE KINASE; CELL-CYCLE CONTROL; SV40 LARGE-T; GENE-PRODUCT; SUSCEPTIBILITY GENE; RB GENE; TRANSCRIPTION FACTOR AB The retinoblastoma gene product (pRB) is a nuclear phosphoprotein that is thought to play a key role in the negative regulation of cellular proliferation. pRB is phosphorylated in a cell cycle dependent manner, and studies in both actively dividing and differentiated cells suggest that this modification may be essential for cells to progress through the cell cycle. Using tryptic phosphopeptide mapping we have shown that pRB is phosphorylated on multiple serine and threonine residues in vivo and that many of these phosphorylation events can be mimicked in vitro using purified p34cdc2. Using synthetic peptides corresponding to potential cdc2 phosphorylation sites, we have developed a strategy which has allowed the identification of five sites. S249, T252, T373, S807 and S811 are phosphorylated in vivo, and in each case these sites correspond closely to the consensus sequence for phosphorylation by p34cdc2. This and the observation that pRB forms a specific complex with p34cdc2 in vivo suggests that p34cdc2 or a p34cdc2-related protein is a major pRB kinase. C1 MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02114 USA. BROOKHAVEN NATL LAB, DEPT BIOL, UPTON, NY 11973 USA. RP COLD SPRING HARBOR LAB, POB 100, COLD SPRING HARBOR, NY 11724 USA. FU NCI NIH HHS [CA13106]; NIAID NIH HHS [AI25170] NR 69 TC 319 Z9 320 U1 0 U2 5 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0261-4189 EI 1460-2075 J9 EMBO J JI Embo J. PD DEC PY 1991 VL 10 IS 13 BP 4279 EP 4290 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA GU645 UT WOS:A1991GU64500034 PM 1756735 ER PT J AU KURODA, T LEE, MM RAGIN, RC HIROBE, S DONAHOE, PK AF KURODA, T LEE, MM RAGIN, RC HIROBE, S DONAHOE, PK TI MULLERIAN INHIBITING SUBSTANCE PRODUCTION AND CLEAVAGE IS MODULATED BY GONADOTROPINS AND STEROIDS SO ENDOCRINOLOGY LA English DT Article ID GROWTH FACTOR-BETA; FOLLICLE-STIMULATING-HORMONE; RIBONUCLEIC-ACID; GRANULOSA-CELLS; OOCYTE MEIOSIS; RAT; EXPRESSION; GENE; INVITRO; BOVINE AB Analysis of the ontogeny and localization of the amino (N)-terminal and carboxy (C)-terminal cleavage products of Mullerian Inhibiting Substance (MIS) and their modulation by hormones of the hypothalamic-pituitary gonadal axis by immunohistochemistry and Northern analysis led to the discovery of a novel mode of posttranslational regulation of this differentiating agent. Antibody to both holo- and C-terminal MIS identically stained the cytosol of testicular Sertoli cells from 21-day fetal rats, whereas staining of antibody to N-terminal MIS localized to the basement membrane of seminiferous tubules. In addition, when studied longitudinally, basement membrane staining for N-terminal MIS persisted; cytosolic staining for C-terminal MIS was no longer detectable in postnatal testes, but marked basement membrane staining for the N-terminal fragment could still be observed in the testes of untreated 7-day postnatal animals. When 19-day fetuses were injected with FSH, testes collected 2 days later showed less immunohistochemical staining for holo-, N-, and C-terminal MIS, and less MIS messenger RNA. This suggested that FSH downregulates MIS transcription, as had been shown previously in neonatal testes treated with FSH. Testes collected at 21 days from fetuses treated at day 19 in utero with human CG or testosterone, also showed less staining for holo-MIS, but, surprisingly, increased staining for the N- and C-terminal fragments. These changes in MIS protein were accompanied by no or minimal changes in MIS messenger RNA levels, indicating that human CG and testosterone do not affect transcription, but may regulate the cleavage and/or dissociation of MIS. This study describes a form of post-translational regulation of MIS and shows that both transcription and processing of MIS may be differentially modulated by gonadotropins and sex steroids. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,PEDIAT SURG RES LAB,WARREN 10,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,PEDIAT ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP DONAHOE, PK (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,PEDIAT SURG RES LAB,WARREN 10,BOSTON,MA 02114, USA. OI Lee, Mary/0000-0002-7204-4884 FU NCI NIH HHS [CA17393] NR 39 TC 35 Z9 35 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD DEC PY 1991 VL 129 IS 6 BP 2985 EP 2992 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GT670 UT WOS:A1991GT67000026 PM 1954882 ER PT J AU MORITA, CT VERMA, S APARICIO, P MARTINEZ, AC SPITS, H BRENNER, MB AF MORITA, CT VERMA, S APARICIO, P MARTINEZ, AC SPITS, H BRENNER, MB TI FUNCTIONALLY DISTINCT SUBSETS OF HUMAN GAMMA-DELTA-T-CELLS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID PERIPHERAL-BLOOD LYMPHOCYTES; RECEPTOR-DELTA; MYCOBACTERIUM-TUBERCULOSIS; CD3+WT31 LYMPHOCYTES; MONOCLONAL-ANTIBODY; ANTIGEN RECEPTOR; GENE ENCODES; HUMAN CD4+; RECOGNITION; CLONES AB To determine if effector subsets exist among human gamma/delta T cells, we examined the cytokine production and cytotoxic activity of gamma/delta T cells clones with different accessory molecule phenotypes, V-delta and V-gamma gene expression, and J-gamma rearrangements. T cell clones bearing gamma/delta T cell receptor produce an array of cytokines like alpha/beta T cell clones. Individual gamma/delta T cells clones produced a characteristic array of cytokines without correlation with V-delta or V-gamma gene expression. However, when phenotypic subsets were considered, CD4+ gamma/delta clones produced significantly higher levels of interleukin 2 and granulocyte-monocyte colony-stimulating factor compared with CD4-CD8- and CD8+ gamma/delta clones. Similarly, when cytotoxic potential was assessed, CD4+ gamma/delta clones exhibited minimal activity when compared with CD4-CD8- and CD8+ adult peripheral blood gamma/delta clones. We conclude that functionally distinct gamma/delta T cell subsets exist and suggest that these subsets may correlate with expression of the CD4 accessory molecule. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT HUMAN IMMUNOL,PALO ALTO,CA. FAC MED MURCIA,DEPT BIOQUIM & BIOL MOLEC,MURCIA,SPAIN. UNIV AUTONOMA MADRID,CSIC,CTR BIOL MOLEC,MADRID 34,SPAIN. RP MORITA, CT (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Morita, Craig/C-1365-2011 NR 62 TC 100 Z9 100 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD DEC PY 1991 VL 21 IS 12 BP 2999 EP 3007 DI 10.1002/eji.1830211215 PG 9 WC Immunology SC Immunology GA GV437 UT WOS:A1991GV43700014 PM 1684157 ER PT J AU JONES, KJ ALBERT, MS DUFFY, FH HYDE, MR NAESER, M ALDWIN, C AF JONES, KJ ALBERT, MS DUFFY, FH HYDE, MR NAESER, M ALDWIN, C TI MODELING AGE USING COGNITIVE, PSYCHOSOCIAL AND PHYSIOLOGICAL VARIABLES - THE BOSTON NORMATIVE AGING STUDY SO EXPERIMENTAL AGING RESEARCH LA English DT Article ID BRAIN ELECTRICAL-ACTIVITY AB A structural equation model is computed for 36 variables from eight domains of data using 100 healthy male subjects whose age varies between 30 and 80 years. Chronological age is required to be an exogenous variable while cognitive function variables are required to be an ultimate endogenous or outcome set. The model suggests that the direct effect of age on cognition is substantially reduced when social, life style, physiological, and brain state variables are allowed to become intervening variables. The study also finds that there is an association between cognitive function and psychosocial measures relating to general psychiatric symptomatology and social support systems. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. VET ADM OUTPATIENT CLIN,BOSTON,MA 02108. BOSTON UNIV,SCH MED,BOSTON,MA 02118. RP JONES, KJ (reprint author), BRANDEIS UNIV,FLORENCE HELLER GRAD SCH ADV STUDIES SOCIAL WELFARE,WALTHAM,MA 02154, USA. FU NIA NIH HHS [P01-AG04953] NR 22 TC 12 Z9 12 U1 0 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 WIN PY 1991 VL 17 IS 4 BP 227 EP 242 PG 16 WC Geriatrics & Gerontology; Psychology SC Geriatrics & Gerontology; Psychology GA HV145 UT WOS:A1991HV14500002 PM 1820288 ER PT J AU CHENG, HM YOSHIDA, A XIONG, H GONZALEZ, RG AF CHENG, HM YOSHIDA, A XIONG, H GONZALEZ, RG TI THE EFFECT OF INSULIN AND ALDOSE REDUCTASE INHIBITION ON THE PHOSPHATE-METABOLISM OF STREPTOZOTOCIN-DIABETIC RAT LENS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE SORBITOL-3-PHOSPHATE; FRUCTOSE-3-PHOSPHATE; [P-31]NMR; STREPTOZOTOCIN-DIABETES; RAT LENS; INSULIN; ALDOSE REDUCTASE INHIBITION ID SORBITOL 3-PHOSPHATE; FRUCTOSE 3-PHOSPHATE; HIGH GLUCOSE; IDENTIFICATION C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. RP CHENG, HM (reprint author), HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY04424] NR 10 TC 10 Z9 10 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD DEC PY 1991 VL 53 IS 6 BP 805 EP 808 DI 10.1016/0014-4835(91)90117-W PG 4 WC Ophthalmology SC Ophthalmology GA GW154 UT WOS:A1991GW15400015 PM 1783017 ER PT J AU MIYAZAWA, K HENDRIE, PC MANTEL, C WOOD, K ASHMAN, LK BROXMEYER, HE AF MIYAZAWA, K HENDRIE, PC MANTEL, C WOOD, K ASHMAN, LK BROXMEYER, HE TI COMPARATIVE-ANALYSIS OF SIGNALING PATHWAYS BETWEEN MAST-CELL GROWTH-FACTOR (C-KIT LIGAND) AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR IN A HUMAN FACTOR-DEPENDENT MYELOID CELL-LINE INVOLVES PHOSPHORYLATION OF RAF-1, GTPASE-ACTIVATING PROTEIN AND MITOGEN-ACTIVATED PROTEIN-KINASE SO EXPERIMENTAL HEMATOLOGY LA English DT Article ID GAP-ASSOCIATED PROTEINS; PDGF BETA-RECEPTOR; FACTOR-I RECEPTOR; TYROSINE KINASE; GM-CSF; MOLECULAR-CLONING; SI-LOCUS; W-LOCUS; INTERLEUKIN-3; PROTOONCOGENE AB Mast cell growth factor (MGF, the ligand for c-kit receptor) can stimulate proliferation of factor dependent myeloid cell line, M07e, and MGF synergizes with granulocyte-macrophage colony-stimulating factor (GM-CSF) or IL-3 in this effect. The effect of MGF on protein tyrosine kinase activity in M07e cells was investigated by immunoblotting with antiphosphotyrosine mAb and this was compared with effects of GM-CSF. MGF stimulation rapidly induced or enhanced at least 12 tyrosine phosphorylated bands. Major bands had molecular weights of 145, 120, 110, 98, 62, 55 and 42 kD. P145, the most prominent phosphorylated protein, was identified as c-kit product using anti-c-kit-mAb (YB5.B8), suggesting ligand-dependent receptor autophosphorylation. Five of six tyrosine phosphorylated bands induced or enhanced by GM-CSF stimulation comigrated with those tyrosine phosphorylated by MGF (138, 120, 76, 55 and 42 kD). P42 was identified, at least in part, as mitogen-activated protein (MAP) kinase. MGF induced tyrosine phosphorylation of a complex of GTPase-activating protein (GAP, 120 kD) and GAP associated proteins (p62/p190) as detected by anti-GAP Ab immunoprecipitation followed by immunoblotting with anti-phosphotyrosine mAb. GM-CSF also stimulated slightly but consistently tyrosine phosphorylation of GAP and p190 but not p62. Both MGF and GM-CSF enhanced Raf-1 phosphorylation and increased Raf-1 associated kinase activity in vitro. Phosphoamino acid analysis-revealed Raf-1 phosphorylation by these two growth factors occurred almost exclusively on serine residues. No tyrosine phosphorylation of Raf-1 protein was detected. These data suggest shared and unshared components of signaling pathways of both factors, which may be involved in cell proliferation. C1 INDIANA UNIV,SCH MED,WALTHER ONCOL CTR,975 W WALNUT,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,DEPT MED HEMATOL ONCOL,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,DEPT MICROBIOL & IMMUNOL,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV ADELAIDE,DEPT MICROBIOL & IMMUNOL,ADELAIDE,SA 5001,AUSTRALIA. RI ASHMAN, LEONIE/G-7631-2013 OI ASHMAN, LEONIE/0000-0003-3559-3611 FU NCI NIH HHS [R37 CA36464, R01 CA36740]; NHLBI NIH HHS [R01 HL46549] NR 58 TC 135 Z9 135 U1 0 U2 1 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 DEC PY 1991 VL 19 IS 11 BP 1110 EP 1123 PG 14 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA GT295 UT WOS:A1991GT29500008 PM 1721591 ER PT J AU FISHER, DE CARR, CS PARENT, LA SHARP, PA AF FISHER, DE CARR, CS PARENT, LA SHARP, PA TI TFEB HAS DNA-BINDING AND OLIGOMERIZATION PROPERTIES OF A UNIQUE HELIX LOOP HELIX LEUCINE-ZIPPER FAMILY SO GENES & DEVELOPMENT LA English DT Article DE TFEB; HELIX LOOP HELIX; LEUCINE ZIPPER; IMMUNOGLOBULIN ENHANCER; PROTEIN DIMER; PROTEIN TETRAMER ID ALTERED PROTEIN CONFORMATION; MAJOR LATE PROMOTER; C-MYC PROTEIN; TRANSCRIPTION FACTOR; IMMUNOGLOBULIN ENHANCER; NEGATIVE REGULATOR; FOS; JUN; SEQUENCE; DOMAINS AB The DNA-binding factor TFEB contains adjacent helix-loop-helix (HLH) and leucine zipper (LZ) domains flanked by an upstream basic region. This arrangement of interactive motifs has recently been observed in several other transcription factors and in the Myc family of oncogenes. TFEB was isolated by virtue of its binding to the major late promoter of adenovirus. DNA binding by a soluble protein was achieved by deleting a hydrophobic amino-terminal domain and permitted the structural analysis of the oligomerization and DNA-binding properties of TFEB. TFEB specifically bound DNA as both a homodimer and a heterodimer with another b-HLH-LZ protein TFE3. The LZ domain was essential for homo- or hetero-oligomerization and high-affinity DNA binding. In the absence of DNA a tetramer-sized form of TFEB was observed that dissociates to bind added DNA as a dimer. Binding by TFEB and TFE3 to related, but different, naturally occurring DNA target sequences was observed with distinct binding preferences. Analysis of basic domain residues in this family of proteins revealed a pattern of sequence conservation predictive of an interacting alpha-helical face. Common oligomerization and DNA-binding features suggest the b-HLH-LZ domain structure to define a distinct family of DNA-binding factors. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,SCH MED,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,SCH MED,DEPT MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT HEMATOL,BOSTON,MA 02115. RP FISHER, DE (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [P01-CA42063, P30-CA14051] NR 38 TC 117 Z9 119 U1 1 U2 7 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD DEC PY 1991 VL 5 IS 12A BP 2342 EP 2352 DI 10.1101/gad.5.12a.2342 PG 11 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA GU846 UT WOS:A1991GU84600017 PM 1748288 ER PT J AU LIAO, SM TAYLOR, ICA KINGSTON, RE YOUNG, RA AF LIAO, SM TAYLOR, ICA KINGSTON, RE YOUNG, RA TI RNA POLYMERASE-II CARBOXY-TERMINAL DOMAIN CONTRIBUTES TO THE RESPONSE TO MULTIPLE ACIDIC ACTIVATORS INVITRO SO GENES & DEVELOPMENT LA English DT Article DE RNA POLYMERASE-II; CARBOXY-TERMINAL DOMAIN; TRANSCRIPTION INITIATION ID LARGEST SUBUNIT; SACCHAROMYCES-CEREVISIAE; TRANSCRIPTION INITIATION; REPEAT DOMAIN; DROSOPHILA-MELANOGASTER; HEPTAPEPTIDE REPEAT; GENE PROMOTER; HSP70 GENE; YEAST; PHOSPHORYLATION AB The largest subunit of RNA polymerase II contains a unique carboxy-terminal domain (CTD) that consists of repeats of the heptapeptide YSPTSPS. RNA polymerase II CTD truncation mutations affect the ability to induce transcription of a subset of yeast genes in vivo, and the lack of response to induction maps to the upstream activating sequences of these genes. Here, we report that progressive truncation of the yeast RNA polymerase II CTD causes progressive loss of trans-activator-dependent transcription in nuclear extracts but has little effect on elongation or termination. Specific transcription, which is reduced by up to 50-fold in these assays, can be restored in the defective nuclear extracts by adding purified wild-type RNA polymerase II. The defects in factor-dependent transcription are observed with templates that are assembled into nucleosomes as well as with templates that are not so assembled. Defects in factor-independent transcription are also observed, but these are not as profound as those observed in the presence of trans-activators. These results indicate that the RNA polymerase II CTD functions during transcription initiation and is required for normal levels of activated transcription in vitro. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP LIAO, SM (reprint author), WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142, USA. RI Young, Richard/F-6495-2012 OI Young, Richard/0000-0001-8855-8647 NR 50 TC 75 Z9 75 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD DEC PY 1991 VL 5 IS 12B BP 2431 EP 2440 DI 10.1101/gad.5.12b.2431 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA GX544 UT WOS:A1991GX54400007 PM 1752437 ER PT J AU WEBSTER, EW AF WEBSTER, EW TI COMPOSITE-MATERIALS FOR X-RAY PROTECTION - ADDENDUM SO HEALTH PHYSICS LA English DT Letter RP WEBSTER, EW (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIOL, BOSTON, MA 02114 USA. NR 4 TC 7 Z9 7 U1 1 U2 3 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD DEC PY 1991 VL 61 IS 6 BP 917 EP 918 PG 2 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA GT922 UT WOS:A1991GT92200032 PM 1955342 ER PT J AU LEVINE, RA DAVIS, PJ AF LEVINE, RA DAVIS, PJ TI ORIGIN OF THE CLICK-EVOKED BINAURAL INTERACTION POTENTIAL, BETA, OF HUMANS SO HEARING RESEARCH LA English DT Article DE BRAIN-STEM AUDITORY EVOKED POTENTIALS; BINAURAL INTERACTION; DERIVED POTENTIALS; MASKING; CLICK POLARITY ID SUPERIOR OLIVARY COMPLEX; INTERAURAL TIME; CAT; LATERALIZATION; SENSITIVITY; COMPONENT; POLARITY; STIMULI AB The human click-evoked binaural difference waveform has as its most prominent feature the peak, beta, which has been shown to be related to binaural perception. In normal human subjects, we investigated the effect upon beta of (1) delivering the clicks in the presence of high passed masking noise (4000 Hz cut-off) and (2) reversing click polarity. In the presence of the masker, little activity occurs at the time the click-evoked-beta would be expected. No significant change in beta-latency occurs when the click polarity is inverted. We conclude that beta is principally due to the high-frequency components of the broad band click, so that it is through the activity in high characteristic frequency auditory nerve fibers that click-evoked-beta is generated. Because the medial superior olive is the major nucleus of the human superior olivary complex, our results suggest that beta is possibly generated by the high-frequency cells of the medial superior olive. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP LEVINE, RA (reprint author), MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,EATON PEABODY LAB AUDITORY PHYSIOL,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC 00119] NR 30 TC 20 Z9 20 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-5955 J9 HEARING RES JI Hear. Res. PD DEC PY 1991 VL 57 IS 1 BP 121 EP 128 DI 10.1016/0378-5955(91)90081-J PG 8 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA GV065 UT WOS:A1991GV06500014 PM 1774203 ER PT J AU MARKS, LB ANSCHER, MS SHIPLEY, WU AF MARKS, LB ANSCHER, MS SHIPLEY, WU TI THE ROLE OF RADIATION-THERAPY IN THE TREATMENT OF TESTICULAR GERM-CELL TUMORS SO HEMATOLOGY-ONCOLOGY CLINICS OF NORTH AMERICA LA English DT Review ID PRIMARY MEDIASTINAL SEMINOMA; STAGE-I SEMINOMA; METASTATIC SEMINOMA; PURE SEMINOMA; COMBINATION CHEMOTHERAPY; MEGAVOLTAGE IRRADIATION; ADJUVANT CHEMOTHERAPY; DENMARK 1976-1980; INITIAL TREATMENT; TESTIS TUMORS C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. RP MARKS, LB (reprint author), DUKE UNIV,MED CTR,DEPT RADIAT ONCOL,BOX 3085,DURHAM,NC 27710, USA. NR 102 TC 4 Z9 4 U1 0 U2 2 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 1991 VL 5 IS 6 BP 1143 EP 1172 PG 30 WC Oncology; Hematology SC Oncology; Hematology GA GU853 UT WOS:A1991GU85300004 PM 1663938 ER PT J AU LEIGHTON, JA BAY, MK MALDONADO, AL SCHENKER, S SPEEG, KV AF LEIGHTON, JA BAY, MK MALDONADO, AL SCHENKER, S SPEEG, KV TI COLCHICINE CLEARANCE IS IMPAIRED IN ALCOHOLIC CIRRHOSIS SO HEPATOLOGY LA English DT Article ID PRIMARY BILIARY-CIRRHOSIS; TRIAL; PHARMACOKINETICS; VOLUNTEERS; LIVER AB Colchicine may have benefit in primary biliary cirrhosis and alcoholic liver disease. It is currently used in patients with impaired liver function, yet little is known about its elimination in such patients. Colchicine clearance in the rat is significantly impaired in various models of liver disease. To study this in human beings, colchicine pharmacokinetics were compared in normal subjects and patients with alcoholic cirrhosis. Colchicine clearance was impaired in the cirrhotic patients. Normal subjects had a mean clearance of 10.65 +/- 1.82 ml/min.kg, whereas cirrhotic patients had a mean clearance of 4.22 +/- 0.45 ml/min.kg (p < 0.01). The half-life was 57.4 +/- 14.2 min in control subjects vs. 114.4 +/- 19.7 min in cirrhotic patients (p = 0.054). Volume of distribution was not different in the two groups (0.718 +/- 0.1 L/kg in control subjects; 0.716 +/- 0.158 L/kg in cirrhotic patients, p > 0.99). No correlation was seen between colchicine clearance and bilirubin, albumin, prothrombin time or Child-Pugh classification, but this may be the result of the small number of patients studied. Based on the values measured, it is estimated that colchicine steady state would change from an average 1.12 ng/ml in normal individuals to 2.82 ng/ml in the cirrhotic patients if 0.6 mg were taken every 12 hr. It is unknown whether this change would be clinically significant. These data show that cirrhosis impairs colchicine clearance and demonstrates that the liver is a major route of colchicine elimination. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GASTROENTEROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. FU NCRR NIH HHS [MO1-RR-01346] NR 15 TC 23 Z9 23 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD DEC PY 1991 VL 14 IS 6 BP 1013 EP 1015 DI 10.1016/0270-9139(91)90121-B PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GT559 UT WOS:A1991GT55900010 PM 1959847 ER PT J AU FRISMAN, DM FALLON, JT HURWITZ, AA DEC, WG KURNICK, JT AF FRISMAN, DM FALLON, JT HURWITZ, AA DEC, WG KURNICK, JT TI CYTOTOXIC ACTIVITY OF GRAFT-INFILTRATING LYMPHOCYTES CORRELATES WITH CELLULAR REJECTION IN CARDIAC TRANSPLANT PATIENTS SO HUMAN IMMUNOLOGY LA English DT Article ID ENDOMYOCARDIAL BIOPSIES; T-CELLS; ALLOGRAFTS; PROPAGATION AB Lymphocytes propagated from allografts have shown a wide spectrum of activity during rejection including cytotoxicity, proliferation, and lymphokine production. It is necessary to correlate these activities to the rejection process to understand the in vivo immune response. The frequent need to obtain a biopsy of human cardiac allografts permits the evaluation of the function of the graft-infiltrating lymphocytes (GIL) as related to development of the rejection process. Lymphocyte cultures established from biopsies taken before, during, and after rejection episodes of grade 1.0 or greater were assayed for surface antigen expression using flow cytometry, proliferative activity using a primed lymphocyte test (PLT), and cytotoxicity using a cell-mediated lympholysis assay. Fifteen rejection episodes were followed from 10 patients. Two patients were followed through two different rejection episodes and one patient through four rejection episodes. CD8+ cells usually predominated during the rejection episode. Following the rejection episodes the GIL showed a shift toward higher proportion of CD4+ cells. Most cultures taken prior to and during rejection episodes (8/9 and 12/13 assayed, respectively) demonstrated > 30% killing of targets bearing donor-related HLA antigens. Seven of 15 cultures remained cytotoxic after a rejection episode whereas 8 of 15 lost cytotoxicity. The patients whose cultures remained cytotoxic after a rejection episode went on to further rejection episodes at 6, 7, 11, 20, 37, or 118 days later. Those patients whose cultures were no longer cytotoxic did not experience any subsequent rejection episode until at least 257 days later. Persistence of alloreactivity, as indicated by the ability to proliferate in a PLT, did not predict future rejection episodes. These results suggest that the cytotoxic activity of the interleukin-2 responsive T lymphocytes in the biopsies is closely related to clinical rejection, and continued cytotoxicity may be a useful prognostic indicator of future rejection episodes. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL & CARDIOL,BOSTON,MA 02114. FU NCI NIH HHS [CA44324]; NHLBI NIH HHS [HL 43793, HL18646] NR 16 TC 14 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0198-8859 J9 HUM IMMUNOL JI Hum. Immunol. PD DEC PY 1991 VL 32 IS 4 BP 241 EP 245 DI 10.1016/0198-8859(91)90086-O PG 5 WC Immunology SC Immunology GA GY263 UT WOS:A1991GY26300002 PM 1686025 ER PT J AU ZUKERBERG, LR KAYNOR, BL SILVERMAN, ML HARRIS, NL AF ZUKERBERG, LR KAYNOR, BL SILVERMAN, ML HARRIS, NL TI SPLENIC HAMARTOMA AND CAPILLARY HEMANGIOMA ARE DISTINCT ENTITIES - IMMUNOHISTOCHEMICAL ANALYSIS OF CD8 EXPRESSION BY ENDOTHELIAL-CELLS SO HUMAN PATHOLOGY LA English DT Article DE SPLEEN; HEMANGIOMA; HAMARTOMA; IMMUNOPHENOTYPE ID LYMPHOCYTE SUBSETS; SPLEEN C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LAB,WARREN 2,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. LAHEY CLIN FDN,DEPT PATHOL,BURLINGTON,MA. NR 14 TC 34 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 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD DEC PY 1991 VL 22 IS 12 BP 1258 EP 1261 DI 10.1016/0046-8177(91)90108-2 PG 4 WC Pathology SC Pathology GA GX837 UT WOS:A1991GX83700010 PM 1748432 ER PT J AU SNOEK, M GROOT, PC SPIES, T CAMPBELL, RD DEMANT, P AF SNOEK, M GROOT, PC SPIES, T CAMPBELL, RD DEMANT, P TI FINE MAPPING OF THE CROSSOVER-SITES IN THE C4-H-2D REGION OF H-2 RECOMBINANT MOUSE STRAINS SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; TUMOR NECROSIS FACTOR; CLEFT-PALATE; MAP POSITION; E-ALPHA; GENES; LOCUS; INTERVAL; SUSCEPTIBILITY; IDENTIFICATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. UNIV OXFORD,DEPT BIOCHEM,MRC,IMMUNOCHEM UNIT,OXFORD,ENGLAND. RP SNOEK, M (reprint author), NETHERLANDS CANC INST,DEPT MOLEC GENET,PLESMANLAAN 121,1066 CX AMSTERDAM,NETHERLANDS. NR 23 TC 27 Z9 27 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 DEC PY 1991 VL 34 IS 6 BP 409 EP 412 DI 10.1007/BF01787492 PG 4 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA GT095 UT WOS:A1991GT09500009 PM 1684177 ER PT J AU PEYRON, JF VERMA, S MALEFYT, RD SANCHO, J TERHORST, C SPITS, H AF PEYRON, JF VERMA, S MALEFYT, RD SANCHO, J TERHORST, C SPITS, H TI THE CD45 PROTEIN TYROSINE PHOSPHATASE IS REQUIRED FOR THE COMPLETION OF THE ACTIVATION PROGRAM LEADING TO LYMPHOKINE PRODUCTION IN THE JURKAT HUMAN T-CELL LINE SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE T-CELL ACTIVATION; TYROSINE PHOSPHORYLATION; CD45 PROTEIN TYROSINE PHOSPHATASE ID COLONY-STIMULATING FACTOR; LEUKOCYTE-COMMON ANTIGEN; SIGNAL TRANSDUCTION; KINASE-ACTIVITY; INOSITOL PATHWAY; LYMPHOCYTE-T; C-FOS; PHOSPHORYLATION; RECEPTOR; EXPRESSION AB Stimulation of the T cell antigen receptor, TCR - CD3, induces tyrosine phosphorylation of specific cellular proteins through activation of a tyrosine kinase. The possible regulatory role of the CD45 protein tyrosine phosphatase in this process was explored by studying the functional properties of cellular variants of the Jurkat T cell line which have been selected to have normal levels of the TCR - CD3 complex, but low or negative expression of CD45. These variants had < 20% of the normal membrane tyrosine phosphatase activity. Triggering the TCR - CD3 receptor on the CD45 variants with anti-CD3 mAb induced the activation of a tyrosine kinase. Tyrosine phosphorylation of cellular substrates as well as of the CD3-zeta chain was qualitatively comparable to normal cells although the extent of stimulation was lower. No differences were observed between the variants and the normal cells in the duration of the tyrosine phosphorylation signal. The increase in intracellular calcium concentration following receptor stimulation was also less efficient, suggesting that CD45 is necessary for optimal generation of the second messengers of the activation. The CD45 deficient cells secreted highly reduced levels of lymphokines (IL-2, IL-3 or GM-CSF) after activation by anti-CD3 mAb combined with the phorbol ester TPA. This impaired lymphokines production is related to the absence of CD45 since a CD45+ revertant subclone, isolated from one CD45- clone, produced normal levels of cytokines upon activation via CD3, while CD45- subclones were unable to secrete cytokines following activation via CD3. However, upon activation with Ca2+ ionophore and PMA, all CD45- (sub)clones secreted cytokines at levels comparable to those produced by CD45+ cells. These results show that CD45 is required for cytokine production after activation via the TCR - CD3 complex. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. RP PEYRON, JF (reprint author), DNAX RES INST MOLEC & CELLULAR BIOL INC,DEPT HUMAN IMMUNOL,901 CALIF AVE,PALO ALTO,CA 94304, USA. RI Sancho, Jaime/O-3228-2013; Jean-Francois, PEYRON/M-5682-2016 OI Sancho, Jaime/0000-0003-3852-7951; Jean-Francois, PEYRON/0000-0001-6113-916X NR 35 TC 66 Z9 66 U1 1 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD DEC PY 1991 VL 3 IS 12 BP 1357 EP 1366 DI 10.1093/intimm/3.12.1357 PG 10 WC Immunology SC Immunology GA GV851 UT WOS:A1991GV85100019 PM 1838006 ER PT J AU STEPINSKI, J ZAJACZKOWSKI, I KAZEMBEK, D TEMERIUSZ, A LIPKOWSKI, AW TAM, SW AF STEPINSKI, J ZAJACZKOWSKI, I KAZEMBEK, D TEMERIUSZ, A LIPKOWSKI, AW TAM, SW TI USE OF HYDROPHILIC DIAMINES FOR BRIDGING OF 2 OPIOID PEPTIDE PHARMACOPHORES - SYNTHESIS AND RECEPTOR-BINDING OF 2 NEW ANALOGS SO INTERNATIONAL JOURNAL OF PEPTIDE AND PROTEIN RESEARCH LA English DT Article DE BIVALENT OPIOIDS; ENKEPHALIN ANALOGS; OPIOID RECEPTOR SELECTIVITY ID CENTRAL-NERVOUS-SYSTEM; DELTA-OPIATE RECEPTOR; BIVALENT LIGANDS; BIOLOGICAL-ACTIVITY; ENKEPHALINS; SELECTIVITY; ANTAGONIST; KAPPA; TRANSPORT; DESIGN AB The bivalent ligand approach, which assumes that two pharmacophores are connected by a spacer, was used to design receptor type-selective ligands for opioid receptors. The first two opioid peptide bivalent ligands with different spacer lengths containing different numbers of hydroxyl groups, (Tyr-D-Ala-Gly-Phe-NH-CH2-CHOH-)2 and (Tyr-D-Ala-Gly-Phe-NH-CH2-CHOH-CHOH-)2, were synthesized and their binding to mu, delta, and kappa opioid receptors was characterized. Both analogues were found to possess high opioid in vitro activities. The length of the hydrophilic spacer does not affect the affinity for delta receptors, whereas shorter spacer length increases affinity for mu and even more so for kappa receptors. Thus receptor type-selective peptides for opioid receptors can be designed using the bivalent approach. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. DUPONT MERCK PHARMACEUT CO,WILMINGTON,DE. RP STEPINSKI, J (reprint author), UNIV WARSAW,DEPT CHEM,UL PASTEURA 1,PL-02093 WARSAW,POLAND. NR 31 TC 8 Z9 8 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0367-8377 J9 INT J PEPT PROT RES JI Int. J. Pept. Protein Res. PD DEC PY 1991 VL 38 IS 6 BP 588 EP 592 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HB398 UT WOS:A1991HB39800013 PM 1668098 ER PT J AU TALAMO, JH STEINERT, RF PULIAFITO, CA AF TALAMO, JH STEINERT, RF PULIAFITO, CA TI UPDATE ON LASER CORNEAL SURGERY SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP TALAMO, JH (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,50 STANIFORD ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD WIN PY 1991 VL 31 IS 1 BP 13 EP 23 DI 10.1097/00004397-199103110-00005 PG 11 WC Ophthalmology SC Ophthalmology GA EZ716 UT WOS:A1991EZ71600004 PM 1997448 ER PT J AU KORNMEHL, EW AF KORNMEHL, EW TI RADIAL KERATOTOMY - INCISION NUMBER, INCISION DIRECTION, PERIPHERAL REDEEPENING, AND MULTIPLE-DEPTH INCISIONS SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP KORNMEHL, EW (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,636 BEACON ST,BOSTON,MA 02115, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD WIN PY 1991 VL 31 IS 1 BP 101 EP 107 DI 10.1097/00004397-199103110-00013 PG 7 WC Ophthalmology SC Ophthalmology GA EZ716 UT WOS:A1991EZ71600012 PM 1997447 ER PT J AU MATSUBARA, M ZIESKE, JD FINI, ME AF MATSUBARA, M ZIESKE, JD FINI, ME TI MECHANISM OF BASEMENT-MEMBRANE DISSOLUTION PRECEDING CORNEAL ULCERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE COLLAGENASE; GELATINASE; METALLOPROTEINASE; BASEMENT MEMBRANE; CORNEAL ULCERATION; THERMAL BURN ID EXTRACELLULAR-MATRIX; IV COLLAGENASE; EXPRESSION; METALLOPROTEINASE; RABBIT; FIBROBLASTS; COMPONENTS AB In animal models for corneal ulceration, the degradation of extracellular matrix components of the stroma does not occur until after the basement membrane underlying the corneal epithelium has disappeared. Using a thermal-burn model, it was demonstrated that epithelial basement membrane is degraded actively by products of corneal cells in a process that does not require the participation of polymorphonuclear leukocytes. A new gelatinolytic metalloproteinase, preliminarily identified as the matrix metalloproteinase, MMP-9, is synthesized and secreted by corneal cells with a timing appropriate for a role in basement membrane degradation. During healing of ulcers, when new matrix is being deposited actively in the burned tissue, a second new gelatinase appears in the cornea, preliminarily identified as a stable activated form of the matrix metalloproteinase, MMP-2. The timing of expression suggests a role for this enzyme in appropriate deposition and remodeling of new matrix in the regenerating corneal tissue. C1 EYE RES INST,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. RP FINI, ME (reprint author), MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BLDG 149,3RD FLOOR,BOSTON,MA 02129, USA. FU NEI NIH HHS [EY05665, EY08408] NR 42 TC 130 Z9 132 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 1991 VL 32 IS 13 BP 3221 EP 3237 PG 17 WC Ophthalmology SC Ophthalmology GA GV121 UT WOS:A1991GV12100013 PM 1660857 ER PT J AU CROFT, MA KAUFMAN, PL ERICKSONLAMY, K POLANSKY, JR AF CROFT, MA KAUFMAN, PL ERICKSONLAMY, K POLANSKY, JR TI ACCOMMODATION AND CILIARY MUSCLE MUSCARINIC RECEPTORS AFTER ECHOTHIOPHATE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE ACCOMMODATION; CHOLINERGIC SENSITIVITY; CHOLINESTERASE INHIBITORS; CILIARY MUSCLE; ECHOTHIOPHATE; GLAUCOMA; MONKEY EYE; MUSCARINIC CHOLINERGIC RECEPTORS; PILOCARPINE; QUINUCLIDINYL BENZILATE ID TOPICAL ANTICHOLINESTERASE TREATMENT; AQUEOUS OUTFLOW SYSTEM; CHOLINERGIC SENSITIVITY; CYNOMOLGUS MONKEY; SUBSENSITIVITY; PILOCARPINE; DRUGS; MECHANISM; EYES AB Twice daily topical administration of echothiophate for 2 weeks to the eyes of living cynomologus monkeys produced profound subsensitivity of the accommodative response to pilocarpine and an approximately 50% decrease in the number of specific binding sites for H-3-quinuclidinyl benzilate (H-3-QNB) in the ciliary muscle without a change in their affinity. When echothiophate treatment was discontinued, functional cholinergic sensitivity and the number of QNB binding sites both returned to normal over a similar 4-8 week period. Most animals had a modest overshoot of both functional sensitivity and number of binding sites for at least several weeks thereafter. The treated to control eye ratios for the number of binding sites and accommodative response to pilocarpine were correlated and the plot of log treated to control binding site ratio versus treated to control accommodation ratio resembled a dose-response curve. Similarly, the treated versus control eye differences for the two parameters were correlated, with the regression line passing through the 0-0 axis intercept. Collectively, these findings suggest that agonist-induced modulation of functional cholinergic sensitivity in the parasympathetically innervated (as opposed to denervated) ciliary muscle occurs by a muscarinic receptor-mediated mechanism. This system appears to provide a useful model to study the regulation of ciliary muscle cholinergic sensitivity. C1 UNIV WISCONSIN,SCH MED,DEPT OPHTHALMOL,MADISON,WI 53706. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT OPHTHALMOL,SAN FRANCISCO,CA 94143. RP KAUFMAN, PL (reprint author), UNIV WISCONSIN,CTR CLIN SCI,DEPT OPHTHALMOL,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NEI NIH HHS [EY03980, EY07321, EY02698] NR 30 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD DEC PY 1991 VL 32 IS 13 BP 3288 EP 3297 PG 10 WC Ophthalmology SC Ophthalmology GA GV121 UT WOS:A1991GV12100021 PM 1748559 ER PT J AU BLOCH, KJ BUCKLEY, RH KOHLER, PF AF BLOCH, KJ BUCKLEY, RH KOHLER, PF TI DIAGNOSTIC LABORATORY IMMUNOLOGY - A SUBSPECIALTY THAT ENCOMPASSES CLINICAL AS WELL AS LABORATORY IMMUNOLOGY SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,ALLERGY UNIT,BOSTON,MA 02114. DUKE UNIV,MED CTR,DIV PEDIAT ALLERGY & IMMUNOL,DURHAM,NC 27710. TULANE UNIV,SCH MED,DEPT MED,NEW ORLEANS,LA 70112. RP BLOCH, KJ (reprint author), MASSACHUSETTS GEN HOSP,CLIN IMMUNOL UNIT,BOSTON,MA 02114, USA. NR 1 TC 3 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD DEC PY 1991 VL 88 IS 6 BP 961 EP 963 DI 10.1016/0091-6749(91)90254-L PG 3 WC Allergy; Immunology SC Allergy; Immunology GA GW262 UT WOS:A1991GW26200018 PM 1744367 ER PT J AU JANSSENS, SP THOMPSON, BT SPENCE, CR HALES, CA AF JANSSENS, SP THOMPSON, BT SPENCE, CR HALES, CA TI POLYCYTHEMIA AND VASCULAR REMODELING IN CHRONIC HYPOXIC PULMONARY-HYPERTENSION IN GUINEA-PIGS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE PULMONARY HEART DISEASE; HYPERVISCOSITY; PULMONARY VASCULAR RESISTANCE; PULMONARY VASCULAR SMOOTH MUSCLE PROLIFERATION ID RATS; CIRCULATION; HEPARIN; DISEASE; GROWTH; LUNGS AB Chronic hypoxia increases pulmonary arterial pressure (PAP) as a result of vasoconstriction, polycythemia, and vascular remodeling with medial thickening. To determine whether preventing the polycythemia with repeated bleeding would diminish the pulmonary hypertension and remodeling, we compared hemodynamic and histological profiles in hypoxic bled (HB, n = 6) and hypoxic polycythemic guinea pigs (H, n = 6). After 10 days in hypoxia (10% O2), PAP was increased from 10 +/- 1 (SE) mmHg in room air controls (RA, n = 5) to 20 +/- 1 mmHg in H (P < 0.05) but was lower in HB (15 +/- 1 mmHg, P < 0.05 vs. H). Cardiac output and pulmonary artery vasoreactivity did not differ among groups. Total pulmonary vascular resistance increased from 0.072 +/- 0.011 mmHg.ml-1.min in RA to 0.131 mmHg.ml-1.min in H but was significantly lower in HB (0.109 +/- 0.006 mmHg.ml-1.min). Hematocrit increased with hypoxia (57 +/- 3% in H vs. 42 +/- 1% in RA, P < 0.05), and bleeding prevented the increase (46 +/- 4% in HB, P < 0.05 vs. H only). The proportion of thick-walled peripheral pulmonary vessels (53.2 +/- 2.9% in HB and 50.6 +/- 4.8% in H vs. 31.6 +/- 2.6% in RA, P < 0.05) and the percent medial thickness of pulmonary arteries adjacent to alveolar ducts (7.2 +/- 0.6% in HB and 7.0 +/- 0.4% in H vs. 5.2 +/- 0.4% in RA, P < 0.05) increased to a similar degree in both hypoxic groups. A similar tendency was present in larger bronchiolar vessels. We conclude that pulmonary vascular remodeling in chronic hypoxic guinea pigs occurs to the same degree despite a normal hematocrit and a 50% reduction in the PAP rise, suggesting that the level of pressure or polycythemia may not be the sole stimulus to remodeling. C1 MASSACHUSETTS GEN HOSP,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-39150] NR 29 TC 26 Z9 27 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD DEC PY 1991 VL 71 IS 6 BP 2218 EP 2223 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA GW105 UT WOS:A1991GW10500022 PM 1778916 ER PT J AU FLEMING, H BURTON, M JOHNSON, DC KAZEMI, H AF FLEMING, H BURTON, M JOHNSON, DC KAZEMI, H TI SODIUM-SALICYLATE CENTRALLY AUGMENTS VENTILATION THROUGH CHOLINERGIC MECHANISMS SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE CENTRAL CONTROL OF BREATHING; ATROPINE ID DOGS; CHEMOSENSITIVITY; INTOXICATION AB Several different stimuli, including hydrogen ions, may exert their effect on central ventilatory control through cholinergic mechanisms. Salicylates are known to be central respiratory stimulants. Therefore this study explored whether the ventilatory effect of sodium salicylate (SAL) is through cholinergic mechanisms. Ventriculocisternal perfusion was used in spontaneously breathing anesthetized (pentobarbital sodium, 30 mg/kg) mongrel dogs to study the effects of SAL (50 mM), atropine (ATR, 4.8 mM), and SAL-ATR on ventilation. After 15 min of perfusion with mock cerebrospinal fluid, each test agent was perfused for 15 min at a rate of 1 ml/min. Cardiovascular and ventilatory parameters were monitored. Values at 15 min of test agent perfusion were compared with values at 15 min of mock cerebrospinal fluid perfusion, with each animal used as its own control. Body temperature was kept between 37.5 and 39.0-degrees-C. Perfusion with SAL increased minute ventilation (VE) by 54% (P < 0.005) and respiratory frequency by 50% (P < 0.005). Tidal volume was not changed, but mean inspiratory flow rate increased (P < 0.05). Perfusion with ATR decreased VE by 22% (P < 0.1), and perfusion with SAL-ATR decreased VE by 20% (P = 0.01). No significant cardiovascular changes were noted in any group. We conclude that SAL increases VE centrally, primarily by increasing respiratory frequency. Because ATR blocked this effect, cholinergic mechanisms are probably involved in the salicylates' central stimulation of ventilation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [F32-HL-07665, HL-07354] NR 29 TC 5 Z9 5 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD DEC PY 1991 VL 71 IS 6 BP 2299 EP 2303 PG 5 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA GW105 UT WOS:A1991GW10500033 PM 1778926 ER PT J AU BERRY, DJ CHANDLER, HP REILLY, DT AF BERRY, DJ CHANDLER, HP REILLY, DT TI THE USE OF BONE ALLOGRAFTS IN 2-STAGE RECONSTRUCTION AFTER FAILURE OF HIP REPLACEMENTS DUE TO INFECTION SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID FEMORAL-HEAD ALLOGRAFTS; DEEP INFECTION; ARTHROPLASTY; DEFICIENCY; SALVAGE AB Bone allografts were used to reconstruct deficient acetabular and femoral bone in eighteen patients during two-stage revision of a hip arthroplasty that had failed due to infection. At a mean of 4.2 years after reimplantation, only two patients had had recurrence of the infection. Four patients needed another revision arthroplasty for reasons other than infection. These results suggest that allografts of bone are useful for the reconstruction of osseous deficiencies in carefully selected patients who have a hip arthroplasty after infection. The results do not support the concern that allografts that are used under these circumstances necessarily lead to a high rate of recurrence of infection. However, the long-term results of the use of allografts in hip arthroplasty after infection remain unknown. C1 BRIGHAM & WOMENS HOSP,DEPT ORTHOPAED SURG,75 FRANCIS ST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. NR 62 TC 84 Z9 86 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. Vol. PD DEC PY 1991 VL 73A IS 10 BP 1460 EP 1468 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA GX803 UT WOS:A1991GX80300003 PM 1748695 ER PT J AU MITLAK, BH RODDA, CP VONDECK, MD DOBROLET, NC NEER, RM NUSSBAUM, SR AF MITLAK, BH RODDA, CP VONDECK, MD DOBROLET, NC NEER, RM NUSSBAUM, SR TI PAMIDRONATE REDUCES PTH-MEDIATED BONE LOSS IN A GENE-TRANSFER MODEL OF HYPERPARATHYROIDISM IN RATS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID DICHLOROMETHYLENE DIPHOSPHONATE; PHOTON-ABSORPTIOMETRY; HYPERCALCEMIA AB We evaluated spinal and femoral bone mass and density utilizing dual-energy x-ray absorptiometry (DEXA) in rats in which severe hyperparathyroidism was produced by the expression of the gene for human PTH-(1-84) (hPTH). This gene was incorporated into a retroviral vector that was transfected into fibroblasts which were subsequently injected into their peritoneal cavities. Further, we examined the effect of the administration of pamidronate on bone mass and density in the presence of extremely high concentrations of hPTH. Three groups of rats were studied. Groups 1 and 2 receive the hPTH-secreting fibroblasts; group 2 subsequently received pamidronate (2.5 mg/kg IV) 18 and 27 days after receiving the fibroblasts. These animals developed levels of hPTH > 1.0-mu-g/liter and became hypercalcemia within 20 days. These animals became lethargic and were significantly lower in weight than age-matched controls (group 3, p < 0.05). After accounting for the animal weight there was a further significant decrease in bone mineral content and density (BMC and BMD) on day 29 attributable to hPTH-mediated bone loss. Treatment with pamidronate resulted in a higher BMC of the lumbar spine than in the untreated animals, with elevated concentrations of hPTH. The BMD was significantly higher at both the lumbar spine and femur in the pamidronate-treated animals (p < 0.05). The CV of paired measurements of BMD was 2.7% at the spine and 1.5% of a femur, respectively. The BMC of the lumbar spine and femur was closely correlated with the ashed weight of the same bones (r = 0.92 and 0.85, respectively). C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 5,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 16 TC 16 Z9 16 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD DEC PY 1991 VL 6 IS 12 BP 1317 EP 1321 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GZ148 UT WOS:A1991GZ14800007 PM 1792942 ER PT J AU ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA AF ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA TI NIFEDIPINE IMPROVES LEFT-VENTRICULAR FUNCTION IN PATIENTS WITH HYPERTENSION SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE CALCIUM CHANNEL BLOCKADE; RADONUCLIDE CINEANGIOGRAPHY; DIASTOLIC; DIASTOLIC FUNCTION; LUSITROPY; CARDIAC PERFORMANCE; EXERCISE ID TRADITIONAL ANTIHYPERTENSIVE THERAPY; DIASTOLIC FUNCTION; VERAPAMIL; DEFENSE AB The effects of the nifedipine gastrointestinal therapeutic system (GITS) on blood pressure (BP), systemic vascular resistance (SVR), and left ventricular (LV) performance were determined in eight patients with essential hypertension. LV systolic and diastolic performance were assessed by first-pass radionuclide cineangiography at rest and during upright bicycle exercise after initial and long-term BP reduction. After initial treatment, end-diastolic volume (LVEDV) increased in association with an increase in stroke volume (SV), cardiac output (CO), and peak ejection rate. After long-term treatment, LVEDV decreased, SV and CO returned to pretreatment values, early diastolic filling fraction increased, and time to peak filling rate decreased. These hemodynamic changes are consistent with an initial predominant effect of vasodilation on LV function. With long-term treatment, the effects on LV diastolic performance are consistent with a positive lusitropic effect of nifedipine GITS. Nifedipine GITS is an effective agent for control of hypertension; its hemodynamic effects are consistent with both an effect on SVR due to decreased vascular smooth muscle contraction and a direct lusitropic effect on myocardial function. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,DIV HYPERTENS & VASC MED,15 PARKMAN ST,ACC 482,BOSTON,MA 02114, USA. NR 22 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD DEC PY 1991 VL 18 IS 6 BP 843 EP 848 DI 10.1097/00005344-199112000-00009 PG 6 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA GW483 UT WOS:A1991GW48300009 PM 1725896 ER PT J AU BACKER, JM SHOELSON, SE HARING, E WHITE, MF AF BACKER, JM SHOELSON, SE HARING, E WHITE, MF TI INSULIN-RECEPTORS INTERNALIZE BY A RAPID, SATURABLE PATHWAY REQUIRING RECEPTOR AUTOPHOSPHORYLATION AND AN INTACT JUXTAMEMBRANE REGION SO JOURNAL OF CELL BIOLOGY LA English DT Article ID GROWTH-FACTOR RECEPTOR; TYROSINE KINASE-ACTIVITY; CELL-FREE SYSTEM; DENSITY-LIPOPROTEIN RECEPTOR; COATED PIT FORMATION; ATP-BINDING-SITE; CYTOPLASMIC DOMAIN; MEDIATED ENDOCYTOSIS; DOWN-REGULATION; TRANSFECTED CELLS AB The effect of receptor occupancy on insulin receptor endocytosis was examined in CHO cells expressing normal human insulin receptors (CHO/IR), autophosphorylation- and internalization-deficient receptors (CHO/IR(A1018)), and receptors which undergo autophosphorylation but lack a sequence required for internalization (CHO/IR(DELTA-960)). The rate of [I-125]insulin internalization in CHO/IR cells at 37-degrees-C was rapid at physiological concentrations, but decreased markedly in the presence of increasing unlabeled insulin (ED50 = 1-3 nM insulin, or 75,000 occupied receptors/cell). In contrast, [I-125]insulin internalization by CHO/IR(A1018) and CHO/IR(DELTA-960) cells was slow and was not inhibited by unlabeled insulin. At saturating insulin concentrations, the rate of internalization by wild-type and mutant receptors was similar. Moreover, depletion of intracellular potassium, which has been shown to disrupt coated pit formation, inhibited the rapid internalization of [I-125]insulin at physiological insulin concentrations by CHO/IR cells, but had little or no effect on [I-125]insulin uptake by CHO/IR(DELTA-960) and CHO/IR(A1018) cells or wild-type cells at high insulin concentrations. These data suggest that the insulin-stimulated entry of the insulin receptor into a rapid, coated pit-mediated internalization pathway is saturable and requires receptor autophosphorylation and an intact juxtamembrane region. Furthermore, CHO cells also contain a constitutive nonsaturable pathway which does not require receptor autophosphorylation or an intact juxtamembrane region; this second pathway is unaffected by depletion of intracellular potassium, and therefore may be independent of coated pits. Our data suggest that the ligand-stimulated internalization of the insulin receptor may require specific saturable interactions between the receptor and components of the endocytic system. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BACKER, JM (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK36836, DK38712] NR 70 TC 78 Z9 78 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD DEC PY 1991 VL 115 IS 6 BP 1535 EP 1545 DI 10.1083/jcb.115.6.1535 PG 11 WC Cell Biology SC Cell Biology GA GW007 UT WOS:A1991GW00700005 PM 1757462 ER PT J AU RITTENBERG, T LONGAKER, MT ADZICK, NS EHRLICH, HP AF RITTENBERG, T LONGAKER, MT ADZICK, NS EHRLICH, HP TI SHEEP AMNIOTIC-FLUID HAS A PROTEIN FACTOR WHICH STIMULATES HUMAN FIBROBLAST POPULATED COLLAGEN LATTICE CONTRACTION SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID DERMAL FIBROBLASTS; SKIN WOUNDS; FETAL; PROLIFERATION; INVITRO; MUSCLE; RAT AB Sutured incisional wounds made in fetal sheep and rabbits heal without scarring. Fetal sheep excisional wounds can close by contraction, but those in fetal rabbits do not. In vivo and in vitro evidence suggests that rabbit amniotic fluid inhibits wound contraction. The question arises: does sheep amniotic fluid promote wound contraction because their fetal wounds close by contraction? Sheep amniotic fluid (SAF) from 100 and 125 days gestation was tested in fibroblast populated collagen lattice (FPCL) system, an in vitro model of wound contraction. SAF stimulated FPCL contraction in a dose responsive manner. SAF from a 100 day fetus was more stimulating than a 125 day SAF. SAF enhanced FPCL contraction in the presence or absence of serum. SAF was fractionated by size, using column chromatography. It yielded a fraction with an estimated molecular weigh near 40,000 daltons, which stimulated FPCL contraction. The factor was inactivated by proteolytic digestion and heat denaturation. This protein fraction which stimulates FPCL contraction is not related to 1) actin-myosin filaments enhanced contraction by ATP-induced cell contraction, 2) promotion of fibroblast elongation on glass surface or in collagen, or 3) increased cell number by enhanced fibroblast duplication in a collagen matrix. A mechanism for SAF promotion of FPCL contraction was investigated but not identified. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SHRINERS BURN INST,WOUND HEALING LAB,51 BLOSSOM ST,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,DEPT SURG,FETAL TREATMENT PROGRAM,SAN FRANCISCO,CA 94143. NR 23 TC 17 Z9 17 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD DEC PY 1991 VL 149 IS 3 BP 444 EP 450 DI 10.1002/jcp.1041490313 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA GU237 UT WOS:A1991GU23700012 PM 1744173 ER PT J AU CASTANO, L RUSSO, E ZHOU, L LIPES, MA EISENBARTH, GS AF CASTANO, L RUSSO, E ZHOU, L LIPES, MA EISENBARTH, GS TI IDENTIFICATION AND CLONING OF A GRANULE AUTOANTIGEN (CARBOXYPEPTIDASE-H) ASSOCIATED WITH TYPE-I DIABETES SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID INSULIN-SECRETORY-GRANULE; ENKEPHALIN CONVERTASE; SEQUENCE-ANALYSIS; ANTIBODIES; CDNA; ANTIGEN; CELL; RAT; AUTOANTIBODIES; ACID AB Using serum from a prediabetic patient as a probe, we screened 0.5 x 10(6) recombinants from a rat islet lambda-gt11 expression library. One plaque-producing antigen reactive with this prediabetic serum was identified, subcloned, and sequenced. Analysis of the sequence reveals that the clone encodes a 136-amino acid fragment of carboxypeptidase-H (enkephalin convertase). Carboxypeptidase-H is a molecule expressed within islet secretory granules and neurendocrine cells. The patient whose antibodies recognize this recombinant molecule (termed DG-1) was negative for anti-DG-1 antibodies in 1984, developed the antibodies by 1986, and remained positive until the development of diabetes in 1988. To date, serum from 5 of 20 cytoplasmic islet cell antibody-positive relatives reacted with the expressed protein, while none of 14 control sera reacted. On Western blotting, the initial patient's serum used for the screening reacts with a 52-kDa antigen corresponding to the mol wt of the membrane form of carboxypeptidase-N. The current study has identified carboxypeptidase-H as an autoantigen recognized by serum of pretype I diabetes, and the methodology used should aid in identification of additional autoantigens associated with type I diabetes. RP CASTANO, L (reprint author), HARVARD UNIV, CHILDRENS HOSP, NEW ENGLAND DEACONESS HOSP, SCH MED, JOSLIN DIABET CTR, BOSTON, MA 02115 USA. RI Castano, Luis/C-3084-2009 FU NIDDK NIH HHS [DK-36836, DK-32083-09] NR 32 TC 150 Z9 159 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 1991 VL 73 IS 6 BP 1197 EP 1201 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GW879 UT WOS:A1991GW87900008 PM 1955501 ER PT J AU KLIBANSKI, A ALEXANDER, JM BIKKAL, HA HSU, DW SWEARINGEN, B ZERVAS, NT AF KLIBANSKI, A ALEXANDER, JM BIKKAL, HA HSU, DW SWEARINGEN, B ZERVAS, NT TI SOMATOSTATIN REGULATION OF GLYCOPROTEIN HORMONE AND FREE SUBUNIT SECRETION IN CLINICALLY NONFUNCTIONING AND SOMATOTROPH ADENOMAS INVITRO SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GONADOTROPH CELL ADENOMAS; PITUITARY-ADENOMAS; ALPHA-SUBUNIT; GROWTH-HORMONE; LUTEINIZING-HORMONE; ANALOG SMS-201-995; BETA-SUBUNIT; TUMORS; THYROTROPIN; RECEPTORS AB There is increasing evidence that clinically non-functioning pituitary tumors produce and secrete glycoprotein hormone and/or free alpha- and beta-subunits. In addition, hypersecretion of free alpha-subunit occurs in up to 37% of patients with somatotroph adenomas. An understanding of glycoprotein hormone regulation is important in developing effective therapeutic strategies for patients with tumors associated with intact glycoprotein hormone and free subunit hypersecretion. We investigated glycoprotein hormone and free subunit secretion by somatostatin in primary dispersed cultures of pituitary tumor cells from 23 patients with pituitary adenomas. Fifteen tumors from patients with clinically nonfunctioning adenomas (group 1) and 8 tumors from patients with somatotroph adenomas and cosecretion of alpha-subunit (group 2) were studied. Cultures were incubated with control or somatostatin-supplemented media for 24 h. Media samples from group 1 tumors were assayed for intact glycoprotein hormones and free alpha- and beta-subunits secretion levels, while media samples from group 2 cultures were assayed for alpha-subunit and GH secretion levels. Significant (P < 0.05-0.001) inhibition of secretion of 1 or more intact hormones and/or free subunits was found in 10 of the 15 group 1 tumors. SRIF[10(-7) M] suppressed intact gonadotropin secretion in 60% of FSH-producing tumors and 30% of LH-producing tumors. Media concentrations of FSH-beta and LH-beta were decreased in 31% and 50% of group 1 tumors, respectively, following somatostatin treatment in those tumors which secreted free beta-subunits. alpha-Subunit was secreted by 12 of the 15 tumors, but significant (P < 0.02-0.01) inhibition by somatostatin was observed in only 2 tumors. In contrast, significant (P < 0.05-0.001) inhibition of alpha-subunit in the somatotroph adenomas was found in 6 of the 8 tumors. Significant decreases in alpha-subunit were observed only in those tumors where GH was also significantly inhibited by somatostatin. We conclude that 1) somatostatin inhibits intact glycoprotein or free subunit secretion in the majority of clinically nonfunctioning pituitary tumors in vitro and 2) alpha-subunit secretion is suppressed in 17% and 69% of clinically nonfunctioning and somatotroph adenomas, respectively, consistent with a differential regulation of alpha-subunit by somatostatin in these two tumor types. C1 MASSACHUSETTS GEN HOSP, DEPT NEUROSURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. RP KLIBANSKI, A (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, NEUROENDOCRINE UNIT, FRUIT ST, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK07028, DK40947] NR 36 TC 36 Z9 36 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 1991 VL 73 IS 6 BP 1248 EP 1255 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GW879 UT WOS:A1991GW87900015 PM 1720125 ER PT J AU DEFRONZO, RA BARZILAI, N SIMONSON, DC AF DEFRONZO, RA BARZILAI, N SIMONSON, DC TI MECHANISM OF METFORMIN ACTION IN OBESE AND LEAN NONINSULIN-DEPENDENT DIABETIC SUBJECTS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HEPATIC GLUCOSE-PRODUCTION; INSULIN RESISTANCE; LACTIC-ACIDOSIS; METABOLISM; MELLITUS; THERAPY; HYPERGLYCEMIA; SECRETION; BINDING; MUSCLE AB The effect of metformin on glucose metabolism was examined in eight obese (percent ideal body weight, 151 +/- 9%) and six lean (percent ideal body weight, 104 +/- 4%) noninsulin-dependent diabetic (NIDD) subjects before and after 3 months of metformin treatment (2.5 g/day). Fasting plasma glucose (11.5-8.8 mmol/L), hemoglobin-A1c (9.8-7.7%), oral glucose tolerance test response (20.0-17.0 mmol/L; peak glucose), total cholesterol (5.67-4.71 mmol/L), and triglycerides (2.77-1.52 mmol/L) uniformly decreased (P < 0.05-0.001) after metformin treatment; fasting plasma lactate increased slightly from baseline (1.4 to 1.7 mmol/L; P = NS). Body weight decreased by 5 kg in obese NIDD subjects, but remained constant in lean NIDD. Basal hepatic glucose production declined in all diabetics from 83 to 61 mg/m2.min (P < 0.01), and the decrease correlated (r = 0.80; P < 0.01) closely with the fall in fasting glucose concentration. Fasting insulin (115 to 79 pmol/L) declined (P < 0.05) after metformin. During a 6.9 mmol/L hyperglycemic clamp, glucose uptake increased in every NIDD subject (113 +/- 15 to 141 +/- 12 mg/m2.min; P < 0.001) without a change in the plasma insulin response. During a euglycemic insulin clamp, total glucose uptake rose in obese NIDD subjects (121 +/- 10 to 146 +/- 9 mmol/m2.min; P < 0.05), but decreased slightly in lean NIDD (121 +/- 10 to 146 +/- 0.5; P = NS). Hepatic glucose production was suppressed by more than 80-90% in all insulin clamp studies before and after metformin treatment. In conclusion, metformin lowers the fasting plasma glucose and insulin concentrations, improves oral glucose tolerance, and decreases plasma lipid levels independent of changes in body weight. The improvement in fasting glucose results from a reduction in basal hepatic glucose production. Metformin per se does not enhance tissue sensitivity to insulin in NIDD subjects. The improvement in glucose metabolism under hyperglycemic, but not euglycemic, conditions suggests that metformin augments glucose-mediated glucose uptake. Metformin has no stimulatory effect on insulin secretion. C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP DEFRONZO, RA (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV DIABET, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. NR 59 TC 267 Z9 268 U1 3 U2 7 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD DEC PY 1991 VL 73 IS 6 BP 1294 EP 1301 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GW879 UT WOS:A1991GW87900022 PM 1955512 ER PT J AU SIMON, S AWDEH, Z CAMPBELL, RD RONCO, P BRINK, SJ EISENBARTH, GS YUNIS, EJ ALPER, CA AF SIMON, S AWDEH, Z CAMPBELL, RD RONCO, P BRINK, SJ EISENBARTH, GS YUNIS, EJ ALPER, CA TI A RESTRICTION FRAGMENT OF THE C2 GENE IS A UNIQUE MARKER FOR C2 DEFICIENCY AND THE UNCOMMON C2-ALLELE C2-STAR-B (A MARKER FOR TYPE-1 DIABETES) SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE HUMAN COMPLEMENT C2; C2-GENE; C2-ALLELE; C2-DEFICIENCY; RESTRICTION FRAGMENT LENGTH POLYMORPHISM ID MAJOR HISTOCOMPATIBILITY COMPLEX; INHERITED STRUCTURAL POLYMORPHISM; 2ND COMPONENT; GEL-ELECTROPHORESIS; FACTOR-B; DNA; HAPLOTYPES; ASSOCIATIONS; LINKAGE; ANTIGEN AB There are three common C2 protein alleles in caucasians, C2*C, C2*B, and C2*Q0, with allele frequencies of 0.96, 0.03,and 0.01, as well as Sst I RFLP variants of 2.75, 2.7, 2.65, 2.55, and 2.4 kb, with frequencies of 0.017, 0.533, 0.358, 0.017, and 0.075. Thus, C2*C is informatively split by the RFLP. Of 94 nonrandomly ascertained caucasian complotypes, 77 contained C2*C, four contained C2*Q0, and 13 had C2*B. None of the C2*C-containing complotypes carried the 2.75 kb Sst I fragment and all of the complotypes with C2*B or C2*Q0 carried it. All of the C2*Q0 alleles were associated with C4A*4, C4B*2 in the complotype S042 as previously reported. C2*B was usually (9/13) in the complotype SB42, occasionally (1/13 each) in SB45, SB41, SB(4,3)0, and SB31. Thus, the association of the C2 2.75-kb fragment was with C2*B and C2*Q0, not with C4A*4, C4B*2, or even C4A*4 alone. The complotype SC42 was associated with the 2.65-kb Sst I fragment in four of five instances and in a single example with the 2.7-kb fragment. C2*B and C2*Q0 possibly had a common evolutionary ancestor complotype which carried the 2.75-kb Sst I fragment, and BF*S, C4A*4, and C4B*2. C2*B (particularly as the haplotype HLA-Bw62, SB42, DR4) is associated with type 1 diabetes but C2*Q0 is protective. C1 CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV OXFORD,OXFORD OX1 3QU,ENGLAND. RP ALPER, CA (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI 14157]; NIDDK NIH HHS [DK 26844] NR 31 TC 8 Z9 8 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD DEC PY 1991 VL 88 IS 6 BP 2142 EP 2145 DI 10.1172/JCI115545 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA GU967 UT WOS:A1991GU96700047 PM 1684365 ER PT J AU CALIGIURI, MA MURRAY, C SOIFFER, RJ KLUMPP, TR SEIDEN, M COCHRAN, K CAMERON, C ISH, C BUCHANAN, L PERILLO, D SMITH, K RITZ, J AF CALIGIURI, MA MURRAY, C SOIFFER, RJ KLUMPP, TR SEIDEN, M COCHRAN, K CAMERON, C ISH, C BUCHANAN, L PERILLO, D SMITH, K RITZ, J TI EXTENDED CONTINUOUS INFUSION LOW-DOSE RECOMBINANT INTERLEUKIN-2 IN ADVANCED CANCER - PROLONGED IMMUNOMODULATION WITHOUT SIGNIFICANT TOXICITY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACTIVATED KILLER-CELLS; REPETITIVE WEEKLY CYCLES; HUMAN PERIPHERAL-BLOOD; METASTATIC CANCER; IL-2; IMMUNOTHERAPY; CARCINOMA; THERAPY; LYMPHOCYTES; INVIVO C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. ROSWELL PK CANC INST,BUFFALO,NY. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HANOVER,NH 03756. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA34183, CA41619]; NIAID NIH HHS [AI29530] NR 30 TC 94 Z9 94 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 1991 VL 9 IS 12 BP 2110 EP 2119 PG 10 WC Oncology SC Oncology GA GT515 UT WOS:A1991GT51500006 PM 1960552 ER PT J AU DECAPRIO, JA MAYER, RJ GONIN, R ARBUCK, SG AF DECAPRIO, JA MAYER, RJ GONIN, R ARBUCK, SG TI FLUOROURACIL AND HIGH-DOSE LEUCOVORIN IN PREVIOUSLY UNTREATED PATIENTS WITH ADVANCED ADENOCARCINOMA OF THE PANCREAS - RESULTS OF A PHASE-II TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ADVANCED COLORECTAL-CARCINOMA; CLINICAL-TRIALS; RANDOMIZED TRIAL; 5-FLUOROURACIL; CANCER; CHEMOTHERAPY; MODULATION; CALCIUM; POOLS; XENOGRAFTS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. ROSWELL PK CANC INST,BUFFALO,NY. NR 33 TC 108 Z9 113 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD DEC PY 1991 VL 9 IS 12 BP 2128 EP 2133 PG 6 WC Oncology SC Oncology GA GT515 UT WOS:A1991GT51500008 PM 1960554 ER PT J AU FALKSON, G GELMAN, R FALKSON, CI GLICK, J HARRIS, J AF FALKSON, G GELMAN, R FALKSON, CI GLICK, J HARRIS, J TI FACTORS PREDICTING FOR RESPONSE, TIME TO TREATMENT FAILURE, AND SURVIVAL IN WOMEN WITH METASTATIC BREAST-CANCER TREATED WITH DAVTH - A PROSPECTIVE EASTERN-COOPERATIVE-ONCOLOGY-GROUP STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COMBINATION CHEMOTHERAPY; PREMENOPAUSAL WOMEN; ADRIAMYCIN; DIBROMODULCITOL; METHOTREXATE; OOPHORECTOMY; TAMOXIFEN; THERAPY; TRIAL; CAF C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. RP FALKSON, G (reprint author), UNIV PRETORIA,DEPT MED ONCOL,POB 667,PRETORIA 0001,SOUTH AFRICA. FU NCI NIH HHS [CA 21115, CA 21692, CA 23318] NR 25 TC 59 Z9 60 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD DEC PY 1991 VL 9 IS 12 BP 2153 EP 2161 PG 9 WC Oncology SC Oncology GA GT515 UT WOS:A1991GT51500012 PM 1960558 ER PT J AU ETCOFF, NL FREEMAN, R CAVE, KR AF ETCOFF, NL FREEMAN, R CAVE, KR TI CAN WE LOSE MEMORIES OF FACES - CONTENT SPECIFICITY AND AWARENESS IN A PROSOPAGNOSIC SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID POSTERIOR CEREBRAL-LESIONS; ASSOCIATIVE VISUAL AGNOSIA; MENTAL-IMAGERY; FACIAL RECOGNITION; REPRESENTATION; ORGANIZATION; KNOWLEDGE; DISORDERS; IDENTITY; CONTOURS AB Prosopagnosia is a neurological syndrome in which patients cannot recognize faces. Recently it has been shown that some prosopagnosics give evidence of "covert" recognition: they show greater autonomic responses to familar faces than to unfamiliar ones, and respond differently to familiar faces in learning and interference tasks. Although some patients do not show covert recognition, this has usually been attributed to an "apperceptive" deficit that impairs perceptual analysis of the input. The implication is that prosopagnosia is a deficit in access to, or awareness of, memories of faces: the inducing brain injury does not destroy the memories themselves. We present a case study that challenges this view. LH suffers from prosopagnosia as the result of a closed head injury. He cannot recognize familiar faces or report that they are familiar, nor answer questions about the faces from memory, though he can (1) recognize common objects and subtly varying shapes, (2) match faces while ignoring irrelevant information such as emotional expression or angle of view, (3) recognize sex, age, and likeability from faces, and (4) recognize people by a number of nonfacial channels. The only other categories of shapes that he has marked trouble recognizing are animals and emotional expressions, though even these impairments were not as severe as the one for faces. Three measures (sympathetic skin response, pupil dilation, and learning correct and incorrect names of faces) failed to show any signs of covert face recognition in LH, though the measures were sensitive enough to reflect autonomic reactions in LH to stimuli other than faces, and face familiarity in normal controls. Thus prosopagnosia cannot always be attributed to a mere absence of awareness (i.e., preserved information about faces whose output is disconnected from conscious congnitive processing), to an apperceptive deficit (i.e., preserved information about faces that cannot be accessed due to improperly analyzed perceptual input), or to an inability to recognize complex or subtly varying shapes (i.e., loss or degradation of shape memory in general). We conclude that it is possible for brain injury to eliminate the storage of information about familiar faces and certain related shapes. C1 MASSACHUSETTS GEN HOSP,NEUROPSYCHOL LAB,BOSTON,MA 02114. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DIV NEUROL,BOSTON,MA 02215. UNIV CALIF SAN DIEGO,DEPT PSYCHOL,SAN DIEGO,CA 92103. RP ETCOFF, NL (reprint author), MIT,DEPT BRAIN & COGNIT SCI,E10-237A,CAMBRIDGE,MA 02139, USA. NR 60 TC 70 Z9 70 U1 4 U2 12 PU MIT PRESS PI CAMBRIDGE PA 55 HAYWARD ST JOURNALS DEPT, CAMBRIDGE, MA 02142 SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD WIN PY 1991 VL 3 IS 1 BP 25 EP 41 DI 10.1162/jocn.1991.3.1.25 PG 17 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA FC735 UT WOS:A1991FC73500004 PM 23964803 ER PT J AU VANHOUTE, J SANSONE, C JOSHIPURA, K KENT, R AF VANHOUTE, J SANSONE, C JOSHIPURA, K KENT, R TI INVITRO ACIDOGENIC POTENTIAL AND MUTANS STREPTOCOCCI OF HUMAN SMOOTH-SURFACE PLAQUE ASSOCIATED WITH INITIAL CARIES LESIONS AND SOUND ENAMEL SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID DENTAL PLAQUE; SELECTIVE MEDIUM; ACID PRODUCTION; CARIOGENICITY; SUSPENSIONS; INVIVO; AREA AB Samples of human dental plaque were pooled from several "white spot" smooth tooth surface areas as well as from several clinically-sound tooth surface areas in each of 12 caries-positive college students. Each of the two samples from each subject was used for the determination of: (1) pH-lowering potential in vitro involving dispersed plaque suspensions, excess glucose supply, and a 60-minute test, and (2) the proportions of mutans streptococci and lactobacilli. When all subjects were considered, plaques from "white spot" areas, as compared with samples from sound surface areas, were characterized by significantly higher proportions of mutans streptococci, a lower starting ("resting") pH, a faster rate of pH drop between pH 6.0 and 5.0, and a lower minimum pH of the suspension; the lactobacillus proportions were generally very low in both types of plaques. For individual subjects, however, the proportions of mutans streptococci in plaque associated with "white spot" areas showed a wide range (0.001-10.0%), and samples with high as well as low levels of these micro-organisms could exhibit a high rate of pH drop and a low pH minimum. This suggests that, besides mutans streptococci and lactobacilli, other bacteria capable of acidogenesis at a low pH may contribute to the high pH-lowering potential exhibited by many plaques. C1 FORSYTH DENT CTR,DEPT CLIN TRIALS & HUMAN EXPERIMENTAT,BOSTON,MA 02115. RP VANHOUTE, J (reprint author), FORSYTH DENT CTR,DEPT ORAL MICROBIOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009] NR 23 TC 42 Z9 42 U1 1 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD DEC PY 1991 VL 70 IS 12 BP 1497 EP 1502 DI 10.1177/00220345910700120501 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HB901 UT WOS:A1991HB90100005 PM 1774380 ER PT J AU VANHOUTE, J SANSONE, C JOSHIPURA, K KENT, R AF VANHOUTE, J SANSONE, C JOSHIPURA, K KENT, R TI MUTANS STREPTOCOCCI AND NON-MUTANS STREPTOCOCCI ACIDOGENIC AT LOW PH, AND INVITRO ACIDOGENIC POTENTIAL OF DENTAL PLAQUE IN 2 DIFFERENT AREAS OF THE HUMAN DENTITION SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID SELECTIVE MEDIUM; CARIES; MITIS AB Samples of human dental plaque were obtained from sound tooth surfaces in the lower anterior and upper posterior areas of each of 11 subjects with various degrees of caries experience. Both types of plaque were compared for: (1) their pH-lowering potential [pH at 10 and 60 min after sugar addition and the pH drop between 0 and 10 min (delta pH) with an in vitro method involving dispersed plaque suspensions and excess glucose supply; (2) the proportions of mutans streptococci; and (3) the distribution of the predominant non-mutans streptococci according to their final pH in glucose broth. Compared with plaque from the lower anterior area, plaque from the upper posterior area exhibited a significantly higher pH-lowering potential, i.e., a lower pH at 10 and 60 min and a greater delta pH and significantly higher levels of mutans streptococci. The final pH values for the non-mutans streptococci exhibited a wide range from about 4.4 to over 5.0. The proportions of such organisms designated as capable of acidogenesis at low pH (final pH < 4.6), whether expressed as a percentage of the total non-mutans streptococci or of the total plaque flora, were significantly increased in plaque from the upper posterior area. The proportions of non-mutans streptococci capable of acidogenesis at low pH in plaque from the upper posterior area were also significantly increased, with decreasing pH values at 10 and 60 min. The findings strengthen the link between the capacity of the plaque flora for acidogenesis at a low pH and its pH-lowering potential as well as the role of bacterial acidogenesis at a low pH as an oral ecological determinant. C1 FORSYTH DENT CTR,DEPT CLIN TRIALS & HUMAN EXPERIMENTAT,BOSTON,MA 02115. RP VANHOUTE, J (reprint author), FORSYTH DENT CTR,DEPT EARTH & PLANETARY SCI,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009] NR 19 TC 49 Z9 50 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD DEC PY 1991 VL 70 IS 12 BP 1503 EP 1507 DI 10.1177/00220345910700120601 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HB901 UT WOS:A1991HB90100006 PM 1774381 ER PT J AU SHIMODA, S AOBA, T MORENO, EC AF SHIMODA, S AOBA, T MORENO, EC TI CHANGES IN ACID-PHOSPHATE CONTENT IN ENAMEL MINERAL DURING PORCINE AMELOGENESIS SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID HYDROXYAPATITE; PROTEINS; APATITES AB The present study was undertaken to investigate changes in the acid-phosphate content of porcine enamel mineral during its development and to assess separately the HPO4(2-) pools in labile and stable forms. Enamel samples at the secretory and maturing stages of amelogenesis were obtained from the permanent incisors of five- to six-month-old slaughtered piglets. Human enamel from erupted, extracted teeth, synthetic hydroxyapatite, and carbonatoapatite containing acid phosphate were included as references. The acid-phosphate content of each sample was determined chemically through its pyrolytic conversion to pyrophosphate. The assessment of HPO4(2-) in labile forms was made by analysis of samples preequilibrated with solutions containing 3 mmol/L phosphate at pH 11 (to de-protonate the HPO4(2-) species on crystal surfaces). The analytical results of porcine enamel samples showed that: (a) the outermost secretory (youngest) enamel contained the highest HPO4(2-), corresponding to about 16% of the total phosphate; (b) the acid-phosphate content decreased gradually to 10% in the inner (older) secretory and to 6% in the maturing tissue; (c) a substantial part of the HPO4(2-) in developing enamel tissue (50-60% of the HPO4(2-) for the secretory enamel) was in labile forms; and (d) the pool of the labile HPO4(2-) decreased with the growth of enamel mineral. In parallel studies with mature human enamel, it was ascertained that the total acid phosphate was only about 3% of the total phosphate, much lower than in developing porcine enamel, and that the labile pool of HPO4(2-) was also small, corresponding to about 15% of the total acid phosphate determined. The overall results indicate that acid phosphate is one of the major constituents of the early enamel crystals formed during amelogenesis and that the surfaces of the growing enamel crystallites are rich in HPO4(2-). C1 FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115. FU NIDCR NIH HHS [DE03187, DE08670] NR 24 TC 23 Z9 23 U1 0 U2 2 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD DEC PY 1991 VL 70 IS 12 BP 1516 EP 1523 DI 10.1177/00220345910700120801 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HB901 UT WOS:A1991HB90100008 PM 1774383 ER PT J AU HAMADAH, I GRANDE, DJ AF HAMADAH, I GRANDE, DJ TI THE USE OF MOHS SURGERY IN FACIAL TUMORS IN A PATIENT WITH DARIERS DISEASE SO JOURNAL OF DERMATOLOGIC SURGERY AND ONCOLOGY LA English DT Article ID SKIN AB A case illustrating the need for the Mohs technique for removing basal cell carcinomas (BCC) in skin involved with Darier's disease is presented. Because of the erythema and scaling secondary to Darier's disease, defining the margins of the tumor clinically is impossible. Therefore, we recommend Mohs micrographic surgery for BCCs that occur in Darier's-involved skin. C1 NEW ENGLAND MED CTR HOSP,DEPT DERMATOL,750 WASHINGTON ST,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DIV DERMATOL,BOSTON,MA 02114. RP GRANDE, DJ (reprint author), NEW ENGLAND MED CTR HOSP,DEPT DERMATOL,750 WASHINGTON ST,BOSTON,MA 02111, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0148-0812 J9 J DERMATOL SURG ONC PD DEC PY 1991 VL 17 IS 12 BP 950 EP 953 PG 4 WC Oncology; Dermatology; Surgery SC Oncology; Dermatology; Surgery GA GU214 UT WOS:A1991GU21400006 PM 1960266 ER PT J AU KALLI, KR HSU, PH BARTOW, TJ AHEARN, JM MATSUMOTO, AK KLICKSTEIN, LB FEARON, DT AF KALLI, KR HSU, PH BARTOW, TJ AHEARN, JM MATSUMOTO, AK KLICKSTEIN, LB FEARON, DT TI MAPPING OF THE C3B-BINDING SITE OF CR-1 AND CONSTRUCTION OF A (CR1)2-F(AB')2 CHIMERIC COMPLEMENT INHIBITOR SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID C3B/C4B RECEPTOR CR-1; EPSTEIN-BARR-VIRUS; FACTOR-H; EFFECTOR FUNCTIONS; PROTEIN; IDENTIFICATION; CONVERTASE; MEMBRANE; PATHWAY; BINDING AB CR1/CR2 chimeric receptors in which various short consensus repeats (SCRs) of CR1 were attached to CR2 were transiently expressed on COS cells, and assessed for the binding of polymerized C3b (pC3b) and anti-CR2 by immunofluorescence. Of COS cells expressing chimeras containing SCR 1-4, 1-3, 2-4, 1-2, and 2-3 of the long homologous repeats (LHRs) -B or -C, 96%, 66%, 23%, 0%, and 0%, respectively, bound pC3b. K562 cells were stably transfected with wild-type CR1, deletion mutants of CR1, and the CR1/CR2 chimeras, respectively, and assayed for binding of I-125-pC3b. The dissociation constants (K(d)) for pC3b of wild-type CR1 and the LHR-BD and -CD constructs were in the range of 1.0-2.7 nM, and of the CR1/CR2 chimeras containing SCRs 1-4, 1-3, and 2-4 of LHR-B or -C were 1.8-2.4, 6-9, and 22-36 nM, respectively. The factor I-cofactor function of the CR1/CR2 chimeras paralleled the C3b-binding function of the constructs. A CR1/immunoglobulin (1g) chimeric protein was prepared by fusing SCRs 1-4 of LHR-B to the heavy chains of a murine F(ab')2 anti-nitrophenacetyl (NP) monoclonal antibody. The (CR1)2-F(ab')2 chimera, which retained its specificity for NP, was as effective as soluble, full-length CR1 in binding pC3b, serving as a cofactor for factor I-mediated cleavage of C3b, and inhibiting activation of the alternative pathway, indicating that the bivalent expression of these SCRs reconstitutes the alternative pathway inhibitory function of CR1. The feasibility of creating CR1/Ig chimeras makes possible a new strategy of targeting complement inhibition by the use of Ig fusion partners having particular antigenic specificities. C1 JOHNS HOPKINS UNIV,SCH MED,IMMUNOL POLIKLIN,1059-S ROSS RES BLDG,720 RUTLAND AVE,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,DIV MOLEC & CLIN RHEUMATOL,BALTIMORE,MD 21205. MARSHFIELD CLIN FDN MED RES & EDUC,MARSHFIELD,WI 54449. CTR BLOOD RES,BOSTON,MA 02115. FU NIAID NIH HHS [AI-28191, AI-22833, AI-07247] NR 32 TC 86 Z9 87 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD DEC 1 PY 1991 VL 174 IS 6 BP 1451 EP 1460 DI 10.1084/jem.174.6.1451 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA GU644 UT WOS:A1991GU64400018 PM 1836011 ER PT J AU HARRISON, L TEPLOW, DB RINALDI, M STROBEL, G AF HARRISON, L TEPLOW, DB RINALDI, M STROBEL, G TI PSEUDOMYCINS, A FAMILY OF NOVEL PEPTIDES FROM PSEUDOMONAS-SYRINGAE POSSESSING BROAD-SPECTRUM ANTIFUNGAL ACTIVITY SO JOURNAL OF GENERAL MICROBIOLOGY LA English DT Article ID DUTCH ELM DISEASE; BIOLOGICAL-CONTROL; PV-SYRINGAE; SYRINGOMYCIN; FLUORESCENS; SYRINGOTOXIN; BACTERIA; ROT AB A family of peptide antimycotics, termed pseudomycins, has been isolated from liquid cultures of Pseudomonas syringae, a plant-associated bacterium. These compounds were purified using Amberlite XAD-2 and reverse-phase liquid chromatography. Pseudomycin A, the predominant peptide in a family of four, showed selective phytotoxicity, and had impressive activity against the human pathogen Candida albicans. Amino acid, mass spectroscopic, and comparative electrophoretic and chromatographic analyses revealed that the pseudomycins are different from previously described antimycotics from P. syringae, including syringomycin, syringotoxin and syringostatins. Pseudomycins A-C contain hydroxyaspartic acid, aspartic acid, serine, arginine, lysine and diaminobutyric acid. The molecular masses of pseudomycins A-C, as determined by plasma desorption mass spectrometry, are 1224, 1208 and 1252 Da, respectively. Pseudomycin D, on the other hand, has a molecular mass of 2401 Da and is more complex than pseudomycins A-C. C1 MONTANA STATE UNIV,DEPT PLANT PATHOL,BOZEMAN,MT 59717. CALTECH,BECKMAN INST,PASADENA,CA 91125. CALTECH,DIV BIOL,PASADENA,CA 91125. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 23 TC 47 Z9 50 U1 1 U2 4 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1287 J9 J GEN MICROBIOL JI J. Gen. Microbiol. PD DEC PY 1991 VL 137 BP 2857 EP 2865 PN 12 PG 9 WC Microbiology SC Microbiology GA GX946 UT WOS:A1991GX94600023 PM 1791440 ER PT J AU ASSAD, JA COREY, DP AF ASSAD, JA COREY, DP TI AN ACTIVE MOTOR REGULATES GATING-SPRING TENSION IN BULLFROG SACCULAR HAIR-CELLS SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. NR 4 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1991 VL 98 IS 6 BP A24 EP A25 PG 2 WC Physiology SC Physiology GA GW479 UT WOS:A1991GW47900057 ER PT J AU COREY, DP SHEPHERD, GMG ASSAD, JA AF COREY, DP SHEPHERD, GMG ASSAD, JA TI TIP LINKS AND ADAPTATION IN VERTEBRATE HAIR-CELLS SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1991 VL 98 IS 6 BP A10 EP A11 PG 2 WC Physiology SC Physiology GA GW479 UT WOS:A1991GW47900028 ER PT J AU SHEPHERD, GMG ASSAD, JA PARAKKEL, M KACHAR, B COREY, DP AF SHEPHERD, GMG ASSAD, JA PARAKKEL, M KACHAR, B COREY, DP TI MOVEMENT OF THE TIP-LINK ATTACHMENT IS CORRELATED WITH ADAPTATION IN BULLFROG SACCULAR HAIR-CELLS SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. NIDCD,MOLEC OTOL LAB,BETHESDA,MD. RI Shepherd, Gordon/F-2679-2010 NR 6 TC 3 Z9 3 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1991 VL 98 IS 6 BP A25 EP A25 PG 1 WC Physiology SC Physiology GA GW479 UT WOS:A1991GW47900058 ER PT J AU TEETER, JH KUMAZAWA, T BRAND, JG HONDA, E KALINOSKI, DL SMUTZER, G AF TEETER, JH KUMAZAWA, T BRAND, JG HONDA, E KALINOSKI, DL SMUTZER, G TI AMINO-ACID RECEPTOR CHANNELS IN TASTE CELLS SO JOURNAL OF GENERAL PHYSIOLOGY LA English DT Meeting Abstract C1 MONELL CHEM SENSES CTR,PHILADELPHIA,PA 19104. UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1295 J9 J GEN PHYSIOL JI J. Gen. Physiol. PD DEC PY 1991 VL 98 IS 6 BP A9 EP A10 PG 2 WC Physiology SC Physiology GA GW479 UT WOS:A1991GW47900026 ER PT J AU MONTGOMERY, LB KAO, CYY VERDIN, E CAHILL, C MARATOSFLIER, E AF MONTGOMERY, LB KAO, CYY VERDIN, E CAHILL, C MARATOSFLIER, E TI INFECTION OF A POLARIZED EPITHELIAL-CELL LINE WITH WILD-TYPE REOVIRUS LEADS TO VIRUS PERSISTENCE AND ALTERED CELLULAR FUNCTION SO JOURNAL OF GENERAL VIROLOGY LA English DT Article ID CANINE KIDNEY-CELLS; ADHESION MOLECULE UVOMORULIN; VIRAL-INFECTION; PLASMA-MEMBRANE; GROWTH-FACTOR; GENOME RNAS; SEROTYPES 1; MAINTENANCE; RECEPTOR; PROTEIN AB The mechanisms and consequences of persistence of non-transforming viruses are poorly understood. Reovirus infections are usually regarded as cytocidal and infection is associated with inhibition of cellular protein and DNA synthesis. Reovirus infection of the polarized epithelial MDCK cell line is not associated with inhibition of protein synthesis, and cells become persistently infected and continue to grow without c.p.e. after infection. After several passages, virus persistence is associated with profound morphological and functional changes. The cells lose their usual cobblestone appearance and acquire a fibroblastic, undifferentiated morphology. This is associated with an inability to form tight junctions. In addition, expression of epidermal growth factor receptors and one adhesion protein is altered in the persistently infected cells. These results demonstrate that reovirus persistence will occur readily, and that infection of differentiated cells with a non-transforming virus can lead to loss of differentiation and abnormal protein expression. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABETES CTR,RES DIV,BOSTON,MA 02215. OI Verdin, Eric/0000-0003-3703-3183 NR 44 TC 15 Z9 15 U1 0 U2 0 PU SOC GENERAL MICROBIOLOGY PI READING PA HARVEST HOUSE 62 LONDON ROAD, READING, BERKS, ENGLAND RG1 5AS SN 0022-1317 J9 J GEN VIROL JI J. Gen. Virol. PD DEC PY 1991 VL 72 BP 2939 EP 2946 DI 10.1099/0022-1317-72-12-2939 PN 12 PG 8 WC Biotechnology & Applied Microbiology; Virology SC Biotechnology & Applied Microbiology; Virology GA GY555 UT WOS:A1991GY55500010 PM 1765767 ER PT J AU TAYLOR, E AF TAYLOR, E TI JAMES,WILLIAM AND THE HUMANISTIC TRADITION SO JOURNAL OF HUMANISTIC PSYCHOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,HIST PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,AIKIDO CLUB,CAMBRIDGE,MA 02138. NR 47 TC 7 Z9 7 U1 1 U2 1 PU SAGE SCIENCE PRESS PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 SN 0022-1678 J9 J HUMANIST PSYCHOL JI J. Humanist. Psychol. PD WIN PY 1991 VL 31 IS 1 BP 56 EP 74 DI 10.1177/0022167891311006 PG 19 WC Psychology, Multidisciplinary SC Psychology GA EP244 UT WOS:A1991EP24400005 ER PT J AU NUSSBERGER, J FLUCKIGER, JP HUI, KY EVEQUOZ, D WAEBER, B BRUNNER, HR AF NUSSBERGER, J FLUCKIGER, JP HUI, KY EVEQUOZ, D WAEBER, B BRUNNER, HR TI ANGIOTENSIN-I AND ANGIOTENSIN-II DISAPPEAR COMPLETELY FROM CIRCULATING BLOOD WITHIN 48 HOURS AFTER BINEPHRECTOMY - IMPROVED MEASUREMENT OF ANGIOTENSINS IN RAT PLASMA SO JOURNAL OF HYPERTENSION LA English DT Article; Proceedings Paper CT 5TH EUROPEAN MEETING ON HYPERTENSION CY JUN 07-10, 1991 CL MILAN, ITALY SP CIBA GEIGY, HOECHST, KNOLL, KONTRON INSTRUMENTS, PRODOTTI ROCHE, SCHERING PLOUGH INT DE RAT RENIN INHIBITOR; ANEPHRIC RATS; RENAL HYPERTENSIVE RATS; SALT DEPLETION; NORMAL VALUES; TISSUE RENIN ANGIOTENSIN SYSTEM; BLOOD SAMPLING; HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY; SOLID-PHASE EXTRACTION; RADIOIMMUNOASSAY C1 MASSACHUSETTS GEN HOSP,CELLULAR & MOLEC RES LAB,BOSTON,MA 02114. RP NUSSBERGER, J (reprint author), CHU VAUDOIS,DIV HYPERTENS,CH-1011 LAUSANNE,SWITZERLAND. NR 6 TC 6 Z9 8 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0263-6352 J9 J HYPERTENS JI J. Hypertens. PD DEC PY 1991 VL 9 SU 6 BP S230 EP S231 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HD147 UT WOS:A1991HD14700099 PM 1818955 ER PT J AU DAUM, RS SIBER, GR BALLANCO, GA SOOD, SK AF DAUM, RS SIBER, GR BALLANCO, GA SOOD, SK TI SERUM ANTICAPSULAR ANTIBODY-RESPONSE IN THE 1ST WEEK AFTER IMMUNIZATION OF ADULTS AND INFANTS WITH THE HAEMOPHILUS-INFLUENZAE TYPE-B-NEISSERIA-MENINGITIDIS OUTER-MEMBRANE PROTEIN COMPLEX CONJUGATE VACCINE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HEMOPHILUS-INFLUENZAE; POLYSACCHARIDE VACCINE; EFFICACY; DISEASE; CHILDREN; ANTIGEN AB Eight healthy adults and 48 infants 2 and 4 months old were immunized with Haemophilus influenzae type b-Neisseria meningitidis outer membrane protein complex conjugate vaccine (PRP-OMP) to evaluate antibody kinetics in the first days after immunization. Five adults (63%) had some decrease in antibody, although the geometric mean did not decrease significantly. With one exception, the nadir occurred on postimmunization day 3. Seven had an antibody increase by day 7. Of the children, 6 (75%) of 8 and 17 (77%) of 23 had a decrease in antibody in serum obtained on day 2-3 after the first or second dose, respectively, the magnitude of which directly correlated with the preimmunization antibody concentration. However, the geometric mean did not decrease significantly. Within 1 week of immunization, 85% of infants had an increase in antibody, significantly greater after the second dose than after the first. A high concentration of maternally derived antibody before immunization correlated negatively with antibody response. Thus, a transient decrease in antibody occurs in most adults and infants 2-3 days after immunization with PRP-OMP followed by a prompt increase by day 7. C1 HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02115. ALBERT EINSTEIN COLL MED,LONG ISL JEWISH MED CTR,SCHNEIDER CHILDRENS HOSP,DIV INFECT DIS,NEW HYDE PK,NY. LOUISIANA STATE UNIV,DEPT PEDIAT,BATON ROUGE,LA 70803. RP DAUM, RS (reprint author), UNIV CHICAGO,WYLER CHILDRENS HOSP,DEPT PEDIAT,INFECT DIS SECT,BOX 286,CHICAGO,IL 60637, USA. FU NIAID NIH HHS [AI-18125] NR 20 TC 14 Z9 15 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD DEC PY 1991 VL 164 IS 6 BP 1154 EP 1159 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA GR660 UT WOS:A1991GR66000016 PM 1955715 ER PT J AU RABINOWITZ, JL AF RABINOWITZ, JL TI [2-C-14] 5-FLUOROURACIL METABOLISM TO [(CO2)-C-14] SO JOURNAL OF LABELLED COMPOUNDS & RADIOPHARMACEUTICALS LA English DT Article DE FLUOROURACIL; NOVIKOFF ASCITES; TUMOR TREATMENT; FIBROSARCOMA ID F-19 NMR; PHARMACOKINETICS; INVIVO AB The rate of (CO2)-C-14 production from 2-C-14-5-FU was measured in rats bearing the Novikoff ascites hepatoma. Tracer amounts were injected and (CO2)-C-14 collected over a 6-hour period. As the tumor cells proliferated the rate of 2-C-14-5-FU oxidation decreased markedly over the approximately 12 +/- 2 days between implantation of tumor cells and death. On the day of innoculation of tumor cells, oxidation proceeded nearly linearly until almost 50% of the injected 2-C-14-5-FU was converted to (CO2)-C-14 in about 4 hours. With time after tumor innoculation, the rate of (CO2)-C-14 collection declined; ten days after innoculation only about 27% was oxidized by 4 hours, and at the terminal stage it declined to about 18% over 4 hours. Calculated from the time curves, the time oxidation of 25% of the injected trace dose increased from 88 +/- 27 min to 195 +/- 42 min after ten days, to 300 +/- 59 min at the moribund state after 12 +/- 2 days. Similar decreases in oxidation rate of 5-FU were observed during growth of a solid implanted mammary carcinoma and for two other 2-C-14-labelled pyrimidines, uracil and thymine injected in trace quantities. By comparing cancer subjects with themselves at different time-intervals from the onset of the disease and treatment, it might be possible to guage treatment dosages in the progress of the disease. RP RABINOWITZ, JL (reprint author), UNIV PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 14 TC 0 Z9 0 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0362-4803 J9 J LABELLED COMPD RAD JI J. Label. Compd. Radiopharm. PD DEC PY 1991 VL 29 IS 12 BP 1277 EP 1282 DI 10.1002/jlcr.2580291203 PG 6 WC Biochemical Research Methods; Chemistry, Medicinal; Chemistry, Analytical; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Chemistry GA GV770 UT WOS:A1991GV77000002 ER PT J AU GRUBER, ML HOCHBERG, FH AF GRUBER, ML HOCHBERG, FH TI VISUAL SCOTOMAS RESULTING FROM LUPUS ANTICOAGULANT IN A PATIENT WITH LYMPHOMA IN REMISSION SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE LYMPHOMA; CIRCULATING ANTICOAGULANT; LUPUS ANTICOAGULANT ID ANTIPHOSPHOLIPID ANTIBODIES; ANTICARDIOLIPIN ANTIBODIES; DISEASE AB Episodic cerebro or retinovascular ischemic events without apparent cause occur in patients with cancer. We report a patient in remission from lymphoma whose multiple episodes of presumed ocular ischemia occurred in the setting of a circulating lupus anticoagulant. Symptoms resolved following therapy with Warfarin. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 14 TC 7 Z9 7 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD DEC PY 1991 VL 11 IS 3 BP 255 EP 257 DI 10.1007/BF00165534 PG 3 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA GN896 UT WOS:A1991GN89600009 PM 1726657 ER PT J AU FERRANTE, RJ KOWALL, NW RICHARDSON, EP AF FERRANTE, RJ KOWALL, NW RICHARDSON, EP TI PROLIFERATIVE AND DEGENERATIVE CHANGES IN STRIATAL SPINY NEURONS IN HUNTINGTONS-DISEASE - A COMBINED STUDY USING THE SECTION GOLGI METHOD AND CALBINDIN-D28K IMMUNOCYTOCHEMISTRY SO JOURNAL OF NEUROSCIENCE LA English DT Article ID CALCIUM-BINDING PROTEIN; QUINOLINIC ACID; SUBSTANCE-P; NEUROPEPTIDE-Y; HUMAN NEOSTRIATUM; MESSENGER-RNA; BASAL GANGLIA; GLUTAMATE NEUROTOXICITY; IMMUNOREACTIVE NEURONS; HIPPOCAMPAL-NEURONS AB Dysmorphic alterations of dendritic arbors and spines in spiny striatal neurons were identified in section-Golgi impregnations of moderate and severe grades of Huntington's disease (HD). These alterations could be characterized as either proliferative or degenerative changes. Proliferative changes included prominent recurving of distal dendritic segments, short-segment branching along dendrites, and increased numbers and size of dendritic spines. Degenerative alterations consisted of truncated dendritic arborizations, occasional focal dendritic swellings, and marked spine loss. Proliferative changes were found primarily in moderate grades of HD, while degenerative changes were predominantly found in severe grades. Cytopathologic changes increased with neuropathologic severity. Similar morphologic alterations were observed in calbindin D28k (Calb) stained neurons in HD striatum. The immunoreactive intensity of Calb staining was increased in the distal dendrites of positive neurons in HD striatum. The present findings provide morphologic and quantitative evidence that confirms an early and marked involvement of spiny striatal neurons in HD and suggest that neuronal growth, rather than degeneration, may be the harbinger of cell death in this disorder. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL NEUROPATHOL,BOSTON,MA 02115. RP FERRANTE, RJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NINDS NIH HHS [NS25588-04] NR 76 TC 181 Z9 183 U1 0 U2 5 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD DEC PY 1991 VL 11 IS 12 BP 3877 EP 3887 PG 11 WC Neurosciences SC Neurosciences & Neurology GA GV176 UT WOS:A1991GV17600019 PM 1836019 ER PT J AU LEIDENHEIMER, NJ HARRIS, RA AF LEIDENHEIMER, NJ HARRIS, RA TI A TRANSIENT OSMOTIC PERMEABILIZATION METHOD FOR THE INTRODUCTION OF IMPERMEANT MOLECULES INTO FUNCTIONAL BRAIN MEMBRANE-VESICLES SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Article DE BRAIN MEMBRANE VESICLES; MICROSACS; GABA-A RECEPTOR; PHOSPHORYLATION; PERMEABILIZATION ID CALCIUM-TRANSPORT; RECEPTOR FUNCTION; GABAA-RECEPTOR; GAINING ACCESS; RAT-BRAIN; PHOSPHORYLATION; SYNAPTOSOMES; DESENSITIZATION; CELLS AB Mouse brain membrane vesicles (microsacs) were transiently permeabilized by hypo-osmotic shock. This permeabilization method resulted in the encapsulation of both [C-14]sucrose and exogenous alkaline phosphatase. The efficiency of this method was estimated by [C-14]sucrose encapsulation experiments to be approximately 81%. External membrane binding experiments with the lectin [H-3]concanavalin A demonstrate that the microsacs were not inverted by permeabilization. Following permeabilization, the functional integrity of a ligand-gated ion channel, the GABA(A) receptor complex, was investigated. Muscimol-stimulated Cl-36- uptake experiments show that this receptor retains its functional properties including blockade by the receptor antagonist bicuculline and potentiation by the allosteric modulators flunitrazepam and pentobarbital. The osmotic permeabilization technique described here provides several advantages over other permeabilization methods. These advantages include a high trapping efficiency, the encapsulation of not only small solutes but large membrane impermeant compounds such as enzymes and the functional preservation of at least one transmembrane protein. Furthermore, this method does not require specialized equipment and does not result in large, permanent holes in the plasma membrane. C1 DENVER VET AFFAIRS MED CTR, DENVER, CO USA. RP UNIV COLORADO, HLTH SCI CTR, DEPT PHARMACOL, 4200 E 9TH AVE, DENVER, CO 80262 USA. FU NIAAA NIH HHS [AA06399, AA03527] NR 28 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0270 EI 1872-678X J9 J NEUROSCI METH JI J. Neurosci. Methods PD DEC PY 1991 VL 40 IS 2-3 BP 233 EP 241 DI 10.1016/0165-0270(91)90072-8 PG 9 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA GY148 UT WOS:A1991GY14800017 PM 1666165 ER PT J AU MACFARLANE, R MOSKOWITZ, MA SAKAS, DE TASDEMIROGLU, E WEI, EP KONTOS, HA AF MACFARLANE, R MOSKOWITZ, MA SAKAS, DE TASDEMIROGLU, E WEI, EP KONTOS, HA TI THE ROLE OF NEUROEFFECTOR MECHANISMS IN CEREBRAL HYPERPERFUSION SYNDROMES SO JOURNAL OF NEUROSURGERY LA English DT Review DE ISCHEMIA; HYPERPERFUSION SYNDROME; TRIGEMINAL NERVE; CALCITONIN GENE-RELATED PEPTIDE; SUBSTANCE-P ID PERFUSION-PRESSURE BREAKTHROUGH; GENE-RELATED PEPTIDE; NEUROGENIC PLASMA EXTRAVASATION; TRANSIENT FOREBRAIN ISCHEMIA; TRIGEMINAL GANGLION-CELLS; BLOOD-BRAIN-BARRIER; CAROTID ENDARTERECTOMY; SUBSTANCE-P; ARTERIOVENOUS-MALFORMATIONS; VASCULAR HEADACHES AB Cerebral hyperperfusion, a state in which blood flow exceeds the metabolic needs of brain, may complicate a number of neurological and neurosurgical conditions. It may account for the propensity with which hemorrhage, cerebral edema, or seizures follow embolic stroke, carotid endarterectomy, or the excision of large arteriovenous malformations, and for some of the morbidity that accompanies acute severe head injury, prolonged seizures, and acute severe hypertension. Hyperperfusion syndromes have in common acute increases in blood pressure, vasodilatation, breakdown of the blood-brain barrier, and the development of cerebral edema. These common features suggest the possibility that they share the same pathogenic mechanisms. It was believed until recently that reactive hyperemia was caused primarily by the generation of vasoactive metabolites, which induced vasodilatation through relaxation of vascular smooth muscle. However, the authors have recently established that the release of vasoactive neuropeptides from perivascular sensory nerves via axon reflex-like mechanisms has a significant bearing upon a number of hyperperfusion syndromes. In this article, the authors summarize their data and discuss possible therapeutic implications for blockade of these nerves or their constituent neuropeptides. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV, STROKE RES LAB, BOSTON, MA 02114 USA. VIRGINIA COMMONWEALTH UNIV, MED COLL VIRGINIA, DEPT MED, DIV CARDIOL, RICHMOND, VA 23298 USA. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS21558, NS26361] NR 160 TC 85 Z9 87 U1 0 U2 1 PU AMER ASSOC NEUROLOGICAL SURGEONS PI ROLLING MEADOWS PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA SN 0022-3085 EI 1933-0693 J9 J NEUROSURG JI J. Neurosurg. PD DEC PY 1991 VL 75 IS 6 BP 845 EP 855 DI 10.3171/jns.1991.75.6.0845 PG 11 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GQ946 UT WOS:A1991GQ94600001 PM 1941113 ER PT J AU ROSENBERG, WS ROSENBERG, AE POLETTI, CE AF ROSENBERG, WS ROSENBERG, AE POLETTI, CE TI CERVICAL DISK HERNIATION PRESENTING AS A MASS LESION POSTERIOR TO THE ODONTOID PROCESS - REPORT OF 2 CASES SO JOURNAL OF NEUROSURGERY LA English DT Article DE HERNIATED DISK, ODONTOID; INTERVERTEBRAL DISK; CERVICAL SPINE; CRANIOVERTEBRAL JUNCTION ID CRYSTAL DEPOSITION DISEASE; CRANIOVERTEBRAL JUNCTION; SURGICAL-TREATMENT; PSEUDOGOUT; LIGAMENT AB The authors report two cases of herniated intervertebral disc presenting as a mass posterior to the odontoid process and causing myelopathy in previously healthy elderly women. The differential diagnosis of a mass at the craniovertebral junction is reviewed, and the implications of these cases are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP ROSENBERG, WS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 27 TC 31 Z9 31 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD DEC PY 1991 VL 75 IS 6 BP 954 EP 959 DI 10.3171/jns.1991.75.6.0954 PG 6 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA GQ946 UT WOS:A1991GQ94600017 PM 1941124 ER EF