FN Thomson Reuters Web of Science™ VR 1.0 PT J AU MANSCHRECK, TC MAHER, B CELADA, MT SCHNEYER, M FERNANDEZ, R AF MANSCHRECK, TC MAHER, B CELADA, MT SCHNEYER, M FERNANDEZ, R TI OBJECT CHAINING AND THOUGHT-DISORDER IN SCHIZOPHRENIC SPEECH SO PSYCHOLOGICAL MEDICINE LA English DT Article AB The phenomenon of object chaining was investigated to determine its relationship to thought disorder in schizophrenia. Samples from thought-disordered schizophrenics (N = 12) and controls (10 non-thought-disordered schizophrenics and 10 normals) were analysed. Using the object subject ratio (OSR) to measure object chaining, we found higher OSRs in the speech of thought-disordered subjects than in that of subjects free of thought disorder. Object chaining correlated with low predictability of speech. We conclude that object chaining is associated with reduced speech comprehensibility and probably contributes to the judgement that thought disorder is present. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 12 TC 5 Z9 5 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD MAY PY 1991 VL 21 IS 2 BP 443 EP 446 PG 4 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA FR873 UT WOS:A1991FR87300019 PM 1876648 ER PT J AU SILVA, JA LEONG, GB SHANER, AL AF SILVA, JA LEONG, GB SHANER, AL TI THE SYNDROME OF INTERMETAMORPHOSIS SO PSYCHOPATHOLOGY LA English DT Article ID CAPGRAS SYNDROME; MISIDENTIFICATION SYNDROMES; CONTRIBUTORS AB A series of 15 patients suffering from the syndrome of intermetamorphosis or its variants is discussed in terms of this misidentification syndrome's historical, classification, diagnostic, and psychosocial aspects. One case is presented in detail. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED CTR,PSYCHIAT SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 38 TC 16 Z9 16 U1 1 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-JUN PY 1991 VL 24 IS 3 BP 158 EP 165 PG 8 WC Psychiatry SC Psychiatry GA GL243 UT WOS:A1991GL24300006 PM 1754646 ER PT J AU GERWECK, LE RHEE, JG KOUTCHER, JA SONG, CW URANO, M AF GERWECK, LE RHEE, JG KOUTCHER, JA SONG, CW URANO, M TI REGULATION OF PH IN MURINE TUMOR AND MUSCLE SO RADIATION RESEARCH LA English DT Article ID NUCLEAR MAGNETIC-RESONANCE; EXTRACELLULAR PH; INTRACELLULAR PH; MOUSE-TUMOR; MISONIDAZOLE; HYPERTHERMIA; ANALOGS RP GERWECK, LE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-13353, CA-22860, CA-44056] NR 14 TC 36 Z9 36 U1 0 U2 0 PU RADIATION RESEARCH SOC PI OAK BROOK PA 2021 SPRING RD, STE 600, OAK BROOK, IL 60521 SN 0033-7587 J9 RADIAT RES JI Radiat. Res. PD MAY PY 1991 VL 126 IS 2 BP 206 EP 209 DI 10.2307/3577819 PG 4 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA FK351 UT WOS:A1991FK35100012 PM 2023990 ER PT J AU STARK, DD AF STARK, DD TI HEPATIC IRON OVERLOAD - PARAMAGNETIC PATHOLOGY SO RADIOLOGY LA English DT Editorial Material DE HEMOCHROMATOSIS; LIVER, DISEASES; LIVER, IRON CONTENT; LIVER, MR STUDIES; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT ID NUCLEAR MAGNETIC-RESONANCE; LIVER; HEMOCHROMATOSIS; FERRITIN; RELAXATION; DISEASE C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP STARK, DD (reprint author), HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA50353] NR 35 TC 54 Z9 55 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 MAY PY 1991 VL 179 IS 2 BP 333 EP 335 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH130 UT WOS:A1991FH13000004 PM 2014271 ER PT J AU LEE, MJ HAHN, PF PAPANICOLAOU, N EGGLIN, TK SAINI, S MUELLER, PR SIMEONE, JF AF LEE, MJ HAHN, PF PAPANICOLAOU, N EGGLIN, TK SAINI, S MUELLER, PR SIMEONE, JF TI BENIGN AND MALIGNANT ADRENAL MASSES - CT DISTINCTION WITH ATTENUATION COEFFICIENTS, SIZE, AND OBSERVER ANALYSIS SO RADIOLOGY LA English DT Article DE ADRENAL GLAND; ADRENAL GLAND, NEOPLASMS; RECEIVER OPERATING CHARACTERISTIC CURVE (ROC) ID COMPUTED-TOMOGRAPHY; MR; TUMORS; GLAND AB In a retrospective study of adrenal masses evaluated with computed tomography (CT), lesion x-ray attenuation was compared with size and radiologists' interpretations in discriminating benign lesions from malignant ones. Unenhanced CT attenuation coefficient and size were analyzed electronically in 55 patients with 66 adrenal masses. There were 38 nonhyperfunctioning adenomas in 33 patients and 28 malignant masses in 22 patients. Primary extraadrenal malignancies were present in 45 of the 55 patients. Three blinded readers characterized the adrenal masses using a seven-point scale of certainty. Results were subjected to receiver operating characteristic (ROC) analysis. The mean CT attenuation coefficient for benign adrenal masses was -2.2 HU +/- 16.0 and was significantly different from the mean for malignant lesions (28.9 HU +/- 10.6). The area under the ROC curve for CT attenuation coefficients (0.91 +/- 0.04) was significantly larger than that for lesion size (0.84 +/- 0.05) or best observer interpretation (0.84 +/- 0.05). A threshold CT attenuation value of 0 HU had a sensitivity-to-specificity ratio of 47%:100% for characterizing benign adrenal masses, whereas a threshold attenuation of 10 HU had a ratio of 79%:96%. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 24 TC 257 Z9 277 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 MAY PY 1991 VL 179 IS 2 BP 415 EP 418 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH130 UT WOS:A1991FH13000020 PM 2014283 ER PT J AU YUCEL, EK FISHER, JS EGGLIN, TK GELLER, SC WALTMAN, AC AF YUCEL, EK FISHER, JS EGGLIN, TK GELLER, SC WALTMAN, AC TI ISOLATED CALF VENOUS THROMBOSIS - DIAGNOSIS WITH COMPRESSION US SO RADIOLOGY LA English DT Article DE THROMBOSIS, VENOUS; VEINS, EXTREMITIES; VEINS, US STUDIES ID DEEP-VEIN THROMBOSIS; IMPEDANCE PLETHYSMOGRAPHY; PULMONARY-EMBOLISM; DOPPLER ULTRASOUND; LEG; THROMBOPHLEBITIS AB Compression ultrasound (US) is an excellent means of evaluating the femoral and popliteal veins but is generally regarded as inadequate for the diagnosis of calf vein thrombosis. This prospective study evaluated compression sonography of the calf veins in 45 symptomatic patients with normal femoral and popliteal veins. All patients underwent correlative venography. Compression US enabled identification of 15 to 17 patients with calf vein thrombosis (sensitivity, 88%). The two false-negative results were in patients with small isolated thrombi. Compression US results were true-negative in 26 to 27 patients with normal venograms (specificity, 96%). If these results can be duplicated by other investigators in larger series of patients, compression US will be an adequate screening modality for calf vein thrombosis. RP YUCEL, EK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114, USA. NR 27 TC 76 Z9 76 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 MAY PY 1991 VL 179 IS 2 BP 443 EP 446 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH130 UT WOS:A1991FH13000026 PM 2014289 ER PT J AU SENETERRE, E WEISSLEDER, R JARAMILLO, D REIMER, P LEE, AS BRADY, TJ WITTENBERG, J AF SENETERRE, E WEISSLEDER, R JARAMILLO, D REIMER, P LEE, AS BRADY, TJ WITTENBERG, J TI BONE-MARROW - ULTRASMALL SUPERPARAMAGNETIC IRON-OXIDE FOR MR IMAGING SO RADIOLOGY LA English DT Article DE BONE MARROW, MR STUDIES; CONTRAST MEDIA; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT; MAGNETIC RESONANCE (MR), EXPERIMENTAL ID SINUSOIDAL ENDOTHELIUM; RELAXATION-TIMES; DISORDERS; LYMPHOMA; DISEASES; RAT AB An ultrasmall superparamagnetic iron oxide (USPIO) preparation was evaluated as a potential intravenous contrast agent for magnetic resonance (MR) imaging of bone marrow. One hour after administration of USPIO (40, 80, and 160-mu-mol of iron per kilogram body weight) in rats and rabbits, T1 and T2 relaxation times were, respectively, approximately 30%, 50%, and 65% lower than precontrast relaxation times. Maximum decrease in relaxation times of marrow occurred within 1-24 hours after intravenous administration; thereafter, relaxation times slowly returned to normal within 7 days. In vivo MR imaging of rabbits and rats confirmed that USPIO decreases signal intensity of red and yellow marrow. The decrease was most marked with gradient echo pulse sequences. An animal model of intramedullary tumor demonstrated the potential of USPIO to enable differentiation between tumor and normal red marrow. USPIO-enhanced MR imaging improves detection of smaller tumors and allows differentiation of tumor deposits from islands of hyperplastic or normal red marrow. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR NUCL MAGNET RESONANCE,13TH ST,BLDG 149,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NCI NIH HHS [CA 48279] NR 33 TC 80 Z9 81 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAY PY 1991 VL 179 IS 2 BP 529 EP 533 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH130 UT WOS:A1991FH13000043 PM 2014305 ER PT J AU TAKAYAMA, K DATTA, AK AF TAKAYAMA, K DATTA, AK TI STRUCTURE-TO-FUNCTION RELATIONSHIP OF MYCOBACTERIAL CELL-ENVELOPE COMPONENTS SO RESEARCH IN MICROBIOLOGY LA English DT Article; Proceedings Paper CT 6TH INTERNATIONAL SYMP ON THE GENETICS OF INDUSTRIAL MICROORGANISMS CY AUG 12-18, 1990 CL STRASBOURG, FRANCE ID TUMOR NECROSIS FACTOR; MYCOLIC ACID SYNTHESIS; HUMAN MACROPHAGES; AVIUM COMPLEX; FACTOR-ALPHA; TUBERCULOSIS; WALL; INHIBITION; ETHAMBUTOL; INFECTION C1 UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. RP TAKAYAMA, K (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 37 TC 6 Z9 7 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2508 J9 RES MICROBIOL JI Res. Microbiol. PD MAY PY 1991 VL 142 IS 4 BP 443 EP 448 DI 10.1016/0923-2508(91)90118-T PG 6 WC Microbiology SC Microbiology GA FN625 UT WOS:A1991FN62500015 PM 1871431 ER PT J AU DRAPER, P BARROW, W LANEELLE, G DAFFE, M NIKAIDO, H TAKAYAMA, K HOFFNER, SE SVENSON, SB RASTOGI, N AF DRAPER, P BARROW, W LANEELLE, G DAFFE, M NIKAIDO, H TAKAYAMA, K HOFFNER, SE SVENSON, SB RASTOGI, N TI RECENT OBSERVATIONS CONCERNING STRUCTURE AND FUNCTION RELATIONSHIPS IN THE MYCOBACTERIAL CELL-ENVELOPE - ELABORATION OF A MODEL IN TERMS OF MYCOBACTERIAL PATHOGENICITY, VIRULENCE AND DRUG-RESISTANCE - DISCUSSION SO RESEARCH IN MICROBIOLOGY LA English DT Discussion DE MYCOBACTERIUM; CELL MEMBRANE; CELL WALL; DRUG RESISTANCE; VIRULENCE; FORUM ID AVIUM C1 TEXAS COLL OSTEOPATH MED,DEPT MICROBIOL & IMMUNOL,FT WORTH,TX 76107. CNRS,CTR RECH BIOCHIM GENET CELLULAIRES,F-31062 TOULOUSE,FRANCE. UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. NATL BACTERIOL LAB,DIV MYCOBACTERIOL,S-10521 STOCKHOLM,SWEDEN. NATL BACTERIOL LAB,DEPT VACCINE & DEV PROD,S-10521 STOCKHOLM,SWEDEN. INST PASTEUR,UNITE TUBERCULOSE & MYCOBACTERIES,F-75724 PARIS 15,FRANCE. RP DRAPER, P (reprint author), NATL INST MED RES,MILL HILL,LONDON NW7 1AA,ENGLAND. NR 9 TC 1 Z9 1 U1 0 U2 2 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2508 J9 RES MICROBIOL JI Res. Microbiol. PD MAY PY 1991 VL 142 IS 4 BP 477 EP 481 PG 5 WC Microbiology SC Microbiology GA FN625 UT WOS:A1991FN62500019 ER PT J AU ROBINSON, DR AF ROBINSON, DR TI ALLEVIATION OF AUTOIMMUNE-DISEASE BY DIETARY LIPIDS CONTAINING OMEGA-3-FATTY-ACIDS SO RHEUMATIC DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID EICOSAPENTAENOIC ACID; FISH OIL; MICE; SUPPLEMENTATION; ENRICHMENT; GENERATION; ARTHRITIS; INVITRO; CELLS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ROBINSON, DR (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,ARTHRITIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 18 TC 15 Z9 15 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-857X J9 RHEUM DIS CLIN N AM JI Rheum. Dis. Clin. North Am. PD MAY PY 1991 VL 17 IS 2 BP 213 EP 222 PG 10 WC Rheumatology SC Rheumatology GA GL844 UT WOS:A1991GL84400004 PM 1862233 ER PT J AU ROSSITER, A GUELRUD, M SOUNEY, PF MENDOZA, S ROSSITER, G GELRUD, D AF ROSSITER, A GUELRUD, M SOUNEY, PF MENDOZA, S ROSSITER, G GELRUD, D TI HIGH VASOACTIVE INTESTINAL POLYPEPTIDE PLASMA-LEVELS IN PATIENTS WITH BARRETTS-ESOPHAGUS SO SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY LA English DT Article DE ESOPHAGEAL MANOMETRY; GASTROESOPHAGEAL REFLUX; VASOACTIVE INTESTINAL POLYPEPTIDE ID VIP-IMMUNOREACTIVE NERVES; HIRSCHSPRUNGS-DISEASE; PEPTIDERGIC INNERVATION; GASTROINTESTINAL-TRACT; REGULATORY PEPTIDES; SPHINCTER; NEUROTRANSMITTER; ACHALASIA; ABNORMALITIES; RELAXATION AB We have evaluated the correlation between vasoactive intestinal polypeptide (VIP) plasma concentration and severity of gastroesophageal reflux in patients with Barrett's esophagus and the possible differences in the VIP values of these patients compared with healthy volunteers. We also evaluated the relation between VIP plasma concentration and lower esophageal sphincter (LES) pressure in 24 patients with Barrett's esophagus. The mean VIP plasma concentration in 14 patients with severe gastroesophageal reflux was 25.6 +/- 0.75 pg/ml, significantly higher than the mean value observed in 10 patients with moderate reflux (18.9 +/- 0.67 pg/ml) (p < 0.01). The mean LES resting pressure was significantly lower in the group of patients with severe gastroesophageal reflux than that observed in patients with moderate reflux (3 +/- 0.64 and 10.3 +/- 0.69 mm Hg, respectively; p < 0.01). The mean VIP plasma concentration in 11 healthy volunteers (20.6 +/- 0.65 pg/ml) was significantly lower than the mean value observed in the subgroup of patients with severe gastroesophageal reflux (p < 0.01). VIP values in patients with moderate reflux were not significantly different from those observed in our volunteers. There was a significant correlation between LES pressure and VIP plasma level (r = -0.9253; p < 0.01). In conclusion, it is possible that the decreased LES resting pressure observed in patients with Barrett's esophagus and severe gastroesophageal reflux may be due to impairment of the VIPergic innervation, resulting in an increased local VIP release with possible overflow to peripheral plasma. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PHARM,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HOSP GEN OESTE,DEPT GASTROENTEROL,CARACAS,VENEZUELA. NR 31 TC 3 Z9 3 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0036-5521 J9 SCAND J GASTROENTERO JI Scand. J. Gastroenterol. PD MAY PY 1991 VL 26 IS 5 BP 572 EP 576 DI 10.3109/00365529108998582 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FL133 UT WOS:A1991FL13300018 PM 1871550 ER PT J AU KAHN, RS DAVIDSON, M GABRIEL, S DUMONT, K DUBIE, CR MOORE, C APTER, S SIEVER, L DAVIS, KL AF KAHN, RS DAVIDSON, M GABRIEL, S DUMONT, K DUBIE, CR MOORE, C APTER, S SIEVER, L DAVIS, KL TI SEROTONIN RECEPTOR SENSITIVITY IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 BRONX VET ADM MED CTR, MT SINAI HOSP, DEPT PSYCHIAT, BRONX, NY 10468 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 EI 1573-2509 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAY-JUN PY 1991 VL 4 IS 3 BP 347 EP 348 PG 2 WC Psychiatry SC Psychiatry GA FD743 UT WOS:A1991FD74300174 ER PT J AU FABER, R COSTELLO, R MITZEL, H SCHNEIDER, S AF FABER, R COSTELLO, R MITZEL, H SCHNEIDER, S TI DIMENSIONALITY OF A NEUROPSYCHIATRIC SOFT SIGN BATTERY SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD MAY-JUN PY 1991 VL 4 IS 3 BP 382 EP 383 DI 10.1016/0920-9964(91)90317-K PG 2 WC Psychiatry SC Psychiatry GA FD743 UT WOS:A1991FD74300229 ER PT J AU KATKOV, WN DIENSTAG, JL AF KATKOV, WN DIENSTAG, JL TI PREVENTION AND THERAPY OF VIRAL-HEPATITIS SO SEMINARS IN LIVER DISEASE LA English DT Review ID B SURFACE-ANTIGEN; RECOMBINANT ALPHA INTERFERON; CHRONIC ACTIVE HEPATITIS; PLACEBO-CONTROLLED TRIAL; RENAL-TRANSPLANT RECIPIENTS; RANDOMIZED CONTROLLED TRIAL; HUMAN-LEUKOCYTE INTERFERON; HUMORAL IMMUNE-RESPONSE; HEALTH-CARE PERSONNEL; PRE-S-REGION C1 MASSACHUSETTS GEN HOSP, MED SERV, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CTR LIVER BILIARY PANCREAS, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. NR 80 TC 25 Z9 26 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 333 SEVENTH AVE, NEW YORK, NY 10001 USA SN 0272-8087 EI 1098-8971 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD MAY PY 1991 VL 11 IS 2 BP 165 EP 174 DI 10.1055/s-2008-1040433 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GN065 UT WOS:A1991GN06500009 PM 1716004 ER PT J AU DIENSTAG, JL AF DIENSTAG, JL TI VIRAL-HEPATITIS AND SEMINARS-IN-LIVER-DISEASE - A DECADE ANNIVERSARY SO SEMINARS IN LIVER DISEASE LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,CTR LIVER BILIARY PANCREAS,MED SERV,GASTROINTESTINAL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0272-8087 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD MAY PY 1991 VL 11 IS 2 BP R3 EP R6 DI 10.1055/s-2008-1040425 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA GN065 UT WOS:A1991GN06500001 ER PT J AU ABBOUD, HE AF ABBOUD, HE TI RESIDENT GLOMERULAR CELLS IN GLOMERULAR INJURY - MESANGIAL CELLS SO SEMINARS IN NEPHROLOGY LA English DT Article ID REACTIVE OXYGEN METABOLITES; GROWTH-FACTOR; PROLIFERATIVE GLOMERULONEPHRITIS; RAT; INFLAMMATION; GLOMERULOSCLEROSIS; PROTEOGLYCANS; PROGRESSION; EXPRESSION; INDUCTION C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV RENAL,SAN ANTONIO,TX. RP ABBOUD, HE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK 33665] NR 56 TC 30 Z9 31 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD MAY PY 1991 VL 11 IS 3 BP 304 EP 311 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA FK642 UT WOS:A1991FK64200009 PM 2057645 ER PT J AU KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S AF KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S TI LEUKOARAIOSIS CORRELATES WITH CEREBRAL HYPOPERFUSION IN VASCULAR DEMENTIA SO STROKE LA English DT Article DE CEREBRAL BLOOD FLOW; LEUKOENCEPHALOPATHY; DEMENTIA ID WHITE MATTER LUCENCIES; SCAN LEUKO-ARAIOSIS; BLOOD-FLOW; RISK-FACTORS; NEUROLOGIC FINDINGS; NORMAL INDIVIDUALS; LESIONS; ATROPHY; COGNITION AB Leukoaraiosis quantified by computerized densitometric measurements of reduced Hounsfield numbers was correlated with local cerebral blood flow on the same computed tomographic images of 35 patients with multi-infarct dementia and 16 age-matched elderly normal volunteers. The ratio for area of frontal leukoaraiosis to total area of parenchyma among the patients was significantly greater than that among the normal volunteers (5.8 +/- 2.3% compared with 3.1 +/- 1.3%, p < 0.001). Severity of leukoaraiosis around the frontal horns of the lateral ventricles correlated significantly with severity of leukoaraiosis of the centrum semiovale adjacent to the bodies of the lateral ventricles. Cerebral blood flow values for all representative cerebral regions except the parietal white matter were reduced among the patients compared with the normal volunteers. Multivariate regression analysis revealed that reduced cerebral perfusion in the putamen and thalamus correlated significantly with the severity of leukoaraiosis. Cerebral hypoperfusion in territories supplied by deep penetrating arteries may contribute to the pathogenesis of leukoaraiosis. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR UNIV,DEPT NEUROL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT RADIOL,HOUSTON,TX 77030. NR 27 TC 86 Z9 91 U1 1 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAY PY 1991 VL 22 IS 5 BP 609 EP 614 PG 6 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA FL344 UT WOS:A1991FL34400008 PM 2028490 ER PT J AU PEI, J CHOO, SY SPIES, T STROMINGER, JL HANSEN, JA AF PEI, J CHOO, SY SPIES, T STROMINGER, JL HANSEN, JA TI ASSOCIATION OF 4 HLA CLASS-III REGION GENOMIC MARKERS WITH HLA HAPLOTYPES SO TISSUE ANTIGENS LA English DT Article DE GENOMIC MARKER; HLA-B-ASSOCIATED TRANSCRIPT; HLA CLASS-III REGION; LINKAGE DISEQUILIBRIUM; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; TUMOR-NECROSIS FACTOR ID MAJOR HISTOCOMPATIBILITY COMPLEX; LENGTH-POLYMORPHISM RFLP; NECROSIS FACTOR GENES; GEL-ELECTROPHORESIS; HEALTHY DANES; FRAGMENTS; CLUSTER AB We have studied restriction fragment length polymorphism (RFLP) in the region 300 kb centromeric to the HLA-B locus. Four probes were used: one was genomic DNA derived from the tumor-necrosis factor (TNF)-beta gene, one was a cDNA for the BAT3 gene, and two single-copy genomic probes, R5A and M20A. The order of these markers from HLA-B towards the centromere is M20A, R5A, TNF and BAT3. The BAT3 and TNF-beta probes each detected two allelic bands with Taq I and Nco I digestion, respectively; the R5A and M20A probes each detected three polymorphic allelic bands with BstEII digestion. To determine if these restriction polymorphisms are preferentially associated with certain HLA-B and -DR haplotypes, a total of 153 HLA haplotypes was analyzed. The haplotypes Al, B8, DR3 and A3, B7, DR2 were each associated with a distinct combination of polymorphisms identified at these four sites, thereby demonstrating that the strong linkage disequilibrium characteristic of these haplotypes extends also to this segment of the class III region. In contrast, haplotypes that are not in positive linkage disequilibrium, such as A1, B8, DR4 and A2, B7, DR3, showed no preferential association with any of these polymorphisms. The antigens HLA-B27 and B35 were also found to be in positive linkage disequilibrium with RFLP patterns at three of these sites, and HLA-B14, B35, B44, Bw57 and Bw62 were found preferentially associated with polymorphisms at one or two of these sites, independent of the DR antigen present. These data further demonstrate that genetic linkage disequilibrium in the HLA class III region is complex and variable among different HLA halpotypes. C1 FRED HUTCHINSON CANC RES CTR,1124 COLUMBIA ST,SEATTLE,WA 98104. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,BOSTON,MA 02115. UNIV WASHINGTON,SCH MED,SEATTLE,WA 98195. FU NCI NIH HHS [CA 18029] NR 18 TC 10 Z9 10 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD MAY PY 1991 VL 37 IS 5 BP 191 EP 196 DI 10.1111/j.1399-0039.1991.tb01871.x PG 6 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA FW370 UT WOS:A1991FW37000001 PM 1685263 ER PT J AU ABE, K TANZI, RE KOGURE, K AF ABE, K TANZI, RE KOGURE, K TI INDUCTION OF HSP70 MESSENGER-RNA AFTER TRANSIENT ISCHEMIA IN GERBIL BRAIN SO NEUROSCIENCE LETTERS LA English DT Article DE HEAT SHOCK PROTEIN; SELECTIVE VULNERABILITY; ISCHEMIA; GERBIL; NORTHERN BLOT ANALYSIS ID HEAT-SHOCK PROTEIN; DELAYED NEURONAL DEATH; ALZHEIMERS-DISEASE; LOCALIZATION; EXPRESSION; INVITRO; CELLS; GENE AB Heat shock protein (HSP) plays an important role in stress responses of cells. Inductions of HSP70 mRNA, amyloid precursor protein (APP) mRNA, and tubulin mRNA within hippocampal CA1 and parietal cortex in gerbil brains were examined at 1 h to 7 days after 10 min of bilateral common carotid artery occlusion using Northern blot analyses. In contrast to the induction of HSP70 mRNA, no induction was observed in APP mRNA or tubulin mRNA. Regional differences in the induction of HSP70 mRNA were found. CA1 cells produced less amount of HSP70 mRNA than cortical cells at 8 h after the transient ischemia. Transient global ischemia is known to result in the selective neuronal death of hippocampal CA1 cells days after reperfusion. Our results suggest that the regional difference in the induction of HSP70 mRNA may relate to the regional difference of the vulnerability of neuronal cells after transient ischemia. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP ABE, K (reprint author), TOHOKU UNIV,SCH MED,INST BRAIN DIS,DEPT NEUROL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. NR 24 TC 96 Z9 97 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 29 PY 1991 VL 125 IS 2 BP 166 EP 168 DI 10.1016/0304-3940(91)90018-O PG 3 WC Neurosciences SC Neurosciences & Neurology GA FL176 UT WOS:A1991FL17600018 PM 1908957 ER PT J AU ABE, K STGEORGEHYSLOP, PH TANZI, RE KOGURE, K AF ABE, K STGEORGEHYSLOP, PH TANZI, RE KOGURE, K TI INDUCTION OF AMYLOID PRECURSOR PROTEIN MESSENGER-RNA AFTER HEAT-SHOCK IN CULTURED HUMAN LYMPHOBLASTOID-CELLS SO NEUROSCIENCE LETTERS LA English DT Article DE AMYLOID PRECURSOR PROTEIN; HEAT SHOCK PROTEIN; LYMPHOBLASTOID CELL ID ALZHEIMERS-DISEASE; EXPRESSION; GENE AB In an attempt to examine a possible relationship between heat shock stress and an induction of amyloid precursor protein, cultured lymphoblastoid cells established from 12 human subjects were treated with heat shock at 42-degrees-C for 30 min. The levels of mRNA for amyloid precursor protein (APP), heat shock protein (HSP) 70, and actin were examined by Northern blot at 1, 3, 8, 24, and 48 h after the heat shock treatment. HSP70 mRNA was induced at 1 and 3 h, and became undetectable again by 8 h. APP mRNA was also induced at 3 and 8 h, and recovered to the steady level by 48 h. No induction was observed in actin mRNA. These results indicate that APP mRNA is induced by heat shock treatment after the induction of HSP70 mRNA, suggesting a role of heat shock response in an induction of APP. C1 UNIV TORONTO,CTR RES NEURODEGENERAT DIS,TORONTO M5S 1A1,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP ABE, K (reprint author), TOHOKU UNIV,SCH MED,INST BRAIN DIS,DEPT NEUROL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. NR 16 TC 80 Z9 80 U1 1 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 29 PY 1991 VL 125 IS 2 BP 169 EP 171 DI 10.1016/0304-3940(91)90019-P PG 3 WC Neurosciences SC Neurosciences & Neurology GA FL176 UT WOS:A1991FL17600019 PM 1652710 ER PT J AU ABE, K TANZI, RE KOGURE, K AF ABE, K TANZI, RE KOGURE, K TI SELECTIVE INDUCTION OF KUNITZ-TYPE PROTEASE INHIBITOR DOMAIN-CONTAINING AMYLOID PRECURSOR PROTEIN MESSENGER-RNA AFTER PERSISTENT FOCAL ISCHEMIA IN RAT CEREBRAL-CORTEX SO NEUROSCIENCE LETTERS LA English DT Article DE AMYLOID PRECURSOR PROTEIN; ISCHEMIA; ALZHEIMERS DISEASE ID ALZHEIMERS-DISEASE; NEXIN-II; BRAIN; EXPRESSION; DAMAGE AB An induction of amyloid precursor protein (APP) mRNA was examined in a middle cerebral artery occlusion model of rats using Northern blot analyses. The level of tubulin mRNA was measured as an internal standard. With persistent focal ischemia, APP mRNA species which contain a Kunitz-type protese inhibitor (KPI) domain were induced in the rat cerebral cortex from 1 to 21 days after the insult with a maximum of 4 days, while total amounts of APP mRNA did not change. No change was observed in the level of tubulin mRNA. These results suggest a selective role of APP species which contain the KPI domain in focal cerebral ischemia. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP ABE, K (reprint author), TOHOKU UNIV,SCH MED,INST BRAIN DIS,DEPT NEUROL,1-1 SEIRYO MACHI,AOBA KU,SENDAI,MIYAGI 980,JAPAN. NR 20 TC 204 Z9 205 U1 2 U2 4 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD APR 29 PY 1991 VL 125 IS 2 BP 172 EP 174 DI 10.1016/0304-3940(91)90020-T PG 3 WC Neurosciences SC Neurosciences & Neurology GA FL176 UT WOS:A1991FL17600020 PM 1908958 ER PT J AU WEINER, HL HAUSER, SL DAWSON, DM HAFLER, DA MACKIN, GA ORAV, EJ AF WEINER, HL HAUSER, SL DAWSON, DM HAFLER, DA MACKIN, GA ORAV, EJ TI CYCLOPHOSPHAMIDE AND PLASMA-EXCHANGE IN MULTIPLE-SCLEROSIS SO LANCET LA English DT Letter ID IMMUNOSUPPRESSION; EXPERIENCE; ACTH C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP WEINER, HL (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115, USA. RI Hauser, Stephen/J-2978-2016 NR 9 TC 15 Z9 15 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 27 PY 1991 VL 337 IS 8748 BP 1033 EP 1034 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FJ135 UT WOS:A1991FJ13500025 ER PT J AU PARK, JK ROSENSTEIN, YJ REMOLDODONNELL, E BIERER, BE ROSEN, FS BURAKOFF, SJ AF PARK, JK ROSENSTEIN, YJ REMOLDODONNELL, E BIERER, BE ROSEN, FS BURAKOFF, SJ TI ENHANCEMENT OF T-CELL ACTIVATION BY THE CD43 MOLECULE WHOSE EXPRESSION IS DEFECTIVE IN WISKOTT-ALDRICH SYNDROME SO NATURE LA English DT Article ID LYMPHOCYTE SURFACE SIALOGLYCOPROTEIN; MONOCLONAL-ANTIBODY; SIALOPHORIN CD43; HUMAN-LEUKOCYTES; LEUKOSIALIN; PROLIFERATION; ANTIGEN; CD2; PHOSPHORYLATION; RECEPTOR AB CD43 (sialophorin, leukosialin, leukocyte large sialoglycoprotein), a heavily sialylated molecule found on most leukocytes and platelets, was initially identified as a major glycoprotein of mouse, rat and human T cells 1-8. CD43 expression is defective on the T cells of males with the Wiskott-Aldrich syndrome, an X chromosome-linked recessive immunodeficiency disorder 9. Affected males are susceptible to opportunistic infections and do not respond to polysaccharide antigens, reflecting defects in cytotoxic and helper T-cell functions. Anti-CD43 monoclonal antibodies have a modest costimulatory effect on T cells, natural killer cells, B cells and monocytes 10-14, and one such antibody has been shown to activate T cells directly 15. To investigate a possible physiological role for CD43, a complementary DNA encoding the human protein 16,17 was introduced into an antigen-responsive murine T-cell hybridoma 18. We observed that CD43 enhances the antigen-specific activation of T cells and that the intracellular domain of CD43, which is hyperphosphorylated during T-cell activation 19-21, is required for this function. We also found that antigen-presenting cells can bind specifically to immobilized purified CD43 and that the binding can be inhibited by liposomes containing CD43 as well as by anti-CD43 monoclonal antibodies. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,SCH MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP PARK, JK (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. NR 26 TC 131 Z9 131 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD APR 25 PY 1991 VL 350 IS 6320 BP 706 EP 709 DI 10.1038/350706a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FJ130 UT WOS:A1991FJ13000060 PM 2023632 ER PT J AU VECSEI, L BEAL, MF AF VECSEI, L BEAL, MF TI COMPARATIVE BEHAVIORAL AND PHARMACOLOGICAL STUDIES WITH CENTRALLY ADMINISTERED KYNURENINE AND KYNURENIC ACID IN RATS SO EUROPEAN JOURNAL OF PHARMACOLOGY LA English DT Article DE ATAXIA; KYNURENIC ACID; KYNURENINE; LEARNING; MEMORY; OPEN-FIELD ACTIVITY; STEREOTYPY ID WORKING MEMORY VERSIONS; D-ASPARTATE ANTAGONIST; OPEN-FIELD ACTIVITY; WATER MAZE TASK; STEREOTYPED BEHAVIOR; QUINOLINIC ACID; BINDING-SITES; BRAIN-DAMAGE; GLUTAMATE; KETAMINE AB In the present study the effects of kynurenine and its metabolite kynurenic acid were compared in different behavioral and pharmacological tests. Kynurenic acid administered i.c.v. resulted in ataxia and sterotype in a dose-dependent manner (0.025-1.6-mu-mol). Administration of 0.8-mu-mol of kynurenic acid resulted in sleeping and an approximate 25% mortality of the animals. At a dose of 1.6-mu-mol all of the animals died within 2-5 min from cardiorespiratory failure. One hour after lower doses of kynurenic acid the behavior of the rats appeared normal (neither stereotypy nor ataxia were observed in their familiar environment), but their exploratory activity (0.025-0.2-mu-mol) was significantly lower in a novel environment (open-field box) compared to the control group. Twenty four hours after the injection of kynurenic acid the exploratory activity of the animals did not differ from the control group. Kynurenine administered i.c.v. in equimolar doses did not result in stereotypy, ataxia, sleeping or mortality of the animals although, immediately after high doses short-lasting (1-2 min) immobility was observed. The rearing activity of the high dose kynurenine-treated animals was lower 1 h after injection, but this effect disappeared 24 h after the treatment. Post-trial injection of kynurenic acid (0.2-mu-mol) slightly, but not significantly, inhibited the learning ability of the rats in an active avoidance paradigm. Kynurenine administered in an equimolar dose had no effect on the speed of learning, but significantly attenuated the intertrial activity of the rats. Kynurenic acid (0.2-mu-mol, 0.4-mu-mol) did not significantly inhibit the passive avoidance latency of the animals after post-trial treatment. These findings suggest that i.c.v. administration of kynurenic acid results in marked acute behavioral changes while equimolar doses of kynurenine had only slight behavior effects. The present experiments and earlier behavioral data suggest that the NMDA receptor complex plays a role in specific cognitive functions. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP VECSEI, L (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROL SERV,NEUROL RES 4,EDWARDS 410,FRUIT ST,BOSTON,MA 02114, USA. RI Vecsei, Laszlo/B-2066-2010 OI Vecsei, Laszlo/0000-0001-8037-3672 FU DS NIH HHS [NINCDS 16367] NR 33 TC 32 Z9 32 U1 2 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-2999 J9 EUR J PHARMACOL JI Eur. J. Pharmacol. PD APR 24 PY 1991 VL 196 IS 3 BP 239 EP 246 DI 10.1016/0014-2999(91)90436-T PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FK979 UT WOS:A1991FK97900004 PM 1893912 ER PT J AU KALLINOWSKI, F WILKERSON, R MOORE, R STRAUSS, W VAUPEL, P AF KALLINOWSKI, F WILKERSON, R MOORE, R STRAUSS, W VAUPEL, P TI VASCULARITY, PERFUSION RATE AND LOCAL TISSUE OXYGENATION OF TUMORS DERIVED FROM RAS-TRANSFORMED FIBROBLASTS SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID BLOOD-FLOW; EMBRYO CELLS; ONCOGENES; MICROENVIRONMENT; ANGIOGENESIS; METABOLISM; XENOGRAFTS; RESISTANCE; INDUCTION; RADIATION AB Tumors derived from ras-transformed rat fibroblasts were investigated in order to gain insight into possible interrelationships between oncogenic transformations and therapeutically relevant parameters of the metabolic micromilieu of solid tumors in vivo. Tumors grew in nude mice after injection of in vitro-passaged cells. Growth rates, early stages of angiogenesis, perfusion and tissue oxygenation were assessed. Compared with the parental cell line, both ras transformants grew very rapidly and exhibited an early onset of angiogenesis. Perfusion rates of one ras-transformed tumor line were similar to those of the parental tumors whereas reduced flow values were detected in tumors of the other ras line. The better perfused tumors exhibited more adequate tissue oxygen levels whereas reduced oxygen levels were obvious in the poorly perfused ras line. These results indicate that ras transformation alters therapeutically relevant parameters of the tumor micromilieu. However, the tumor phenotype cannot be predicted even if the transforming oncogene is known. C1 UNIV MAINZ,INST PHYSIOL & PATHOPHYSIOL,W-6500 MAINZ,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NUCL MED,BOSTON,MA 02114. NR 35 TC 13 Z9 13 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 22 PY 1991 VL 48 IS 1 BP 121 EP 127 PG 7 WC Oncology SC Oncology GA FH936 UT WOS:A1991FH93600021 PM 1708361 ER PT J AU MAZIARZ, RT GROH, V PRENDERGAST, M FABBI, M STROMINGER, JL BURAKOFF, SJ AF MAZIARZ, RT GROH, V PRENDERGAST, M FABBI, M STROMINGER, JL BURAKOFF, SJ TI NON-MHC-RESTRICTED TARGET-CELL LYSIS BY A CD4-CD8-TCR-ALPHA-BETA T-CELL LINE, AS WELL AS BY TCR-GAMMA-DELTA T-CELL LINES, RESULTS FROM LYMPHOKINE-ACTIVATED KILLING SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID RECEPTOR-ALPHA-BETA; NATURAL-KILLER; LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; ADHESION MOLECULES; CD4-8 THYMOCYTES; ANTIGEN RECEPTOR; CYTO-TOXICITY; INTERLEUKIN-2; CLONES AB A long-term CD4-CD8-TCR-alpha-beta human T-cell line, as well as similar CD4-CD8-TCR-gamma-delta T-cell lines for comparison, were generated from various tissues by negative selection using anti-CD4 and anti-CD8 monoclonal antibodies (MAbs) followed by positive selection with specific anti-TCR MAb and then repeated in vitro stimulation with interleukin-enriched media and lectin. These cell lines all demonstrated non-MHC-restricted cytolysis on a variety of human tumor cell lines. However, removal of lymphokines from the culture media for 24 hr abrogated most of the non-MHC-restricted target-cell lysis without affecting TCR-alpha-beta or TCR-gamma-delta cell viability or TCR function as determined by antibody-triggered redirected target-cell lysis. Subsequent re-exposure to lymphokines reconstituted non-MHC-restricted cytolysis by these cell lines. Thus, much of the non-specific, non-MHC-restricted cytolytic activity generated by CD4-CD8-TCR-alpha-beta or TCR-gamma-delta cells is secondary to lymphokine-activated killing (LAK) activity. These cells have potent LAK activity and may be prominent in LAK-cell populations. In addition, after lymphokine deprivation, both CD4-CD8-TCR-alpha-beta and TCR-gamma-delta cells showed residual activity against some tumor-cell targets, the nature of which remains to be defined. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. RP MAZIARZ, RT (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PEDIAT,DIV HEMATOL,BOSTON,MA 02115, USA. RI Fabbi, Marina/I-1290-2012 FU NCI NIH HHS [CA34129]; NIAID NIH HHS [AI-15669]; NIDDK NIH HHS [DK13230] NR 37 TC 8 Z9 8 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 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD APR 22 PY 1991 VL 48 IS 1 BP 142 EP 147 PG 6 WC Oncology SC Oncology GA FH936 UT WOS:A1991FH93600024 PM 1902200 ER PT J AU HART, PJ MONZINGO, AF DONOHUEROLFE, A KEUSCH, GT CALDERWOOD, SB ROBERTUS, JD AF HART, PJ MONZINGO, AF DONOHUEROLFE, A KEUSCH, GT CALDERWOOD, SB ROBERTUS, JD TI CRYSTALLIZATION OF THE B-CHAIN OF SHIGA-LIKE TOXIN-I FROM ESCHERICHIA-COLI SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Note ID SHIGELLA-DYSENTERIAE TYPE-1; NUCLEOTIDE-SEQUENCE; STRUCTURAL GENES; PATHOGENESIS; DIARRHEA; IDENTIFICATION; RECEPTOR; CLONING C1 UNIV TEXAS,DEPT CHEM & BIOCHEM,CLAYTON FDN,INST BIOCHEM,AUSTIN,TX 78712. TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DIV GEOG MED & INFECT DIS,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [AI20325]; NIGMS NIH HHS [GM30048, GM35989] NR 21 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD APR 20 PY 1991 VL 218 IS 4 BP 691 EP 694 DI 10.1016/0022-2836(91)90256-6 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK564 UT WOS:A1991FK56400006 PM 2023244 ER PT J AU TANZI, RE HYMAN, BT AF TANZI, RE HYMAN, BT TI ALZHEIMERS MUTATION SO NATURE LA English DT Letter ID PRECURSOR; DISEASE; PROTEIN C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. RP TANZI, RE (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET LAB,FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 54 Z9 54 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 18 PY 1991 VL 350 IS 6319 BP 564 EP 564 DI 10.1038/350564a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FH112 UT WOS:A1991FH11200041 PM 1901961 ER PT J AU COPELAND, PM AF COPELAND, PM TI HORMONAL EVALUATION OF PATIENTS WITH AN INCIDENTALLY DISCOVERED ADRENAL MASS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP COPELAND, PM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 18 PY 1991 VL 324 IS 16 BP 1135 EP 1135 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FG912 UT WOS:A1991FG91200017 ER PT J AU ROSS, NS ARON, DC AF ROSS, NS ARON, DC TI HORMONAL EVALUATION OF PATIENTS WITH AN INCIDENTALLY DISCOVERED ADRENAL MASS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID CUSHINGS-SYNDROME; TUMORS C1 VET AFFAIRS MED CTR,CLEVELAND,OH 44106. RP ROSS, NS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 18 PY 1991 VL 324 IS 16 BP 1135 EP 1136 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FG912 UT WOS:A1991FG91200018 ER PT J AU STRONG, RK CAMPBELL, R ROSE, DR PETSKO, GA SHARON, J MARGOLIES, MN AF STRONG, RK CAMPBELL, R ROSE, DR PETSKO, GA SHARON, J MARGOLIES, MN TI 3-DIMENSIONAL STRUCTURE OF MURINE ANTI-PARA-AZOPHENYLARSONATE FAB-36-71 .1. X-RAY CRYSTALLOGRAPHY, SITE-DIRECTED MUTAGENESIS, AND MODELING OF THE COMPLEX WITH HAPTEN SO BIOCHEMISTRY LA English DT Article ID CROSS-REACTIVE IDIOTYPE; CHAIN-VARIABLE REGIONS; AMINO-ACID-SEQUENCE; ARS-A ANTIBODIES; IMMUNE-RESPONSE; CROSSREACTIVE IDIOTYPE; MONOCLONAL-ANTIBODIES; JUNCTIONAL DIVERSITY; IMMUNOGLOBULIN FAB; ARSONATE IDIOTYPE AB The structure of the antigen-binding fragment (Fab) of an anti-p-azophenylarsonate monoclonal antibody, 36-71, bearing a major cross-reactive idiotype of A/J mice has been refined to an R factor of 24.8% at a resolution of 1.85 angstrom. The previously solved partial structure of this Fab at a resolution of 2.9 angstrom (Rose et al., 1990) was used as an initial model for refinement against the high-resolution data. The complex with hapten has been modeled by docking the small-molecule crystal structure of phenylarsonic acid into the structure of the native Fab on the basis of a low-resolutionelectron density map of the complex. In this model, residue Arg-96 in the light chain and residues Asn-35, Trp-47, and Ser-99 in the heavy chain contact the arsonate moiety of the hapten; an additional bond is found between the arsonate group and a tightly bound water molecule. The phenyl moiety of the hapten packs against two tyrosine side chains at positions 50 and 106 in the heavy chain. Residue Arg-96 in the light chain had been implicated as involved in hapten binding on the basis of previous experiments, and indeed, this residue appears to play a crucial role in this model. Experiments employing site-directed mutagenesis directly support this conclusion. The heavy-chain complementarity-determining regions have novel conformations not previously observed in immunoglobulins except for the recently solved anti-p-azophenylarsonate Fab R19.9 (Lascombe et al., 1989). C1 NATL RES COUNCIL CANADA,DIV BIOL SCI,OTTAWA K1A 0R6,ONTARIO,CANADA. BRANDEIS UNIV,ROSENSTIEL BASIC MED SCI RES CTR,WALTHAM,MA 02254. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP STRONG, RK (reprint author), CALTECH,MAIL STOP 156-29,PASADENA,CA 91125, USA. FU NCI NIH HHS [CA 24432]; NHLBI NIH HHS [HL 19259]; NIAID NIH HHS [AI 23909] NR 76 TC 97 Z9 97 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 16 PY 1991 VL 30 IS 15 BP 3739 EP 3748 DI 10.1021/bi00229a022 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG730 UT WOS:A1991FG73000022 PM 2015229 ER PT J AU STRONG, RK PETSKO, GA SHARON, J MARGOLIES, MN AF STRONG, RK PETSKO, GA SHARON, J MARGOLIES, MN TI 3-DIMENSIONAL STRUCTURE OF MURINE ANTI-PARA-AZOPHENYLARSONATE FAB-36-71 .2. STRUCTURAL BASIS OF HAPTEN BINDING AND IDIOTYPY SO BIOCHEMISTRY LA English DT Article ID CROSS-REACTIVE IDIOTYPE; CHAIN VARIABLE REGIONS; AMINO-ACID-SEQUENCE; ARS-A ANTIBODIES; ARSONATE IDIOTYPE; GENETIC-BASIS; J MICE; STRAIN; HEAVY; MOUSE AB Comparisons between the structures and solvent-accessible surfaces of the antigen-binding fragments of two murine anti-p-azophenylarsonate monoclonal antibodies, one bearing a major cross-reactive idiotype of A/J strain mice (36-71) and one lacking the idiotype (R19.9; Lascombe et al., 1989), highlight the structural basis for the determination of hapten affinity and idiotypy. Since the sequence of R19.9 is identical with the germline-encoded sequence at 16 positions in both heavy-chain and light-chain variable regions where somatic mutations and junctional differences have occurred to produce the 36-71 sequence, the structure of R19.9 can be used to model the structure of the germline-encoded antibody (36-65) in the regions around these sites. These 16 sequence differences exclude the third heavy-chain complementarity-determining region because R19.9 utilizes a D gene segment not associated with the predominant idiotype, which is 4 residues longer than the canonical D gene segment utilized in the sequences of 36-71 and 36-65. This difference between the structures of R19.9 and 36-71 does not affect the validity of using the structure of R 19.9 to model the structure of 36-65 since the third heavy-chain complementarity-determining region is highly solvent-exposed in both 36-71 and R19.9, and does not interact with any of these 16 sites. Comparing the structures of 36-71 and R19.9 suggests that only three of the differences in the heavy-chain sequences, and three of the differences in the light-chain sequences of 36-71 and 36-65, increase the affinity for hapten. The substitutions in the light chain appear to affect the binding constant for hapten by altering the overall conformation of the third heavy-chain complementarity-determining region. Regions where the solvent-accessible surfaces of 36-71 and R19.9 differ have been located. Presumably, these differences in accessible surface area account for the lack of reactivity with anti-idiotypic antibodies for R19.9 versus 36-71. Positions in the sequence where differences are known to affect the binding of anti-p-azophenylarsonate antibodies to monoclonal anti-idiotope antibodies generally map to the region around the hapten-binding site. Not unexpectedly, substitutions at these locations in the sequence do not always appear to affect anti-idiotope binding directly but may alter idiotype/anti-idiotype affinity indirectly by altering the conformation of contact residues. C1 BRANDEIS UNIV,ROSENSTIEL BASIC MED SCI RES CTR,WALTHAM,MA 02254. BOSTON UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT BIOCHEM,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP STRONG, RK (reprint author), CALTECH,MAIL STOP 156-29,PASADENA,CA 91125, USA. FU NCI NIH HHS [CA 24432]; NHLBI NIH HHS [HL 19259]; NIAID NIH HHS [AI 23909] NR 33 TC 43 Z9 43 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 16 PY 1991 VL 30 IS 15 BP 3749 EP 3757 DI 10.1021/bi00229a023 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG730 UT WOS:A1991FG73000023 PM 2015230 ER PT J AU ARONEY, CN SEMIGRAN, MJ DEC, GW BOUCHER, CA FIFER, MA AF ARONEY, CN SEMIGRAN, MJ DEC, GW BOUCHER, CA FIFER, MA TI LEFT-VENTRICULAR DIASTOLIC FUNCTION IN PATIENTS WITH LEFT-VENTRICULAR SYSTOLIC DYSFUNCTION DUE TO CORONARY-ARTERY DISEASE AND EFFECT OF NICARDIPINE SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID HEART-FAILURE; HEMODYNAMIC DETERMINANTS; ISOVOLUMIC RELAXATION; TIME-COURSE; BLOOD-FLOW; PRESSURE; NIFEDIPINE; NITROPRUSSIDE; VERAPAMIL; CARDIOMYOPATHY AB To assess the effect of nicardipine on left ventricular (LV) diastolic function independent of concurrent effects on loading conditions in patients with LV systolic dysfunction due to coronary artery disease, equihypotensive doses of intravenous nitroprusside and nicardipine were administered to 12 patients with congestive heart failure due to previous myocardial infarction (LV ejection fraction < 0.40). LV micromanometer pressure and simultaneous radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during nicardipine infusion. Mean systemic arterial pressure decreased an average of 21 mm Hg with nitroprusside and 19 mm Hg with nicardipine. A greater decrease in LV end-diastolic pressure was observed with nitroprusside (29 +/- 2 to 15 +/- 2 mm Hg, p < 0.01) than with nicardipine (29 +/- 2 to 25 +/- 3 mm Hg, p < 0.05). There was a decrease in the time constant of relaxation during nitroprusside but not during nicardipine infusion. There was enough overlap in LV volumes in the baseline and nitroprusside periods to compare diastolic pressure-volume relations over a common range of volumes in 4 patients, and enough overlap in the baseline and nicardipine periods in 11 patients. The relation was shifted downward in 3 of 4 patients taking nitroprusside and in 6 of 11 patients taking nicardipine. The relation between end-diastolic pressure and volume was not shifted with nicardipine. Thus, in patients with LV systolic dysfunction due to coronary artery disease, nicardipine shifted the diastolic pressure-volume relation downward in some patients, but did not alter the relation between end-diastolic pressure and volume, and, unlike nitroprusside, did not increase the rate of isovolumic relaxation. With regard to acute effects on diastolic function, nicardipine did not offer an advantage over nitroprusside in this patient group. C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,WACC 478,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Aroney, Constantine/A-7672-2013 OI Aroney, Constantine/0000-0002-0908-7179 NR 29 TC 7 Z9 7 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 APR 15 PY 1991 VL 67 IS 9 BP 823 EP 829 DI 10.1016/0002-9149(91)90614-Q PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FF799 UT WOS:A1991FF79900006 PM 2011984 ER PT J AU GELBER, RD GOLDHIRSCH, A CAVALLI, F AF GELBER, RD GOLDHIRSCH, A CAVALLI, F TI QUALITY-OF-LIFE-ADJUSTED EVALUATION OF ADJUVANT THERAPIES FOR OPERABLE BREAST-CANCER SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID ENDPOINT; WOMEN AB Objective: To evaluate a single cycle of adjuvant chemotherapy compared with longer duration chemotherapy for premenopausal women or chemoendocrine therapy for postmenopausal women with operable breast cancer using a quality-of-life-oriented end point, Q-TWiST (quality-adjusted analysis of TWiST: Time Without Symptoms and Toxicity). Design: Multicenter randomized clinical trial-International Breast Cancer Study Group (IBCSG: formerly Ludwig Group) Trial V. Setting: IBCSG participating centers in Sweden, Switzerland, Australia, Yugoslavia, Spain, New Zealand, Italy, Germany, and South Africa. Patients: Data were available for 1229 eligible patients with node-positive breast cancer who were randomized to receive one of three adjuvant treatments after at least a total mastectomy and axillary clearance. Interventions: Patients received either a single cycle of perioperative chemotherapy consisting of cyclophosphamide, methotrexate, fluorouracil, and leucovorin; or six cycles (6 months) of a conventionally timed chemotherapy consisting of cyclophosphamide, methotrexate, fluorouracil, and prednisone for premenopausal women or this combination plus tamoxifen for postmenopausal women; or both perioperative and conventionally timed chemotherapy for a 7-month course of adjuvant therapy. Results: At 5 years of median follow-up, patients who received the longer duration therapies had an improved 5-year disease-free survival percentage (53% compared with 36%; P < 0.001) and 5-year overall survival percentage (73% compared with 63%; P = 0.001) compared with those who received the single perioperative cycle alone. By 3.5 years, the greater burden of toxic effects associated with the longer duration treatments was balanced by their superior control of disease. Within 5 years of follow-up, even after subtracting time with adjuvant treatment toxicity, patients gained an average of 2.2 months of Q-TWiST if treated with the longer duration therapies compared with the single cycle (P = 0.03). The gain for premenopausal patients was 2.8 months (P = 0.05), whereas the gain for postmenopausal women was 1.5 months (P > 0.2). Conclusions: Six or seven months of adjuvant chemotherapy or chemoendocrine therapy improve both the quantity and quality of life for patients with node-positive breast cancer compared with a single short course of perioperative combination chemotherapy. C1 INT BREAST CANC STUDY GRP,OPERAT OFF,BERN,SWITZERLAND. RP GELBER, RD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 17 TC 129 Z9 129 U1 2 U2 3 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1991 VL 114 IS 8 BP 621 EP 628 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FG031 UT WOS:A1991FG03100002 PM 2003707 ER PT J AU SOMAN, G HAREGEWOIN, A HOM, RC FINBERG, RW AF SOMAN, G HAREGEWOIN, A HOM, RC FINBERG, RW TI GUANIDINE GROUP-SPECIFIC ADP-RIBOSYLTRANSFERASE IN MURINE CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID ADENYLATE-CYCLASE; TURKEY ERYTHROCYTES; SKELETAL-MUSCLE; RIBOSYLATION; DIFFERENTIATION; MEMBRANES; PROTEINS; ACID; NAD; PURIFICATION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SOMAN, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU PHS HHS [A1 20382] NR 34 TC 26 Z9 26 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 APR 15 PY 1991 VL 176 IS 1 BP 301 EP 308 DI 10.1016/0006-291X(91)90924-V PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FG328 UT WOS:A1991FG32800045 PM 1902105 ER PT J AU FAZELY, F DEZUBE, BJ ALLENRYAN, J PARDEE, AB RUPRECHT, RM AF FAZELY, F DEZUBE, BJ ALLENRYAN, J PARDEE, AB RUPRECHT, RM TI PENTOXIFYLLINE (TRENTAL) DECREASES THE REPLICATION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN HUMAN PERIPHERAL-BLOOD MONONUCLEAR-CELLS AND IN CULTURED T-CELLS SO BLOOD LA English DT Note ID TUMOR NECROSIS FACTOR; LONG TERMINAL REPEAT; FACTOR-ALPHA; FACTOR CACHECTIN; KAPPA-B; INTERLEUKIN-1; EXPRESSION; INDUCTION; BINDING; CLONE C1 BETH ISRAEL HOSP,DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02215. BETH ISRAEL HOSP,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIAID NIH HHS [1-RO1-AI25847, UO1-AI24845] NR 26 TC 115 Z9 115 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 APR 15 PY 1991 VL 77 IS 8 BP 1653 EP 1656 PG 4 WC Hematology SC Hematology GA FG728 UT WOS:A1991FG72800003 PM 1707692 ER PT J AU PAUL, SR YANG, YC DONAHUE, RE GOLDRING, S WILLIAMS, DA AF PAUL, SR YANG, YC DONAHUE, RE GOLDRING, S WILLIAMS, DA TI STROMAL CELL-ASSOCIATED HEMATOPOIESIS - IMMORTALIZATION AND CHARACTERIZATION OF A PRIMATE BONE MARROW-DERIVED STROMAL CELL-LINE SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTORS; HUMAN ADENOSINE-DEAMINASE; MEDIATED GENE-TRANSFER; LONG-TERM CULTURE; LARGE T-ANTIGEN; STEM-CELLS; SIMIAN VIRUS-40; ADHERENT CELLS; GROWTH-FACTOR; GM-CSF C1 CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,ENDERS 7,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DANA FARBER CANC INST,BOSTON,MA 02114. GENET INST,CAMBRIDGE,MA. FU NCI NIH HHS [CA39542-05]; NHLBI NIH HHS [5 K08 HL01554-02, 5T32 HL07574] NR 58 TC 79 Z9 79 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1991 VL 77 IS 8 BP 1723 EP 1733 PG 11 WC Hematology SC Hematology GA FG728 UT WOS:A1991FG72800013 PM 2015398 ER PT J AU JANSON, CH GRUNEWALD, J OSTERBORG, A DERSIMONIAN, H BRENNER, MB MELLSTEDT, H WIGZELL, H AF JANSON, CH GRUNEWALD, J OSTERBORG, A DERSIMONIAN, H BRENNER, MB MELLSTEDT, H WIGZELL, H TI PREDOMINANT T-CELL RECEPTOR-V GENE USAGE IN PATIENTS WITH ABNORMAL CLONES OF B-CELLS SO BLOOD LA English DT Article ID BENIGN MONOCLONAL GAMMOPATHY; ANTIGEN RECEPTOR; MULTIPLE-MYELOMA; BLOOD-LYMPHOCYTES; PERIPHERAL-BLOOD; THERAPY; ANTIBODY; LEUKEMIA; ALPHA C1 KAROLINSKA HOSP,RADIUM HEMMET,S-10401 STOCKHOLM,SWEDEN. KAROLINSKA HOSP,IMMUNOL RES LAB,S-10401 STOCKHOLM 60,SWEDEN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. RP JANSON, CH (reprint author), KAROLINSKA INST,DEPT IMMUNOL,BOX 60400,S-10401 STOCKHOLM 60,SWEDEN. FU NIAMS NIH HHS [AR39582] NR 25 TC 47 Z9 47 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 APR 15 PY 1991 VL 77 IS 8 BP 1776 EP 1780 PG 5 WC Hematology SC Hematology GA FG728 UT WOS:A1991FG72800020 PM 1901744 ER PT J AU RABINOWE, SN SOIFFER, RJ TARBELL, NJ NEUBERG, D FREEDMAN, AS SEIFTER, J BLAKE, KW GRIBBEN, JG ANDERSON, KC TAKVORIAN, T RITZ, J NADLER, LM AF RABINOWE, SN SOIFFER, RJ TARBELL, NJ NEUBERG, D FREEDMAN, AS SEIFTER, J BLAKE, KW GRIBBEN, JG ANDERSON, KC TAKVORIAN, T RITZ, J NADLER, LM TI HEMOLYTIC-UREMIC SYNDROME FOLLOWING BONE-MARROW TRANSPLANTATION IN ADULTS FOR HEMATOLOGIC MALIGNANCIES SO BLOOD LA English DT Article ID TOTAL-BODY IRRADIATION; RADIATION NEPHRITIS; CYCLOSPORIN-A; RENAL-FAILURE; NEPHROTOXICITY; RECIPIENTS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL & BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT THERAPY,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT NEPHROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP RABINOWE, SN (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 06516, CA 34183]; NIAID NIH HHS [AI 29530] NR 31 TC 116 Z9 117 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 APR 15 PY 1991 VL 77 IS 8 BP 1837 EP 1844 PG 8 WC Hematology SC Hematology GA FG728 UT WOS:A1991FG72800028 PM 2015407 ER PT J AU CHIN, TW PARRY, RL DONAHOE, PK AF CHIN, TW PARRY, RL DONAHOE, PK TI HUMAN MULLERIAN INHIBITING SUBSTANCE INHIBITS TUMOR-GROWTH INVITRO AND INVIVO SO CANCER RESEARCH LA English DT Article ID HUMAN OVARIAN-CANCER; HUMAN-MELANOMA CELLS; PRIMARY BIOASSAY; COLONY GROWTH; FACTOR-BETA; STEM-CELLS; ASSAY; MODEL; SPHEROIDS; CULTURE AB Mullerian inhibiting substance (MIS) causes regression of the mullerian duct in the male fetus. Bovine MIS has been reported to inhibit the growth of some gynecological tumors. Recombinant human MIS (rhMIS) produced in transfected Chinese hamster ovary cells has been highly purified by immunoaffinity chromatography. The introduction of a salt wash prior to elution of MIS from the affinity column removes a growth-stimulating factor(s) derived from Chinese hamster ovary cells. This immunopurified rhMIS caused significant inhibition (34-59% survival) of A431 (a vulvar epidermoid carcinoma), HT-3 (a cervical carcinoma), HEC-1-A (an endometrial adenocarcinoma), NIH:OVCAR-3 (an ovarian adenocarcinoma), and OM431 (an ocular melanoma) human cell lines in colony inhibition assays. Two cell lines, Hep 3B (a hepatocellular carcinoma) and RT4 (a bladder transitional cell papilloma), were unresponsive to immunopurified rhMIS. Using an in vivo subrenal capsule assay in irradiated CD-1 mice, the growth of A431 and OM431 cells was inhibited by immunopurified rhMIS. We conclude that rhMIS inhibits the growth of certain tumor cell lines in vitro and in vivo. C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,WARREN 11,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NATL NAVAL MED CTR,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TAIPEI VET GEN HOSP,DEPT SURG,TAIPEI 11217,TAIWAN. FU NCI NIH HHS [CA 17393] NR 33 TC 53 Z9 56 U1 2 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1991 VL 51 IS 8 BP 2101 EP 2106 PG 6 WC Oncology SC Oncology GA FG082 UT WOS:A1991FG08200024 PM 2009529 ER PT J AU SWACK, JA MIER, JW ROMAIN, PL HULL, SR RUDD, CE AF SWACK, JA MIER, JW ROMAIN, PL HULL, SR RUDD, CE TI BIOSYNTHESIS AND POSTTRANSLATIONAL MODIFICATION OF CD6, A T-CELL SIGNAL-TRANSDUCING MOLECULE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ANTIGEN-RECEPTOR COMPLEX; HUMAN LYMPHOCYTES-T; HUMAN INTERLEUKIN-2 RECEPTOR; RAT MAMMARY ADENOCARCINOMA; PROTEIN KINASE-C; MONOCLONAL-ANTIBODIES; MEMBRANE-PROTEINS; CROSS-LINKING; ACTIVATION; PHOSPHORYLATION AB CD6 (T12) is a 130-kDa glycoprotein present on the surface of human T cells. Previously, we demonstrated that the anti-T12 and anti-2H1 monoclonal antibodies recognized different epitopes on CD6, and both were capable of transducing activation signals to T cells. Anti-T12 augmented suboptimal signaling via the TCR/CD3 complex and directly activated separated CD4+ but not CD8+ cells. Structural characterization of CD6 revealed that it contained intrachain disulfide bonds, was N-glycosylated, and in activated cells was phosphorylated on serine. Given the functional significance of CD6 and its involvement in signaling via CD3 and CD2 pathways, we examined in detail the biosynthesis, structural characteristics, and phosphorylation properties of this receptor-like molecule. These studies demonstrate that the nascent CD6 polypeptide on both T cells and thymocytes is 88 kDa, and the immature N-glycosylated form is 110 kDa. After maturation of N-linked glycan and addition of sulfated O-linked oligosaccharide, CD6 appears on the cell surface as a molecule of 130 kDa. CD6 is phosphorylated in resting cells and can be hyperphosphorylated when stimulated by phorbol 12-myristate 13-acetate, indicating that it may participate in the major common signaling pathway mediated through protein kinase C. Concanavalin A-activated cells are phosphorylated at an additional site(s) on the molecule and cannot be hyperphosphorylated with phorbol 12-myristate 13-acetate. These physical features reveal additional clues about the physiological role of CD6 and its mechanism of signal transduction and strongly suggest that CD6 represents a physiologically important membrane receptor involved in T cell activation. C1 NEW ENGLAND MED CTR HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,BOSTON,MA 02111. UNIV MASSACHUSETTS,MED CTR,DIV RHEUMATOL & IMMUNOL,WORCESTER,MA 01655. UNIV MIAMI,SCH MED,DEPT ANAT & CELL BIOL,MIAMI,FL 33101. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FU NCI NIH HHS [CA43590, CA08248]; NIAMS NIH HHS [AR01590] NR 66 TC 35 Z9 36 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1991 VL 266 IS 11 BP 7137 EP 7143 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG727 UT WOS:A1991FG72700077 PM 2016320 ER PT J AU FLESCHER, E FOSSUM, D GRAY, PJ FERNANDES, G HARPER, MJK TALAL, N AF FLESCHER, E FOSSUM, D GRAY, PJ FERNANDES, G HARPER, MJK TALAL, N TI ASPIRIN-LIKE DRUGS PRIME HUMAN T-CELLS - MODULATION OF INTRACELLULAR CALCIUM CONCENTRATIONS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID BLOOD MONONUCLEAR-CELLS; RABBIT BLASTOCYSTS; MEMBRANE FLUIDITY; ARACHIDONIC-ACID; ANTIGEN RECEPTOR; IL-2 PRODUCTION; PROSTAGLANDIN; LYMPHOCYTES; ACTIVATION; INTERLEUKIN-2 AB Aspirin-like drugs (ALD) enhance T cell proliferation by suppressing PG production in monocytes. Normal human T cells do not produce any eicosanoids. Therefore we studied whether ALD would affect purified T cells directly. We found that ALD enhanced the proliferation and IL-2 production of T cells in the absence of monocytes. This effect did not depend on arachidonic acid metabolism as no lipoxygenase products and only nonsuppressive levels of cyclooxygenase products were detected in T cell cultures. Several possible mechanisms of the ALD effect were ruled out including 1) enhanced mitogen binding, 2) induction of activation markers (IL-2R, transferrin receptor, HLA-DR) on the cell surface, 3) down-regulation of suppressor cells. ALD caused a rise in [Ca2+]i which appeared to reflect an influx of Ca2+ from the extracellular milieu and was more pronounced in CD4+ cells. The rise in intracellular levels of Ca2+, that is considered a necessary second messenger for T cell activation, may prime these cells for an enhanced response to mitogens. In addition, ALD increased T cell membrane fluidity but only at higher concentrations than those found to enhance proliferation. The pharmacologic effect of ALD on T cells presents a possible new immunoenhancing potential of these drugs and may have therapeutic use in immunosuppressed individuals. C1 UNIV TEXAS,HLTH SCI CTR,DEPT OBSTET & GYNECOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. FU NIA NIH HHS [AG03417]; NICHD NIH HHS [HD14048]; NIDCR NIH HHS [R01 DE09311-01] NR 37 TC 64 Z9 64 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 15 PY 1991 VL 146 IS 8 BP 2553 EP 2559 PG 7 WC Immunology SC Immunology GA FG729 UT WOS:A1991FG72900010 PM 1901879 ER PT J AU MOTOKURA, T BLOOM, T KIM, HG JUPPNER, H RUDERMAN, JV KRONENBERG, HM ARNOLD, A AF MOTOKURA, T BLOOM, T KIM, HG JUPPNER, H RUDERMAN, JV KRONENBERG, HM ARNOLD, A TI A NOVEL CYCLIN ENCODED BY A BCL1-LINKED CANDIDATE ONCOGENE SO NATURE LA English DT Article ID CELL-CYCLE; SACCHAROMYCES-CEREVISIAE; MOLECULAR-CLONING; MESSENGER-RNA; GENE; AMPLIFICATION; DIVISION; KINETICS; MEIOSIS; BCL-1 AB WE have previously identified a candidate oncogene (PRAD1 or D11S287E) on chromosome 11q13 which is clonally rearranged with the parathyroid hormone locus in a subset of benign parathyroid tumours 1,2. We now report that a cloned human placental PRAD1 complementary DNA encodes a protein of 295 amino acids with sequence similarities to the cyclins. Cyclins can form a complex with and activate p34 cdc2 protein kinase, thereby regulating progress through the cell cycle (reviewed in refs 3-5). PRAD1 messenger RNA levels vary dramatically across the cell cycle in HeLa cells. Addition of the PRAD1 protein to interphase clam embryo lysates containing inactive p34cdc2 kinase and lacking endogenous cyclins allows it to be isolated using beads bearing p13suc1, a yeast protein that binds cdc2 and related kinases with high affinity and coprecipitates kinase-associated proteins. Addition of PRAD1 also induces phosphorylation of histone H1, a preferred substrate of cdc2. These data suggest that PRAD1 encodes a novel cyclin whose overexpression may play an important part in the development of various tumours with abnormalities in 11q13. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. NR 33 TC 1215 Z9 1238 U1 0 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 APR 11 PY 1991 VL 350 IS 6318 BP 512 EP 515 DI 10.1038/350512a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FG143 UT WOS:A1991FG14300055 PM 1826542 ER PT J AU MCKINNEY, RE MAHA, MA CONNOR, EM FEINBERG, J SCOTT, GB WULFSOHN, M MCINTOSH, K BORKOWSKY, W MODLIN, JF WEINTRUB, P ODONNELL, K GELBER, RD ROGERS, GK LEHRMAN, SN WILFERT, CM AF MCKINNEY, RE MAHA, MA CONNOR, EM FEINBERG, J SCOTT, GB WULFSOHN, M MCINTOSH, K BORKOWSKY, W MODLIN, JF WEINTRUB, P ODONNELL, K GELBER, RD ROGERS, GK LEHRMAN, SN WILFERT, CM TI A MULTICENTER TRIAL OF ORAL ZIDOVUDINE IN CHILDREN WITH ADVANCED HUMAN-IMMUNODEFICIENCY-VIRUS DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; INFECTION; AZT; SURVIVAL; TYPE-1 AB Background and Methods. Zidovudine has been shown to be an effective antiretroviral treatment in adults with human immunodeficiency virus (HIV) infection. We examined the safety of zidovudine and the tolerance of and therapeutic response to the drug in 88 children with advanced HIV disease. During a 24-week outpatient trial, zidovudine (180 mg per square meter of body-surface area per dose) was given by mouth every six hours and serial measurements were made of clinical, immunologic, and virologic indexes. Children who completed 24 weeks of treatment were permitted to continue receiving zidovudine. Results. Of the 88 children (mean age, 3.9 years; range, 4 months to 11 years), 61 completed the initial 24-week trial, and 49 continued to receive zidovudine for up to 90 weeks (median follow-up, 56 weeks). The patients generally tolerated zidovudine well. One or more episodes of hematologic toxicity occurred in 54 children (61 percent) - anemia (hemoglobin level, < 75 g per liter) in 23 children (26 percent) and neutropenia (neutrophil count, < 0.75 X 10(9) per liter) in 42 (48 percent). Many of these abnormalities resolved spontaneously, but 30 children required transfusions or a modification of the dose of zidovudine. Only three children had to stop receiving the drug because of hematologic toxicity. Kaplan-Meier analysis demonstrated that the probability of survival was 0.89 after 24 weeks and 0.79 after 52 weeks. There was marked improvement in weight gain, cognitive function (mainly in children < 3 years old), serum and cerebrospinal fluid concentrations of p24 antigen, and the proportion of cerebrospinal fluid cultures negative for HIV. CD4+ lymphocyte counts (mean at base line, 0.263 X 10(9) per liter) improved during the first 12 weeks, although the improvement was not sustained through the 24th week. Conclusions. Zidovudine in a dose of 180 mg per square meter every six hours can be safely administered to children with advanced HIV disease. The resultant clinical, immunologic, and virologic improvements in children are similar to those reported with zidovudine in adults. C1 BURROUGHS WELLCOME CO,RES TRIANGLE PK,NC 27709. NEW JERSEY CHILDRENS HOSP,NEWARK,NJ. NIAID,DIV AIDS,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,DEPT PEDIAT,SAN FRANCISCO,CA 94143. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. UNIV MIAMI,SCH MED,DEPT PEDIAT,MIAMI,FL 33152. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NYU,SCH MED,DEPT PEDIAT,NEW YORK,NY 10003. JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT,BALTIMORE,MD 21205. RP MCKINNEY, RE (reprint author), DUKE UNIV,MED CTR,SCH MED,DEPT PEDIAT,BOX 3461,DURHAM,NC 27710, USA. NR 23 TC 190 Z9 191 U1 1 U2 3 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 11 PY 1991 VL 324 IS 15 BP 1018 EP 1025 DI 10.1056/NEJM199104113241503 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FF771 UT WOS:A1991FF77100003 PM 1672443 ER PT J AU WAIN, JC MARK, EJ MCLOUD, TC JACOBY, GA AF WAIN, JC MARK, EJ MCLOUD, TC JACOBY, GA TI A 48-YEAR-OLD MAN WITH DYSPHAGIA, CHEST PAIN, FEVER, AND A SUBCARINAL MASS ... CHRONIC-HISTOPLASMOSIS OF MEDIASTINAL LYMPH-NODES, WITH RUPTURE INTO ESOPHAGUS AND SECONDARY ACUTE STREPTOCOCCAL LYMPHADENITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID GRANULOMA; TUBERCULOSIS; FIBROSIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WAIN, JC (reprint author), MASSACHUSETTS GEN HOSP,SURG,BOSTON,MA 02114, USA. NR 24 TC 3 Z9 3 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 11 PY 1991 VL 324 IS 15 BP 1049 EP 1056 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FF771 UT WOS:A1991FF77100008 ER PT J AU RUBIN, RH AF RUBIN, RH TI PREEMPTIVE THERAPY IN IMMUNOCOMPROMISED HOSTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ALLOGENEIC MARROW TRANSPLANTATION; INTRAVENOUS IMMUNE GLOBULIN; CYTOMEGALO-VIRUS INFECTION; PNEUMONIA; GANCICLOVIR; PREVENTION RP RUBIN, RH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 10 TC 119 Z9 119 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 11 PY 1991 VL 324 IS 15 BP 1057 EP 1059 DI 10.1056/NEJM199104113241509 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FF771 UT WOS:A1991FF77100009 PM 1848680 ER PT J AU TZALL, S MARTINIUK, F OZELIUS, L GUSELLA, J HIRSCHHORN, R AF TZALL, S MARTINIUK, F OZELIUS, L GUSELLA, J HIRSCHHORN, R TI FURTHER CHARACTERIZATION OF PSTI RFLPS AT THE ACID ALPHA-GLUCOSIDASE (GAA) LOCUS SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP TZALL, S (reprint author), NYU MED CTR,DEPT MED,550 1ST AVE,NEW YORK,NY 10016, USA. NR 6 TC 3 Z9 3 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 APR 11 PY 1991 VL 19 IS 7 BP 1727 EP 1727 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FG762 UT WOS:A1991FG76200082 PM 1674147 ER PT J AU KOCHOYAN, M HAVEL, TF NGUYEN, DT DAHL, CE KEUTMANN, HT WEISS, MA AF KOCHOYAN, M HAVEL, TF NGUYEN, DT DAHL, CE KEUTMANN, HT WEISS, MA TI ALTERNATING ZINC FINGERS IN THE HUMAN MALE ASSOCIATED PROTEIN ZFY - 2D NMR STRUCTURE OF AN EVEN FINGER AND IMPLICATIONS FOR JUMPING-LINKER DNA RECOGNITION SO BIOCHEMISTRY LA English DT Article ID TRANSCRIPTION FACTOR-IIIA; NUCLEAR MAGNETIC-RESONANCE; SEX-DETERMINING REGION; Y-CHROMOSOME ENCODES; SECONDARY STRUCTURE; DISTANCE GEOMETRY; ANTENNAPEDIA HOMEODOMAIN; BINDING DOMAINS; FACTOR TFIIIA; MOTIF AB ZFY, a sex-related Zn-finger protein encoded by the human Y chromosome, is distinguished from the general class of Zn-finger proteins by the presence of a two-finger repeat. Whereas odd-numbered domains and linkers fit a general consensus, even-numbered domains and linkers exhibit systematic differences. Because this alternation may have fundamental implications for the mechanism of protein-DNA recognition, we have undertaken biochemical and structural studies of fragments of ZFY. We describe here the solution structure of a representative nonconsensus (even-numbered) Zn finger based on 2D NMR studies of a 30-residue peptide. Structural modeling by distance geometry and simulated annealing (DG/SA) demonstrates that this peptide folds as a miniglobular domain containing a C-terminal beta-hairpin and N-terminal alpha-helix (beta-beta-alpha-motif). These features are similar to (but not identical with) those previously described in consensus-type Zn fingers (derived from ADR1 and Xfin); the similarities suggest that even and odd ZFY domains bind DNA by a common mechanism. A model of the protein-DNA complex (designated the "jumping-linker" model) is presented and discussed in terms of the ZFY two-finger repeat. In this model every other linker is proposed to cross the minor groove by means of a putative finger/linker submotif HX4HX3-hydrophobic residue-X3. Analogous use of a hydrophobic residue in a linker that spans the minor groove has recently been described in crystallographic and 3D NMR studies of homeodomain-DNA complexes. The proposed model of ZFY is supported in part by the hydroxyl radical footprint of the TFIIIA-DNA complex [Churchill, M. E. A., Tullius, T. D., & Klug, A. (1990) Proc. Natl. Acad. Sci. U.S.A. 87, 5528-5532]. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NCRR NIH HHS [1 S10RR-02301]; NICHD NIH HHS [HD 26465]; NIGMS NIH HHS [GM 38221] NR 60 TC 75 Z9 76 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD APR 9 PY 1991 VL 30 IS 14 BP 3371 EP 3386 DI 10.1021/bi00228a004 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FF646 UT WOS:A1991FF64600004 PM 1849423 ER PT J AU QURESHI, N TAKAYAMA, K MEYER, KC KIRKLAND, TN BUSH, CA CHEN, L WANG, R COTTER, RJ AF QURESHI, N TAKAYAMA, K MEYER, KC KIRKLAND, TN BUSH, CA CHEN, L WANG, R COTTER, RJ TI CHEMICAL-REDUCTION OF 3-OXO AND UNSATURATED GROUPS IN FATTY-ACIDS OF DIPHOSPHORYL LIPID-A FROM THE LIPOPOLYSACCHARIDE OF RHODOPSEUDOMONAS-SPHAEROIDES - COMPARISON OF BIOLOGICAL PROPERTIES BEFORE AND AFTER REDUCTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; COMPLETE STRUCTURAL DETERMINATION; NUCLEAR MAGNETIC-RESONANCE; SALMONELLA-TYPHIMURIUM; MASS-SPECTROMETRY; ESCHERICHIA-COLI; MACROPHAGES; MUTANT; PURIFICATION; DESORPTION AB Unlike the diphosphoryl lipid A (DPLA) derived from toxic lipopolysaccharide of Escherichia coli and Salmonella strains, the DPLA from nontoxic lipopolysaccharide of Rhodopseudomonas sphaeroides ATCC 17023 is biologically inactive. This could be due to the presence of 3-oxotetradecanoic and DELTA-7-tetradecenoic acids. These two fatty acids in R. sphaeroides DPLA were catalytically reduced in platinum oxide/H-2 to the 3-hydroxy and saturated fatty acids, respectively. The biologically active E. coli DPLA was also treated with platinum oxide/H-2, but as expected, the reduction step did not change the structure. These two preparations were then compared with the untreated samples for biological activity in three select in vitro assays. Over a range of 0.01-100 ng/ml, both normal and reduced DPLA from R. sphaeroides were inactive in priming phorbol myristate acetate-stimulated superoxide anion release in human alveolar macrophages. Over a range of 10-10(3) ng/ml, both samples failed to induce tumor necrosis factor in the RAW 264.7 murine macrophage cell line. The reduced DPLA marginally activated 70Z/3 pre-B cells at concentrations of 0.1-30-mu-g/ml. In every case, both normal and platinum oxide/H-2-treated E. coli DPLA were biologically active. These results indicate that the lack of biological activity of R. sphaeroides DPLA is not due to the presence of 3-oxo and unsaturated fatty acids, but rather to one or more of the following: (i) presence of only five fatty acyl groups (compared to six in active lipid A); (ii) presence of 3-hydroxydecanoic acids (rather than 3-hydroxytetradecanoic, in active lipid A); (iii) greater variation in size of the fatty acids. C1 UNIV WISCONSIN,SCH MED,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53706. VET ADM MED CTR,DIV INFECT DIS,SAN DIEGO,CA 92161. UNIV CALIF SAN DIEGO,DEPT PATHOL & MED,LA JOLLA,CA 92093. UNIV MARYLAND,DEPT CHEM & BIOCHEM,CATONSVILLE,MD 21228. JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,BALTIMORE,MD 21205. RP QURESHI, N (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705, USA. RI Wang, Rong/A-8721-2009 FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 28 TC 65 Z9 68 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6532 EP 6538 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300079 PM 2007601 ER PT J AU FORCE, T KYRIAKIS, JM AVRUCH, J BONVENTRE, JV AF FORCE, T KYRIAKIS, JM AVRUCH, J BONVENTRE, JV TI ENDOTHELIN, VASOPRESSIN, AND ANGIOTENSIN-II ENHANCE TYROSINE PHOSPHORYLATION BY PROTEIN KINASE-C-DEPENDENT AND KINASE-C-INDEPENDENT PATHWAYS IN GLOMERULAR MESANGIAL CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTOR; PHOSPHOLIPASE-C; SIGNAL TRANSDUCTION; PHOSPHATIDYLINOSITOL KINASE; HUMAN-PLATELETS; THROMBIN; PDGF; ACTIVATION; CALCIUM; IDENTIFICATION AB Protein tyrosine phosphorylation has not been considered to be important for cellular activation by phospholipase C-linked vasoactive peptides. We found that endothelin, angiotensin II, and vasopressin (AVP), peptides that signal via phospholipase C activation, rapidly enhanced tyrosine phosphorylation of proteins of approximate molecular mass 225, 190, 135, 120, and 70 kDa in rat renal mesangial cells. The phosphorylated proteins were cytosolic or membrane-associated, and none were integral to the membrane, suggesting that the peptide receptors are not phosphorylated on tyrosine. Epidermal growth factor (EGF), which does not activate phospholipase C in these cells, induced the tyrosine phosphorylation of its own 175-kDa receptor, in addition to five proteins of identical molecular mass to those phosphorylated in response to endothelin, AVP, and angiotensin II. This suggests that in mesangial cells there is a common signaling pathway for phospholipase C-coupled agonists and agonists classically assumed to signal via receptor tyrosine kinase pathways, such as EGF. The phorbol ester, phorbol 12-myristate 13-acetate, and the synthetic diacylglycerol, oleoyl acetylglycerol, stimulated the tyrosine phosphorylation of proteins identical to those phosphorylated by the phospholipase C-linked peptides, suggesting that protein kinase C (PKC) activation is sufficient to active tyrosine phosphorylation. However, the PKC inhibitor, staurosporine, and down-regulation of PKC activity by prolonged exposure to phorbol esters completely inhibited tyrosine phosphorylation in response to PMA but not to endothelin, AVP, or EGF. In conclusion, endothelin, angiotensin II, and AVP enhances protein tyrosine phosphorylation via at least two pathways, PKC-dependent and PKC-independent. Although activation of PKC may be sufficient to enhance protein tyrosine phosphorylation, PKC is not necessary and may not be the primary route by which these agents act. At least one of these pathways is shared with the growth factor EGF, suggesting not only common intermediates in the signaling pathways for growth factors and vasoactive peptides but also perhaps common cellular tyrosine kinases which phosphorylate these intermediates. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PREVENT MED,BOSTON,MA 02115. RP FORCE, T (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,BIGELOW 840,BOSTON,MA 02114, USA. OI Force, Thomas/0000-0002-0450-8659 FU NIDDK NIH HHS [DK 39773, DK 01986, DK 38452] NR 43 TC 209 Z9 209 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1991 VL 266 IS 10 BP 6650 EP 6656 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FE373 UT WOS:A1991FE37300095 PM 1706722 ER PT J AU BRESSAC, B KEW, M WANDS, J OZTURK, M AF BRESSAC, B KEW, M WANDS, J OZTURK, M TI SELECTIVE G-MUTATION TO T-MUTATION OF P53 GENE IN HEPATOCELLULAR-CARCINOMA FROM SOUTHERN AFRICA SO NATURE LA English DT Article ID HEPATITIS-B VIRUS; CELL-LINE; LIVER; DNA; ESTABLISHMENT AB HEPATOCELLULAR carcinoma (HCC) is a prevalent cancer in sub-Saharan Africa and eastern Asia 1. Hepatitis B virus and aflatoxins are risk factors for HCC 2, but the molecular mechanism of human hepatocellular carcinogenesis is largely unknown 3. Abnormalities in the structure and expression of the tumour-suppressor gene p53 are frequent in HCC cell lines 4, and allelic losses from chromosome 17p have been found in HCCs from China 5 and Japan 6. Here we report on allelic deletions from chromosome 17p and mutations of the p53 gene found in 50% of primary HCCs from southern Africa. Four of five mutations detected were G --> T substitutions, with clustering at codon 249. This mutation specificity could reflect exposure to a specific carcinogen, one candidate being aflatoxin B1 (ref. 7), a food contaminant in Africa 8, which is both a mutagen that induces G to T substitution 9 and a liver-specific carcinogen 10. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,MGH E,149 13TH ST,BOSTON,MA 02129. UNIV WITWATERSRAND,PARKTOWN 2193,SOUTH AFRICA. RI ozturk, mehmet/G-3330-2014 NR 29 TC 1165 Z9 1192 U1 4 U2 38 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD APR 4 PY 1991 VL 350 IS 6317 BP 429 EP 431 DI 10.1038/350429a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FF042 UT WOS:A1991FF04200052 PM 1672732 ER PT J AU WEICHSELBAUM, RR HALLAHAN, DE SUKHATME, V DRITSCHILO, A SHERMAN, ML KUFE, DW AF WEICHSELBAUM, RR HALLAHAN, DE SUKHATME, V DRITSCHILO, A SHERMAN, ML KUFE, DW TI BIOLOGICAL CONSEQUENCES OF GENE-REGULATION AFTER IONIZING-RADIATION EXPOSURE SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Review ID TUMOR NECROSIS FACTOR; DNA DAMAGE; SACCHAROMYCES-CEREVISIAE; NEOPLASTIC TRANSFORMATION; INCREASED RESISTANCE; PROMOTER REGION; CELLS INVITRO; RAS ONCOGENES; RAD9 GENE; DOSE-RATE AB Ionizing radiation is a ubiquitous environmental mutagen and carcinogen widely used in cancer therapy. However, little is known about the induction of cellular signaling events and specific gene expression after radiation exposure. We review the accumulating evidence that ionizing radiation induces signal transduction pathways involving activation of protein kinase C and a program of genetic events that may contribute to the biological effects of x rays. C1 UNIV CHICAGO HOSP & CLIN,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. UNIV CHICAGO HOSP & CLIN,DEPT MED,CHICAGO,IL 60637. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA-41068, CA-42596] NR 50 TC 158 Z9 159 U1 1 U2 5 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD APR 3 PY 1991 VL 83 IS 7 BP 480 EP 484 DI 10.1093/jnci/83.7.480 PG 5 WC Oncology SC Oncology GA FE173 UT WOS:A1991FE17300008 PM 2005631 ER PT J AU HENDERSON, GI BASKIN, GS FROSTO, TA SCHENKER, S AF HENDERSON, GI BASKIN, GS FROSTO, TA SCHENKER, S TI INTERACTIVE EFFECTS OF ETHANOL AND CAFFEINE ON RAT FETAL HEPATOCYTE REPLICATION AND EGF RECEPTOR EXPRESSION SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article ID AMINO-ACID-UPTAKE; PROTEIN-KINASE; GROWTH-FACTOR; ALCOHOL; PREGNANCY; TRANSPORT; EXPOSURE; PHOSPHORYLATION; CONSUMPTION; INHIBITION AB This study reports on the interactive effects of ethanol and caffeine on growth of rat fetal hepatocytes. Exposure of cultured rat fetal hepatocytes (RFH) to ethanol in concentrations above 1 mg/ml, causes a blockade of EGF-dependent cell replication along with an overexpression of surface EGF receptors (EGF-R). However, RFHs exposed for 24 hours to ethanol at a concentration of 1 mg/ml alone had little effect on cell replication. Caffeine, when combined with this concentration of alcohol, progressively impaired RFH growth by up to 100%. Caffeine alone up to 10-mu-g/ml, on the other hand, caused a progressive increase in RFH replication associated with a 69% enhancement of DNA synthesis. Caffeine concentrations in excess of 50-mu-g/ml had no effect on replicative capacity. Concomitant caffeine exposure had no effect on the ethanol-related increase in cell DNA content, yet it caused a further enhancement of the cell protein accrual induced by ethanol alone. Caffeine (10-mu-g/ml) alone had no effect on EGF-R expression, while ethanol (2 mg/ml) increased it by almost 200%. Addition of caffeine to ethanol reduced this enhanced EGF binding by 45%. Scatchard analysis indicated that no treatment altered ligand affinity for the receptor, but that the alterations in binding caused by ethanol and the caffeine/ethanol combination reflected changes in binding capacity, in both low and high affinity components. It is concluded that (1) ethanol blocks EGF-mediated replication accompanied by a reduction in DNA synthesis, (2) caffeine alone at low concentrations has the opposite effect and can actually potentiate the EGF-mediated mitogenic response, (3) caffeine in combination with ethanol acts synergistically to reduce RFH replication. We suggest that the ethanol-induced perturbation of the EGF-R may be due to an altered cAMP kinase that plays a regulatory role in EFG-R expression. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,DIV GASTROENTEROL & NUTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HENDERSON, GI (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 36 TC 10 Z9 10 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD APR PY 1991 VL 15 IS 2 BP 175 EP 180 DI 10.1111/j.1530-0277.1991.tb01850.x PG 6 WC Substance Abuse SC Substance Abuse GA FG761 UT WOS:A1991FG76100005 PM 2058791 ER PT J AU LAWRENCE, DL SHENKER, Y AF LAWRENCE, DL SHENKER, Y TI EFFECT OF HYPOXIC EXERCISE ON ATRIAL-NATRIURETIC-FACTOR AND ALDOSTERONE REGULATION SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE ALDOSTERONE REGULATION; PHYSICAL ACTIVITY; HORMONE STIMULATION; PLASMA RENIN ACTIVITY AB To evaluate the possible physiologic role of atrial natriuretic factor (ANF) in the observed dissociation of aldosterone secretion from the renin-angiotensin system during hypoxic exercise, 12 untrained men, ages 18 to 24, were studied on two separate days for 30 min during hypoxic (16% 0(2)) and normoxic (room air exercise on a bicycle ergometer. Workloads were adjusted to produce individual heart rates that remained within 70 to 75% of their previously measured maximum. Hemoglobin saturation decreased during hypoxia from 98 +/- 0.1% to 90 +/- 0.4% (P < .01). Plasma aldosterone levels increased significantly (P < .01) under both breathing conditions, yet were on average 36% lower during hypoxia than during normoxia (P < .001). Plasma ANF levels increased during exercise under both conditions (P < .01), yet levels were 45% greater during hypoxia than during normoxia (P < .001). Plasma renin activity, adrenocorticotropic hormone, cortisol, potassium, and systolic blood pressure increased during exercise on both study days (P < .01, compared to basal level), and showed no difference between normoxic and hypoxic conditions. Plasma pH was slightly higher during hypoxic exercise (P < .05, compared to normoxia). We conclude that acute hypoxemia is a potent enhancing stimulus for ANF release during dynamic exercise and that ANF is probably a contributing factor in the dissociation of aldosterone secretion from the renin-angiotensin system under these conditions. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [1-R29-DK-38444] NR 0 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1991 VL 4 IS 4 BP 341 EP 347 PN 1 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FG949 UT WOS:A1991FG94900009 PM 1829370 ER PT J AU MURPHY, RL LAVELLE, JP ALLAN, JD GORDIN, FM DUPLISS, R BOSWELL, SL WASKIN, HA DAVIES, SF GRAZIANO, FM SAAG, MS WALTER, JB CRANE, LR MACDONELL, KB HODGES, TL PIERCE, PF AF MURPHY, RL LAVELLE, JP ALLAN, JD GORDIN, FM DUPLISS, R BOSWELL, SL WASKIN, HA DAVIES, SF GRAZIANO, FM SAAG, MS WALTER, JB CRANE, LR MACDONELL, KB HODGES, TL PIERCE, PF TI AEROSOL PENTAMIDINE PROPHYLAXIS FOLLOWING PNEUMOCYSTIS-CARINII PNEUMONIA IN AIDS PATIENTS - RESULTS OF A BLINDED DOSE-COMPARISON STUDY USING AN ULTRASONIC NEBULIZER SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; BLOOD-INSTITUTE WORKSHOP; PULMONARY COMPLICATIONS; NATIONAL-HEART; SULFAMETHOXAZOLE; LUNG AB PURPOSE: To compare the efficacy and safety of three different doses of prophylactic aerosol pentamidine in patients with one prior episode of Pneumocystis carinii pneumonia (PCP) and the acquired immunodeficiency syndrome. PATIENTS AND METHODS: The design of the study was a double-blind, randomized, dose-comparison clinical trial conducted at 13 medical centers within the United States. In stage I of the trial, patients were randomized to receive either 5 mg, 60 mg, or 120 mg of aerosol pentamidine delivered biweekly with the Fisoneb (Fisons, Inc., Rochester, New York) ultrasonic nebulizer. After 24 weeks of therapy, patients entered stage II of the trial, where the 5-mg group was re-randomized to either the 60-mg or 120-mg group. RESULTS: One hundred seventy-five patients entered stage I of the trial and received prophylaxis for a mean of 123.6 days. Seven assigned to the 5-mg biweekly dosing schedule had a confirmed recurrence of PCP, compared with none in the 60-mg group (p = 0.007) and three in the 120-mg group (p = 0.304). During stage II of the trial, eight patients in the 60-mg group and one additional patient in the 120-mg group had recurrent PCP. After 52 weeks of observation, the likelihood of being PCP-free was 88.0% in the 60-mg group and 93% in the 120-mg group (p = 0.712). Minor adverse events related to aerosol pentamidine administration included cough, taste perversion, chest pain, bronchospasm, and dyspnea. These side effects were more common in the 60-mg and 120-mg treatment groups and resulted in withdrawal from the study by one patient. Serious events were more common after 24 weeks of therapy and included asymptomatic hypoglycemia (five), pancreatitis (two), pneumothorax (one), and extrapulmonary pneumocystosis (one). CONCLUSIONS: These results demonstrate that biweekly administration of 60 mg or 120 mg of aerosol pentamidine significantly decreases PCP recurrence when compared with a 5-mg regimen or findings in historic controls and is generally well tolerated. There is no significant difference in effect or safety between these two dosing regimens in patients followed for at least 52 weeks of therapy. C1 GEORGIA BAPTIST HOSP,ATLANTA,GA 30312. UNIV ALABAMA,BIRMINGHAM MED CTR,BIRMINGHAM,AL. WAYNE STATE UNIV,SCH MED,DETROIT,MI 48201. VET ADM MED CTR,WASHINGTON,DC 20422. HENNEPIN CTY MED CTR,MINNEAPOLIS,MN 55415. UNIV WISCONSIN,SCH MED,MADISON,WI 53706. HHCS RES INST INC,ORLAND,FL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. DUKE UNIV,MED CTR,DURHAM,NC 27710. RP MURPHY, RL (reprint author), NORTHWESTERN UNIV,SCH MED,303 E SUPER ST,ROOM 828,CHICAGO,IL 60611, USA. OI Murphy, Robert/0000-0003-3936-2052 NR 26 TC 40 Z9 40 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD APR PY 1991 VL 90 IS 4 BP 418 EP 426 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA FG905 UT WOS:A1991FG90500002 PM 2012082 ER PT J AU HSU, DW HOOI, SC HEDLEYWHYTE, ET STRAUSS, RM KAPLAN, LM AF HSU, DW HOOI, SC HEDLEYWHYTE, ET STRAUSS, RM KAPLAN, LM TI COEXPRESSION OF GALANIN AND ADRENOCORTICOTROPIC HORMONE IN HUMAN PITUITARY AND PITUITARY-ADENOMAS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; GROWTH-HORMONE; ANTERIOR-PITUITARY; POSSIBLE INVOLVEMENT; RAT; IMMUNOREACTIVITY; RELEASE; CHOLECYSTOKININ; SECRETION; PEPTIDE AB Galanin is a neuropeptide that regulates the secretion of several pituitary hormones, including prolactin (PRL) and growth hormone (GH). Galaninlike immunoreactivity (Gal-IR) and galanin mRNA in the rat anterior pituitary is cell lineage specific, with predominant expression in lactotrophs and somatotrophs. The authors examined the cellular distribution of human Gal-IR in seven normal postmortem pituitaries and 62 pituitary tumors by immunoperoxidase staining. In contrast to the rat, Gal-IR in human anterior pituitaries was present in corticotrophs scattered throughout the gland, but not in lactotrophs, somatotrophs, thyrotrophs, or gonadotrophs. Distinct Gal-IR also was present in hyperplastic and neoplastic corticotrophs in 19 of 22 patients with Cushing's disease. In noncorticotroph cell tumors, unequivocal Gal-IR was present in 5 of 11 GH-secreting tumors associated with clinical acromegaly, 9 of 18 nonfunctioning pituitary adenomas, and 2 of 14 prolactinomas. Of these galanin-positive tumors, four of the five GH-secreting adenomas, six of the nine nonfunctioning adenomas, and both of the prolactinomas also contained adrenocorticotropic hormone immunoreactivity (ACTH-IR). Immunostaining and in situ hybridization on adjacent sections using an S-35-labeled probe complementary to human galanin mRNA demonstrated predominant galanin expression in normal corticotrophs. Immunoelectron microscopy confirmed the presence of Gal-IR in pituitary cells characteristic of corticotrophs in both normal and neoplastic pituitaries. Thus, as in the rat, galanin gene expression in the human pituitary is cell-type specific. Unlike the rat, however, human galanin gene expression is restricted to the corticotroph lineage. Studies of tumors confirmed the observed coexpression of galanin and adrenocorticotropic hormone. The divergent cell type specificity of galanin production in human and rat pituitaries reflects different patterns of gene activation in these two species. In addition, these results suggest that galanin in the human pituitary may participate locally in the regulation of the hypothalamic-pituitary-adrenal axis. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. RP HSU, DW (reprint author), MASSACHUSETTS GEN HOSP,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114, USA. RI Hooi, Shing/C-8588-2012 FU NIDDK NIH HHS [DK42189] NR 39 TC 51 Z9 52 U1 0 U2 2 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1991 VL 138 IS 4 BP 897 EP 909 PG 13 WC Pathology SC Pathology GA FF067 UT WOS:A1991FF06700014 PM 1707237 ER PT J AU CLINTON, SK FLEET, JC LOPPNOW, H SALOMON, RN CLARK, BD CANNON, JG SHAW, AR DINARELLO, CA LIBBY, P AF CLINTON, SK FLEET, JC LOPPNOW, H SALOMON, RN CLARK, BD CANNON, JG SHAW, AR DINARELLO, CA LIBBY, P TI INTERLEUKIN-1 GENE-EXPRESSION IN RABBIT VASCULAR TISSUE INVIVO SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID TUMOR NECROSIS FACTOR; SMOOTH-MUSCLE CELLS; HUMAN-ENDOTHELIAL CELLS; HUMAN MONONUCLEAR-CELLS; DERMAL FIBROBLASTS; IL-1; RECEPTOR; NEUTROPHILS; CONTRACTION; ENDOTOXIN AB Cultured human vascular endothelial and smooth muscle cells express interleukin-1 (IL-1) genes when exposed to bacterial lipopolysaccharides (LPS) and a variety of inflammatory mediators. Local production of IL-1 may contribute to the pathogenesis of various vascular diseases. Therefore the ability of intact vascular tissue to accumulate IL-1 mRNA and synthesize de novo biologically active IL-1 protein was examined. Escherichia coli LPS (10-mu-g/kg) was administered intravenously to adult rabbits and total RNA was isolated from aortic tissue at various times after LPS injection. In saline-injected rabbits, RNA extracted from the thoracic aorta contained little or no IL-1 message detected by Northern analysis using IL-1 alpha and beta cDNA probes cloned from an LPS-stimulated rabbit splenic macrophage library. Lipopolysaccharide treatment promptly induced transient accumulation of mRNA for IL-1 alpha and IL-1 beta within the aorta (maximal 1-hour after injection). Short-term organoid cultures of rabbit aorta exposed to LPS in vitro synthesized immunoprecipitable IL-1 alpha protein. Extracts of aortic tissue excised 1.5 to 3.0 hours after intravenous LPS administration contained immunoreactive and biologically active IL-1 alpha Anti-rabbit IL-1 alpha antibody neutralized the biologic activity (more than 90%). Microscopic and immunohistochemical studies did not disclose adherent or infiltrating macrophages in rabbit aorta at the time of maximal IL-1 mRNA accumulation after LPS administration (1.5 hours), indicating that intrinsic vascular wall cells rather than mononuclear phagocytes probably account for the IL-1 activity induced by LPS. In addition, aortic tissue from rabbits fed an atherogenic diet showed an enhanced ability to accumulate IL-1 alpha and beta mRNA and produce immunodetectible protein in response to LPS administration. These studies demonstrate inducible IL-1 gene expression in rabbit vascular tissue in vivo and support a local role for this cytokine in vascular pathophysiology. C1 GLAXO IMB,GENEVA,SWITZERLAND. BRIGHAM & WOMENS HOSP,VASC MED UNIT,BOSTON,MA 02115. TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111. NEW ENGLAND MED CTR HOSP,BOSTON,MA 02111. TUFTS UNIV,DEPT MED,BOSTON,MA 02111. TUFTS UNIV,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02111. RP CLINTON, SK (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02117, USA. NR 42 TC 86 Z9 90 U1 0 U2 2 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1991 VL 138 IS 4 BP 1005 EP 1014 PG 10 WC Pathology SC Pathology GA FF067 UT WOS:A1991FF06700024 PM 2012168 ER PT J AU DEALMEIDA, JB STOW, JL AF DEALMEIDA, JB STOW, JL TI DISRUPTION OF MICROTUBULES ALTERS POLARITY OF BASEMENT-MEMBRANE PROTEOGLYCAN SECRETION IN EPITHELIAL-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE POLARIZED SECRETION; HEPARAN SULFATE PROTEOGLYCANS; SORTING; GOLGI PROCESSING ID DARBY CANINE KIDNEY; PLASMA-MEMBRANE; GOLGI-APPARATUS; PROTEIN SECRETION; SURFACE; DELIVERY; COLCHICINE; TRANSPORT; COMPLEX; LOCALIZATION AB Basement membrane proteins such as the heparan sulfate proteoglycan (HSPG) are secreted in a polarized fashion from the basolateral membrane of epithelial cells. We have used the microtubule-disrupting drug colchicine to study the role of the microtubule network in directing constitutive secretion to the basolateral membrane of LLC-PK1 renal epithelial cells. Microtubule depolymerization induced by colchicine resulted in fragmentation and redistribution of fluorescently labeled trans-Golgi membranes. Increased immunofluorescent staining of HSPG was associated with these dispersed Golgi cisternae. The biosynthetic processing of HSPG was not significantly altered by the loss of microtubules or by the dispersal of the Golgi elements. The most striking effect of microtubule disruption was the loss of polarity of HSPG secretion. Immunoprecipitation studies showed that HSPG was secreted from both apical and basolateral surfaces of LLC-PK1 cells treated with colchincine, and a similar result was found for the delivery of laminin, another basement membrane protein. In contrast, there was no change in the distribution of an integral basolateral membrane protein, Na+-K+-ATPase, following colchicine treatment. Our results provide the first demonstration that microtubules are involved in the constitutive trafficking of basolateral secretory proteins. These data also suggest that there may be an inherent difference in the targeting or delivery of membrane and secretory proteins to the basolateral cell surface. C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 30 TC 31 Z9 31 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP C691 EP C700 PN 1 PG 10 WC Physiology SC Physiology GA FG541 UT WOS:A1991FG54100003 ER PT J AU TOMPKINS, RG AF TOMPKINS, RG TI QUANTITATIVE-ANALYSIS OF BLOOD-VESSEL PERMEABILITY OF SQUIRREL-MONKEYS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE LOW-DENSITY LIPOPROTEIN; MACROMOLECULAR PERMEABILITY; AORTA; ARTERIES; ATHEROSCLEROSIS ID LOW-DENSITY LIPOPROTEIN; MACROMOLECULAR TRANSPORT; ARTERIAL-WALL; ENDOTHELIUM; ALBUMIN; INVIVO; AORTA; SERUM AB A mathematical transport model was derived to analyze in vivo low-density lipoprotein (LDL) transport across the aorta, peripheral muscular arteries, and major veins of squirrel monkeys (primates that develop diet-induced atherosclerosis similar to humans). Parameters determining the relative magnitudes of intimal permeability and diffusion within the vascular wall were optimized by nonlinear regression methods. Transmural LDL concentrations demonstrating discrete spatial resolution along the endothelial surface were previously obtained after 30 min of tracer circulation using quantitative autoradiography. In this study, intimal mass transfer coefficient (k1) was determined in 87 vascular regions representing 280 transmural profiles. As a result of this analysis, the value of k1 was 1.7 +/- 0.4 x 10(-9) cm/s for arteries, 2.9 +/- 0.3 x 10(-9) cm/s for veins, and 60 +/- 120 x 10(-9) cm/s for enhanced LDL uptake regions, which was a significant increase (P < 0.01). The effective diffusion coefficient was 6.2 +/- 3.7 x 10(-10) cm2/s for all vascular regions examined. As a result of this analysis, focal regions of enhanced LDL uptake were explained solely on the basis of intimal permeability. C1 MIT,DEPT CHEM ENGN,CAMBRIDGE,MA 02139. RP TOMPKINS, RG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT SURG,SURG SERV,BOSTON,MA 02114, USA. NR 30 TC 16 Z9 16 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1991 VL 260 IS 4 BP H1194 EP H1204 PN 2 PG 11 WC Physiology SC Physiology GA FG542 UT WOS:A1991FG54200023 ER PT J AU TORRY, DS COOPER, GM AF TORRY, DS COOPER, GM TI PROTOONCOGENES IN DEVELOPMENT AND CANCER SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE ONCOGENES; CELLULAR REGULATION; PROTOONCOGENE ACTIVATION ID CHRONIC MYELOGENOUS LEUKEMIA; KIRSTEN SARCOMA-VIRUSES; TRANSFORMING GENES; VIRAL ONCOGENES; HUMAN BLADDER; CELL-LINE; ONC GENE; ABL GENE; ACTIVATION; HARVEY AB Although analogies are often made comparing development to cancer, there is of course a major difference. Normal development requires complex patterns of rigidly controlled cell proliferation and differentiation. In contrast, cancer represents the pathological condition that results when normal cell growth patterns are uncoupled from their regulatory influences. Genetic studies of RNA tumor viruses have provided insights into the relationships and differences of the genes responsible for normal development and cancer. The presence of discrete genes (oncogenes) within the genome of oncogenic retroviruses is responsible for their tumor-igenic potential. Molecular genetic studies have found that normal eukaryotic cells possess genes that are quite homologous to the retroviral oncogenes. These normal cellular genes (proto-oncogenes) are involved in the regulation of proliferation and differentiation. However, if mutated, proto-oncogenes have the potential for inducing neoplastic transformation. The conversion of a proto-oncogene to an oncogene is called activation. Proto-oncogenes can become activated by a variety of genetic mechanisms including transduction, insertional mutagenesis, amplification, point mutations, and chromosomal translocations. In each instance the genetic aberration results in a proto-oncogene that is now free of its normal regulatory constraints. Such deregulation of function imparts a distinct growth advantage to the cell. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP TORRY, DS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC CARCINOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 34 TC 4 Z9 4 U1 0 U2 3 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 8755-8920 J9 AM J REPROD IMMUNOL JI Am. J. Reprod. Immunol. PD APR PY 1991 VL 25 IS 3 BP 129 EP 132 PG 4 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA GC163 UT WOS:A1991GC16300009 PM 1930640 ER PT J AU PALMER, WE GERARDMCFARLAND, EL CHEW, FS AF PALMER, WE GERARDMCFARLAND, EL CHEW, FS TI ADRENAL MYELOLIPOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 14 Z9 14 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 APR PY 1991 VL 156 IS 4 BP 724 EP 724 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC830 UT WOS:A1991FC83000009 PM 2003434 ER PT J AU FERRUCCI, JT AF FERRUCCI, JT TI CT VS MR IN IMAGING LIVER-TUMORS - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter ID ARTERIAL PORTOGRAPHY RP FERRUCCI, JT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 5 TC 3 Z9 3 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 APR PY 1991 VL 156 IS 4 BP 867 EP 868 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC830 UT WOS:A1991FC83000046 ER PT J AU FERRUCCI, JT AF FERRUCCI, JT TI SCREENING METHODS FOR HEPATOCELLULAR-CARCINOMA - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP FERRUCCI, JT (reprint author), MASSACHUSETTS GEN HOSP,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 APR PY 1991 VL 156 IS 4 BP 869 EP 869 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC830 UT WOS:A1991FC83000049 ER PT J AU PAIEMENT, GD WESSINGER, SJ HARRIS, WH AF PAIEMENT, GD WESSINGER, SJ HARRIS, WH TI COST-EFFECTIVENESS OF PROPHYLAXIS IN TOTAL HIP-REPLACEMENT SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 18TH WORLD CONGRESS OF THE SOC-INTERNATIONALE-DE-CHIRURGIE-ORTHOPEDIQUE-ET-DE-TRAUMATOLOGIE : VENOUS THROMBOEMBOLISM IN SURGERY CY SEP 10, 1990 CL MONTREAL, CANADA SP SOC INT CHIRURG ORTHOPED & TRAUMATOL, RHONE POULENC ID VENOUS THROMBOSIS; PREVENTION; DIAGNOSIS AB A theoretical analysis was performed regarding the cost-effectiveness in terms of lives saved (reduction of fatal pulmonary embolism [PE]) and in terms of money (dollars spent for prevention and treatment) of seven strategies in the management of venous thromboembolic disease in patients over 39 years of age undergoing elective total hip replacement (THR). Strikingly, this theoretical analysis suggests that low-dose warfarin combined with clinical surveillance of deep vein thrombosis would reduce the incidence of fatal PE from 20 per 1,000 patients to 4 per 1,000 patients and simultaneously reduce the charges for venous thromboembolic disease from $550,000 to about $400,000 per 1,000 patients. Based on this analysis, we strongly recommend this measure on a routine basis. Adding venography or duplex sonography routinely to this prophylactic regimen would, in this theoretical analysis, reduce the incidence of fatal PE from 4 per 1,000 patients to 0.15 per 1,000, but adds charges of $200,000 per extra life saved in the case of routine venography and $50,000 in the case of routine sonogrphy. Low-dose warfarin prophylaxis combined with routine sonography does not generate more charges than no prophylaxis with no screening while drastically reducing the incidence of fatal PE from 20 to 0.3 per 1,000 patients. Where duplex sonography is not easily available, a 12-week postoperative course of low-dose warfarin for every patient with no routine screening will be efficacious in reducing fatal PE and as cost-effective. C1 UNIV MONTREAL,SCH MED,DIV ORTHOPED,MONTREAL H3C 3J7,QUEBEC,CANADA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV ORTHOPED,BOSTON,MA 02114. NR 14 TC 55 Z9 58 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 APR PY 1991 VL 161 IS 4 BP 519 EP 524 DI 10.1016/0002-9610(91)91124-2 PG 6 WC Surgery SC Surgery GA FG784 UT WOS:A1991FG78400023 PM 1903606 ER PT J AU SPRINCE, NL OLIVER, LC MCLOUD, TC EISEN, EA CHRISTIANI, DC GINNS, LC AF SPRINCE, NL OLIVER, LC MCLOUD, TC EISEN, EA CHRISTIANI, DC GINNS, LC TI ASBESTOS EXPOSURE AND ASBESTOS-RELATED PLEURAL AND PARENCHYMAL DISEASE - ASSOCIATIONS WITH IMMUNE IMBALANCE SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID LYMPHOCYTE-T SUBSETS; BRONCHOALVEOLAR LAVAGE; MONOCLONAL-ANTIBODIES; FLOW-CYTOMETRY; PERIPHERAL-BLOOD; CELL SUBSETS; LUNG; WORKERS; SMOKING; SUBPOPULATIONS AB The study hypothesis was that asbestos exposure and asbestos-related pleural plaques and interstitial disease are associated with (1) immune imbalances favoring helper-inducer T-cell subsets in blood and bronchoalveolar lavage (BAL) and (2) T-lymphocyte accumulation in BAL. One hundred twenty-two asbestos-exposed subsets (AES), including 27 nonsmokers (NS), were evaluated and compared with 10 unexposed normal subjects. Data were collected on medical, smoking, and occupational histories, physical examination, spirometry, lung volumes, single-breath DL(CO), chest films read by a "B" reader, and T-lymphocyte characterization in blood and BAL using flow cytometry analysis of monoclonal-antibody-treated cells. On average, AES were 47 yr of age and had 23 yr of asbestos exposure. Fifty-eight (48%) had pleural thickening, and seven (6%) had profusion greater-than-or-equal-to 1/0. In blood, asbestos-exposed NS had lower total and percent CD8 and lower total CD3 than did normal subjects. In BAL, asbestos-exposed NS had higher total CD3 than did normal subjects. Among AES, increased asbestos exposure was associated with increased percent CD8 in BAL and decreases in both percent lymphocytes and total CD8 in blood. Increases in CD4/CD8 ratio in BAL were associated with pleural thickening. In those seven with profusion greater-than-or-equal-to 1/0, there was increased percent CD4 in blood and decreased percent CD8 in BAL. These results suggest immune imbalance favoring helper-inducer T-cell subsets in association with asbestos exposure systemically and with pleural plaques in BAL. In addition, our results suggest possible redistribution of T-lymphocytes and CD8 from blood to lungs in association with asbestos exposure. Longitudinal studies will determine whether these imbalances signal later asbestos-related diseases such as asbestosis, lung cancer, or mesothelioma. C1 MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM SCI & PHYSIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-07354]; NIEHS NIH HHS [ES-03301] NR 38 TC 23 Z9 23 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD APR PY 1991 VL 143 IS 4 BP 822 EP 828 PN 1 PG 7 WC Respiratory System SC Respiratory System GA FE781 UT WOS:A1991FE78100022 PM 1826194 ER PT J AU SWEADNER, KJ AF SWEADNER, KJ TI TRYPSIN-INHIBITOR PARADOXICALLY STABILIZES TRYPSIN ACTIVITY IN SODIUM DODECYL-SULFATE, FACILITATING PROTEOLYTIC FINGERPRINTING SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID OUTER MEDULLA; ALPHA-SUBUNIT; CATALYTIC SUBUNIT; CRYSTAL-STRUCTURE; NA,K-ATPASE; PROTEINS; KIDNEY; ELECTROPHORESIS; DENATURATION; ASSOCIATION C1 HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RP SWEADNER, KJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 36271] NR 28 TC 20 Z9 21 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD APR PY 1991 VL 194 IS 1 BP 130 EP 135 DI 10.1016/0003-2697(91)90159-Q PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FE430 UT WOS:A1991FE43000017 PM 1867377 ER PT J AU HICKEY, R HOFFMAN, J RAMAMURTHY, S AF HICKEY, R HOFFMAN, J RAMAMURTHY, S TI A COMPARISON OF ROPIVACAINE 0.5-PERCENT AND BUPIVACAINE 0.5-PERCENT FOR BRACHIAL-PLEXUS BLOCK SO ANESTHESIOLOGY LA English DT Article DE ANESTHETIC TECHNIQUES, BRACHIAL PLEXUS BLOCK; ANESTHETICS, LOCAL, BUPIVACAINE; ROPIVACAINE ID LIDOCAINE; TOXICITY; AGENT AB This study compared the effectiveness of 0.5% ropivacaine and 0.5% bupivacaine for brachial plexus block. Forty-eight patients received a subclavian perivascular brachial plexus block for upper-extremity surgery. One group (n = 24) received ropivacaine 0.5% (175 mg) and a second group (n = 24) received bupivacaine 0.5% (175 mg), both without epinephrine. Onset times for analgesia and anesthesia in each of the C5 through T1 brachial plexus dermatomes did not differ significantly between groups. Duration of analgesia and anesthesia was long (mean duration of analgesia, 13-14 h; mean duration of anesthesia, 9-11 h) and also did not differ significantly between groups. Motor block was profound, with shoulder paralysis as well as hand paresis developing in all of the patients in both groups. Two patients in each group required supplemental blocks before surgery. Ropivacaine 0.5% and bupivacaine 0.5% appeared equally effective in providing brachial plexus anesthesia. C1 MED CTR HOSP,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP HICKEY, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT ANESTHESIOL,SAN ANTONIO,TX 78284, USA. NR 11 TC 75 Z9 77 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1991 VL 74 IS 4 BP 639 EP 642 DI 10.1097/00000542-199104000-00002 PG 4 WC Anesthesiology SC Anesthesiology GA FE106 UT WOS:A1991FE10600002 PM 2008942 ER PT J AU DERSHWITZ, M ROSOW, CE DIBIASE, PM ZASLAVSKY, A AF DERSHWITZ, M ROSOW, CE DIBIASE, PM ZASLAVSKY, A TI COMPARISON OF THE SEDATIVE EFFECTS OF BUTORPHANOL AND MIDAZOLAM SO ANESTHESIOLOGY LA English DT Article DE ANALGESICS, INTRAVENOUS, BUTORPHANOL; ANTAGONISTS, OPIOID; HYPNOTICS, INTRAVENOUS, MIDAZOLAM; INTERACTION, DRUG; PREMEDICATION; TOXICITY, DRUG ID MORPHINE AB Although kappa opioid agonists and certain agonist-antagonists are known to be sedating, this effect has not been well characterized in a drug-naive population. We compared the sedative properties of intravenous butorphanol with those of midazolam or the combination in 126 healthy preoperative patients. Subjects were randomly assigned to receive one of nine treatments in a double-blind fashion: 7.1, 22.5, or 71.4-mu-g/kg butorphanol; 4.3, 13.6, or 42.9-mu-g/kg midazolam; or 3.6 + 2.2, 11.3 + 6.8, or 35.7 + 21.5-mu-g/kg butorphanol and midazolam in combination. Eight visual analogue scales (VAS) were completed by the subject and an observer. The subject then performed two psychomotor tests (the Trieger dot test and the Halstead trail-making test) and was shown two playing cards in order to assess memory. The test drug was administered, and 5 min later the evaluations were repeated and two more cards were shown. On the following day the subjects were asked to recall the names of the playing cards. Butorphanol, midazolam, and their combination produced dose-related changes in VAS scores that were significant and qualitatively similar: subjects became sleepy, less nervous, weak, and less clear-thinking. There was no significant euphoria or dysphoria. The sedative and depressant effects on respiratory rate of the high-dose combination were significantly greater than those predicted by simple additivity: 14 of 14 subjects receiving the high dose of the butorphanol/midazolam combination had lid droop and marked sedation, and 2 of 14 subjects had respiratory rates of less than 4 breaths per min. All three drug treatments caused significant, dose-dependent impairment of psychomotor function. Subjects usually remembered cards seen prior to drug treatment, but not those seen afterward. The amnesic effects of midazolam were dose-related, profound, and much greater than those of butorphanol. In a 70-kg subject, a dose as low as 0.5 mg butorphanol (lower than the usual analgesic dose) provided clinically useful sedative effects. At this dose, however, butorphanol caused no significant amnesic effect or psychomotor impairment. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANESTHESIA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. HARVARD UNIV,DEPT STAT,CAMBRIDGE,MA 02138. NR 22 TC 27 Z9 28 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD APR PY 1991 VL 74 IS 4 BP 717 EP 724 DI 10.1097/00000542-199104000-00016 PG 8 WC Anesthesiology SC Anesthesiology GA FE106 UT WOS:A1991FE10600016 PM 2008954 ER PT J AU POTTS, JT AF POTTS, JT TI NIH CONFERENCE - DIAGNOSIS AND MANAGEMENT OF ASYMPTOMATIC PRIMARY HYPERPARATHYROIDISM - CONSENUS DEVELOPMENT CONFERENCE STATEMENT SO ANNALS OF INTERNAL MEDICINE LA English DT Article AB Endocrinologists, surgeons, radiologists, epidemiologists, and primary health care providers convened to address both indications for surgery in asymptomatic patients with hyperparathyroidism as well as how patients who do not have surgery should be monitored and managed to minimize the risk for complications. The National Institutes of Health Consensus Development Conference Panel concluded that a diagnosis of hyperparathyroidism is established by showing persistent hypercalcemia and an elevated serum parathyroid hormone concentration; that the current and acceptable treatment for hyperparathyroidism is surgery; that the diagnosis of hyperparathyroidism in an asymptomatic patient does not in all cases mandate referral for surgery; that conscientious surveillance may be justified in patients whose calcium levels are only mildly elevated and whose renal and bone status are close to normal; and that preoperative localization in patients without previous neck operation is rarely indicated and has not proved to be cost effective. RP POTTS, JT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 1 TC 275 Z9 281 U1 0 U2 2 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1991 VL 114 IS 7 BP 593 EP 597 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FD661 UT WOS:A1991FD66100013 ER PT J AU THEDINGER, BA MONTGOMERY, WW CHENEY, ML GOODMAN, M AF THEDINGER, BA MONTGOMERY, WW CHENEY, ML GOODMAN, M TI LEIOMYOSARCOMA OF THE TRACHEA - CASE-REPORT SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE LEIOMYOSARCOMA; TRACHEAL RECONSTRUCTION; TRACHEAL TUMORS AB Leiomyosarcoma of the trachea is a rare primary tumor of the upper airway. Twelve cases have been reported in the English-language literature. Our experience with a patient with leiomysarcoma of the cervical trachea is presented. The classic symptoms, diagnosis, and surgical management of this case are contrasted with those of the previously reported cases. The surgical technique used for our patient, primary tumor resection with skin grafting and placement of a Montgomery(R) Laryngeal Stent, is a unique and effective treatment. RP THEDINGER, BA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02114, USA. NR 11 TC 8 Z9 8 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD APR PY 1991 VL 100 IS 4 BP 337 EP 340 PN 1 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA FF485 UT WOS:A1991FF48500014 PM 2018295 ER PT J AU STEINBERG, JB DOHERTY, NE MUNFAKH, NA GEFFIN, GA TITUS, JS HOAGLIN, DC DENENBERG, AG DAGGETT, WM AF STEINBERG, JB DOHERTY, NE MUNFAKH, NA GEFFIN, GA TITUS, JS HOAGLIN, DC DENENBERG, AG DAGGETT, WM TI OXYGENATED CARDIOPLEGIA - THE METABOLIC AND FUNCTIONAL-EFFECTS OF GLUCOSE AND INSULIN SO ANNALS OF THORACIC SURGERY LA English DT Article ID ISCHEMIC CARDIAC-ARREST; PERFUSED RAT-HEART; MYOCARDIAL PROTECTION; PRESERVATION; SUBSTRATE; CALCIUM AB Reports differ as to the efficacy of glucose and insulin as cardioplegic additives. Although deliberate oxygenation of crystalloid cardioplegic solutions improves myocardial protection, little is known about the protection afforded by glucose and insulin in such oxygenated solutions. In the isolated working rat heart, we studied the addition of oxygen, glucose, and insulin, separately and together, to a cardioplegic solution. The solution was equilibrated with O2 or N2, with glucose added as a substrate or sucrose as a nonmetabolizable osmotic control, with or without insulin. Hearts were arrested for 2 hours at 8-degrees-C by multidose infusions. Oxygenation decreased lactate production and improved high-energy phosphate and glycogen preservation during arrest, prevented ischemic contracture, and improved functional recovery. The addition of glucose to the oxygenated solution increased the level of adenosine triphosphate at end-arrest from 10.5 +/- 0.5 to 13.9 +/- 0.6 nmol/mg dry weight and glycogen stores from 18.7 +/- 2.5 to 35.7 +/- 5.5 nmol/mg dry weight. The further addition of insulin did not better preserve these metabolities. Improvements in functional recovery due to glucose or insulin in the oxygenated solution attained statistical significance when both additives were included. Glucose increased lactate production significantly only when the solution was nitrogenated. Insulin added to the nitrogenated glucose-containing solution increased adenosine triphosphate and glycogen levels after 1 hour of arrest; and, although insulin did not prevent ischemic contracture from developing during the latter part of arrest with profound depletion of these metabolites, functional recovery was improved. The mechanism of improved functional recovery by insulin is not clear. Whether aerobic or anaerobic metabolism is favored during arrest modifies the effects of glucose and insulin. The data support the use of a fully oxygenated cardioplegic solution containing glucose, and perhaps insulin, for myocardial protection, and suggest that these additives may be beneficial whether the cardioplegic solution is deliberately oxygenated or not. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,DEPT STAT,CAMBRIDGE,MA 02138. FU NHLBI NIH HHS [HL 12777] NR 26 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD APR PY 1991 VL 51 IS 4 BP 620 EP 629 PG 10 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FF788 UT WOS:A1991FF78800018 PM 2012422 ER PT J AU SHARKEY, PK RINALDI, MG DUNN, JF HARDIN, TC FETCHICK, RJ GRAYBILL, JR AF SHARKEY, PK RINALDI, MG DUNN, JF HARDIN, TC FETCHICK, RJ GRAYBILL, JR TI HIGH-DOSE ITRACONAZOLE IN THE TREATMENT OF SEVERE MYCOSES SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; KETOCONAZOLE THERAPY; FUNGAL-INFECTIONS; SYNDROME AIDS; INVITRO; ENZYMES AB Eight patients with systemic mycoses and with prior treatment failures were treated with itraconazole (600 mg/day) for a mean duration of 5.5 months. All six patients without AIDS experienced improvement or stabilization of their fungal infections while receiving high-dose itraconazole, although two patients later experienced treatment failures, one by relapse and one by progression, on lower doses. Treatment failures also occurred in the two patients with AIDS and cryptococcal meningitis. The failures were associated with low serum itraconazole concentrations (< 2.5-mu-g/ml) in both patients. All other patients had mean trough levels in serum above 5-mu-g/ml. One patient who was improving on 600 mg/day developed a progressive infection after reduction of the dose to 400 mg/day. Side effects included reversible adrenal insufficiency in one patient; severe hypokalemia, mild diastolic hypertension, and rhabdomyolysis in one patient; mild hypokalemia and hypertension in four other patients; and breast tenderness in one patient. The mean decrease in serum potassium during treatment was statistically significant (P = 0.05). Selected patients with severe systemic mycoses may benefit from prolonged high-dose itraconazole treatment. However, 600 mg/day may be approaching the upper limits of acceptable dosing for long-term treatment. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP SHARKEY, PK (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [MO1-RR-01346] NR 40 TC 88 Z9 92 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1991 VL 35 IS 4 BP 707 EP 713 PG 7 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA FF789 UT WOS:A1991FF78900018 PM 1648887 ER PT J AU ALLENDOERFER, R MARQUIS, AJ RINALDI, MG GRAYBILL, JR AF ALLENDOERFER, R MARQUIS, AJ RINALDI, MG GRAYBILL, JR TI COMBINED THERAPY WITH FLUCONAZOLE AND FLUCYTOSINE IN MURINE CRYPTOCOCCAL MENINGITIS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; AMPHOTERICIN-B; CEREBROSPINAL-FLUID; KETOCONAZOLE; COMBINATION; PENETRATION; INFECTIONS AB To assess the possible beneficial effects of combined therapy (fluconazole and flucytosine) in the treatment of cryptococcal meningitis in the immunocompromised host, we compared therapy with fluconazole and flucytosine, individually and combined, in the experimental murine model. BALB/c athymic (nu/nu) mice were infected intracerebrally with 150 to 300 CFU of Cryptococcus neoformans. In mortality studies, treatment was initiated 24 h postinfection and continued for 10 to 14 days with either fluconazole (1 to 15 mg/kg of body weight per day), flucytosine (60 to 120 mg/kg/8 h), both drugs, or 0.3% Noble agar (control). Combined therapy delayed mortality significantly when compared with controls and single-drug regimens. This was observed over a broad range of doses. Quantitative determinations of CFU in brain tissue demonstrated a significantly lower burden of C. neoformans in mice receiving combined therapy. The results indicate that combined therapy with fluconazole and flucytosine is superior to single-drug therapy. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ALLENDOERFER, R (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. NR 22 TC 63 Z9 63 U1 1 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD APR PY 1991 VL 35 IS 4 BP 726 EP 729 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA FF789 UT WOS:A1991FF78900021 PM 2069378 ER PT J AU MOORE, MR SAVER, JL JOHNSON, KA ROMERO, JA AF MOORE, MR SAVER, JL JOHNSON, KA ROMERO, JA TI RIGHT PARIETAL STROKE WITH GERSTMANN SYNDROME - APPEARANCE ON COMPUTED-TOMOGRAPHY, MAGNETIC-RESONANCE-IMAGING, AND SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY SO ARCHIVES OF NEUROLOGY LA English DT Article ID CEREBRAL ASYMMETRIES AB We examined a patient who exhibited Gerstmann's syndrome (left-right disorientation, finger agnosia, dyscalculia, and dysgraphia) in association with a perioperative stroke in the right parietal lobe. This is the first description of the Gerstmann tetrad occurring in the setting of discrete right hemisphere pathologic findings. A well-localized vascular lesion was demonstrated by computed tomography, magnetic resonance imaging, and single-photon emission computed tomographic studies. The patient had clinical evidence of reversed fucntional cerebral dominance and radiologic evidence of reversed anatomic cerebral asymmetries. C1 BRIGHAM & WOMENS HOSP,DEPT NEUROSURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 21 TC 14 Z9 14 U1 1 U2 1 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 APR PY 1991 VL 48 IS 4 BP 432 EP 435 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA FF073 UT WOS:A1991FF07300020 PM 2012521 ER PT J AU MAFUNE, K WONG, JM STANIUNAS, RJ LU, ML RAVIKUMAR, TS CHEN, LB STEELE, GD AF MAFUNE, K WONG, JM STANIUNAS, RJ LU, ML RAVIKUMAR, TS CHEN, LB STEELE, GD TI UBIQUITIN HYBRID PROTEIN GENE-EXPRESSION DURING HUMAN COLON CANCER PROGRESSION SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 43RD ANNUAL CANCER SYMP OF THE SOC OF SURGICAL ONCOLOGY CY MAY 29, 1990 CL WASHINGTON, DC SP SOC SURG ONCOL ID C-FOS GENE; COLORECTAL CARCINOMAS; BINDING-PROTEIN; JUN ENCODES; 3T3 CELLS; SEQUENCE; ONCOGENE; AP-1; TRANSCRIPTION; MYC AB Ubiquitin is involved in cell-cycle control and DNA replication through a specific proteolytic pathway. Our previous studies demonstrated selected higher expression of a gene encoding ubiquitin-ribosomal protein S27a in poorly differentiated colon carcinoma cell lines. In this study, we evaluated this ubiquitin hybird protein gene expression in surgical specimens of colon cancers. Northern blot analysis showed that ubiquitin hybrid protein messenger RNA was overexpressed in primary colon cancers compared with adjacent normal colon mucosae in 17 of 20 patients. Dot blot analysis of RNA of 27 tumor samples revealed significantly greater expression in higher Dukes' stage primary colon tumors and liver metastases. These data imply that protein translation machinery is highly activated during progression and metastasis of colon tumors, and that ubiquitin hybrid protein may be useful as a marker of biological aggressiveness. C1 NEW ENGLAND DEACONESS HOSP,DEPT SURG,110 FRANCIS ST 3A,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [P01-CA 44704-02] NR 42 TC 20 Z9 20 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD APR PY 1991 VL 126 IS 4 BP 462 EP 466 PG 5 WC Surgery SC Surgery GA FE876 UT WOS:A1991FE87600011 PM 2009061 ER PT J AU ZIMNIAK, P HOLSZTYNSKA, EJ RADOMINSKA, A ISCAN, M LESTER, R WAXMAN, DJ AF ZIMNIAK, P HOLSZTYNSKA, EJ RADOMINSKA, A ISCAN, M LESTER, R WAXMAN, DJ TI DISTINCT FORMS OF CYTOCHROME-P-450 ARE RESPONSIBLE FOR 6-BETA-HYDROXYLATION OF BILE-ACIDS AND OF NEUTRAL STEROIDS SO BIOCHEMICAL JOURNAL LA English DT Article ID RAT-LIVER MICROSOMES; HEPATIC CYTOCHROME-P-450; TESTOSTERONE 6-BETA-HYDROXYLASE; DIFFERENTIAL REGULATION; HORMONAL-REGULATION; NIFEDIPINE OXIDASE; CATALYTIC ACTIVITY; GENE CONVERSION; MESSENGER-RNA; METABOLISM AB Cytochrome P-450-dependent 6-beta-hydroxylation of bile acids in rat liver contributes to the synthesis of the quantitatively important pool of 6-hydroxylated bile acids, as well as to the detoxification of hydrophobic bile acids. The lithocholic acid 6-beta-hydroxylation reaction was investigated and compared with androstenedione 6-beta-hydroxylation. Differential responses of these two activities to inducers and inhibitors of microsomal P-450 enzymes, lack of mutual inhibition by the two substrates and differential inhibition by antibodies raised against several purified hepatic cytochromes P-450 were observed. From these results it was concluded that 6-beta-hydroxylation of lithocholic acid is catalysed by P-450 form(s) different from the subfamily IIIA cytochromes P-450 which are responsible for the bulk of microsomal androstenedione 6-beta-hydroxylation. Similar, but more tentative, results revealed that the 7-alpha-hydroxylation of lithocholic acid and of androstenedione may be also catalysed by distinct P-450 enzymes. The results indicate that cytochromes P-450 hydroxylating bile acids are distinct from analogous enzymes that carry out reactions of the same regio- and stereo-specificity on neutral steroids (steroid hormones). A comparison of pairs of cytochromes P-450 that catalyse the same reaction on closely related steroid molecules will help to define those structural elements in the proteins that determine the recognition of their respective substrates. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ZIMNIAK, P (reprint author), UNIV ARKANSAS MED SCI HOSP,DEPT INTERNAL MED,DIV GASTROENTEROL,4301 W MARKHAM,SLOT 567,LITTLE ROCK,AR 72205, USA. FU NICHD NIH HHS [HD-14198]; NIDDK NIH HHS [DK-33765, DK-38678] NR 58 TC 15 Z9 15 U1 0 U2 1 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD APR 1 PY 1991 VL 275 BP 105 EP 111 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FF870 UT WOS:A1991FF87000017 PM 2018466 ER PT J AU WARD, JM MARTYN, J AF WARD, JM MARTYN, J TI ALTERATIONS IN NEUROMUSCULAR FUNCTION FOLLOWING THERMAL-INJURY SO BIOCHEMICAL SOCIETY TRANSACTIONS LA English DT Meeting Abstract ID CLINICAL-PHARMACOLOGY; MUSCLE; RESPONSES; BURNS C1 MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. SHRINERS BURN INST,ANESTHESIA SERV,BOSTON,MA 02114. RP WARD, JM (reprint author), HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0300-5127 J9 BIOCHEM SOC T JI Biochem. Soc. Trans. PD APR PY 1991 VL 19 IS 2 BP S191 EP S191 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FQ821 UT WOS:A1991FQ82100215 PM 1889571 ER PT J AU SULLIVAN, EV SAGAR, HJ AF SULLIVAN, EV SAGAR, HJ TI DOUBLE DISSOCIATION OF SHORT-TERM AND LONG-TERM-MEMORY FOR NONVERBAL MATERIAL IN PARKINSONS-DISEASE AND GLOBAL AMNESIA - A FURTHER ANALYSIS SO BRAIN LA English DT Article ID ALZHEIMERS-DISEASE; BASAL GANGLIA; PREFRONTAL CORTEX; FRONTAL LOBES; DISCRIMINATION; ORGANIZATION; IMPAIRMENTS; RECOGNITION; DIAGNOSIS; DEFICITS AB The traditional concept of memory disorder is deficiency of the long-term (LTM) but not short-term (STM) component of memory. STM impairment with LTM sparing is seldom reported. The present study investigated STM and LTM for nonverbal material in three neurological conditions associated with memory impairment: bilateral medial temporal lobe lesions (patient H.M.), Parkinson's disease (PD) and Alzheimer's disease (AD). Subjects received 3 tests of nonverbal memory: forward block span, immediate and delayed recall of the Wechsler Memory Scale drawings, and immediate and delayed recognition of abstract designs. Compared with the normal control group, the patient groups displayed different patterns of sparing and loss of the two components of memory: in PD, only STM was impaired; in medial temporal lobe amnesia, only LTM was impaired; and in AD, STM and LTM were both impaired. The contrasting patterns of sparing and loss of STM and LTM in PD and global amnesia were present for both recognition and recall. These results provide evidence that STM and LTM are dissociable processes and are served by separate neurological systems: STM depends upon intact corticostriatal systems, whereas LTM depends upon intact medial temporal lobe systems. C1 MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. MIT, CLIN RES CTR, CAMBRIDGE, MA 02139 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR 00088]; NIMH NIH HHS [MH 2433, MH 32724] NR 74 TC 45 Z9 45 U1 6 U2 10 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0006-8950 J9 BRAIN JI Brain PD APR PY 1991 VL 114 BP 893 EP 906 DI 10.1093/brain/114.2.893 PN 2 PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FQ675 UT WOS:A1991FQ67500015 PM 2043956 ER PT J AU Lipton, SA AF Lipton, Stuart A. TI HIV-Related Neurotoxicity SO BRAIN PATHOLOGY LA English DT Article AB The central nervous system manifestations of AIDS were originally thought to consist solely of white matter lesions, but recent evidence has shown that a substantial degree of neuronal loss can also occur. This review presents evidence for HIV-related toxic factors that may account at least in part for this newly-recognized neuronal injury. One potential neurotoxin is the HIV-1 envelope glycoprotein gp120 or a fragment of this molecule. This coat protein is shed by the virus and potentially released from HN-infected immune cells. In tissue culture experiments on rodent neurons, gp120 produces an early rise in intracellular calcium concentration and, subsequently, delayed-onset neurotoxicity. In addition, HIV-infected macrophages or microglia release as yet undefined toxic factor(s) that kill rodent, chick, and human neurons in vitro. It is as yet unknown if one of these macrophage toxic factors might represent a gp120 fragment, or alternatively, if gp120, in the absence of HIV-1 infection, might be capable of activating macrophages to release these toxic factor(s). In at least some neuronal cell types, gp120-induced neurotoxicity can be prevented by antagonists of L-type voltage-dependent calcium channels or by antagonists of N-methyl-D-aspartate (NMDA, a subtype of glutamate receptor). Degradation of endogenous glutamate also protects neurons from gp120-related neuronal injury, suggesting that gp120 and glutamate are both necessary for neuronal cell death as synergistic effectors. Antagonists acting at the other types of glutamate receptors (non-NMDA antagonists) are ineffective in affording protection from gp120. Interestingly, NMDA, but not non-NMDA, antagonists also block the lethal effects of the macrophage toxic factor(s). The similar profile of pharmacological protection may possibly reflect the fact that at least one of the macrophage toxic factors is related to gp120, as suggested above. However, molecular-sieving and protease-digestion experiments suggest that the macrophage toxic factor(s) does not appear to be intact gp120, although a gp120 fragment remains a possibility. Alternatively, it is plausible that macrophages secrete several unrelated neurotoxic factors. Astrocytes may also be important in mediating HIV-related neurotoxicity. For example, in some neuronal cultures gp120-induced toxicity can be prevented by vasoactive intestinal polypeptide (VIP) or by a five amino acid substance with sequence homology, peptide T. VIP has been found to act on astrocytes to increase oscillations in intracellular calcium and to release factors necessary for normal neuronal outgrowth and survival. These results raise the possibility that gp120 may compete with endogenous VIP for a receptor, most likely on astrocytes, that is important for neuronal function. In summary, toxic factor(s) from HIV-infected human monocytoid cells may lead to neuronal damage in vitro. It is as yet unknown if these factors include a gp120 fragment or if gp120 may trigger the release of these neurotoxic factors. Based upon in vitro studies, calcium channel antagonists or NMDA antagonists may represent promising forms of pharmacological intervention to protect neurons from HIV-related injury. In the brains of AIDS patients, neuronal injury may be mediated by several separate pathways that most likely originate from toxins released by HIV-infected macrophages. Alternatively, there may be an intricate web of neurotoxic factors interacting with macrophages/microglia, astrocytes, and neurons; this complex may be amenable to pharmacotherapy because of common finalpathways of attack involving growth factors, NMDA receptors, and deleteriously high levels of intracellular calcium ions. C1 [Lipton, Stuart A.] Childrens Hosp, Lab Cellular & Mol Neurosci, Dept Neurol, Boston, MA 02115 USA. [Lipton, Stuart A.] Beth Israel Hosp, Boston, MA 02115 USA. [Lipton, Stuart A.] Brigham & Womens Hosp, Boston, MA 02115 USA. [Lipton, Stuart A.] Massachusetts Gen Hosp, Boston, MA 02115 USA. [Lipton, Stuart A.] Harvard Univ, Sch Med, Neurosci Program, Boston, MA 02115 USA. RP Lipton, SA (reprint author), Childrens Hosp, Lab Cellular & Mol Neurosci, Dept Neurol, Enders Bldg,Room 350, Boston, MA 02115 USA. FU NIH [EY05477, EY09024, NS07264]; American Foundation for AIDS Research (AmFAR) FX Work in the author's laboratory referred to in this article is supported by NIH grants EY05477, EY09024, and NS07264, and by the American Foundation for AIDS Research (AmFAR). The author is an established investigator of the American Heart Association. In performing these experiments and in developing the ideas described herein, the author gratefully acknowledges the intensive and insightful efforts of his co-workers, E. B. Dreyer, N.J. Sucher, P. K. Kaiser, J.T. Offermann, M. Oyola, V. H. S. Chen, S. Lei, J. Pelligrini and L. A. Wong. I thank D. Leifer for comments on the manuscript. NR 30 TC 102 Z9 102 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1015-6305 J9 BRAIN PATHOL JI Brain Pathol. PD APR PY 1991 VL 1 IS 3 BP 193 EP 199 DI 10.1111/j.1750-3639.1991.tb00659.x PG 7 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA V16GZ UT WOS:000207859400007 PM 1669708 ER PT J AU CANELLOS, GP AF CANELLOS, GP TI HAS THE MOPP ERA ENDED SO BRITISH JOURNAL OF CANCER LA English DT Editorial Material ID ADVANCED HODGKINS-DISEASE; COMBINATION CHEMOTHERAPY; CHLORAMBUCIL; PROCARBAZINE; VINBLASTINE; ABVD C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. RP CANELLOS, GP (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD APR PY 1991 VL 63 IS 4 BP 483 EP 483 DI 10.1038/bjc.1991.115 PG 1 WC Oncology SC Oncology GA FH596 UT WOS:A1991FH59600003 PM 2021529 ER PT J AU BAKER, AS HEMADY, R AF BAKER, AS HEMADY, R TI BACILLUS-INDUCED ENDOPHTHALMITIS SO BRITISH JOURNAL OF OPHTHALMOLOGY LA English DT Letter RP BAKER, AS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,243 CHARLES ST,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0007-1161 J9 BRIT J OPHTHALMOL JI Br. J. Ophthalmol. PD APR PY 1991 VL 75 IS 4 BP 255 EP 255 DI 10.1136/bjo.75.4.255 PG 1 WC Ophthalmology SC Ophthalmology GA FE471 UT WOS:A1991FE47100024 PM 2021602 ER PT J AU KALLINOWSKI, F BROWNELL, AL VAUPEL, P BROWNELL, GL AF KALLINOWSKI, F BROWNELL, AL VAUPEL, P BROWNELL, GL TI COMBINED TISSUE OXYGEN-TENSION MEASUREMENT AND POSITRON EMISSION TOMOGRAPHY STUDIES ON GLUCOSE-UTILIZATION IN ONCOGENE-TRANSFORMED CELL-LINE TUMOR XENOGRAFTS IN NUDE-MICE SO BRITISH JOURNAL OF RADIOLOGY LA English DT Article DE GLUCOSE UTILIZATION; POSITRON EMISSION TOMOGRAPHY; TISSUE OXYGENATION; ONCOGENE-TRANSFORMED TUMORS ID ENERGY-METABOLISM; BLOOD-FLOW; HEXOKINASE; MICROENVIRONMENT; BINDING; RAT AB Glucose utilization studies using high resolution positron emission tomography and tissue oxygenation measurements using microelectrode techniques were carried out in nude mice bearing oncogene-transformed (RatlpEJ6.6 and REFpneoMYCrasEpool) cell line tumours and a non-transformed (Ratl) cell line tumour to determine the correlation between glucose utilization, tissue oxygenation and tumour growth rate. Control measurements were performed in the subcutis of tumour-free animals. Accelerated growth rates were observed in both ras-transformed cell lines with tumour doubling times of 2.5-4 days while Ratl tumours had a doubling time of 28 days. Since rapid growth rates necessitate elevated consumption of oxygen and nutrients, severe tumour hypoxia was observed in tumours from both ras-transformed cell lines; median pO2 being 1-5 mmHg (tumour sizes ca. 400 mm3). Size-matched Ratl tumours exhibited a median pO2 value of 12 mmHg corresponding to the slow growth rate. Comparing both ras-transformed cell lines, RatlpEJ6.6 tumours had a more adequate vascularization than REFpneoMYCrasEpool tumours indicated by a better tissue oxygenation (5 mmHg versus 1 mmHg) and higher glucose metabolic rates (13.4 +/- 2.2-mu-mol/min/100 cm3 versus 9.7 +/- 1.3-mu-mol/min/100 cm3). At advanced growth stages, a reduction of tissue oxygen levels is obtained which is accompanied by a 30% elevation of glucose metabolic rate. The data presented here demonstrate for the first time an impact of well defined oncogenic alterations on the therapeutically relevant parameters of the micromilieu of malignant tumours. C1 UNIV HEIDELBERG,DEPT SURG,W-6900 HEIDELBERG,GERMANY. UNIV MAINZ,INST PHYSIOL & PATHOPHYSIOL,W-6500 MAINZ,GERMANY. RP KALLINOWSKI, F (reprint author), MASSACHUSETTS GEN HOSP,PHYS RES LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA32873] NR 31 TC 16 Z9 16 U1 0 U2 0 PU BRITISH INST RADIOLOGY PI LONDON PA 36 PORTLAND PLACE, LONDON, ENGLAND W1N 4AT SN 0007-1285 J9 BRIT J RADIOL JI Br. J. Radiol. PD APR PY 1991 VL 64 IS 760 BP 350 EP 359 PG 10 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH495 UT WOS:A1991FH49500012 PM 2025776 ER PT J AU BASTILLE, JD AF BASTILLE, JD TI HILL,BARBARA,M. 1924-1990 - OBITUARY SO BULLETIN OF THE MEDICAL LIBRARY ASSOCIATION LA English DT Item About an Individual RP BASTILLE, JD (reprint author), MASSACHUSETTS GEN HOSP,HLTH SCI LIB,BOSTON,MA 02114, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU MED LIBRARY ASSN PI CHICAGO PA SUITE 300 6 N MICHIGAN AVE, CHICAGO, IL 60602 SN 0025-7338 J9 B MED LIBR ASSOC JI Bull. Med. Libr. Assoc. PD APR PY 1991 VL 79 IS 2 BP 256 EP 257 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA FF428 UT WOS:A1991FF42800021 ER PT J AU MENON, AG PONDER, BAJ SEIZINGER, BR AF MENON, AG PONDER, BAJ SEIZINGER, BR TI THE NEUROFIBROMATOSIS GENES - FROM MOLECULAR-CLONING TO CELLULAR FUNCTION SO CANCER CELLS-A MONTHLY REVIEW LA English DT Article ID BILATERAL ACOUSTIC NEUROFIBROMATOSIS; VON RECKLINGHAUSEN NEUROFIBROMATOSIS; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; CHROMOSOME-17; 17Q11.2; REGION; TRANSLOCATION; LINKAGE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CAMBRIDGE,DEPT PATHOL,CANC RES CAMPAIGN,CAMBRIDGE CB2 1QP,ENGLAND. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. RP MENON, AG (reprint author), MASSACHUSETTS GEN HOSP,MOLEC GENET LAB,BOSTON,MA 02114, USA. NR 34 TC 7 Z9 7 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 APR PY 1991 VL 3 IS 4 BP 147 EP 152 PG 6 WC Oncology; Medicine, Research & Experimental SC Oncology; Research & Experimental Medicine GA FH975 UT WOS:A1991FH97500006 PM 1909154 ER PT J AU OBERLEY, TD GONZALEZ, A LAUCHNER, LJ OBERLEY, LW LI, JJ AF OBERLEY, TD GONZALEZ, A LAUCHNER, LJ OBERLEY, LW LI, JJ TI CHARACTERIZATION OF EARLY KIDNEY LESIONS IN ESTROGEN-INDUCED TUMORS IN THE SYRIAN-HAMSTER SO CANCER RESEARCH LA English DT Article ID SUPEROXIDE-DISMUTASE ACTIVITY; RENAL TUMOR; CARCINOGENESIS; TISSUES; CELL AB Syrian hamsters were treated with diethylstilbestrol (DES), a potent estrogen and kidney carcinogen, or ethinyl estradiol (EE), a strong estrogen but weak carcinogen, for 1-9 months. At monthly intervals their kidneys were studied using light, immunoperoxidase, and electron microscopic techniques. At 5 months, DES-treated animals exhibited interstitial lesions composed of small round cells with a high nuclear:cytoplasmic ratio. Immunoperoxidase and ultrastructural studies showed these cells to be similar to cells in fully formed tumors at 9 months. Early lesions in EE-treated animals (seen as early as 1 month) were dissimilar; these lesions appeared in the deep cortex adjacent to the renal pelvis, where proximal tubules underwent hyperplastic changes, showing columnar cells with large nuclei, occasional mitoses, and sloughing of apical cytoplasm. Cells in early lesions of EE-treated animals did not resemble the fully developed tumor in either immunoperoxidase or ultrastructural features; although with longer treatment these tubular lesions progressed to dysplasia (3-5 months) and severe dysplasia/carcinoma in situ (7 months), they did not form grossly visible tumors during the 9-month study. Both early lesions identified were specific, inasmuch as they were not observed in control animals and animals treated with beta-dienestrol and 17-alpha-estradiol (noncarcinogenic weak estrogens). Animals given a combination of DES and EE showed tubular hyperplasia but not interstitial lesions; this finding was of particular interest because hamsters given this combination of estrogens do not develop gross renal tumors. These results strongly implicate the primitive interstitial cell in the hamster kidney as the cell of origin of the DES-induced neoplasm. C1 UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53706. WASHINGTON STATE UNIV,COLL PHARM,HORMONAL CARCINOGENESIS LAB,PULLMAN,WA 99164. UNIV IOWA,COLL MED,RADIAT RES LAB,IOWA CITY,IA 52242. VET AFFAIRS MED CTR,PATHOL SERV,SALT LAKE CITY,UT 84121. RP OBERLEY, TD (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NCI NIH HHS [CA-22008, CA-41267] NR 24 TC 51 Z9 51 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1991 VL 51 IS 7 BP 1922 EP 1929 PG 8 WC Oncology SC Oncology GA FE041 UT WOS:A1991FE04100027 PM 2004377 ER PT J AU PALACIOS, IF TUZCU, EM ZISKIND, AA YOUNGER, J BLOCK, PC AF PALACIOS, IF TUZCU, EM ZISKIND, AA YOUNGER, J BLOCK, PC TI PERCUTANEOUS BALLOON PERICARDIAL WINDOW FOR PATIENTS WITH MALIGNANT PERICARDIAL-EFFUSION AND TAMPONADE SO CATHETERIZATION AND CARDIOVASCULAR DIAGNOSIS LA English DT Article DE PERCUTANEOUS PERICARDIAL WINDOW; PERICARDIAL FLUID; PIGTAIL CATHETER; PERICARDIAL TAMPONADE AB We performed percutaneous balloon pericardial window (PBPW) in 8 patients (age 40 to 70 yrs; 4 men, 4 women) with malignant pericardial effusion and tamponade. Pericardial window was indicated because they continued to drain > 100 ml/day of pericardial fluid through the pigtail catheter for greater-than-or-equal-to 3 days. A 0.038 inch guidewire was advanced through the pigtail catheter into the pericardial space and then the catheter was removed. A 20 mm diameter, 3 cm long balloon dilating catheter was advanced to straddle the parietal pericardium. Manual inflations were performed until the waist produced by the pericardium disappeared. All patients tolerated the procedure well with minimal discomfort and with no complications. A left or bilateral pleural effusion occurred in all patients after PBPW. No patient developed recurrent pericardial tamponade at a mean follow-up of 6 +/- 2 months. Thus, PBPW is a useful and safe technique to avoid surgery in patients with malignant pericardial effusion and tamponade. RP PALACIOS, IF (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 11 TC 60 Z9 62 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 0098-6569 J9 CATHETER CARDIO DIAG JI Catheter. Cardiovasc. Diagn. PD APR PY 1991 VL 22 IS 4 BP 244 EP 249 DI 10.1002/ccd.1810220403 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FD206 UT WOS:A1991FD20600002 PM 2032271 ER PT J AU BERTAGNOLLI, MM TAKAI, Y HERRMANN, SH AF BERTAGNOLLI, MM TAKAI, Y HERRMANN, SH TI IL-4-SUPPORTED INDUCTION OF CYTOLYTIC LYMPHOCYTES-T REQUIRES IL-2 AND IL-6 SO CELLULAR IMMUNOLOGY LA English DT Article ID CELL-STIMULATORY FACTOR; CYTO-TOXIC LYMPHOCYTES; FACTOR-I INTERLEUKIN-4; PLASMACYTOMA GROWTH-FACTOR; TUMOR NECROSIS FACTOR; PROMOTES GROWTH; DIFFERENTIATION; PROLIFERATION; THYMOCYTES; INVITRO C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP BERTAGNOLLI, MM (reprint author), BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 47831, 2T32CA0935-05] NR 43 TC 11 Z9 12 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 APR 1 PY 1991 VL 133 IS 2 BP 327 EP 341 DI 10.1016/0008-8749(91)90108-N PG 15 WC Cell Biology; Immunology SC Cell Biology; Immunology GA FA011 UT WOS:A1991FA01100006 PM 1901767 ER PT J AU ISHIBASHI, M TAMAKI, N YASUDA, T TAKI, J STRAUSS, HW AF ISHIBASHI, M TAMAKI, N YASUDA, T TAKI, J STRAUSS, HW TI ASSESSMENT OF VENTRICULAR-FUNCTION WITH AN AMBULATORY LEFT-VENTRICULAR FUNCTION MONITOR SO CIRCULATION LA English DT Article; Proceedings Paper CT SYMP ON MENTAL STRESS AS A TRIGGER OF CARDIOVASCULAR EVENTS CY OCT, 1989 CL VERUNO, ITALY SP CLIN LAVORO FDN PAVIA, BOEHRINGER INGELHEIM DE VENTRICULAR FUNCTION; STRESS; TESTING ID CORONARY-ARTERY DISEASE; SILENT MYOCARDIAL ISCHEMIA; EJECTION FRACTION; CARDIAC RESPONSE; MENTAL STRESS; EXERCISE AB Changes in ventricular function caused by activities of daily living, including standing, walking, stair climbing, and mental stress, were evaluated using a radionuclide device that recorded left ventricular function on a beat-by-beat basis. The ambulatory monitor was positioned over the patient's left ventricle after a gated blood pool scan. Monitoring revealed a 10% increase of left ventricular ejection fraction from baseline to brisk walking, an 18% increase during stair climbing, and a 6% increase with mental stress. In some subjects, however, the increase in ejection fraction during mental stress exceeded that during exercise. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. RI Yasuda, Kazunori/D-4156-2012 NR 19 TC 5 Z9 5 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 APR PY 1991 VL 83 IS 4 SU S BP 166 EP 172 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FH047 UT WOS:A1991FH04700021 ER PT J AU SANFILIPPO, AJ WEYMAN, AE AF SANFILIPPO, AJ WEYMAN, AE TI ATRIAL ENLARGEMENT AS A CONSEQUENCE OF ATRIAL-FIBRILLATION - REPLY SO CIRCULATION LA English DT Letter C1 MASSACHUSETTS GEN HOSP,DEPT CARDIOL,ECHOCARDIOG LAB,BOSTON,MA 02114. RP SANFILIPPO, AJ (reprint author), QUEENS UNIV,DEPT MED,KINGSTON K7L 3N6,ONTARIO,CANADA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1991 VL 83 IS 4 BP 1458 EP 1458 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FF419 UT WOS:A1991FF41900035 ER PT J AU SCHNEYER, AL SLUSS, PM WHITCOMB, RW HALL, JE CROWLEY, WF FREEMAN, RG AF SCHNEYER, AL SLUSS, PM WHITCOMB, RW HALL, JE CROWLEY, WF FREEMAN, RG TI DEVELOPMENT OF A RADIOLIGAND RECEPTOR ASSAY FOR MEASURING FOLLITROPIN IN SERUM - APPLICATION TO PREMATURE OVARIAN FAILURE SO CLINICAL CHEMISTRY LA English DT Article DE PITUITARY HORMONES; MENSTRUAL CYCLE; RADIOIMMUNOASSAY COMPARED; COMPETITORS FOR RECEPTOR BINDING ID FOLLICLE-STIMULATING-HORMONE; CELL AROMATASE BIOASSAY; GROWTH-FACTORS; FSH; SECRETION; REGULATORS; INHIBITION; AMENORRHEA; BINDING; INVITRO AB We have developed a radioligand receptor assay (RRA) with sufficient sensitivity and specificity for quantifying follitropin (FSH) in unextracted serum samples. Standard curves prepared by adding pituitary FSH to either buffer or gonadotropin-free serum were parallel and statistically indistinguishable in this assay, whereas gonadotropinfree serum alone had no activity. Cross-reactivity with related pituitary hormones was negligible. Pituitary FSH was calibrated with commonly used reference preparations so that RRA results could be compared with RIA results for identical standards. The patterns in daily blood samples in six normal menstrual cycles were similar by both methods. The mean RIA:RIA ratio in both the follicular and luteal phases was between 0.6 and 0.7, and at mid-cycle decreased to 0.48, suggesting an alteration of isohormone composition at mid-cycle. In 27 women with premature ovarian failure, RRA:RIA ratios ranged from below the RRA minimum detectable dose to 4.6, suggesting that immunoreactive FSH might not be capable of binding to the FSH receptor in some patients, whereas in patients with high RRA:RIA ratios, circulating inhibitors of FSH receptor binding might be present and perhaps contributing to the observed ovarian failure. Use of this RRA in conjunction with RIA and in vitro bioassays may better define the relative contribution of FSH isohormones, autocrine or paracrine modulators of FSH bioactivity, and FSH-receptor binding competitors to the "total FSH biological signal" as detected by the gonadal FSH receptor. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT OBSTET & GYNECOL,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. UNIV ROCHESTER,MED CTR,DEPT UROL,ROCHESTER,NY 14642. RP SCHNEYER, AL (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD-15080, HD-15788, HD-25941] NR 35 TC 11 Z9 11 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1991 VL 37 IS 4 BP 508 EP 514 PG 7 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FH316 UT WOS:A1991FH31600008 PM 1901773 ER PT J AU VARGA, L ALPER, CA ZAM, Z FUST, G AF VARGA, L ALPER, CA ZAM, Z FUST, G TI DECREASED INHIBITION OF IMMUNE PRECIPITATION BY SERA WITH THE C2-B ALLOTYPE SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID INHERITED STRUCTURAL POLYMORPHISM; COMPLEMENT-MEDIATED INHIBITION; 4TH COMPONENT; C-4 C1 CTR BLOOD RES,BOSTON,MA 02115. NATL INST HAEMATOL & BLOOD TRANSFUS,BUDAPEST,HUNGARY. RI Varga, Lilian/F-2491-2010 FU NIAID NIH HHS [AI 14157] NR 19 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 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD APR PY 1991 VL 59 IS 1 BP 65 EP 71 DI 10.1016/0090-1229(91)90082-L PG 7 WC Immunology; Pathology SC Immunology; Pathology GA FB565 UT WOS:A1991FB56500006 PM 2019011 ER PT J AU RUOFF, KL AF RUOFF, KL TI NUTRITIONALLY VARIANT STREPTOCOCCI SO CLINICAL MICROBIOLOGY REVIEWS LA English DT Article AB Streptococci requiring either pyridoxal or L-cysteine for growth were first observed 30 years ago as organisms forming satellite colonies adjacent to colonies of "helper" bacteria. Although they were previously considered nutritional mutants of viridans streptococcal species, the nutritionally variant streptococci (NVS) are currently thought to belong to distinct species of the genus Streptococcus. NVS strains may display pleomorphic cellular morphologies, depending on their growth conditions, and are distinguished from most other streptococci by enzymatic and serological characteristics and the presence of a cell wall chromophore. NVS are found as normal inhabitants of the oral cavity, and in addition to their participation in endocarditis, they have been isolated from a wide range of clinical specimens. Endocarditis caused by NVS is often difficult to eradicate; combinations of penicillin and an aminoglycoside are recommended for treatment. The unique physiological features of the NVS contribute to the difficulties encountered in their recovery from clinical specimens and may play a role in the problems associated with successful treatment of NVS endocarditis. RP RUOFF, KL (reprint author), MASSACHUSETTS GEN HOSP,FRANCIS BLAKE BACTERIOL LABS,BOSTON,MA 02114, USA. NR 0 TC 103 Z9 108 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0893-8512 J9 CLIN MICROBIOL REV JI Clin. Microbiol. Rev. PD APR PY 1991 VL 4 IS 2 BP 184 EP 190 PG 7 WC Microbiology SC Microbiology GA FG203 UT WOS:A1991FG20300005 PM 2070344 ER PT J AU ABOUSAMRA, AB JUEPPNER, H FREEMAN, MW KONG, X SCHIPANI, E RICHARDS, J HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV AF ABOUSAMRA, AB JUEPPNER, H FREEMAN, MW KONG, X SCHIPANI, E RICHARDS, J HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV TI EXPRESSION CLONING OF THE PARATHYROID-HORMONE (PTH) BONE RECEPTOR CDNA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. TUPTS DENT SCH,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A342 EP A342 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301134 ER PT J AU ALCANTARA, O SUNVISON, R BOLDT, DH AF ALCANTARA, O SUNVISON, R BOLDT, DH TI DIFFERENTIAL REGULATION OF PROTEIN-KINASE-C ISOFORMS BY IRON IN HEMATOPOIETIC-CELL LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A269 EP A269 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300743 ER PT J AU BALLANTYNE, J DEAR, K CARR, D JACOX, A MALVENHOLZ, D CHALMERS, T AF BALLANTYNE, J DEAR, K CARR, D JACOX, A MALVENHOLZ, D CHALMERS, T TI MANAGEMENT OF POSTOPERATIVE PAIN - METAANALYSIS OF RANDOMIZED CONTROL TRIALS OF PATIENT CONTROLLED ANALGESIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,VET ADM HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA 02114. JOHNS HOPKINS UNIV,BALTIMORE,MD 21218. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A459 EP A459 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301814 ER PT J AU BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G DIEHL, AK AF BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G DIEHL, AK TI AMBULATORY CARE IN THE 3RD YEAR CLERKSHIP - EFFECT ON CAREER CHOICE - A RANDOMIZED TRIAL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A614 EP A614 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302723 ER PT J AU BAUER, RL AF BAUER, RL TI CHARACTERISTICS OF FALLS AND FALLERS - AGE-RELATED-CHANGES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A409 EP A409 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301516 ER PT J AU BIERER, MF GIOANNETTI, CM JUTRAS, SA AF BIERER, MF GIOANNETTI, CM JUTRAS, SA TI THE USE OF EMERGENCY SERVICES BY HOMELESS PEOPLE AT AN ACADEMIC TEACHING HOSPITAL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A597 EP A597 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302619 ER PT J AU CARSON, MR LIND, SE SHASBY, DM AF CARSON, MR LIND, SE SHASBY, DM TI HISTAMINE DECREASES ACTIN GELSOLIN BINDING IN HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV IOWA,IOWA CITY,IA 52242. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A219 EP A219 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300447 ER PT J AU CHATILA, T MOODY, C FINBERG, R HAMMELL, C GEHA, RS AF CHATILA, T MOODY, C FINBERG, R HAMMELL, C GEHA, RS TI IMMUNODEFICIENCY WITH DEFECTIVE MATURATION OF NATURAL-KILLER (NK) CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02115. CHILDRENS HOSP,DIV IMMUNOL,LOS ANGELES,CA 90027. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RI Finberg, Robert/E-3323-2010 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A212 EP A212 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300409 ER PT J AU CHATZIPANTELI, K RUDOLPH, S AXELROD, L AF CHATZIPANTELI, K RUDOLPH, S AXELROD, L TI COORDINATE CONTROL OF LIPOLYSIS BY PROSTAGLANDIN-E2 AND PROSTACYCLIN IN RAT ADIPOSE-TISSUE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A277 EP A277 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300794 ER PT J AU COLES, NA HIBBERD, M RUSSELL, M LOVE, T ORY, D FIELD, T EAGLE, R AF COLES, NA HIBBERD, M RUSSELL, M LOVE, T ORY, D FIELD, T EAGLE, R TI POTENTIAL IMPACT OF PA LINE PLACEMENT ON SHORT-TERM MANAGEMENT CHANGES IN THE MEDICAL ICU SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A421 EP A421 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301589 ER PT J AU DEWOOD, MA YOUNG, C KAPSCH, S JESBERGE, A SHORT, R SHIELDS, P SHELL, WE AF DEWOOD, MA YOUNG, C KAPSCH, S JESBERGE, A SHORT, R SHIELDS, P SHELL, WE TI CARDIAC NMR AND ULTRA FAST CT IN THE DETERMINATION OF CARDIAC VOLUMES - A COMPARATIVE-STUDY USING PHANTOM HEART MODELS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 DEACONESS MED CTR,SPOKANE,WA. SPOKANE CARDIOL,SPOKANE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A233 EP A233 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300531 ER PT J AU ETOH, T BYERS, HR AF ETOH, T BYERS, HR TI LOCALIZATION AND EXPRESSION OF ALPHA-ACTININ IN CULTURED HUMAN PRIMARY, RECURRENT PRIMARY AND METASTATIC MELANOMA CELL-LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A561 EP A561 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302407 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI FUNCTIONAL RECEPTORS FOR GLUCAGONLIKE PEPTIDE-1(7-37) ON SOMATOSTATIN AND INSULIN SECRETING CELL-LINES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. HOWARD HUGHES MED INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A154 EP A154 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300077 ER PT J AU FINE, MJ HANUSA, BH SINGER, DE LAVE, JR KAPOOR, WN AF FINE, MJ HANUSA, BH SINGER, DE LAVE, JR KAPOOR, WN TI VALIDATION OF A PNEUMONIA MORTALITY RISK INDEX USING THE MEDISGROUPS COMPARATIVE HOSPITAL DATABASE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV PITTSBURGH,PITTSBURGH,PA 15260. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A574 EP A574 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302484 ER PT J AU FINKELSTEIN, J NEER, R BILLER, B CRAWFORD, J KLIBANSKI, A AF FINKELSTEIN, J NEER, R BILLER, B CRAWFORD, J KLIBANSKI, A TI PUBERTAL DELAY IS ASSOCIATED WITH OSTEOPENIA IN ADULT MEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301744 ER PT J AU FUKUDA, M HORIO, F RITTERHAUS, C KATO, H HATTORI, M AF FUKUDA, M HORIO, F RITTERHAUS, C KATO, H HATTORI, M TI MHC CLASS-II I-A RESTRICTION OF FREE-RADICAL OXYGEN PRODUCTION IN ISLET BETA-CELLS BY PERITONEAL-EXUDATE CELLS OF THE DIABETIC NOD MOUSE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOSLIN DIABETES CTR,BOSTON,MA. CENT INST EXPTL ANIM,KAWASAKI,JAPAN. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A246 EP A246 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300608 ER PT J AU GOLDFINE, A MAGRE, J GOLDSTEIN, BJ KROLEWSKI, AS KAHN, CR AF GOLDFINE, A MAGRE, J GOLDSTEIN, BJ KROLEWSKI, AS KAHN, CR TI DENATURING GRADIENT GEL-ELECTROPHORESIS OF GLUCOSE TRANSPORTER AND INSULIN-RECEPTOR GENES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. RI MAGRE, Jocelyne/D-4788-2015 NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A383 EP A383 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301365 ER PT J AU GRABBE, S BRUVERS, S LINDGREN, AM GRANSTEIN, RD AF GRABBE, S BRUVERS, S LINDGREN, AM GRANSTEIN, RD TI REGULATION OF EPIDERMAL-CELL TUMOR-ANTIGEN PRESENTATION BY TNF-ALPHA GM-CSF AND ULTRAVIOLET-RADIATION SO CLINICAL RESEARCH 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A532 EP A532 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302236 ER PT J AU HAFFNER, SM BAUER, RL AF HAFFNER, SM BAUER, RL TI RELATIONSHIP OF FASTING INSULIN TO BONE-DENSITY IN NONDIABETIC WOMEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301746 ER PT J AU HILKERT, RJ LEE, ME BLOCH, KD YUN, JS WAGNER, TE QUERTERMOUS, T AF HILKERT, RJ LEE, ME BLOCH, KD YUN, JS WAGNER, TE QUERTERMOUS, T TI EXPRESSION OF ENDOTHELIN-1 (ET-1) REPORTER CONSTRUCTS IN TRANSGENIC MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A224 EP A224 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300475 ER PT J AU HOLLENBERG, A KLIBANSKI, A NEER, R CRAWFORD, J FINKELSTEIN, J AF HOLLENBERG, A KLIBANSKI, A NEER, R CRAWFORD, J FINKELSTEIN, J TI PUBERTAL DELAY IS ASSOCIATED WITH DECREASED ADULT HEIGHT IN MEN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A166 EP A166 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300148 ER PT J AU HORVATH, K GRANSTEIN, RD AF HORVATH, K GRANSTEIN, RD TI EXPOSURE TO PSORALEN PLUS LONGWAVE ULTRAVIOLET-RADIATION POTENTIATES CYCLOSPORINE-MEDIATED PROLONGATION OF RAT CARDIAC ALLOGRAFT SURVIVAL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MGH HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A546 EP A546 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302317 ER PT J AU HUSAIN, Z CHOW, MP WICK, MM AF HUSAIN, Z CHOW, MP WICK, MM TI CORRELATION BETWEEN INVIVO AND INVITRO MODELS FOR THE ROLE OF EGFR ACTIVATION IN EPIDERMAL NEOPLASIA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A482 EP A482 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301936 ER PT J AU KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM AF KAELIN, WG PALLAS, DC DECAPRIO, JA KAYE, FJ LIVINGSTON, DM TI CELLULAR PROTEINS THAT INTERACT SPECIFICALLY WITH THE RETINOBLASTOMA GENE-PRODUCT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NCI,BETHESDA,MD 20892. RI kaye, frederic/E-2437-2011 NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A339 EP A339 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301117 ER PT J AU KANG, S BARNHILL, RL MIHM, MC DUNCAN, LM SOBER, AJ AF KANG, S BARNHILL, RL MIHM, MC DUNCAN, LM SOBER, AJ TI MELANOMA RISK IS INCREASED IN PATIENTS WITH ATYPICAL NEVI EVEN WITH CLOSE FOLLOW-UPS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL & PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A506 EP A506 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302078 ER PT J AU KOKA, P CHOI, SY VANDEMARK, K FALLER, DV AF KOKA, P CHOI, SY VANDEMARK, K FALLER, DV TI TRANSACTIVATION OF GENES ENCODING HUMAN T-LYMPHOCYTE CELL-SURFACE ACTIVATION PROTEINS BY RETROVIRAL SEQUENCES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A341 EP A341 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301131 ER PT J AU KOLLIAS, N YOUN, J GANGE, R ANDERSON, RR AF KOLLIAS, N YOUN, J GANGE, R ANDERSON, RR TI SUPPRESSION OF THE ERYTHEMA REACTION TO UVB BY A 2ND EXPOSURE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114. SEOUL NATL UNIV,DEPT DERMATOL,SEOUL 151,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A546 EP A546 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302322 ER PT J AU KOUREMBANAS, S MARSDEN, P MCQUILLAN, LP FALLER, DV AF KOUREMBANAS, S MARSDEN, P MCQUILLAN, LP FALLER, DV TI MOLECULAR MECHANISMS BY WHICH ENDOTHELIAL-CELLS CONTROL VASCULAR TONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A317 EP A317 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301002 ER PT J AU LERNER, EA AF LERNER, EA TI MAXADILAN, A NOVEL POTENT VASODILATORY PEPTIDE FROM THE SAND FLY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A322 EP A322 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301028 ER PT J AU LIAO, JK HOMCY, CJ AF LIAO, JK HOMCY, CJ TI DISTINCT-GI PROTEIN ISOFORMS MEDIATE THE RELEASE OF ENDOTHELIUM-DERIVED RELAXING FACTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A147 EP A147 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300032 ER PT J AU LIN, HYF HARRIS, TL FLANNERY, MS ARUFFO, A KAJI, EH GORN, AH LODISH, HF GOLDRING, SR AF LIN, HYF HARRIS, TL FLANNERY, MS ARUFFO, A KAJI, EH GORN, AH LODISH, HF GOLDRING, SR TI EXPRESSION CLONING OF THE RENAL CALCITONIN RECEPTOR SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A330 EP A330 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301071 ER PT J AU LOVE, TW RUNGE, MS MATSUEDA, GR MICHELSON, KD QUERTERMOUS, T HABER, E AF LOVE, TW RUNGE, MS MATSUEDA, GR MICHELSON, KD QUERTERMOUS, T HABER, E TI STRUCTURE-FUNCTION COMPARISON OF 3 ANTIFIBRIN ANTIBODY-TPA RECOMBINANT PROTEINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A198 EP A198 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300333 ER PT J AU MANGIONE, CM PHILLIPS, RS GILBERT, MM SEDDON, J COOK, EF GOLDMAN, L AF MANGIONE, CM PHILLIPS, RS GILBERT, MM SEDDON, J COOK, EF GOLDMAN, L TI CHANGE IN VISUAL FUNCTIONAL STATUS FOLLOWING CATARACT-EXTRACTION AND INTRAOCULAR-LENS IMPLANTATION IN ELDERLY ADULTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A604 EP A604 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302664 ER PT J AU MANGIONE, CM PHILLIPS, RS SEDDON, J COOK, EF GOLDMAN, L AF MANGIONE, CM PHILLIPS, RS SEDDON, J COOK, EF GOLDMAN, L TI DEVELOPMENT OF THE ACTIVITIES OF DAILY VISION SCALE TO ASSESS VISUAL FUNCTION IN PATIENTS UNDERGOING CATARACT-SURGERY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 1 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A188 EP A188 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300278 ER PT J AU MAYTIN, EV MENARD, S WIMBERLY, JM AF MAYTIN, EV MENARD, S WIMBERLY, JM TI STRESS PROTEINS IN MOUSE KERATINOCYTES - ALTERED PATTERNS OF SYNTHESIS AFTER HEAT-SHOCK OR UVB LIGHT (290-320 NM) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A566 EP A566 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302438 ER PT J AU MCCORMICK, ML OBERLEY, LW OBERLEY, TD CIHLA, HP BRITIGAN, BE AF MCCORMICK, ML OBERLEY, LW OBERLEY, TD CIHLA, HP BRITIGAN, BE TI ASSOCIATION OF MANGANESE SUPEROXIDE-DISMUTASE WITH THE PLASMA-MEMBRANE OF HUMAN NEUTROPHILS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT MED,IOWA CITY,IA 52240. VET ADM MED CTR,DEPT RADIOL,IOWA CITY,IA 52240. UNIV WISCONSIN,MADISON,WI 53706. VET ADM MED CTR,RES SERV,IOWA CITY,IA 52240. UNIV IOWA,COLL MED,IOWA CITY,IA 52242. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT ANESTHESIOL,MADISON,WI. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A353 EP A353 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301191 ER PT J AU MORAN, M GANGE, RW LYON, N SIEBERT, B KOCHEVAR, IE AF MORAN, M GANGE, RW LYON, N SIEBERT, B KOCHEVAR, IE TI EFFECTS OF SYSTEMIC INDOMETHACIN, BW755C, AND MECLIZINE ON CHRONIC UVB-INDUCED EFFECTS IN HAIRLESS MOUSE SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A548 EP A548 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302330 ER PT J AU MORT, EA GUADAGNOLI, E SCHROEDER, SA GREENFIELD, S MULLEY, AG MCNEIL, BJ AF MORT, EA GUADAGNOLI, E SCHROEDER, SA GREENFIELD, S MULLEY, AG MCNEIL, BJ TI THE INFLUENCE OF AGE ON CLINICAL AND PATIENT REPORTED OUTCOMES AFTER CHOLECYSTECTOMY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,NEW ENGLAND MED CTR,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A605 EP A605 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302671 ER PT J AU MOTOKURA, T KIM, HG KRONENBERG, HM ARNOLD, A AF MOTOKURA, T KIM, HG KRONENBERG, HM ARNOLD, A TI A NEW CANDIDATE ONCOGENE, REARRANGED IN PARATHYROID ADENOMAS AND LINKED TO BCL1, ENCODES A PROTEIN RELATED TO THE CYCLIN FAMILY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A339 EP A339 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301122 ER PT J AU MUCCINI, J KOLLIAS, N PHILLIPS, S ANDERSON, R SOBER, A DRAKE, L AF MUCCINI, J KOLLIAS, N PHILLIPS, S ANDERSON, R SOBER, A DRAKE, L TI ASSESSABLE PHOTOGRAPHIC RECORDS OF THE CLINICAL-FEATURES ASSOCIATED WITH PHOTOAGING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST CLIN,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A508 EP A508 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302090 ER PT J AU MULROW, CD TULEY, MR AGUILAR, C AF MULROW, CD TULEY, MR AGUILAR, C TI SUSTAINED BENEFITS OF HEARING-AIDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,AMBULATORY CARE & GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A593 EP A593 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302597 ER PT J AU PIKE, MC COSTELLO, K AF PIKE, MC COSTELLO, K TI INTERLEUKIN-8 (IL-8) ACTIVATES PHOSPHATIDYLINOSITOL-4-PHOSPHATE (PIP) KINASE IN HUMAN POLYMORPHONUCLEAR LEUKOCYTES (PMN) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A291 EP A291 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300867 ER PT J AU RABINOWE, SL MYEROV, A BROWN, F AF RABINOWE, SL MYEROV, A BROWN, F TI ANTIGANGLIOSIDE GT1B IGG ANTIBODIES IN TYPE-I DIABETES - ORTHOSTATIC BLOOD-PRESSURE AND AUTONOMIC AUTOANTIBODIES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A364 EP A364 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301254 ER PT J AU REED, GL MATSUEDA, GR HABER, E AF REED, GL MATSUEDA, GR HABER, E TI ACCELERATED FIBRIN-FIBRIN AND ALPHA-2-ANTIPLASMIN CROSS-LINKING BY PLATELET FACTOR-XIII ENHANCES THE FIBRINOLYTIC RESISTANCE OF PLATELET CLOTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 PRINCETON UNIV,PRINCETON,NJ 08544. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A198 EP A198 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300332 ER PT J AU ROSENBERG, CL WONG, E BALE, A TSUJIMOTO, Y HARRIS, NL ARNOLD, A AF ROSENBERG, CL WONG, E BALE, A TSUJIMOTO, Y HARRIS, NL ARNOLD, A TI OVEREXPRESSION OF D11S287E, A CANDIDATE BCL1 REGION ONCOGENE IN CENTROCYTIC LYMPHOMAS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. WISTAR INST,PHILADELPHIA,PA 19104. NR 0 TC 1 Z9 1 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A339 EP A339 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301121 ER PT J AU SAMET, JH CRAVEN, DE LIBMAN, H CHEN, J SHEVITZ, AH STEGER, K DEWEESDUNK, B LEVENSON, S DHAWAN, RK KUFE, D AF SAMET, JH CRAVEN, DE LIBMAN, H CHEN, J SHEVITZ, AH STEGER, K DEWEESDUNK, B LEVENSON, S DHAWAN, RK KUFE, D TI COMPLIANCE WITH ZIDOVUDINE THERAPY IN PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS, TYPE-1 - A CROSS-SECTIONAL STUDY IN A MUNICIPAL HOSPITAL CLINIC SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BOSTON CITY HOSP,BOSTON,MA 02118. BOSTON UNIV,SCH MED,BOSTON,MA 02118. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A161 EP A161 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300118 ER PT J AU SCHEURICH, JW WRAY, NP AF SCHEURICH, JW WRAY, NP TI SUBJECTIVE ASSESSMENT OF ILLNESS SEVERITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BAYLOR UNIV,HOUSTON VET ADM MED CTR,GEN MED SECT,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A608 EP A608 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302688 ER PT J AU SILVERMAN, LB SANCHO, J CASTIGLI, E TERHORST, C GEHA, RS CHATILA, TA AF SILVERMAN, LB SANCHO, J CASTIGLI, E TERHORST, C GEHA, RS CHATILA, TA TI DEVELOPMENTAL REGULATION OF TRANSMEMBRANE SIGNALING VIA TCR/CD3 IN HUMAN T-LYMPHOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RI Sancho, Jaime/O-3228-2013 OI Sancho, Jaime/0000-0003-3852-7951 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A155 EP A155 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300080 ER PT J AU SOIFFER, R MURRAY, C RITZ, J AF SOIFFER, R MURRAY, C RITZ, J TI CLINICAL AND IMMUNOLOGICAL EFFECTS OF CONTINUOUS INFUSION INTERLEUKIN-2 AFTER ALLOGENEIC AND AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO CLINICAL RESEARCH 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A431 EP A431 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301651 ER PT J AU THOMAS, L ETOH, T MIHM, MC BYERS, HR AF THOMAS, L ETOH, T MIHM, MC BYERS, HR TI ATTACHMENT STUDIES OF HUMAN PRIMARY, RECURRENT CUTANEOUS AND METASTATIC MELANOMA ON HYALURONIC-ACID COATED SUBSTRATES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A569 EP A569 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32302455 ER PT J AU URAKAZE, M SUGIYAMA, E XU, L AURON, P YEH, E ROBINSON, D AF URAKAZE, M SUGIYAMA, E XU, L AURON, P YEH, E ROBINSON, D TI DIETARY MARINE LIPIDS SUPPRESS IL-1-BETA MESSENGER-RNA LEVELS IN LIPOPOLYSACCHARIDE STIMULATED MONOCYTES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MED SERV,ARTHRITIS UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A182 EP A182 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300241 ER PT J AU VATNER, DE KIUCHI, K UEMURA, N MANDERS, WT CHEN, L HOMCY, CJ VATNER, SF AF VATNER, DE KIUCHI, K UEMURA, N MANDERS, WT CHEN, L HOMCY, CJ VATNER, SF TI INDEPENDENT MECHANISMS OF UNCOUPLING OF THE BETA-ADRENERGIC-RECEPTOR AND DECREASE IN GS IN CORONARY REPERFUSION AND ISOPROTERENOL DESENSITIZATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. NR 0 TC 0 Z9 0 U1 0 U2 4 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A154 EP A154 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300076 ER PT J AU WU, YJ THORENS, B LEAHY, JL LODISH, HF WEIR, GC AF WU, YJ THORENS, B LEAHY, JL LODISH, HF WEIR, GC TI INCREASED BASAL AND NORMAL GLUCOSE-POTENTIATED ARGININE-INDUCED INSULIN-SECRETION IN THE PRESENCE OF REDUCED GLUT-2 EXPRESSION IN THE DB/DB MOUSE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOSLIN DIABETES CTR,WHITEHEAD INST,BOSTON,MA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A307 EP A307 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32300950 ER PT J AU ZUSMAN, RM HIGGINS, J CHRISTENSEN, D BOUCHER, CA AF ZUSMAN, RM HIGGINS, J CHRISTENSEN, D BOUCHER, CA TI BEPRIDIL IMPROVES LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC PERFORMANCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1991 VL 39 IS 2 BP A408 EP A408 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FH323 UT WOS:A1991FH32301512 ER PT J AU WATERS, G CAPLAN, D HILDEBRANDT, N AF WATERS, G CAPLAN, D HILDEBRANDT, N TI ON THE STRUCTURE OF VERBAL SHORT-TERM-MEMORY AND ITS FUNCTIONAL-ROLE IN SENTENCE COMPREHENSION - EVIDENCE FROM NEUROPSYCHOLOGY SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID STORE; SPEECH AB We present a case of a patient with a disorder of short-term memory. BO has a reduced span (2 to 3 items), no recency effect in free recall, and rapid forgetting in Brown-Peterson tasks, establishing her as a patient with impaired short-term verbal memory functions. She shows no effect of either phonological similarity or word length in recall of auditory or written word lists, but some recency effect under recall-from-end conditions and better performance on Brown-Peterson tasks in an unfilled than in a filled condition. This pattern of performance is interpreted as being consistent with a primary disturbance of the articulatory rehearsal processes of S.T.M. and possibly some impairment of the phonological store (using Baddeley's 1986 terminology). Her aphasic disturbance - apraxia of speech - is also consistent with a disturbance of articulatory rehearsal. BO shows a retained ability to extract phonology from print, including an ability to apply sublexical grapheme-phoneme correspondences, thus indicating that the rehearsal and transcoding functions associated with articulatory mechanisms are dissociable. Her improved performance on unfilled delays in Brown-Peterson testing, as well as her overt attempts to rehearse in this condition, also establishes a dissociation between rehearsal in span and in delayed recall tasks. BO shows excellent comprehension of a wide variety of syntactic structures with auditory, written, and speeded written presentations, indicating that articulatory rehearsal is not needed for the assignment of syntactic structure and its utilisation to establish aspects of propositional semantics (thematic roles and co-indexation of noun phrases). BO makes errors referable to the maintenance of particular items in propositional memory systems, consistent with the view that the role of articulatory rehearsal mechanisms in sentence comprehension involves maintenance of items in an interpreted (semantic) structure. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROPSYCHOL LAB,BOSTON,MA 02114. RP WATERS, G (reprint author), MCGILL UNIV,SCH HUMAN COMMUN DISORDERS,BEATTY HALL,1266 PINE AVE W,MONTREAL H36 1A8,QUEBEC,CANADA. NR 55 TC 67 Z9 68 U1 1 U2 2 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0264-3294 J9 COGNITIVE NEUROPSYCH JI Cogn. Neuropsychol. PD APR PY 1991 VL 8 IS 2 BP 81 EP 126 DI 10.1080/02643299108253368 PG 46 WC Psychology; Psychology, Experimental SC Psychology GA FG462 UT WOS:A1991FG46200001 ER PT J AU JOHNSON, M CHEN, A EPSTEIN, DL KAMM, RD AF JOHNSON, M CHEN, A EPSTEIN, DL KAMM, RD TI THE PRESSURE AND VOLUME DEPENDENCE OF THE RATE OF WASH-OUT IN THE BOVINE EYE SO CURRENT EYE RESEARCH LA English DT Note AB The rate of increase of outflow facility (the wash-out rate) was measured in bovine eyes at 6 and 15 mm Hg. The time-rate-of-change of facility was less at 6 mm Hg (0.20: DELTA-facility/hour) than at 15 mm Hg (0.44). However, when the data was analyzed as a function of volume passing through the outflow system, the volume-rate-of-change of facility was the same at 6 (0.35: DELTA-facility/ml) and 15 mm Hg (0.34). This was consistent with the hypothesis of macromolecules "washing-out" of the aqueous outflow system, if these macromolecules were saturable in the perfusate. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JOHNSON, M (reprint author), MIT,ROOM 3-160,77 MASSACHUSETTS AVE,CAMBRIDGE,MA 02139, USA. RI Johnson, Mark/B-6921-2009 FU NEI NIH HHS [EY05503, EY01894] NR 7 TC 17 Z9 17 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1991 VL 10 IS 4 BP 373 EP 375 DI 10.3109/02713689108996343 PG 3 WC Ophthalmology SC Ophthalmology GA FM937 UT WOS:A1991FM93700011 PM 2070641 ER PT J AU PRAVTCHEVA, DD ADRA, CN RUDDLE, FH AF PRAVTCHEVA, DD ADRA, CN RUDDLE, FH TI TIMING OF PATERNAL PGK-1 EXPRESSION IN EMBRYOS OF TRANSGENIC MICE SO DEVELOPMENT LA English DT Article DE PHOSPHOGLYCERATE KINASE-1; TRANSGENE; CHROMOSOME IMPRINTING; MOUSE ID X-CHROMOSOME INACTIVATION; PREIMPLANTATION MOUSE EMBRYOS; LINKED PHOSPHOGLYCERATE KINASE; GLUCOSE-PHOSPHATE-ISOMERASE; FEMALE MOUSE; DETERMINES METHYLATION; CONTROLLING ELEMENTS; NUCLEOTIDE-SEQUENCE; DNA METHYLATION; IMPLANTATION AB In mouse development, the paternal allele of the X-linked gene Pgk-1 initiates expression on day 6, two days later than the maternal allele, which is activated on day 4. The different timing of expression of the maternal and paternal alleles may be determined by (i) imprinting of the chromosome region in which the gene resides, but not aimed specifically at the Pgk-1 gene; (ii) gene specific imprinting, acting on Pgk-1 irrespective of the chromosomal localization of the gene; (iii) an interplay between embryo cell differentiation, timing of X-inactivation and Pgk-1 expression, without the involvement of imprinting at the Pgk-1 locus itself (Fundele R., Illmensee, K., Jagerbauer, E. M., Fehlau, M. and Krietsch, W. K. (1987) Differentiation 35, 31-36). Our findings in transgenic mouse lines, carrying Pgk-1 on autosomes, indicate the importance of the X chromosomal location for the delayed expression of the paternal Pgk-1 allele, and are in agreement with the first of the explanations listed above. We propose that the late activation of the paternal Pgk-1 locus is a consequence of imprinting targeted at, and centered around, the X chromosome controlling element (Xce). C1 MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. KING FAISAL SPECIALIST HOSP & RES CTR,RIYADH 11211,SAUDI ARABIA. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP PRAVTCHEVA, DD (reprint author), YALE UNIV,DEPT BIOL,NEW HAVEN,CT 06511, USA. FU NIGMS NIH HHS [GM 9966] NR 81 TC 24 Z9 24 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD APR PY 1991 VL 111 IS 4 BP 1109 EP 1120 PG 12 WC Developmental Biology SC Developmental Biology GA FK576 UT WOS:A1991FK57600025 PM 1879353 ER PT J AU ERLICH, HA GRIFFITH, RL BUGAWAN, TL ZIEGLER, R ALPER, C EISENBARTH, G AF ERLICH, HA GRIFFITH, RL BUGAWAN, TL ZIEGLER, R ALPER, C EISENBARTH, G TI IMPLICATION OF SPECIFIC DQB1 ALLELES IN GENETIC SUSCEPTIBILITY AND RESISTANCE BY IDENTIFICATION OF IDDM SIBLINGS WITH NOVEL HLA-DQB1 ALLELE AND UNUSUAL DR2 AND DR1 HAPLOTYPES SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; ENZYMATIC AMPLIFICATION; BETA-GLOBIN; HLA; DISEASE; DNA; SITE AB Genetic susceptibility to insulin-dependent diabetes mellitus (IDDM) is associated with the HLA-DR3 and DR4 haplotypes. The HLA-DR2 haplotype is negatively associated with IDDM, an association that has been interpreted as dominant protection. Here, we describe the molecular analysis of the HLA class II genes in an unusual family with three HLA-DR1/2 siblings, all of whom have IDDM. With polymerase chain reaction amplification and sequence analysis to characterize the class II alleles, we identified a novel DQB1 allele on the DR1 haplotype and an unusual DQB1 allele on the DR2 haplotype. However, the DRB1 alleles on these DR1 and DR2 haplotypes are the conventional alleles (*0101 and *1501, respectively). These results suggest that it is the conventional DQB1 allele (*0602) not the DRB1 allele (*1501) on the protective DR2 haplotype that confers protection in the general population and, furthermore, that these unusual DQB1 alleles may confer susceptibility to IDDM in this family. The unusual DQB1 allele on this DR2 haplotype encodes Asp at position 57, indicating that it is the allele DQB1*0602 and not simply the presence of this residue that is responsible for the protective effect. C1 JOSLIN DIABET CTR,BOSTON,MA. CTR BLOOD RES,BOSTON,MA. RP ERLICH, HA (reprint author), CETUS CORP,DEPT HUMAN GENET,1400 53RD ST,EMERYVILLE,CA 94608, USA. NR 20 TC 73 Z9 73 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 APR PY 1991 VL 40 IS 4 BP 478 EP 481 DI 10.2337/diabetes.40.4.478 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FE091 UT WOS:A1991FE09100012 PM 2010048 ER PT J AU ALARCON, B LEY, SC SANCHEZMADRID, F BLUMBERG, RS JU, ST FRESNO, M TERHORST, C AF ALARCON, B LEY, SC SANCHEZMADRID, F BLUMBERG, RS JU, ST FRESNO, M TERHORST, C TI THE CD3-GAMMA AND CD3-DELTA SUBUNITS OF THE T-CELL ANTIGEN RECEPTOR CAN BE EXPRESSED WITHIN DISTINCT FUNCTIONAL TCR/CD3 COMPLEXES SO EMBO JOURNAL LA English DT Article DE CD3; STOICHIOMETRY; T-CELL RECEPTOR ID CD3 COMPLEX; ZETA-CHAIN; MONOCLONAL-ANTIBODY; SURFACE EXPRESSION; ETA-CHAIN; PROTEINS; LINKAGE; CLONES; ALPHA; GENES AB The T cell receptor for antigen (TCR) consists of two glycoproteins containing variable regions (TCR-alpha/beta or TCR-gamma/delta) which are expressed on the cell surface in association with at least four invariant proteins (CD3-gamma, -delta, -epsilon and -zeta). CD3-gamma and CD3-delta chains are highly homologous, especially in the cytoplasmic domain. The similarity observed in their genomic organization and their proximity in the chromosome indicate that both genes arose from duplication of a single gene. Here, we provide several lines of evidence which indicate that in human and murine T cells which expressed both the CD3-gamma and CD3-delta chains on their surface, the TCR/CD3 complex consisted of a mixture of alpha-beta-gamma-epsilon-zeta and alpha-beta-delta-epsilon-zeta complexes rather than a single alpha-beta-gamma-delta-epsilon-zeta complex. First, a CD3-gamma specific antibody failed to co-immunoprecipitate CD3-delta and conversely, several CD3-delta specific antibodies did not coprecipitate CD3-gamma. Secondly, analysis of a panel of human and murine T cell lines demonstrated that CD3-gamma and CD3-delta were expressed at highly variable ratios on their surface. This suggested that these chains were not expressed as a single complex. Thirdly, CD3-gamma and CD3-delta competed for binding to CD3-epsilon in transfected COS cells, suggesting that CD3-gamma and CD3-delta formed mutually exclusive complexes. The existence of these two forms of TCR/CD3 complexes could have important implications in the understanding of T cell receptor function and its role in T cell development. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. HOSP PRINCESA,DEPT IMMUNOL,E-28006 MADRID,SPAIN. BOSTON UNIV,SCH MED,CTR ARTHRITIS,BOSTON,MA 02118. RI SANZ, MAGDALENA/L-4825-2013; Sanchez-Madrid, Francisco/M-7889-2016; Alarcon, Balbino/N-9648-2016 OI SANZ, MAGDALENA/0000-0002-3106-2680; Sanchez-Madrid, Francisco/0000-0001-5303-0762; Alarcon, Balbino/0000-0001-7820-1070 FU NIAID NIH HHS [AI-15066, AI-17651]; NIDDK NIH HHS [1 KO8 DKO1886 01] NR 44 TC 101 Z9 101 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR PY 1991 VL 10 IS 4 BP 903 EP 912 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FE950 UT WOS:A1991FE95000020 PM 1826255 ER PT J AU MAITER, D KOENIG, JI KAPLAN, LM AF MAITER, D KOENIG, JI KAPLAN, LM TI SEXUALLY DIMORPHIC EXPRESSION OF THE GROWTH HORMONE-RELEASING HORMONE GENE IS NOT MEDIATED BY CIRCULATING GONADAL-HORMONES IN THE ADULT-RAT SO ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT 72ND ANNUAL MEETING OF THE ENDOCRINE SOC CY JUN 20-23, 1990 CL ATLANTA, GA SP ENDOCRINE SOC ID PERIVENTRICULAR NUCLEUS; MONOSODIUM GLUTAMATE; SECRETION; SOMATOSTATIN; HYPOTHALAMUS; INVITRO; CELLS; DNA AB The sexual dimorphism characterizing GH secretion in the rat is thought to be related to differences in the hypothalamic synthesis and release of the GH-regulating peptides, GH-releasing hormone (GHRH), and somatostatin. Therefore, the influence of gender and sex steroid hormones on hypothalamic expression of the GHRH gene in adult rats were examined. GHRH messenger RNA (mRNA) levels were measured in individual rat hypothalami by Northern hybridization analysis using a P-32-labeled complementary DNA encoding rat GHRH. Destruction of hypothalamic GHRH neurons by neonatal treatment with monosodium glutamate caused similar 3-fold reductions in the levels of GHRH mRNA in adult male and female animals. In three separate experiments, hypothalamic GHRH mRNA concentrations in male rats were 2- to 3-fold greater than in randomly cycling females (four or five rats per group; P < 0.01). In spite of the greater abundance of GHRH mRNA abundance in the male rat hypothalamus, circulating gonadal steroids lacked the ability to modulate GHRH gene expression in adult animals, since neither gonadectomy nor pharmacological sex steroid replacement changed GHRH mRNA levels in the hypothalamus of male and female adult rats. Furthermore, GHRH mRNA concentrations in female rats were similar during the proestrus, estrus, and diestrus phases of the estrous cycle. Also, GH inhibited hypothalamic GHRH gene expression in a sex-specific manner. Exposure to high levels of GH secreted by the MtTW 15 tumor for 4 weeks reduced GHRH mRNA concentrations 7-fold in male rats (P < 0.001) but only 2-fold in females (P < 0.05). These studies demonstrate that GHRH gene expression in the rat hypothalamus is sexually dimorphic. Basal mRNA levels are greater in male rats, and expression in male hypothalami is more sensitive to feedback inhibition by GH than expression in females. There is no evidence for regulation of GHRH mRNA levels by either testosterone or estrogen in adult rats. These gender differences in GHRH gene expression likely contribute to the generation of a sex-specific pattern of GH secretion. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,NEUROENDOCRINOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MAITER, D (reprint author), CATHOLIC UNIV LOUVAIN,UNITE DIABETOL & NUTR,UCL DIAB 54-74,AVE HIPPOCRATE 54,B-1200 BRUSSELS,BELGIUM. FU NIDDK NIH HHS [DK-42189, DK-40788] NR 45 TC 46 Z9 46 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD APR PY 1991 VL 128 IS 4 BP 1709 EP 1716 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FD869 UT WOS:A1991FD86900004 PM 2004597 ER PT J AU HOOPER, DC WOLFSON, JS AF HOOPER, DC WOLFSON, JS TI MODE OF ACTION OF THE NEW QUINOLONES - NEW DATA SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 3RD INTERNATIONAL SYMP ON NEW QUINOLONES CY JUL, 1990 CL VANCOUVER, CANADA ID ESCHERICHIA-COLI K-12; DNA GYRASE; NALIDIXIC-ACID; SOS RESPONSE; PSEUDOMONAS-AERUGINOSA; ANTIMICROBIAL AGENTS; ANTIBACTERIAL AGENTS; RESISTANT MUTATIONS; TOPOISOMERASE-II; CALF THYMUS AB New details of the molecular interactions of quinolones with their target DNA gyrase and DNA have come from the nucleotide sequences of the gyrA genes from resistant mutants of Escherichia coli and wild-type strains of other bacteria and studies of gyrase A tryptic fragments, all suggesting the importance of an amino-terminal domain in quinolone action. Alterations in DNA supertwisting were also associated with altered quinolone susceptibility, possibly by indirect effects on DNA gyrase expression. Specific binding of relevant concentrations of norfloxacin to a complex of DNA gyrase and DNA in the presence of ATP, the cooperativity of DNA binding, and the crystalline structure of nalidixic acid have led to a model in which quinolones bind cooperatively to a pocket of single-strand DNA created by DNA gyrase. Quinolones vary in their relative activity against DNA gyrase and its eukaryotic homolog topoisomerase II, and in some assays increased action against the eukaryotic enzyme was associated with genotoxicity. Inhibition of bacterial DNA synthesis by quinolones may correlate with MICs in some species, but comparisons of drug accumulation and inhibition of DNA synthesis in permeabilized cells among species have been difficult to interpret. The specific factors necessary for bacterial killing by quinolones in addition to interaction with DNA gyrase have remained elusive, but include oxygen and new protein synthesis. The coordinate expression of the SOS proteins appears not to be necessary for quinolone lethality. Two independent mutants with selective reduced killing by quinolones and beta-lactams indicate overlap in the pathways of bactericidal activity of these classes of agents with distinct targets. RP HOOPER, DC (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 52 TC 51 Z9 52 U1 0 U2 1 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PD APR PY 1991 VL 10 IS 4 BP 223 EP 231 DI 10.1007/BF01966994 PG 9 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA FQ032 UT WOS:A1991FQ03200002 PM 1650698 ER PT J AU WOLFSON, JS HOOPER, DC AF WOLFSON, JS HOOPER, DC TI PHARMACOKINETICS OF QUINOLONES - NEWER ASPECTS SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT 3RD INTERNATIONAL SYMP ON NEW QUINOLONES CY JUL, 1990 CL VANCOUVER, CANADA ID INTRAVENOUSLY ADMINISTERED CIPROFLOXACIN; TISSUE PENETRATION; INTERPRETIVE CRITERIA; HEALTHY-VOLUNTEERS; ANTIMICROBIAL AGENTS; INVITRO ACTIVITY; THEOPHYLLINE PHARMACOKINETICS; ANTIBACTERIAL ACTIVITY; DOSE PHARMACOKINETICS; DISK SUSCEPTIBILITY AB Differences in pharmacokinetic properties are emerging as important determinants in distinguishing among clinical uses of individual new quinolone antimicrobial agents. Selected data on pharmacokinetics, new pharmacokinetic studies, and pharmacodynamics are reviewed, with reference to norfloxacin, ciprofloxacin, ofloxacin, pefloxacin, enoxacin, fleroxacin, lomefloxacin, and other new quinolones. Considering pharmacokinetics, oral bioavailability is excellent (> 95 %) for most quinolones. Differences in peak serum concentrations and beta-half-lives of elimination exist, however, and are reflected in up to ten-fold differences in values of the area under the curve of serum concentration versus time for administration of similar drug doses. As suggested by high apparent volumes of distribution and low binding to serum proteins, penetration into many body tissues and fluids is favorable. Considering new findings, orally administered ciprofloxacin has been found to be absorbed primarily in the duodenum and jejunum. Studies also suggest this drug to be cleared by transepithelial elimination into the bowel lumen as well as by the renal route. Oral bioavailability of quinolones has been demonstrated to be in general good in ill as well as healthy subjects but is reduced on co-administration with magnesium- and aluminum-containing acids, sucralfate (which contains aluminum), or ferrous sulfate. Pharmacodynamic parameters, such as the relationship of serum concentrations and drug potency in vitro to clinical response and suppression of bacterial resistance, have been little studied and merit further investigation. RP WOLFSON, JS (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 84 TC 38 Z9 38 U1 0 U2 2 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PD APR PY 1991 VL 10 IS 4 BP 267 EP 274 DI 10.1007/BF01967000 PG 8 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA FQ032 UT WOS:A1991FQ03200008 PM 1864287 ER PT J AU VIVIER, E MORIN, PM OBRIEN, C SCHLOSSMAN, SF ANDERSON, P AF VIVIER, E MORIN, PM OBRIEN, C SCHLOSSMAN, SF ANDERSON, P TI CD2 IS FUNCTIONALLY LINKED TO THE ZETA-NATURAL KILLER RECEPTOR COMPLEX SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note ID T-CELL RECEPTOR; SHEEP ERYTHROCYTE RECEPTOR; FC-GAMMA-RECEPTOR; LYMPHOCYTES-T; LYMPHOKINE GENES; ACTIVATION; EXPRESSION; PROTEIN; TRANSCRIPTION; INDUCTION AB Natural killer (NK) cells express two distinct surface receptors capable of triggering cytolytic effector function. The first is CD16, an immunoglobulin Fc receptor that allows NK cells to mediate antibody-dependent killing (ADCC). NK cells express CD 16 in association with zeta, a signal-transducing subunit that is also a component of the T cell receptor complex. Activation of NK cells via CD 16 results in tyrosine phosphorylation of zeta. The second NK cell triggering receptor is CD2, a 50-55-kDa cell surface molecule that is also expressed on T cells. Here we show that NK cell activation induced by mAb reactive with CD2 (either anti-T11.1 alone or with anti-T11.2 in combination) also results in the tyrosine phosphorylation of zeta. Our results indicate that CD2 is functionally linked to the CD16-zeta-complex and suggest that the zeta-subunit plays a central role in the signal transduction pathways utilized by NK cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. NR 37 TC 52 Z9 52 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 APR PY 1991 VL 21 IS 4 BP 1077 EP 1080 DI 10.1002/eji.1830210434 PG 4 WC Immunology SC Immunology GA FJ284 UT WOS:A1991FJ28400033 PM 1673433 ER PT J AU MULLENIX, PJ TASSINARI, MS SCHUNIOR, A KERNAN, WJ AF MULLENIX, PJ TASSINARI, MS SCHUNIOR, A KERNAN, WJ TI NO CHANGE IN SPONTANEOUS BEHAVIOR OF RATS AFTER ACUTE ORAL DOSES OF ASPARTAME, PHENYLALANINE, AND TYROSINE SO FUNDAMENTAL AND APPLIED TOXICOLOGY LA English DT Article ID PLASMA PHENYLALANINE; NEUROTRANSMITTER SYNTHESIS; PRECURSOR AVAILABILITY; DL-PHENYLALANINE; MOTOR-ACTIVITY; BRAIN; PHENYLETHYLAMINE; PHENETHYLAMINE; BIOSYNTHESIS; AMPHETAMINE C1 IOWA STATE UNIV SCI & TECHNOL,DEPT PHYS,AMES,IA 50011. IOWA STATE UNIV SCI & TECHNOL,VET DIAGNOST LAB,AMES,IA 50011. RP MULLENIX, PJ (reprint author), FORSYTH RES INST,DEPT TOXICOL,140 FENWAY,BOSTON,MA 02115, USA. NR 54 TC 9 Z9 9 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0272-0590 J9 FUND APPL TOXICOL JI Fundam. Appl. Toxicol. PD APR PY 1991 VL 16 IS 3 BP 495 EP 505 DI 10.1016/0272-0590(91)90090-Q PG 11 WC Toxicology SC Toxicology GA FE983 UT WOS:A1991FE98300011 PM 1677339 ER PT J AU KONIECZNY, A VOYTAS, DF CUMMINGS, MP AUSUBEL, FM AF KONIECZNY, A VOYTAS, DF CUMMINGS, MP AUSUBEL, FM TI A SUPERFAMILY OF ARABIDOPSIS-THALIANA RETROTRANSPOSONS SO GENETICS LA English DT Article ID TRANSPOSABLE GENETIC ELEMENT; COMPLETE NUCLEOTIDE-SEQUENCE; DROSOPHILA-MELANOGASTER; RETROVIRAL PROTEINS; CODING SEQUENCE; YEAST; NUMBER; GYPSY; IDENTIFICATION; ORGANIZATION AB We describe a superfamily of Arabidopsis thaliana retrotransposable elements that consists of at least ten related families designated Ta1-Ta10. The Ta1 family has been described previously. Two genomic clones representing the Ta2 and Ta3 elements were isolated from an A. thaliana (race Landsberg erecta) lambda library using sequences derived from the reverse transcriptase region of Ta1 as hybridization probes. Nucleotide sequence analysis showed that the Ta1, Ta2 and Ta3 families share > 75% amino acid identity in pairwise comparisons of their reverse transcriptase and RNase H genes. In addition to Ta1, Ta2 and Ta3, we identified seven other related retrotransposon families in Landsberg erecta, Ta4-Ta10, using degenerate primers and the polymerase chain reaction to amplify a highly conserved region of retrotransposon-encoded reverse transcriptase. One to two copies of elements Ta2-Ta10 are present in the genomes of the A. thaliana races Landsberg erecta and Columbia indicating that the superfamily comprises at least 0.1% of the A. thaliana genome. The nucleotide sequences of the reverse transcriptase regions of the ten element families place them in the category of copia-like retrotransposons and phylogenetic analysis of the amino acid sequences suggests that horizontal transfer may have played a role in their evolution. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,MUSEUM COMPARAT ZOOL,CAMBRIDGE,MA 02138. RP KONIECZNY, A (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM07620] NR 38 TC 148 Z9 154 U1 0 U2 2 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD APR PY 1991 VL 127 IS 4 BP 801 EP 809 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA FD753 UT WOS:A1991FD75300017 PM 1709409 ER PT J AU BENGER, JC TESHIMA, I WALTER, MA BRUBACHER, MG DAOUK, GH COX, DW AF BENGER, JC TESHIMA, I WALTER, MA BRUBACHER, MG DAOUK, GH COX, DW TI LOCALIZATION AND GENETIC-LINKAGE OF THE HUMAN-IMMUNOGLOBULIN HEAVY-CHAIN GENES AND THE CREATINE-KINASE BRAIN (CKB) GENE - IDENTIFICATION OF A HOT-SPOT FOR RECOMBINATION SO GENOMICS LA English DT Article ID HUMAN DNA; REGION; CHROMOSOME-14; POLYMORPHISMS; SEQUENCE; CLUSTER; LOCUS; ORGANIZATION; EXPRESSION; ASSIGNMENT C1 HOSP SICK CHILDREN,555 UNIV AVE,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV TORONTO,DEPT MED GENET,TORONTO M5G 1X8,ONTARIO,CANADA. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. NR 60 TC 29 Z9 29 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1991 VL 9 IS 4 BP 614 EP 622 DI 10.1016/0888-7543(91)90354-H PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FB629 UT WOS:A1991FB62900008 PM 1674725 ER PT J AU CLEMENTE, C COCHRAN, AJ ELDER, DE LEVENE, A MACKIE, RM MIHM, MC RILKE, F CASCINELLI, N FITZPATRICK, TB SOBER, AJ AF CLEMENTE, C COCHRAN, AJ ELDER, DE LEVENE, A MACKIE, RM MIHM, MC RILKE, F CASCINELLI, N FITZPATRICK, TB SOBER, AJ TI HISTOPATHOLOGIC DIAGNOSIS OF DYSPLASTIC NEVI - CONCORDANCE AMONG PATHOLOGISTS CONVENED BY THE WORLD-HEALTH-ORGANIZATION-MELANOMA-PROGRAM SO HUMAN PATHOLOGY LA English DT Article DE CELLULAR ATYPIA; ARCHITECTURAL ATYPIA; DYSPLASTIC NEVUS; MELANOMA; LENTIGINOUS MELANOCYTIC HYPERPLASIA; CONCORDANCE ID MALIGNANT MELANOMAS; MELANOCYTIC NEVI; CUTANEOUS MELANOMA; PRECURSOR; LESIONS; NAEVI; PHENOTYPE; ATYPIA; RISK C1 NATL TUMOR INST MILAN,DEPT PATHOL,VIA VENEZIAN 1,I-20133 MILAN,ITALY. UNIV CALIF LOS ANGELES,SCH MED,DEPT PATHOL,LOS ANGELES,CA 90024. HOSP UNIV PENN,DEPT PATHOL,PHILADELPHIA,PA 19104. UNIV GLASGOW,DEPT DERMATOL,GLASGOW G12 8QQ,SCOTLAND. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NATL TUMOR INST,DEPT SURG,MILAN,ITALY. HUMANA HOSP WELLINGTON,DEPT PATHOL,LONDON,ENGLAND. NR 20 TC 102 Z9 104 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 APR PY 1991 VL 22 IS 4 BP 313 EP 319 DI 10.1016/0046-8177(91)90078-4 PG 7 WC Pathology SC Pathology GA GJ450 UT WOS:A1991GJ45000003 PM 1741810 ER PT J AU PORCELLI, S BRENNER, MB BAND, H AF PORCELLI, S BRENNER, MB BAND, H TI BIOLOGY OF THE HUMAN GAMMA-DELTA T-CELL RECEPTOR SO IMMUNOLOGICAL REVIEWS LA English DT Review ID VARIABLE-REGION GENES; HUMAN LYMPHOCYTES-T; HUMAN PERIPHERAL-BLOOD; ANTIGEN-MHC RECEPTOR; KILLER-LIKE ACTIVITY; HEAT-SHOCK PROTEIN; ALPHA-BETA; MONOCLONAL-ANTIBODY; MYCOBACTERIUM-TUBERCULOSIS; REARRANGING GENE C1 HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. RP PORCELLI, S (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,BOSTON,MA 02115, USA. NR 171 TC 198 Z9 200 U1 2 U2 4 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0105-2896 J9 IMMUNOL REV JI Immunol. Rev. PD APR PY 1991 VL 120 BP 137 EP 183 DI 10.1111/j.1600-065X.1991.tb00591.x PG 47 WC Immunology SC Immunology GA FL991 UT WOS:A1991FL99100007 PM 1650758 ER PT J AU HUGHES, A BLOCH, KJ BHAN, AK GILLEN, D GIOVINO, VC HARMATZ, PR AF HUGHES, A BLOCH, KJ BHAN, AK GILLEN, D GIOVINO, VC HARMATZ, PR TI EXPRESSION OF MHC CLASS-II (IA) ANTIGEN BY THE NEONATAL ENTEROCYTE - THE EFFECT OF TREATMENT WITH INTERFERON-GAMMA SO IMMUNOLOGY LA English DT Article ID EPITHELIAL-CELLS; DIFFERENTIAL EXPRESSION; SMALL-INTESTINE; GUT EPITHELIUM; RAT; INVIVO; LYMPHOCYTES; ONTOGENY; ORIGIN AB Immunohistochemical techniques were used to probe the expression and inducibility of class II major histocompatibility complex (MHC) (Ia) antigens by the mouse enterocyte at various stages postpartum. Expression of Ia was related to both age and intestinal location. Ia antigen was not detected until at least 1 week post-weaning and was noted thereafter in both proximal and distal intestine. Both crypt and villus enterocytes were stained in the distal small intestine, but staining was restricted to the upper portion of the villus in the proximal small intestine. Moreover, the extent of staining and the intensity of staining were greater in the distal small intestine. The effect of a single injection of recombinant mouse interferon-gamma (IFN-gamma) on Ia expression by enterocytes of 16-day-old, suckling BDF1 mice was examined. Injection of distilled water (DW) or 1 to 2 x 10(4) U IFN-gamma did not induce enterocyte Ia expression. Doses of 4-10 x 10(4) U were effective inducers of Ia on crypt and, occasionally, on lower villus cells examined 24 hr later. Staining did not persist on the enterocyte beyond 48 hr. In conclusion, Ia is not normally expressed on small intestinal enterocytes of the mouse until after weaning; however, Ia expression can be induced earlier by treatment with IFN-gamma. It is not known whether failure to detect Ia expression prior to weaning reflects a lack of positive stimuli and/or the presence of inhibitory stimuli, possibly carried in the breast milk. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CLIN IMMUNOL & ALLERGY UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ALLERGY UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. FU NICHD NIH HHS [HD12437]; NIDDK NIH HHS [DK34854, DK33506] NR 26 TC 27 Z9 27 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0019-2805 J9 IMMUNOLOGY JI Immunology PD APR PY 1991 VL 72 IS 4 BP 491 EP 496 PG 6 WC Immunology SC Immunology GA FJ181 UT WOS:A1991FJ18100006 PM 1903764 ER PT J AU FLESCHER, E FOSSUM, D TALAL, N AF FLESCHER, E FOSSUM, D TALAL, N TI POLYAMINE-DEPENDENT PRODUCTION OF LYMPHOCYTOTOXIC LEVELS OF AMMONIA BY HUMAN PERIPHERAL-BLOOD MONOCYTES SO IMMUNOLOGY LETTERS LA English DT Article DE MACROPHAGE; CYTOTOXICITY; OXIDASE; POLYAMINE; AMMONIA ID OXIDASE; OXIDATION; INVITRO; CELLS AB The activity of polyamine oxidase down-regulates IL-2 production in cultures of peripheral blood mononuclear cells. Monocytes are the main source of this enzymatic activity which generates ammonia. We therefore assessed the production of ammonia by human monocytes. We report that human peripheral blood monocytes produce and secrete ammonia and that this activity peaks after 2 days of incubation in vitro. Ammonia production can be suppressed by inhibiting polyamine biosynthesis and polyamine oxidation; thus, the activity of polyamine oxidase in human monocytes generates ammonia. Ammonia production could serve as a measure of polyamine oxidase activity in human monocytes. The levels of ammonia produced in our system reduce human lymphocyte viability. Therefore, ammonia can be added to the list of macrophage products having cytotoxic and immunosuppressive potential. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FLESCHER, E (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [R01 DEO9311-01] NR 15 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-2478 J9 IMMUNOL LETT JI Immunol. Lett. PD APR PY 1991 VL 28 IS 1 BP 85 EP 90 DI 10.1016/0165-2478(91)90131-S PG 6 WC Immunology SC Immunology GA FH787 UT WOS:A1991FH78700013 PM 2071175 ER PT J AU BRUNKHORST, B NIEDERMAN, R AF BRUNKHORST, B NIEDERMAN, R TI AMMONIUM DECREASES HUMAN POLYMORPHONUCLEAR LEUKOCYTE CYTOSKELETAL ACTIN SO INFECTION AND IMMUNITY LA English DT Article ID PHAGOSOME-LYSOSOME FUSION; HUMAN NEUTROPHIL CHEMOTAXIS; LYSOSOMOTROPIC WEAK BASES; INTRACELLULAR PH; CYTOCHALASIN-B; MACROPHAGES; INHIBITION; MODULATION; PROTEINS; CALCIUM AB Ammonium, a weak base produced as a metabolic by-product of urea metabolism by bacterial pathogens, inhibits a variety of motile polymorphonuclear leukocyte (PMN) functions. It was initially assumed that the mechanism of leukocyte inhibition was due to cytoplasmic alkalinization. However, while it is clear that ammonium can effect cytoplasmic alkalinization, current data indicate that alterations in chemotaxis, degranulation, and receptor recycling occur independently of cytoplasmic alkalinization. Since these are motility-related events, we examined the possibility that alterations in cytoskeletal actin may account for the effects of ammonium on PMN function. The results indicate that ammonium can inhibit degranulation, decrease cytoskeletal actin, and increase actin depolymerization rates. These findings are supported by five lines of evidence. First, formylmethionyl-leucyl-phenylalanine (fMLP)-induced elastase release was inhibited by 85% +/- 3% in the presence of ammonium, and ammonium by itself did not stimulate elastase release. Second, ammonium treatment of resting PMNs caused a rapid 38% +/- 6% decrease in cytoskeletal actin. Third, ammonium treatment accelerated the fMLP-induced depolymerization phase of the cytoskeletal actin transient by 150% +/- 12%. Fourth, in resting PMNs treated with cytochalasin B or D, ammonium induced a 21% +/- 4% and a 25% +/- 5% decrease in cytoskeletal actin, respectively. Conversely, ammonium did not affect the ability of the cytochalasins to inhibit an fMLP-induced cytoskeletal actin transient. Fifth, pertussis toxin treatment of neutrophils did not affect the ammonium-stimulated decrease in cytoskeletal actin. These results suggest that ammonium can inhibit neutrophil function by altering cytoskeletal actin and therefore provide new information regarding potential pathogenic mechanisms for bacterial pathogens. RP BRUNKHORST, B (reprint author), FORSYTH RES INST,DEPT CELL BIOL,140 FENWAY,BOSTON,MA 02115, USA. NR 61 TC 15 Z9 15 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1991 VL 59 IS 4 BP 1378 EP 1386 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FD915 UT WOS:A1991FD91500024 PM 2004818 ER PT J AU YAMASHITA, K EASTCOTT, JW TAUBMAN, MA SMITH, DJ COX, DS AF YAMASHITA, K EASTCOTT, JW TAUBMAN, MA SMITH, DJ COX, DS TI EFFECT OF ADOPTIVE TRANSFER OF CLONED ACTINOBACILLUS-ACTINOMYCETEMCOMITANS-SPECIFIC T-HELPER CELLS ON PERIODONTAL-DISEASE SO INFECTION AND IMMUNITY LA English DT Article ID HUMAN IMMUNE-RESPONSES; FUNCTIONAL-HETEROGENEITY; BONE LOSS; ORAL MICROORGANISMS; ANTIBODY-RESPONSES; LYMPHOCYTES-T; B-CELLS; INTERLEUKIN-2; RAT; BACTEROIDES AB Previously we isolated several Actinobacillus actinomycetemcomitans-specific T-cell clones from the spleens and lymph nodes of immunized Rowett rats. These clones were characterized as W3/13+, W3/25+, OX8-, and OX22-, suggesting a T helper (Th) phenotype. In the current experiments, 10(6) cells from a single A. actinomycetemcomitans-specific clone (A3) were adoptively transferred to a group (AaTh; n = 13) of normal heterozygous rats (rnu/+) at 28 days of age. A second group received no T cells (AaNT; n = 15), and a third group also received no T cells (NAaNT, n = 11). Beginining 1 day after transfer, the first and second groups were infected orally with A. actinomycetemcomitans for 5 consecutive days. The presence of infection was confirmed immediately after challenge and after 5 months, when the experiments were ended. Significantly higher numbers of lymphocytes were recovered from the gingival tissues of the first group than from those of either of the other groups. Also, this group showed significantly elevated (P < 0.01) serum immunoglobulin G and immunoglobulin M antibody to A. actinomycetemcomitans in an enzyme-linked immunosorbent assay when compared with both other groups. Bone loss was significantly lower (P < 0.01) in recipients of A. actinomycetemcomitans-specific cloned cells when compared with the other infected group and was approximately equal to the bone loss of the uninfected group. These results are consistent with the hypothesis that T-cell regulation can affect periodontal disease. In this regulation, T helper cells appear to interfere with periodontal bone loss. C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA 02115. SUNY STONY BROOK,DEPT PERIODONT,STONY BROOK,NY 11794. FU NIDCR NIH HHS [DE 04733, DE 03420, DE 04881] NR 42 TC 59 Z9 61 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD APR PY 1991 VL 59 IS 4 BP 1529 EP 1534 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FD915 UT WOS:A1991FD91500043 PM 1825991 ER PT J AU HALL, C BERKHOUT, B ALARCON, B SANCHO, J WILEMAN, T TERHORST, C AF HALL, C BERKHOUT, B ALARCON, B SANCHO, J WILEMAN, T TERHORST, C TI REQUIREMENTS FOR CELL-SURFACE EXPRESSION OF THE HUMAN TCR/CD3 COMPLEX IN NON-T-CELLS SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE ASSEMBLY; CD3 COMPLEX; EXPRESSION; METABOLISM; T-CELL RECEPTOR ID ANTIGEN RECEPTOR COMPLEX; ENDOPLASMIC-RETICULUM; MOLECULAR-CLONING; ALPHA-CHAINS; CD3 COMPLEX; BETA-CHAINS; ZETA-CHAIN; CDNA; SUBUNIT; DEGRADATION AB The T-cell antigen receptor (TCR) consists of a glycoprotein heterodimer (alpha/beta or gamma/delta) which is non-covalently associated with at least four or five invariant polypeptides (CD3-gamma,delta,epsilon, zeta and eta). In T-cell variants lacking TCR-alpha,beta or zeta, it has been shown that incomplete TCR/CD3 complexes are retained within the cell. To examine requirements for cell surface expression of TCR/CD3, we transfected COS monkey kidney cells with cDNAs encoding TCR-alpha, beta and CD3-gamma, delta, epsilon and zeta. We report that cell surface appearance of TCR/CD3 on COS cells requires coordinate expression of all six proteins. In the absence of the zeta-chain, subcomplexes comprising from two to five chains were readily demonstrable in COS cells, but they failed to reach the cell surface or to acquire N-linked oligosaccharide side chains indicating failure to reach the medial Golgi. Pulse-chase metabolic labelling of transfected COS cells showed that three chains (CD3-gamma, CD3-epsilon, and zeta) were stable while three (TCR-alpha, TCR-beta and CD3-delta) were rapidly degraded. In two- and three-chain co-transfections specific intracellular subcomplexes were formed between TCR-alpha and CD3-gamma, TCR-alpha and CD3-delta, or TCR-beta and CD3-epsilon. Binary subcomplexes having at least one stable chain (CD3-epsilon - TCR-beta) were stable while one formed by two unstable chains (TCR-alpha - CD3-delta) was still degraded. Assembly of the TCR/CD3 complex in COS cells thus appears centered around the metabolically stable CD3-gamma and CD3-epsilon-proteins. Site-specific mutations of the negatively-charged transmembrane amino acid of residues of the CD3 chains to alanines served to either abolish (for TCR-alpha - CD3-delta and TCR-beta - CD3-epsilon) or diminish (for TCR-alpha - CD3-gamma) these TCR-CD3 interactions. These mutations had no effect, however, on CD3 - CD3 interactions or upon synthesis, metabolism, or intracellular distributions of the CD3 proteins. The transmembrane domains of CD3-gamma, delta, and epsilon thus appear to play a major role in associations of CD3 with TCR chains. RP HALL, C (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. RI Sancho, Jaime/O-3228-2013; Alarcon, Balbino/N-9648-2016 OI Sancho, Jaime/0000-0003-3852-7951; Alarcon, Balbino/0000-0001-7820-1070 NR 46 TC 81 Z9 81 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0953-8178 J9 INT IMMUNOL JI Int. Immunol. PD APR PY 1991 VL 3 IS 4 BP 359 EP 368 DI 10.1093/intimm/3.4.359 PG 10 WC Immunology SC Immunology GA FK380 UT WOS:A1991FK38000009 PM 1831654 ER PT J AU GANS, JS AF GANS, JS TI THE LEADERS USE OF METAPHOR IN GROUP-PSYCHOTHERAPY SO INTERNATIONAL JOURNAL OF GROUP PSYCHOTHERAPY LA English DT Article C1 MASSACHUSETTS GEN HOSP,PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 17 TC 12 Z9 12 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 APR PY 1991 VL 41 IS 2 BP 127 EP 143 PG 17 WC Psychology, Clinical SC Psychology GA FV208 UT WOS:A1991FV20800001 PM 2040540 ER PT J AU RUTGERS, JL SCULLY, RE AF RUTGERS, JL SCULLY, RE TI THE ANDROGEN INSENSITIVITY SYNDROME (TESTICULAR FEMINIZATION) - A CLINICOPATHOLOGICAL STUDY OF 43 CASES SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE ANDROGEN INSENSITIVITY SYNDROME; TESTICULAR FEMINIZATION; INTERSEX ID GRANULAR CHANGE; MULLERIAN DUCT; TESTIS; GONADS; TUMORS; CELLS; CHROMOSOME; CARCINOMA; CHILDREN AB Forty-three patients with the androgen insensitivity syndrome (AIS), ages 14 to 83 (average 27) years, were studied. Forty patients had complete AIS and three patients had incomplete AIS. Microscopic examination of the testes revealed immature tubules, which contained rare spermatogonia in 28% of the cases. Prominent Leydig cells and a spindle-cell stroma resembling ovarian stroma were found in a majority of cases. The organization of the testicular parenchyma could be classified into one of four patterns: diffuse tubulostromal, lobular tubulostromal, mixed tubulostromal, or stromal-predominant. Hamartomas were present in 63% and Sertoli cell adenomas in 23% of the cases. Malignant tumors developed in 9% of the patients and comprised two seminomas, one intratubular germ cell neoplasm with early stromal invasion, and a malignant sex cord tumor. At least one fallopian tube was present in 35% of the cases. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. RP RUTGERS, JL (reprint author), UNIV CALIF LOS ANGELES,HARBOR MED CTR,1000 W CARSON ST,TORRANCE,CA 90509, USA. NR 47 TC 110 Z9 116 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1991 VL 10 IS 2 BP 126 EP 144 DI 10.1097/00004347-199104000-00002 PG 19 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA FD055 UT WOS:A1991FD05500002 PM 2032766 ER PT J AU EICHHORN, JH SCULLY, RE AF EICHHORN, JH SCULLY, RE TI OVARIAN MYXOMA - CLINICOPATHOLOGICAL AND IMMUNOCYTOLOGIC ANALYSIS OF 5 CASES AND A REVIEW OF THE LITERATURE SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE OVARY; MYXOMA ID CARDIAC MYXOMA; AGGRESSIVE ANGIOMYXOMA; INTRAMUSCULAR MYXOMA; EDEMA; HISTOGENESIS AB The clinical and pathological features of five personally observed ovarian myxomas and three similar tumors previously described in the literature are analyzed. The patients' ages ranged from 16 to 45 years (mean, 33 years). An asymptomatic unilateral adnexal mass was the usual presentation. The tumors were 5 to 22 cm (mean, 11 cm) in greatest diameter, intraovarian, solid, and cystic, and they were occasionally blood-filled. None had ruptured. The intercellular matrix contained abundant hyaluronic acid in each of the five personally observed cases. The tumor cells were immunoreactive for vimentin and usually for actin, but not for desmin, S100-protein, neuron-specific enolase, neurofilament, Leu-7, epithelial membrane antigen, keratin (AE1/3, CAM5.2, MAK6), or factor VIII-related antigen, and did not bind Ulex europaeus agglutinin 1. Vascularity was a notable feature on microscopic examination. All the patients were treated by a surgical procedure alone, usually a conservative operation, and none of the five tumors with a follow-up period of 1 to 13 years (mean, 5 years) recurred. The ovarian myxoma is a distinctive type of ovarian neoplasm that should be distinguished from massive edema, edematous fibroma, and myxoid sarcomas. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114. RP EICHHORN, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 36 TC 18 Z9 18 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1991 VL 10 IS 2 BP 156 EP 169 DI 10.1097/00004347-199104000-00004 PG 14 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA FD055 UT WOS:A1991FD05500004 PM 2032767 ER PT J AU TEICHER, BA HERMAN, TS HOLDEN, SA AF TEICHER, BA HERMAN, TS HOLDEN, SA TI EFFECT OF PH, OXYGENATION, AND TEMPERATURE ON THE CYTOTOXICITY AND RADIOSENSITIZATION BY ETANIDAZOLE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE ETANIDAZOLE; HYPERTHERMIA; PH; HYPOXIA; COMBINED MODALITIES ID HYPOXIC CELL RADIOSENSITIZER; MOUSE MAMMARY-CARCINOMA; MURINE TUMOR; RADIATION-THERAPY; CYTO-TOXICITY; HYPERTHERMIC POTENTIATION; ELEVATED-TEMPERATURES; FIBRO-SARCOMA; HOECHST 33342; BLOOD-FLOW AB The effect of etanidazole was examined in vitro and in vivo in the FSaIIC tumor system. At pH 7.40 and 37-degrees-C, etanidazole at 5-500-mu-M for 1 hr was minimally cytotoxic. At 42-degrees-C and 43-degrees-C, however, the cytotoxicity of etanidazole increased. Etanidazole was more cytotoxic at pH 6.45 and 37-degrees than at pH 7.40 by about 1 log. Increasing the temperature to 42-degrees-C or 43-degrees-C at pH 6.45 during drug exposure, however, caused little increase in drug killing above the lethality of hyperthermia. When the radiosensitizing abilities of etanidazole were tested in vitro, there was a radiation dose modifying factor of 2.40 at pH 7.40, but only 1.70 at pH 6.45. In vivo, etanidazole (1 g/kg) produced a radiation dose modifying factor of 1.47, whereas 43-degrees-C for 30 min produced a radiation dose modifying factor of 1.38. The combination resulted in a radiation dose modifying factor of 2.29. When the cytotoxicities of hyperthermia (43-degrees-C x 30 min), etanidazole (500 mg/kg or 1 mg/kg), and radiation (10 Gy) combinations were assayed by Hoechst 33342 dye selected tumor subpopulations, 43-degrees-C x 30 min increased the killing of irradiated dim cells by approximately 9.2-fold but by only 2.9-fold in bright cells. Etanidazole (1 g/kg) increased radiation killing of bright cells by about 3-fold and dim cells by about 4.3-fold. The combination of hyperthermia and etanidazole increased the killing of both dim and bright cells exposed to radiation by approximately 10-fold versus 10 Gy alone. C1 JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,BOSTON,MA 02115. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA36508, R01-CA47379] NR 68 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. PD APR PY 1991 VL 20 IS 4 BP 723 EP 731 PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FC806 UT WOS:A1991FC80600012 PM 1825994 ER PT J AU SANDBERG, MA LEE, HY MATTHEWS, GP GAUDIO, AR AF SANDBERG, MA LEE, HY MATTHEWS, GP GAUDIO, AR TI RELATIONSHIP OF OSCILLATORY POTENTIAL AMPLITUDE TO A-WAVE SLOPE OVER A RANGE OF FLASH LUMINANCES IN NORMAL SUBJECTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE A-WAVE; ELECTRORETINOGRAPHY; OSCILLATORY POTENTIALS; RETINAL VASCULAR DISEASE; VITREOUS HEMORRHAGE ID RETINAL VEIN OCCLUSION; HUMAN ROD ERG; DIABETIC-RETINOPATHY; VITREOUS HEMORRHAGE; FOURIER-ANALYSIS; DARK-ADAPTATION; B-WAVE; ELECTRORETINOGRAPHY; PROGRESSION; RESPONSES AB The effect of flash luminance on the relationship of oscillatory potential (OP) amplitude, as a measurement of inner retinal function, to a-wave slope, as a measurement of photoreceptor function, was evaluated in full-field electroretinograms recorded from normal subjects. The ratio of OP amplitude to a-wave slope was found to be independent of flash luminance over a 3000-fold luminance range. This finding raises the possibility that a reduction in the ratio of OP amplitude to a-wave slope in eyes with media opacities may be used as a sign of inner retinal malfunction. Selected cases are presented to illustrate application of this approach. C1 CORNELL UNIV,MED CTR,NEW YORK HOSP,DEPT OPHTHALMOL,NEW YORK,NY 10021. RP SANDBERG, MA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY00169] NR 45 TC 16 Z9 16 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 APR PY 1991 VL 32 IS 5 BP 1508 EP 1516 PG 9 WC Ophthalmology SC Ophthalmology GA FH197 UT WOS:A1991FH19700012 PM 2016132 ER PT J AU ZAMAROCZY, D SCHLUESENER, HJ JOLESZ, FA SOBEL, RA COLUCCI, VM WEINER, HL SANDOR, T AF ZAMAROCZY, D SCHLUESENER, HJ JOLESZ, FA SOBEL, RA COLUCCI, VM WEINER, HL SANDOR, T TI DIFFERENTIATION OF EXPERIMENTAL WHITE MATTER LESIONS USING MULTIPARAMETRIC MAGNETIC-RESONANCE MEASUREMENTS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE BIEXPONENTIAL DECOMPOSITION; DEMYELINATION; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; INVITRO MAGNETIC RESONANCE IMAGING; RAT ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS; MONOCLONAL-ANTIBODY; PROTON RELAXATION; NMR; T2; DEMYELINATION; BRAIN AB The potential of multiparametric proton magnetic resonance (MR) measurements for characterizing white matter lesions was investigated. The authors compared acute experimental allergic encephalomyelitis (EAE), which is distinguished by inflammatory lesions, with an immunologically potentiated hyperacute form of the disease in which demyelinating lesions (DEM) also are present. Tissue samples containing cervical spinal cord and brain stem were excised and in vitro measurements of T1, T2, and two components of T2 were performed. Discriminant analysis was applied using MR parameters singly and in various combinations. When the disease was clearly manifested, discrimination between treated and normal animals was satisfactory with single parameters. The use of biexponential T2 components improved the distinction of normal from treated but asymptomatic animals, and differentiated between EAE and DEM. These results suggest that improved characterization of white matter lesions is possible with multiparametric MR in vivo, especially if sampling is performed with imaging and the T2 decay curves are obtained with a sufficient number of echoes to perform biexponential analysis. C1 BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. MAX PLANCK GESELL,CLIN INST MULTIPLE SCLEROSIS,WURZBURG,GERMANY. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT MED,CTR NEUROL DIS,DIV NEUROL,BOSTON,MA 02115. FU NCI NIH HHS [2 P01 CA41167]; NINDS NIH HHS [1 R01 NS23093, NS 00858] NR 42 TC 11 Z9 12 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 APR PY 1991 VL 26 IS 4 BP 317 EP 324 DI 10.1097/00004424-199104000-00007 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FD829 UT WOS:A1991FD82900005 PM 2032819 ER PT J AU BERDY, SS BLOCH, KJ AF BERDY, SS BLOCH, KJ TI SCHNITZLER SYNDROME - A BROADER CLINICAL SPECTRUM SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID CHRONIC URTICARIA; MONOCLONAL IMMUNOGLOBULINS; MACROGLOBULINEMIA; VASCULITIS; IGM; DEFICIENCY; DISEASE; PATIENT AB Schnitzler's syndrome is characterized by chronic urticaria, recurrent fever, bone pain, and lymphadenopathy in conjunction with a serum IgM M component in a concentration that is usually < 10,000 mg/L. Complement activation and cryoprecipitation do not appear to be involved. We report two additional patients who share many of the characteristics of this entity. These patients differ from patients previously reported because of the markedly elevated IgM M-component concentration in one patient and the severity of anemia in the second patient. An increased frequency of IgG autoantibodies to interleukin-1-alpha has been reported by other investigators; it has been suggested that an antibody-mediated prolongation of the half-life of interleukin-1-alpha might account for some of the symptoms and signs of this disorder. However, neither the mediators involved in the induction of nonpruritic urticaria nor the role of the IgM M component has been established. C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CLIN IMMUNOL UNIT,55 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GEN MED SERV,ALLERGY UNIT,BOSTON,MA 02114. NR 25 TC 39 Z9 39 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 APR PY 1991 VL 87 IS 4 BP 849 EP 854 DI 10.1016/0091-6749(91)90132-8 PG 6 WC Allergy; Immunology SC Allergy; Immunology GA FG059 UT WOS:A1991FG05900015 PM 1826507 ER PT J AU RUSSOTTI, GM HARRIS, WH AF RUSSOTTI, GM HARRIS, WH TI PROXIMAL PLACEMENT OF THE ACETABULAR COMPONENT IN TOTAL HIP-ARTHROPLASTY - A LONG-TERM FOLLOW-UP-STUDY SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID REPLACEMENT; RECONSTRUCTION AB A retrospective review was undertaken of thirty-seven hips (thirty-four patients) that had had a complex cemented total hip arthroplasty. In these hips, circumstances had necessitated that the center of the hip be placed farther proximally, as measured from the interteardrop line, than the anatomical position that is normally used. The mean duration of clinical and roentgenographic follow-up was eleven years (range, seven to seventeen years), and the mean age of the patients was fifty-one years (range, sixteen to seventy-three years). Most of these hips had a major deficiency or defect of the acetabular bone stock, or both. Of the six acetabular components (16 per cent) that became loose and were followed for ten years, only one needed revision. Because this study was aimed specifically at assessment of the acetabular component, if the femoral component alone needed revision, the final clinical rating that was used was the one obtained after the femoral revision. Thirty-one hips (84 per cent) were rated as having a good or excellent result; they had an average Harris hip-rating score of 43 points preoperatively and 93 points postoperatively. Thirty-three of the thirty-seven acetabular components were not substantially displaced laterally as compared with the anatomical location that is normally used. Our findings suggest that, when circumstances dictate, proximal positioning of the acetabular component without lateral displacement can give an acceptable result in cemented total hip-replacement procedures. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 19 TC 198 Z9 211 U1 0 U2 2 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 APR PY 1991 VL 73A IS 4 BP 587 EP 592 PG 6 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FH236 UT WOS:A1991FH23600016 PM 2013598 ER PT J AU JANMEY, PA EUTENEUER, U TRAUB, P SCHLIWA, M AF JANMEY, PA EUTENEUER, U TRAUB, P SCHLIWA, M TI VISCOELASTIC PROPERTIES OF VIMENTIN COMPARED WITH OTHER FILAMENTOUS BIOPOLYMER NETWORKS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID FIBRIN CLOTS; F-ACTIN; INTERMEDIATE FILAMENTS; LIGHT-SCATTERING; UNLIGATED CLOTS; CREEP RECOVERY; MICROTUBULES; RHEOLOGY; INVITRO; MUSCLE AB The cytoplasm of vertebrate cells contains three distinct filamentous biopolymers, the microtubules, microfilaments, and intermediate filaments. The basic structural elements of these three filaments are linear polymers of the proteins tubulin, actin, and vimentin or another related intermediate filament protein, respectively. The viscoelastic properties of cytoplasmic filaments are likely to be relevant to their biologic function, because their extreme length and rodlike structure dominate the rheologic behavior of cytoplasm, and changes in their structure may cause gel-sol transitions observed when cells are activated or begin to move. This paper describes parallel measurements of the viscoelasticity of tubulin, actin, and vimentin polymers. The rheologic differences among the three types of cytoplasmic polymers suggest possible specialized roles for the different classes of filaments in vivo. Actin forms networks of highest rigidity that fluidize at high strains, consistent with a role in cell motility in which stable protrusions can deform rapidly in response to controlled filament rupture. Vimentin networks, which have not previously been studied by rheologic methods, exhibit some unusual viscoelastic properties not shared by actin or tubulin. They are less rigid (have lower shear moduli) at low strain but harden at high strains and resist breakage, suggesting they maintain cell integrity. The differences between F-actin and vimentin are optimal for the formation of a composite material with a range of properties that cannot be achieved by either polymer alone. Microtubules are unlikely to contribute significantly to interphase cell rheology alone, but may help stabilize the other networks. C1 UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,BERKELEY,CA 94720. MAX PLANCK INST CELL BIOL,W-6802 LADENBURG,GERMANY. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. RP JANMEY, PA (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL UNIT,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR38910] NR 45 TC 414 Z9 418 U1 9 U2 58 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 APR PY 1991 VL 113 IS 1 BP 155 EP 160 DI 10.1083/jcb.113.1.155 PG 6 WC Cell Biology SC Cell Biology GA FD834 UT WOS:A1991FD83400015 PM 2007620 ER PT J AU MEYEROVITCH, J ROTHENBERG, P SHECHTER, Y BONNERWEIR, S KAHN, CR AF MEYEROVITCH, J ROTHENBERG, P SHECHTER, Y BONNERWEIR, S KAHN, CR TI VANADATE NORMALIZES HYPERGLYCEMIA IN 2 MOUSE MODELS OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE INSULIN ACTION; INSULIN RECEPTOR KINASE; TYROSINE PHOSPHORYLATION; DIABETES MELLITUS THERAPY ID TYROSINE KINASE-ACTIVITY; PHOSPHOTYROSYL-PROTEIN PHOSPHATASE; GLYCOGEN-SYNTHASE; GLUCOSE-TRANSPORT; SKELETAL-MUSCLE; HUMAN-PLACENTA; BLOOD-GLUCOSE; RECEPTOR; PHOSPHORYLATION; MEMBRANE AB We have studied the effects of oral administration of vanadate, an insulinometic agent and a potent inhibitor of phosphotyrosyl protein phosphatase (PTPase) in vitro, on blood glucose and PTPase action, in two hyperinsulinemic rodent models of non-insulin-dependent diabetes mellitus (NIDDM). Oral administration of vanadate (0.25 mg/ml in the drinking water) to ob/ob mice for 3 wk lowered blood glucose level from 236 +/- 4 to 143 +/- 2 mg/dl without effect on body weight. Administration of vanadate to db/db mice produced a similar effect. Electron microscopic examination revealed no signs of hepatotoxicity after 47 d of treatment. There was a slight reduction in insulin receptor autophosphorylation when tested by immunoblotting with antiphosphotyrosine antibody after in vivo stimulation, and the phosphorylation of the endogenous substrate of the insulin receptor, pp185, was markedly decreased in the ob/ob mice. Both cytosolic and particulate PTPase activities in liver of ob/ob mice measured by dephosphorylation of a P-32-labeled peptide corresponding to the major site of insulin receptor autophosphorylation were decreased by approximately 50% (P < 0.01). In db/db diabetic mice, PTPase activity in the cytosolic fraction was decreased to 53% of control values (P < 0.02) with no significant difference in the particulate PTPase activity. Treatment with vanadate did not alter hepatic PTPase activity as assayed in vitro, or receptor and substrate phosphorylation as assayed in vivo, in ob/ob mice despite its substantial effect on blood glucose. These data indicate that vanadate is an effective oral hypoglycemic treatment in NIDDM states and suggest that its major effects occurs distal to the insulin receptor tyrosine kinase. C1 JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCRR NIH HHS [RR05673]; NIDDK NIH HHS [DK 36836, DK 31036] NR 51 TC 167 Z9 169 U1 1 U2 6 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 APR PY 1991 VL 87 IS 4 BP 1286 EP 1294 DI 10.1172/JCI115131 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FE722 UT WOS:A1991FE72200023 PM 1707061 ER PT J AU DASHEIFF, RM AF DASHEIFF, RM TI SUDDEN UNEXPECTED DEATH IN EPILEPSY - A SERIES FROM AN EPILEPSY SURGERY PROGRAM AND SPECULATION ON THE RELATIONSHIP TO SUDDEN CARDIAC DEATH SO JOURNAL OF CLINICAL NEUROPHYSIOLOGY LA English DT Article DE SUDDEN UNEXPECTED DEATH; SEIZURES; EPILEPSY SURGERY ID EPILEPTOGENIC ACTIVITY; UNEXPLAINED DEATH; AUTONOMIC DYSFUNCTION; NEURAL DISCHARGE; ARRHYTHMIAS; SEIZURES AB Sudden unexpected death represents a significant cause of mortality in people with epilepsy. It derives this significance not because it is the most frequent cause of death but because it is apparently a direct consequence of a seizure. The implication is that epilepsy is an inherently lethal disorder. Seven patients who were studied in an epilepsy surgery program died a sudden unexpected death. This incidence of sudden unexpected death was five times higher than the 1-2/1,000 per year reported in the general epilepsy population. Sudden unexpected death shares some of the characteristics associated with sudden cardiac death, which kills 300,000 people in the United States each year. A cardiac arrhythmia, usually ventricular fibrillation, is the most common terminal event for sudden cardiac death and is the leading candidate as the mechanism for sudden unexpected death. Despite this knowledge, little is known on how to identify a high-risk group of patients for sudden death or how these deaths might be prevented. C1 US DEPT VET AFFAIRS,NEUROL SERV,PITTSBURGH,PA. UNIV PITTSBURGH,CTR EPILEPSY,JOHNSTOWN,PA 15902. US DEPT VET AFFAIRS,SCH MED,DEPT NEUROL,PITTSBURGH,PA. US DEPT VET AFFAIRS,SCH MED,DEPT PSYCHIAT,PITTSBURGH,PA. NR 44 TC 127 Z9 128 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0736-0258 J9 J CLIN NEUROPHYSIOL JI J. Clin. Neurophysiol. PD APR PY 1991 VL 8 IS 2 BP 216 EP 222 DI 10.1097/00004691-199104000-00010 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FK455 UT WOS:A1991FK45500010 PM 2050822 ER PT J AU CUMMINGS, FJ KIM, K NEIMAN, RS COMIS, RL OKEN, MM WEITZMAN, SA MANN, RB OCONNELL, MJ AF CUMMINGS, FJ KIM, K NEIMAN, RS COMIS, RL OKEN, MM WEITZMAN, SA MANN, RB OCONNELL, MJ TI PHASE-II TRIAL OF PENTOSTATIN IN REFRACTORY LYMPHOMAS AND CUTANEOUS T-CELL DISEASE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC LYMPHOCYTIC-LEUKEMIA; CLINICAL CONSEQUENCES; 2'-DEOXYCOFORMYCIN; ADENOSINE; DEOXYCOFORMYCIN; INHIBITION; MALIGNANCY; TOXICITY; CANCER C1 HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. MALLORY INST PATHOL,BOSTON,MA. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. BROWN UNIV,PROVIDENCE,RI 02912. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. NORTHWESTERN UNIV,MED CTR,CHICAGO,IL 60611. RP CUMMINGS, FJ (reprint author), ROGER WILLIAMS GEN HOSP,825 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. FU NCI NIH HHS [CA 21115, CA 15947, CA 23318] NR 34 TC 84 Z9 85 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 APR PY 1991 VL 9 IS 4 BP 565 EP 571 PG 7 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300005 PM 2066753 ER PT J AU GOORIN, AM SHUSTER, JJ BAKER, A HOROWITZ, ME MEYER, WH LINK, MP AF GOORIN, AM SHUSTER, JJ BAKER, A HOROWITZ, ME MEYER, WH LINK, MP TI CHANGING PATTERN OF PULMONARY METASTASES WITH ADJUVANT CHEMOTHERAPY IN PATIENTS WITH OSTEOSARCOMA - RESULTS FROM THE MULTIINSTITUTIONAL OSTEOSARCOMA STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID OSTEOGENIC-SARCOMA; SURVIVAL; THORACOTOMY; RESECTION C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, BOSTON, MA 02115 USA. NCI, PEDIAT BRANCH, BETHESDA, MD 20892 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. STANFORD UNIV, MED CTR, SCH MED, STANFORD, CA 94305 USA. CHILDRENS HOSP STANFORD, PALO ALTO, CA 94304 USA. FU NCI NIH HHS [CA-31566, CA-29139, CA-41573] NR 14 TC 95 Z9 103 U1 0 U2 1 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 APR PY 1991 VL 9 IS 4 BP 600 EP 605 PG 6 WC Oncology SC Oncology GA FD863 UT WOS:A1991FD86300009 PM 2066757 ER PT J AU SANDERS, KM MURRAY, GB CASSEM, NH AF SANDERS, KM MURRAY, GB CASSEM, NH TI HIGH-DOSE INTRAVENOUS HALOPERIDOL FOR AGITATED DELIRIUM IN A CARDIAC PATIENT ON INTRAAORTIC BALLOON PUMP SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter RP SANDERS, KM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 6 TC 23 Z9 23 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD APR PY 1991 VL 11 IS 2 BP 146 EP 147 DI 10.1097/00004714-199104000-00021 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA FG853 UT WOS:A1991FG85300015 PM 2056143 ER PT J AU ARULANANDAM, ARN KOYASU, S REINHERZ, EL AF ARULANANDAM, ARN KOYASU, S REINHERZ, EL TI T-CELL RECEPTOR-INDEPENDENT CD2 SIGNAL TRANSDUCTION IN FCR+ CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NATURAL-KILLER CELLS; ERYTHROCYTE BINDING-PROTEIN; LYMPHOCYTE-T; ALTERNATIVE PATHWAY; MONOCLONAL-ANTIBODY; GAMMA RECEPTOR; MAST-CELL; ACTIVATION; MURINE; EXPRESSION AB CD2 subserves both adhesion and signal transduction functions in T cells, thymocytes, and natural killer (NK) cells. In mature T lymphocytes, CD2-mediated signaling function apparently requires surface expression of T cell receptors (TCRs). In contrast, in CD2+ CD3- NK cells and thymocytes, signal transduction through CD2 is TCR independent. To resolve this paradox and characterize TCR-independent triggering mechanisms, we transfected a human CD2 cDNA into a murine mast cell line, C1.MC/57 (Fc-epsilon-RI+, Fc-gamma-RII+, Fc-gamma-RIII+), which is known to produce interleukin 6 (IL-6) as well as release histamine in response to crosslinking of Fc-epsilon-RI. In the CD2 transfectant, a combination of anti-T11(2) + anti-T11(3) monoclonal antibodies (mAbs) induced a rise in intracellular free calcium ([Ca2+]i), IL-6 production, and histamine release. As expected no activation was mediated by the same mAbs in C1.MC/57. F(ab)'2 fragments of the activatory combination of anti-T11(2) + anti-T11(3) mAbs induced IL-6 in the CD2-transfected mast cells, demonstrating an Fc-gamma-receptor ectodomain-independent triggering mechanism. In addition, either intact anti-T11(2) or anti-T11(3) IgG alone, which failed to induce [Ca2+]i mobilization in the transfectant, was able to induce IL-6 production. A mAb directed against both Fc-gamma-RII (previously denoted as Fc-gamma-RIIb) and Fc-gamma-RIII (previously denoted as Fc-gamma-RIIa) inhibits this induction. These results indicate that: (a) Ca2+ mobilization is not essential for IL-6 production; and (b) crosslinking of CD2 and Fc-gamma receptors via intact anti-CD2 IgG stimulates IL-6 production. Thus, CD2-mediated IL-6 production occurs by both Fc receptor ectodomain-independent as well as Fc receptor ectodomain-dependent mechanisms in these nonlymphoid cells. Northern blot analysis demonstrates that although the mast cells do not express CD3-zeta or CD3-eta mRNA, they express Fc-epsilon-RI-gamma mRNA. The latter is a known component of Fc-gamma-RIII as well as Fc-epsilon-RI, has significant homology to CD3-zeta/eta, and is thought to have a signal transduction function. In these mast cells, CD2 signaling machinery does not require CD3-zeta/eta and may be linked to the Fc-epsilon-RI-gamma-subunit. We predict that this subunit or a related structure may confer a TCR-independent signal transduction pathway upon CD2 in CD3- NK cells, thymocytes, and certain B lymphocytes. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ARULANANDAM, ARN (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-21226] NR 55 TC 23 Z9 23 U1 0 U2 3 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 APR 1 PY 1991 VL 173 IS 4 BP 859 EP 868 DI 10.1084/jem.173.4.859 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FE128 UT WOS:A1991FE12800009 PM 1706751 ER PT J AU PERKINS, DL BERRIZ, G KAMRADT, T SMITH, JA GEFTER, ML AF PERKINS, DL BERRIZ, G KAMRADT, T SMITH, JA GEFTER, ML TI IMMUNODOMINANCE - INTRAMOLECULAR COMPETITION BETWEEN T-CELL EPITOPES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; REPRESSOR CI PROTEIN; ANTIGEN; RECOGNITION; PEPTIDES; DETERMINANT; REPERTOIRE; IDENTIFICATION; SPECIFICITY; RESPONSES AB We have used an approach of linking previously characterized T cell epitopes into immunologically complex synthetic peptides in order to investigate the mechanism of immunodominance. Our results show that first, cI12-26 is highly dominant following immunization with the lambda repressor (cI) protein, but is a minor epitope in the context of the cI:NP peptide. In contrast, the dominant epitope in response to the cI:NP peptide is a new junctional epitope, which is composed of sequences derived from both the cI and influenza nucleoprotein (NP) segments of the composite peptide. Second, T cell recognition of cI:NP is not significantly altered by Ag processing, based on results from glutaraldehyde-fixed APC. Third, the relative affinities of cI and cI:NP for MHC binding are similar, based on in vitro competition, excluding competition at the level of MHC binding as the determinant of immunodominance. Taken together, these results are consistent with the hypothesis that immunodominance of cI:NP is determined by peptide conformation, which affects the configuration of peptide binding to MHC, thus altering T cell recognition. In conclusion, immunodominance is not simply a function of the primary amino acid sequence, but is a function of the context of the epitope within the protein molecule. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP PERKINS, DL (reprint author), BRIGHAM & WOMENS HOSP,IMMUNOGENET & TRANSPLANT LAB,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK01693] NR 26 TC 85 Z9 86 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2137 EP 2144 PG 8 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700010 PM 1706388 ER PT J AU TORIMOTO, Y SUGITA, K WEINBERG, DS DANG, NH DONAHUE, C LETVIN, NL SCHLOSSMAN, SF MORIMOTO, C AF TORIMOTO, Y SUGITA, K WEINBERG, DS DANG, NH DONAHUE, C LETVIN, NL SCHLOSSMAN, SF MORIMOTO, C TI DEVELOPMENT OF A MONOCLONAL-ANTIBODY, ANTI-6C2, WHICH IS INVOLVED IN THE INTERACTION OF CD4 T-HELPER CELLS AND ACTIVATED B-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; LYMPHOCYTES-T; INDUCER CELLS; LFA-1; UCHL1; EXPRESSION; MOLECULES; SUBSET; DIFFERENTIATION; SUBPOPULATIONS AB We have developed a mAb anti-6C2, by immunizing mice with T cell line derived from the Callithrix jacchus (common marmoset). Anti-6C2 is reactive with approximately 50% of unfractionated T cells, 50% of CD4+ cells, and 40% of CD8+ cells. Regarding CD4+ cells, anti-6C2-reactive cells substantially overlap with the CD29+CD45RO+ Th cell population. Moreover, anti-6C2 can divide these T cells into 6C2+ and 6C2- subpopulations. The CD4+ CD45RO+6C2+ cells maximally respond to soluble Ag such as tetanus toxoid and provide strong helper function for PWM-driven B cell IgG synthesis. Most interestingly, anti-6C2 was also reactive against activated B cells but not resting B cells; furthermore, this epitope was inducible through activation of resting B cells or B cell line. Biochemical characterization showed that anti-6C2 precipitated two glycoproteins with the relative molecular weights of 180,000 and 95,000 from I-125-surface labeled cell lysate. Sequential immunoprecipitation studies demonstrated that these two glycoproteins were the lymphocyte function-associated antigen (LFA-1) Ag complex (CD11a/18). Significantly, although this antibody did not inhibit cytotoxic killer T cell responses and Ag-induced T cell proliferation as did conventional anti-LFA-1, it did inhibit PWM-driven B cell IgG synthesis. Because 6C2 expression was induced after B cell activation, the above results strongly suggest that the 6C2 molecule may play a role in the interaction of CD4 helper cells and activated B lymphocytes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-29530, AI-12069]; NIAMS NIH HHS [AR-33713] NR 43 TC 10 Z9 10 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2176 EP 2184 PG 9 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700015 PM 1706389 ER PT J AU YOKOYAMA, S STAUNTON, D FISHER, R AMIOT, M FORTIN, JJ THORLEYLAWSON, DA AF YOKOYAMA, S STAUNTON, D FISHER, R AMIOT, M FORTIN, JJ THORLEYLAWSON, DA TI EXPRESSION OF THE BLAST-1 ACTIVATION/ADHESION MOLECULE AND ITS IDENTIFICATION AS CD48 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LYMPHOMA CELL-LINES; RECEPTOR; ANTIGEN; LFA-3; IL-4; INFECTION; CLONING; PROTEIN; OX-45 AB We have analyzed the induction and expression of Blast-1 at the mRNA and protein levels and demonstrated its identity with CD48. Blast-1/CD48 is expressed on a wider range of cell types, notably T cells and monocytes, than previously thought, but appears to be restricted to lymphoid and myeloid cells. Resting B and T cells express Blast-1/CD48 molecules at the cell surface; however, they lack the epitope recognized by the 17D6 mAb. Resting B cells express no detectable Blast-1/CD48 mRNA. Induction by EBV infection or stimulation with PMA, IL-4, or PHA results in increased levels of Blast-1/CD48 protein (both 6.28 and 17D6 epitopes) at the cell surface. Detailed analysis of EBV-induced expression revealed that it is due to increased steady-state levels of Blast-1/CD48 mRNA induced by transforming but not nontransforming strains of the virus. Induction by IL-1-beta, ionomycin, or suboptimal levels of PMA plus ionomycin results in increased expression of the 17D6 epitope only. In transfected Cos-7 cells Blast-1/CD48 at the cell surface expresses only the 6.28 epitope, whereas cytoplasmic molecules express both 17D6 and 6.28 epitopes. We suggest that these results are most consistent with the idea that Blast-1/CD48 molecules are complexed at the surface of resting cells and Cos-7 cells, resulting in masking of the 17D6 epitope. Activation causes dissociation of the complex, revealing the 17D6 epitope. The existence of 17D6+6.28- Blast-1/CD48 molecules was demonstrated by immunoprecipitation analysis, which also revealed that, unlike the rest of the molecules, this subset was resistant to digestion with glycosylphosphatidylinositol-specific phospholipase C. C1 TUFTS UNIV,SCH MED,DEPT PATHOL,136 HARRISON AVE,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NCI NIH HHS [CA-28737]; NIAID NIH HHS [AI-15310] NR 21 TC 82 Z9 82 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 APR 1 PY 1991 VL 146 IS 7 BP 2192 EP 2200 PG 9 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700017 PM 1848579 ER PT J AU KANSAS, GS WOOD, GS TEDDER, TF AF KANSAS, GS WOOD, GS TEDDER, TF TI EXPRESSION, DISTRIBUTION, AND BIOCHEMISTRY OF HUMAN CD39 - ROLE IN ACTIVATION-ASSOCIATED HOMOTYPIC ADHESION OF LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID N-GLYCOSIDASE-F; NATURAL-KILLER CELLS; HUMAN T-CELLS; FUNCTIONAL-CHARACTERIZATION; MONOCLONAL-ANTIBODIES; GLYCOPROTEINS; INDUCTION; LYMPHOMA; BINDING; ANTIGEN AB The distribution, biochemical properties, and function of CD39 were characterized with the use of a new mAb termed 400. CD39 is an acidic (isoelectric point, approximately 4.2) glycoprotein of M(r) approximately 78,000, containing approximately 24 kDa of N-linked oligosaccharide but no detectable O-linked sugars. CD39 was not expressed by resting blood T, B, or NK cells, neutrophils, or monocytes, but was expressed on activated NK cells, B cells, subsets of T cells, and T cell clones. Furthermore, the pattern of expression of CD39 was distinct from the "classic" activation Ag CD25 and CD71, inasmuch as it was expressed long after expression of CD25 and CD71 had returned to basal levels. CD39 was easily detectable on EBV-transformed B cell lines but was absent from pre-B and non-EBV-transformed B cell lines, most myeloid cell lines, and leukemic T cell lines. In lymphoid tissues, germinal center cells expressed little or no CD39, whereas some paracortical lymphocytes and most macrophages and dendritic cells were positive. CD39 was strongly expressed by endothelium in all tissues examined, including skin, and was present on some, but not all, endothelial cell lines propagated in vitro. Interestingly, mAb binding to certain epitopes on CD39 induced rapid homotypic adhesion that appeared to involve LFA-1 (CD11a/CD18), but was morphologically and kinetically distinct from that induced by PMA. Anti-CD39 mAb also induced homotypic adhesion in an CD11/CD18-EBV-transformed B cell line derived from a patient with severe leukocyte adhesion deficiency. This adhesion was unaffected by EDTA, suggesting that this pathway of anti-CD39-induced homotypic adhesion was not mediated by any of the known integrins. These studies suggest that CD39 is involved in the cellular signaling that regulates adhesion. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,DEPT DERMATOL,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,DEPT PATHOL,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SKIN DIS RES CTR,CLEVELAND,OH 44106. VET ADM MED CTR,CLEVELAND,OH 44106. 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 46 TC 156 Z9 158 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2235 EP 2244 PG 10 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700023 PM 1672348 ER PT J AU KOKA, P VANDEMARK, K FALLER, DV AF KOKA, P VANDEMARK, K FALLER, DV TI TRANSACTIVATION OF GENES ENCODING ACTIVATION-ASSOCIATED HUMAN LYMPHOCYTE-T SURFACE-PROTEINS BY MURINE RETROVIRAL SEQUENCES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CLASS-I ANTIGENS; LEUKEMIA-VIRUS; MOLECULAR-CLONING; TRANSCRIPTIONAL ACTIVATOR; NUCLEOTIDE-SEQUENCE; CELL ACTIVATION; MESSENGER-RNA; EXPRESSION; RECEPTOR; FAMILY AB The mechanisms whereby RNA leukemia viruses cause T lymphocyte leukemias or lymphomas after a long latent period are not understood. We report here that infection of human T lymphocyte lines with a murine leukemia virus results in up-regulation of a number of lymphocyte-specific cell surface Ag. These proteins include CD2, CD3, CD4, the TCR, and MHC class I Ag. The expression of other cell surface proteins, such as LFA-3, are unaffected by the presence of the retrovirus. This up-regulation occurs at the level of the mRNA transcripts encoding these proteins, and is the result of increased transcription of the respective genes. The increases in transcription are the result of a trans-activation process by the leukemia virus. The transient introduction of chimeric genes consisting of MHC class I gene promoter sequences attached to the reporter gene CAT into human T cells containing murine retrovirus produces stimulated transcription of the reporter gene. Subgenomic portions of the murine leukemia virus containing the long terminal repeats and the 5' untranslated region are sufficient to produce transactivation of the same set of T cell genes as the whole leukemia virus. The finding that murine leukemia viruses enhance transcription and expression of a group of T cell surface proteins, all of which have been reported to be capable of transducing an activating signal to the lymphocyte, may be relevant to the pathophysiologic mechanisms whereby these viruses induce leukemias and lymphomas. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,ROOM 1640,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 45 TC 21 Z9 21 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1991 VL 146 IS 7 BP 2417 EP 2425 PG 9 WC Immunology SC Immunology GA FE127 UT WOS:A1991FE12700048 PM 2005405 ER PT J AU HORVATH, K GRANSTEIN, RD AF HORVATH, K GRANSTEIN, RD TI EXPOSURE TO PSORALEN PLUS LONGWAVE ULTRAVIOLET-RADIATION POTENTIATES CYCLOSPORINE-MEDIATED PROLONGATION OF RAT CARDIAC ALLOGRAFT SURVIVAL SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 535 EP 535 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100044 ER PT J AU GRABBE, S BRUVERS, S LINDGREN, AM GRANSTEIN, RD AF GRABBE, S BRUVERS, S LINDGREN, AM GRANSTEIN, RD TI REGULATION OF EPIDERMAL-CELL TUMOR-ANTIGEN PRESENTATION BY TNF-ALPHA, GM-CSF AND ULTRAVIOLET-RADIATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY 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 BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 543 EP 543 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100093 ER PT J AU HUSAIN, Z CHOW, MP WICK, MM AF HUSAIN, Z CHOW, MP WICK, MM TI CORRELATION BETWEEN INVIVO AND INVITRO MODELS FOR THE ROLE OF EGFR ACTIVATION IN EPIDERMAL NEOPLASIA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 543 EP 543 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100094 ER PT J AU KANG, S BARNHILL, RL MIHM, MC DUNCAN, LM SOBER, AJ AF KANG, S BARNHILL, RL MIHM, MC DUNCAN, LM SOBER, AJ TI MELANOMA RISK IS INCREASED IN PATIENTS WITH ATYPICAL NEVI EVEN WITH CLOSE FOLLOW-UPS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 571 EP 571 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100261 ER PT J AU MUCCINI, J KOLLIAS, N PHILLIPS, S ANDERSON, R SOBER, A DRAKE, L AF MUCCINI, J KOLLIAS, N PHILLIPS, S ANDERSON, R SOBER, A DRAKE, L TI ASSESSABLE PHOTOGRAPHIC RECORDS OF THE CLINICAL-FEATURES ASSOCIATED WITH PHOTOAGING SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 571 EP 571 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100263 ER PT J AU MAYTIN, EV MENARD, S WIMBERLY, JM AF MAYTIN, EV MENARD, S WIMBERLY, JM TI STRESS PROTEINS IN MOUSE KERATINOCYTES - ALTERED PATTERNS OF SYNTHESIS AFTER HEAT-SHOCK OR UVB LIGHT (290-320 NM) SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 587 EP 587 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100360 ER PT J AU MORAN, M GANGE, RW LYON, N SIEBERT, B KOCHEVAR, IE AF MORAN, M GANGE, RW LYON, N SIEBERT, B KOCHEVAR, IE TI EFFECTS OF SYSTEMIC INDOMETHACIN, BW755C, AND MECLIZINE ON CHRONIC UVB-INDUCED EFFECTS IN HAIRLESS MOUSE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 588 EP 588 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100363 ER PT J AU KOLLIAS, N YOUN, J GANGE, R ANDERSON, RR AF KOLLIAS, N YOUN, J GANGE, R ANDERSON, RR TI SUPPRESSION OF THE ERYTHEMA REACTION TO UVB BY A 2ND EXPOSURE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114. SEOUL NATL UNIV,DEPT DERMATOL,SEOUL 151,SOUTH KOREA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 590 EP 590 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100376 ER PT J AU THOMAS, L ETOH, T MIHM, MC BYERS, HR AF THOMAS, L ETOH, T MIHM, MC BYERS, HR TI ATTACHMENT STUDIES OF HUMAN PRIMARY, RECURRENT CUTANEOUS AND METASTATIC MELANOMA ON HYALURONIC-ACID COATED SUBSTRATES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 598 EP 598 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100427 ER PT J AU ETOH, T BYERS, HR AF ETOH, T BYERS, HR TI LOCALIZATION AND EXPRESSION OF ALPHA-ACTININ IN CULTURED HUMAN PRIMARY, RECURRENT PRIMARY AND METASTATIC MELANOMA CELL-LINES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1991 VL 96 IS 4 BP 599 EP 599 PG 1 WC Dermatology SC Dermatology GA FE591 UT WOS:A1991FE59100428 ER PT J AU RICHTER, JM AF RICHTER, JM TI TECHNOLOGY-ASSESSMENT - CAN BILIARY LITHOTRIPSY PAY ITS OWN WAY SO JOURNAL OF LITHOTRIPSY & STONE DISEASE LA English DT Editorial Material RP RICHTER, JM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 1040-2152 J9 J LITHOTR STONE DIS PD APR PY 1991 VL 3 IS 2 BP 125 EP 127 PG 3 WC Gastroenterology & Hepatology; Urology & Nephrology SC Gastroenterology & Hepatology; Urology & Nephrology GA FJ941 UT WOS:A1991FJ94100003 PM 10149152 ER PT J AU SIAKOTOS, A HAINES, J DAWSON, G AF SIAKOTOS, A HAINES, J DAWSON, G TI 3RD INTERNATIONAL-SYMPOSIUM ON THE NEURONAL CEROID-LIPOFUSCINOSES (BATTEN DISEASE), INDIANAPOLIS, INDIANA, USA SO JOURNAL OF MEDICAL GENETICS LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129. UNIV CHICAGO,SCH MED,DEPT PEDIAT,CHICAGO,IL 60637. RP SIAKOTOS, A (reprint author), INDIANA UNIV,SCH MED,DEPT PATHOL,INDIANAPOLIS,IN 46202, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD APR PY 1991 VL 28 IS 4 BP 284 EP 285 DI 10.1136/jmg.28.4.284 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA FD304 UT WOS:A1991FD30400016 ER PT J AU PENACRUZ, V REISS, C MCINTOSH, K AF PENACRUZ, V REISS, C MCINTOSH, K TI EFFECT OF RESPIRATORY SYNCYTIAL VIRUS-INFECTION ON MICE WITH PROTEIN-MALNUTRITION SO JOURNAL OF MEDICAL VIROLOGY LA English DT Article DE RSV; NUTRITION; PULMONARY INFECTION ID T-CELLS; LYMPHOCYTES; CHILDREN AB Respiratory syncytial virus (RSV) pulmonary infection was produced in BALB/c mice fed protein-deficient diets in an effort to understand the severity of viral pneumonia in infants in developing countries. As in previously published experiments with Sendai virus, animals on the deficient diet became clinically malnourished, and certain aspects of their cell-mediated immunity were altered. The course of RSV infection in protein-deprived mice was essentially identical to that in normally nourished animals. The titer of virus recovered from lung homogenates over time, as well as the histologic picture of bronchiolitis, were identical under all experimental conditions. This model, unlike that of Sendai virus infection, fails to demonstrate an effect of protein malnutrition on RSV infection. C1 CHILDRENS HOSP MED CTR,DEPT PAEDIAT,DIV INFECT DIS,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. OI Reiss, Carol/0000-0003-4353-8882 FU NIAID NIH HHS [R01 AI 18083, R01 AI 22389] NR 21 TC 2 Z9 2 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 0146-6615 J9 J MED VIROL JI J. Med. Virol. PD APR PY 1991 VL 33 IS 4 BP 219 EP 223 DI 10.1002/jmv.1890330402 PG 5 WC Virology SC Virology GA FJ255 UT WOS:A1991FJ25500001 PM 1906929 ER PT J AU ROSOWSKY, A FORSCH, RA BADER, H FREISHEIM, JH AF ROSOWSKY, A FORSCH, RA BADER, H FREISHEIM, JH TI SYNTHESIS AND INVITRO BIOLOGICAL-ACTIVITY OF NEW DEAZA ANALOGS OF FOLIC-ACID, AMINOPTERIN, AND METHOTREXATE WITH AN L-ORNITHINE SIDE-CHAIN SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID DIHYDROFOLATE-REDUCTASE; FOLYLPOLYGLUTAMATE SYNTHETASE; ANTITUMOR-ACTIVITY; 2,OMEGA-DIAMINOALKANOIC ACIDS; N10-METHYLFOLIC ACID; CELL-GROWTH; INHIBITION; REPLACEMENT; PHOSPHONATE; DERIVATIVES AB The 5-deaza and 5,8-dideaza analogues of N-alpha-pteroyl-L-ornithine (Pter-Orn), the 5-deaza, 8-deaza, and 5,8-dideaza analogues of N-alpha-(4-amino-4-deoxypteroyl)-L-ornithine (APA-Orn), and the N-delta-carboxymethyl derivative of N-alpha-(4-amino-4-deoxy-N-10-methylpteroyl)-L-ornithine (mAPA-Orn) were synthesized and tested as inhibitors of dihydrofolate reductase (DHFR) and as inhibitors of tumor cell growth in culture. Reductive amination of 2-acetamido-6-formylpyrido[2,3-d]pyrimidin-4(H-3)-one with methyl N-alpha-(4-aminobenzoyl)-N-delta-(benzyloxycarbonyl)-L-ornithinate followed by removal of the blocking groups afforded the 5-deaza analogue of Pter-Orn, whereas N-alkylation of methyl N-alpha-(4-aminobenzoyl)-N-delta-(benzyloxycarbonyl)-L-ornithinate with 2-amino-6-(bromomethyl)quinazolin-4(H-3)-one and deprotection gave the corresponding 5,8-dideaza analogue. Reductive coupling of 2,4-diaminopyrido[2,3-d]pyrimidine-6-carbonitrile and 4-aminobenzoic acid followed by reaction with 95-97% formic acid yielded 4-amino-4-deoxy-5-deaza-N-10-formylpteroic acid, which on condensation with methyl N-delta-(benzyloxycarbonyl)-L-ornithinate and deprotection gave the 5-deaza analogue of APA-Orn. A similar sequence starting from 2,4-diaminoquinazoline-6-carbonitrile led to the corresponding 5,8-dideaza compound, whereas treatment of 2,4-diaminopyrido[3,2-d]pyrimidine-6-methanol with phosphorus tribromide followed by condensation with methyl N-alpha-(4-aminobenzoyl)-N-delta-(benzyloxycarbonyl)-L-ornithinate and deprotection afforded the 8-deaza analogue. For the preparation of the N-delta-carboxymethyl derivative of mAPA-Orn, N-alpha-(benzyloxycarbonyl)-L-ornithine was subjected to N-delta-monoalkylation with glyoxylic acid and sodium cyanoborohydride, followed by N-delta-acylation with ethyl trifluoroacetate, N-alpha-deprotection by hydrogenolysis, condensation with 4-amino-4-deoxy-N-10-methylpteroic acid, and N-delta-deprotection by gentle treatment with ammonia. The 2,4-diamino derivatives all inhibited the growth of tumor cells in culture, with IC50 values of 0.2-2-mu-M, and inhibited purified DHFR with IC50 values of 0.02-0.08-mu-M. Deletion of ring nitrogens and N-delta-carboxymethylation both increased potency in the cell growth assay; however, the ornithine derivatives were less potent than aminopterin or methotrexate. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MED COLL OHIO,DEPT BIOCHEM,TOLEDO,OH 43699. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA39867, CA25394, CA41461] NR 30 TC 21 Z9 21 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR PY 1991 VL 34 IS 4 BP 1447 EP 1454 DI 10.1021/jm00108a032 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA FG776 UT WOS:A1991FG77600032 PM 2016722 ER PT J AU RIE, MA AF RIE, MA TI DEFINING THE LIMITS OF INSTITUTIONAL MORAL AGENCY IN HEALTH-CARE - A RESPONSE TO WILDES,KEVIN SO JOURNAL OF MEDICINE AND PHILOSOPHY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP RIE, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 1 TC 2 Z9 2 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0360-5310 J9 J MED PHILOS JI J. Med. Philos. PD APR PY 1991 VL 16 IS 2 BP 221 EP 224 PG 4 WC Ethics; Social Sciences, Biomedical SC Social Sciences - Other Topics; Biomedical Social Sciences GA FK763 UT WOS:A1991FK76300008 PM 11642889 ER PT J AU SEGAL, MM AF SEGAL, MM TI EPILEPTIFORM ACTIVITY IN MICROCULTURES CONTAINING ONE EXCITATORY HIPPOCAMPAL NEURON SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID SUSTAINED POTENTIAL SHIFTS; NMDA RECEPTOR ANTAGONIST; RAT SYMPATHETIC NEURONS; D-ASPARTATE ANTAGONIST; NEOCORTICAL NEURONS; SEIZURE ACTIVITY; MECHANISMS; INVITRO; CELLS; AFTERHYPERPOLARIZATION AB 1. Paroxysmal depolarizing shifts (PDSs) occur during interictal epileptiform activity. Sustained depolarizations are characteristic of ictal activity, and events resembling PDSs also occur during the sustained depolarizations. To study these elements of epileptiform activity in a simpler context, I used the in vitro chronic-excitatory-block model of epilepsy of Furshpan and Potter and the microculture technique of Segal and Furshpan. 2. Intracellular recordings were made from 93 single-neuron microcultures. Forty of these solitary neurons were excitatory; their action potentials were replaced by PDS-like events or sustained depolarizations as kynurenate was removed from the perfusion solution. PDS-like events were similar to PDSs in intact cortex, mass cultures, and microcultures with more than one neuron. Small voltage fluctuations were also seen in solitary excitatory neurons in the absence of recorded action potentials. Sustained depolarizations developed in 5 of the 40 excitatory neurons. Forty-eight of the 93 solitary neurons were inhibitory, with bicuculline-sensitive hyperpolarizations after the action potential (ascribable to gamma-aminobutyric acid-A autapses). None of the solitary inhibitory neurons displayed sustained depolarizations. Five of the 93 neurons were insensitive to both kynurenate and bicuculline and were not placed in either the excitatory or the inhibitory category. 3. Both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors contributed to the PDS-like events and sustained depolarizations. Only a non-NMDA glutamate receptor component was evident for the small voltage fluctuations. 4. Intracellular recordings were also made from two-neuron microcultures, each containing one excitatory neuron and one inhibitory neuron. Sustained depolarizations developed in five microcultures, in each case only in the excitatory neuron. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP SEGAL, MM (reprint author), HARVARD UNIV,SCH MED,DEPT NEUROBIOL,220 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NINDS NIH HHS [NS-01407-01, NS-02253-30] NR 50 TC 82 Z9 84 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3077 J9 J NEUROPHYSIOL JI J. Neurophysiol. PD APR PY 1991 VL 65 IS 4 BP 761 EP 770 PG 10 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA FF973 UT WOS:A1991FF97300001 PM 1646871 ER PT J AU ELLIOTT, ME JONES, HM TOMASKO, S GOODFRIEND, TL AF ELLIOTT, ME JONES, HM TOMASKO, S GOODFRIEND, TL TI SPHINGOSINE INHIBITS ANGIOTENSIN-STIMULATED ALDOSTERONE SYNTHESIS SO JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY LA English DT Article ID ADRENAL GLOMERULOSA CELLS; PROTEIN-KINASE-C; CALCIUM; BINDING; CYTOCHROME-P-450; PHOSPHORYLATION; SPHINGANINE; POTASSIUM; PATHWAY; CORTEX AB Sphingosine and other protein kinase C inhibitors were tested for their ability to inhibit aldosterone synthesis by bovine adrenal glomerulosa cells. Sphingosine inhibited angiotensin (AII)-stimulated aldosterone synthesis (IC50 of 5-mu-M). At doses that totally blocked steroidogenesis, sphingosine did not affect protein synthesis or [I-125]AII binding to cells. Sphingosine also inhibited dibutyryl cyclic AMP (dbcAMP)-stimulated aldosterone synthesis. Sphingosine inhibited pregnenolone synthesis from cholesterol, but not the conversion of progesterone or 20-alpha-hydroxycholesterol to aldosterone. These results suggest that sphingosine inhibits steroidogenesis at a locus close to that where stimulation occurs by AII and dbcAMP. Other protein kinase C inhibitors were tested. Retinal, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), and staurosporine inhibited aldosterone synthesis stimulated by AII and dbcAMP. Retinal and H-7 also inhibited progesterone conversion to aldosterone, and retinal blocked [I-125]AII binding. Staurosporine was more specific, inhibiting AII-stimulated aldosteronogenesis at concentrations which had little effect on conversion of progesterone to aldosterone. Because they inhibited dbcAMP stimulation, none of the inhibitors was sufficiently specific to use as a probe of the role of protein kinase C. The IC50 of sphingosine suggests that this or related products of lipid hydrolysis could act as endogenous regulators of adrenal cell function. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53705. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HYPERTENS RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 28 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-0760 J9 J STEROID BIOCHEM JI J. Steroid Biochem. Mol. Biol. PD APR PY 1991 VL 38 IS 4 BP 475 EP 481 DI 10.1016/0960-0760(91)90335-3 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA FL602 UT WOS:A1991FL60200009 PM 1851631 ER PT J AU KOH, HK CLAPP, RW BARNETT, JM NANNERY, WM TAHAN, SR GELLER, AC BHAWAN, J HARRIST, TJ KWAN, T STADECKER, M OKUN, MR DONG, JA BEATTIE, M PROUT, MN MURPHY, GF LEW, RA AF KOH, HK CLAPP, RW BARNETT, JM NANNERY, WM TAHAN, SR GELLER, AC BHAWAN, J HARRIST, TJ KWAN, T STADECKER, M OKUN, MR DONG, JA BEATTIE, M PROUT, MN MURPHY, GF LEW, RA TI SYSTEMATIC UNDERREPORTING OF CUTANEOUS MALIGNANT-MELANOMA IN MASSACHUSETTS - POSSIBLE IMPLICATIONS FOR NATIONAL INCIDENCE FIGURES SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID CANCER REGISTRATION; COMPLETENESS; TRENDS AB An independent tabulation of incidence of cutaneous malignant melanoma in Massachusetts indicates that 12% and perhaps as many as 19% of new cases of cutaneous malignant melanoma in Massachusetts are not recorded in the Massachusetts Cancer Registry, significantly more than the expected 5% (p = 0.0001). The increasing number of nonhospital medical settings in which melanomas can be diagnosed and/or treated appears to account for this discrepancy. We suspect that these findings in Massachusetts also apply to cancer reporting systems in other regions of the United States. We suggest that the true incidence of cutaneous malignant melanoma in Massachusetts, and perhaps in the United States, may be significantly higher than reported. C1 BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DERMATOPATHOL SECT,BOSTON,MA 02118. BOSTON UNIV,SCH PUBL HLTH,DERMATOPATHOL SECT,BOSTON,MA 02215. FAULKNER HOSP,DEPT PATHOL,BOSTON,MA 02130. BETH ISRAEL HOSP,DEPT DERMATOPATHOL,BOSTON,MA 02215. BOSTON DERMATOPATHOL LAB INC,BOSTON,MA. MASSACHUSETTS CANC REGISTRY,BOSTON,MA. NEW ENGLAND MED CTR HOSP,DEPT PATHOL,BOSTON,MA 02111. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DERMATOPATHOL UNIT,BOSTON,MA 02114. PATHOL SERV INC,BOSTON,MA. RP KOH, HK (reprint author), BOSTON UNIV,SCH MED,DEPT DERMATOL,80 E CONCORD ST,BOSTON,MA 02118, USA. OI Clapp, Richard/0000-0001-8174-0825 FU NCI NIH HHS [5-KO7-CA01380-01] NR 31 TC 41 Z9 41 U1 0 U2 1 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 APR PY 1991 VL 24 IS 4 BP 545 EP 550 DI 10.1016/0190-9622(91)70079-H PG 6 WC Dermatology SC Dermatology GA FD903 UT WOS:A1991FD90300003 PM 2033127 ER PT J AU CAPE, EG YOGANATHAN, AP WEYMAN, AE LEVINE, RA AF CAPE, EG YOGANATHAN, AP WEYMAN, AE LEVINE, RA TI ADJACENT SOLID BOUNDARIES ALTER THE SIZE OF REGURGITANT JETS ON DOPPLER COLOR FLOW MAPS SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MITRAL REGURGITATION; VALVULAR REGURGITATION; ECHOCARDIOGRAPHY; QUANTIFICATION; VISUALIZATION AB Recent studies have attempted to predict the severity of regurgitant lesions from jet size on Doppler flow maps. Jet size is a function of both regurgitant volume and fluid entrained from the receiving chamber and, for a free jet, is a function of its momentum at the orifice. However, regurgitant jets often approach or attach to cardiac walls, potentially altering their momentum and ability to expand by entrainment. Therefore, this study addressed the hypothesis that adjacent walls influence regurgitant jet size as seen on Doppler flow maps. Steady flow was driven through circular orifices (0.02 to 0.05 cm2) at physiologic velocities of 2 to 5 m/s. At a constant flow rate and orifice velocity, orifice position was varied to produce three jet geometries: free jets, jets adjacent to a horizontal chamber wall lying 1 cm below the orifice and wall jets with the orifice at the level of the wall. Doppler color flow imaging was performed at identical instrument settings for all jets. Two long-axis views of the jet were obtained: a vertical view perpendicular to the wall, resembling that most commonly used in patients to image the length of the jet, and a horizontal view parallel to the chamber wall. Velocities along the jet were also measured by Doppler mapping. Jets with their orifices adjacent to the wall but not at its level were deflected toward the wall proximally (the Coanda effect), increasing jet area in the vertical plane by 8 +/- 4% compared with corresponding free jets (p < 0.001), with no change in area in the horizontal plane. Wall jets with their orifices at the level of the wall were 34 +/- 5% smaller in area than free jets in the vertical plane (p < 0.0005) and 13 +/- 6% larger in area in the horizontal plane (p < 0.005). Distal velocities in jets encountering walls were higher than those of free jets (p < 0.0002). Therefore, in the views perpendicular to walls (vertical views) most commonly used in vivo for imaging jets near cardiac structures, a jet lying along the wall will appear smaller than a free jet produced by the same regurgitant flow. The wall jet can entrain fluid and expand only on one side and it spreads laterally over the surface to a greater extent than usual. The area of a deflected jet is slightly increased by the Coanda effect, which draws the proximal jet toward the wall. Therefore, jet size cannot be related to the degree of regurgitation without considering jet geometry and adjacent walls. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,PHILLIPS HOUSE 8,BOSTON,MA 02114. GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332. FU NHLBI NIH HHS [HL38176, HL45485] NR 31 TC 109 Z9 113 U1 1 U2 1 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 APR PY 1991 VL 17 IS 5 BP 1094 EP 1102 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FF474 UT WOS:A1991FF47400017 PM 2007708 ER PT J AU TUZCU, EM BLOCK, PC PALACIOS, IF AF TUZCU, EM BLOCK, PC PALACIOS, IF TI COMPARISON OF EARLY VERSUS LATE EXPERIENCE WITH PERCUTANEOUS MITRAL BALLOON VALVULOPLASTY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID STENOSIS; COMMISSUROTOMY; CATHETER; VALVE; VALVOTOMY; FEATURES; DOPPLER; ADULTS AB The immediate outcome of the first 150 patients (Group 1) and the last 161 patients (Group 2) who underwent percutaneous mitral balloon valvuloplasty was compared. There was no difference between the two groups in age, gender, New York Heart Association functional class, presence of calcification, atrial fibrillation, degree of mitral regurgitation, mean pulmonary artery pressure, left atrial pressure, cardiac output, pulmonary vascular resistance, mitral valve gradient and mitral valve area. Fewer patients in Group 1 than Group 2 had an echocardiographic score less-than-or-equal-to 8 (62% versus 69%, respectively, p = 0.02). The atrial septum was dilated with an 8 mm balloon in 74% of patients in Group 1 and with a 5 mm balloon in all patients in Group 2. Ratio of effective balloon dilating area to body surface area was larger in Group 1 than in Group 2 (4.05 +/- 0.7 versus 3.7 +/- 0.03 cm2/m2, p = 0.0001). A good result (mitral valve area greater-than-or-equal-to 1.5 cm2) was obtained in 77% and 75% in Groups 1 and 2, respectively (p = NS). After percutaneous mitral valvuloplasty, a greater-than-or-equal-to 2 grade increase in mitral regurgitation was noted in 12% of Group 1 and 6% of Group 2 (p = 0.02) and a left to right shunt was detected in 22% of Group 1 and 11% of Group 2 (p = 0.0001). There were three procedure-related deaths in Group 1, but none in Group 2. It is concluded that improvements in technique, patient selection and operator experience have decreased left to right shunting and the incidence of greater-than-or-equal-to 2+ increment in mitral regurgitation and have created a trend toward a lower mortality rate while maintaining the high success rate of percutaneous mitral balloon valvuloplasty. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 18 TC 51 Z9 54 U1 0 U2 1 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 APR PY 1991 VL 17 IS 5 BP 1121 EP 1124 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FF474 UT WOS:A1991FF47400020 PM 2007711 ER PT J AU GARABEDIAN, HD GOLD, HK LEINBACH, RC SVIZZERO, TA FINKELSTEIN, DM GUERRERO, JL COLLEN, D AF GARABEDIAN, HD GOLD, HK LEINBACH, RC SVIZZERO, TA FINKELSTEIN, DM GUERRERO, JL COLLEN, D TI BLEEDING-TIME PROLONGATION AND BLEEDING DURING INFUSION OF RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN DOGS - POTENTIATION BY ASPIRIN AND REVERSAL WITH APROTININ SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; LEFT-VENTRICULAR FUNCTION; INTRAVENOUS STREPTOKINASE; CORONARY THROMBOLYSIS; PLATELET-AGGREGATION; RANDOMIZED TRIAL; PHASE-I; PLASMA; INHIBITION; PA AB Thrombolytic therapy is associated with a bleeding tendency that may be exacerbated by adjunctive antiplatelet agents. The effect of recombinant tissue-type plasminogen activator (rt-PA) alone or in combination with aspirin on serial measurements of template bleeding time, ex vivo platelet aggregation and coagulation factors and the frequency of bleeding was studied in dogs. During infusion of rt-PA (15, 30 or 60-mu-g/kg per min for 90 min), a dose-related increase in bleeding time was observed. In a randomized blinded study of 25 dogs, the baseline bleeding time (mean +/- SD) was 3.5 +/- 1 min in control animals and 4 +/- 2 min after oral aspirin (15 mg/kg body weight). Infusion of rt-PA (15-mu-g/kg per min for 90 min) prolonged the bleeding time to a maximum of 15 +/- 12 min. In contrast, combined aspirin and rt-PA therapy produced an increase to > 30 min during infusion, reverting to 13 +/- 10 min within 2 h after cessation of infusion. Recurrent continuous bleeding from incision sites occurred in one of six dogs given aspirin alone, two of seven given rt-PA alone and all six dogs given both aspirin and rt-PA (p = 0.02). Bleeding time > 9 min correlated significantly with bleeding frequency (p < 0.0001), with a sensitivity of 100% and a specificity of 87%. Intravenous bolus injection of aprotinin (20,000 kallikrein inhibitor units/kg body weight) in six dogs given both rt-PA and aspirin produced a decrease in bleeding time from > 30 min to 9.5 +/- 9 min and resulted in cessation of bleeding. Thus, bleeding and bleeding time prolongation in this canine model are potentiated by a marked interactive effect of rt-PA and aspirin that is rapidly reversible. Template bleeding times may provide a useful quantitative index for monitoring the bleeding tendency associated with thrombolytic therapy. C1 MASSACHUSETTS GEN HOSP,DIV CARDIAC,ACC 4,SUITE 480,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV VERMONT,COLL MED,DEPT BIOCHEM,BURLINGTON,VT 05405. UNIV VERMONT,COLL MED,DEPT MED,BURLINGTON,VT 05405. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 FU NHLBI NIH HHS [HL-35058, HL-26215] NR 35 TC 24 Z9 24 U1 0 U2 1 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 APR PY 1991 VL 17 IS 5 BP 1213 EP 1222 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FF474 UT WOS:A1991FF47400035 PM 1706738 ER PT J AU BOURGOUIN, PM MCLOUD, TC FITZGIBBON, JF MARK, EJ SHEPARD, JO MOORE, EM RUMMENY, E BRADY, TJ AF BOURGOUIN, PM MCLOUD, TC FITZGIBBON, JF MARK, EJ SHEPARD, JO MOORE, EM RUMMENY, E BRADY, TJ TI DIFFERENTIATION OF BRONCHOGENIC-CARCINOMA FROM POSTOBSTRUCTIVE PNEUMONITIS BY MAGNETIC-RESONANCE-IMAGING - HISTOPATHOLOGIC CORRELATION SO JOURNAL OF THORACIC IMAGING LA English DT Article AB Obstructive pneumonitis frequently occurs distal to hilar bronchogenic carcinomas or in lung adjacent to peripheral tumors. The article evaluates the role of MRI in the differentiation of tumor from pneumonitis. Twelve patients underwent MRI of the thorax before surgery. T1-weighted (SE 310/20) and T2-weighted (SE 2000/60-120) images were obtained through the tumor and presumed areas of pneumonitis. Five histologic types of pneumonitis were identified on pathologic examination of the 12 specimens. Cholesterol pneumonitis, found in 7 patients, was the most common type. Organizing pneumonitis, bronchiectasis with mucus plugs, atelectasis, and abscess were found in 3, 4, 2, and 1 patients, respectively. MRI was able to differentiate tumor from pneumonitis in 5 of 6 patients with a hilar mass and in 5 of 6 patients with a peripheral tumor. This was achieved by a visual difference in signal intensity on heavily T2-weighted (SE 2000/120) images. Cholesterol pneumonitis and bronchiectasis with mucus plugs were always hyperintense relative to tumor, and organizing pneumonitis and atelectasis were isointense and indistinguishable from tumor. MRI can differentiate tumor from pneumonitis provided that pneumonitis is of the cholesterol type or if there are mucus plugs in the collapsed lung. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 30 Z9 35 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0883-5993 J9 J THORAC IMAG JI J. Thorac. Imaging PD APR PY 1991 VL 6 IS 2 BP 22 EP 27 DI 10.1097/00005382-199104000-00006 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FD781 UT WOS:A1991FD78100004 PM 1856898 ER PT J AU EBLE, JN YOUNG, RH AF EBLE, JN YOUNG, RH TI STROMAL OSSEOUS METAPLASIA IN CARCINOMA OF THE BLADDER SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; OSTEOSARCOMA; CARCINOSARCOMA; METAPLASIA ID URINARY-BLADDER AB Osseous metaplasia of the stroma of carcinomas of the bladder is a rare finding that must be distinguished from osteosarcoma and carcinosarcoma. We report a case of multifocal osseous metaplasia in a high grade urothelial carcinoma with extensive glandular differentiation, arising in the base of the bladder of an 84-year-old man. Reports of 11 other cases of stromal osseous metaplasia in primary bladder carcinomas and of 5 cases of stromal osseous metaplasia in metastases of bladder carcinoma are reviewed. C1 INDIANA UNIV,SCH MED,DEPT PATHOL,INDIANAPOLIS,IN 46202. INDIANA UNIV,SCH MED,EXPTL ONCOL LAB,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP EBLE, JN (reprint author), RICHARD L ROUDEBUSH VET ADM MED CTR,LAB SERV 113,1481 W 10TH ST,INDIANAPOLIS,IN 46202, USA. NR 17 TC 15 Z9 16 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 APR PY 1991 VL 145 IS 4 BP 823 EP 825 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA FE597 UT WOS:A1991FE59700034 PM 1900893 ER PT J AU BLUM, HE GALUN, E LIANG, TJ VONWEIZSACKER, F WANDS, JR AF BLUM, HE GALUN, E LIANG, TJ VONWEIZSACKER, F WANDS, JR TI NATURALLY-OCCURRING MISSENSE MUTATION IN THE POLYMERASE GENE TERMINATING HEPATITIS-B VIRUS-REPLICATION SO JOURNAL OF VIROLOGY LA English DT Article ID REVERSE TRANSCRIPTION; PLASMID DNA; PROTEIN; ENCAPSIDATION; SQUIRRELS; HEPATOMA; GENOME; RNA AB A hepatitis B virus (HBV) genome was cloned from human liver. Numerous mutations in all viral genes define this HBV DNA as a mutant, divergent from all known HBV DNA sequences. Functional analyses of this mutant demonstrated a defect blocking viral DNA synthesis. The genetic basis of this defect was identified as a single missense mutation in the 5' region of the viral polymerase gene, resulting in the inability to package pregenomic RNA into core particles. The replication defect could be trans-complemented by a full-length wild-type, but not by a full-length mutant or 3'-truncated wild-type, polymerase gene construct. Our findings indicate a critical role of the 5' polymerase gene region in the life cycle of the virus and suggest that introducing missense mutations in this region can be a strategy to terminate viral replication in vivo. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02116. RP BLUM, HE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MOLEC HEPATOL LAB,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-00048, AA-02666] NR 38 TC 143 Z9 146 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 1836 EP 1842 PG 7 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100023 PM 2002544 ER PT J AU FARNET, CM HASELTINE, WA AF FARNET, CM HASELTINE, WA TI DETERMINATION OF VIRAL-PROTEINS PRESENT IN THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 PREINTEGRATION COMPLEX SO JOURNAL OF VIROLOGY LA English DT Article ID MURINE LEUKEMIA-VIRUS; RETROVIRAL DNA; POL GENE; INTEGRATION AB Cytoplasmic extracts prepared from cells infected with metabolically radiolabeled virions of human immunodeficiency virus type 1 contain viral DNA in association with labeled viral proteins. Viral DNA can be purified from these extracts by gel filtration chromatography and sucrose gradient sedimentation as a part of a nucleoprotein complex containing integrase as the only viral protein detectable by immunoprecipitation and gel electrophoretic analysis. The purified complex contains no detectable gag gene products, including p17, p24, p7, or p6, and contains no additional pol gene products, including the p10 protease, p66 and p51 polymerase, or the p15 RNase H. Nearly all of the purified nucleoprotein complexes are capable of integrating into heterologous DNA targets in vitro. These observations demonstrate that integrase is a component of the human immunodeficiency virus type 1 preintegration complex and suggest that integrase may be the only viral protein necessary for the integration of retroviral DNA. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,COMM VIROL,BOSTON,MA 02115. OI Farnet, Chris/0000-0003-4927-198X FU NIAID NIH HHS [AI 24845] NR 15 TC 240 Z9 242 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 1910 EP 1915 PG 6 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100032 PM 2002549 ER PT J AU HELSETH, E OLSHEVSKY, U FURMAN, C SODROSKI, J AF HELSETH, E OLSHEVSKY, U FURMAN, C SODROSKI, J TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 ENVELOPE GLYCOPROTEIN REGIONS IMPORTANT FOR ASSOCIATION WITH THE GP41 TRANSMEMBRANE GLYCOPROTEIN SO JOURNAL OF VIROLOGY LA English DT Note ID HTLV-III/LAV; T4 MOLECULE; AIDS; RETROVIRUS; RECEPTOR; MEMBRANE; ANTIGEN; FUSION; CELLS; LAV AB Insertion of four amino acids into various locations within the amino-terminal halves of the human immunodeficiency virus type 1 gp120 or gp41 envelope glycoprotein disrupts the noncovalent association of these two envelope subunits (M. Kowalski, J. Potz, L. Basiripour, T. Dorfman, W.C. Goh, E. Terwilliger, A. Dayton, C. Rosen, W. A. Haseltine, and J. Sodroski, Science 237:1351-1355, 1987). To localize the determinants on the gp120 envelope glycoprotein important for subunit association, amino acids conserved among primate immunodeficiency viruses were changed. Substitution mutations affecting either of two highly conserved regions located at the amino (residues 36 to 45) and carboxyl (residues 491 to 501) ends of the mature gp120 molecule resulted in nearly complete dissociation of the envelope glycoprotein subunits. Partial dissociation phenotypes were observed for some changes affecting residues in the third and fourth conserved gp120 regions. These results suggest that hydrophobic regions at both ends of the gp120 glycoprotein contribute to noncovalent association with the gp41 transmembrane glycoprotein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-24755] NR 22 TC 254 Z9 255 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1991 VL 65 IS 4 BP 2119 EP 2123 PG 5 WC Virology SC Virology GA FC031 UT WOS:A1991FC03100059 PM 2002555 ER PT J AU SPERTINI, O FREEDMAN, AS BELVIN, MP PENTA, AC GRIFFIN, JD TEDDER, TF AF SPERTINI, O FREEDMAN, AS BELVIN, MP PENTA, AC GRIFFIN, JD TEDDER, TF TI REGULATION OF LEUKOCYTE ADHESION MOLECULE-1 (TQ1, LEU-8) EXPRESSION AND SHEDDING BY NORMAL AND MALIGNANT-CELLS SO LEUKEMIA LA English DT Article ID LYMPHOCYTE HOMING RECEPTOR; HIGH-ENDOTHELIAL VENULES; PROTEIN KINASE-C; DIFFERENTIATION ANTIGENS; SURFACE MOLECULE; MEL-14 ANTIGEN; LFA-1; RECOGNITION; LYMPHOMAS; DISTINCT AB The human leukocyte adhesion molecule-1 (LAM-1, TQ1, Leu-8) is involved in the binding of human leukocytes to high endothelial venules (HEV) of peripheral lymph nodes (LN). The regulation of LAM-1 expression is unique in that leukocyte stimulation induces a rapid down-modulation of LAM-1 from the cell surface. In this study, the regulation and function of LAM-1 was studied in detail in normal lymphocytes and compared with the LAM-1 of malignant leukocytes. Modulation of LAM-1 from the cell surface occurred concomitantly with the appearance of LAM-1 in the culture medium indicating that LAM-1 is cleaved from the cell surface. Shedding of LAM-1 was decreased in the presence of protein kinase C (PKC) inhibitors. As with normal lymphocytes, cells transfected with the LAM-1 cDNA and chronic lymphocytic leukemia (CLL) cells also shed LAM-1 following phorbol myristate acetate (PMA) exposure. CLL cells expressed the same Mr LAM-1 protein as normal lymphocytes and LAM-1+ CLL cells were able to specifically bind to HEV. In addition, normal lymphocytes and LAM-1+ CLL cells were capable of binding polyphosphomonester core polysaccharide (PPME) derived from yeast cell wall, a carbohydrate which mimics an essential component of the natural ligand for LAM-1, and PPME and HEV binding was specifically blocked by a new monoclonal antibody (mAb) reactive with LAM-1. The expression of LAM-1 and other adhesion molecules was examined on cells of 118 hematopoietic malignancies. LAM-1 was most frequently expressed on CLL and follicular or diffuse small cleaved cell lymphomas, whereas most other malignancies were LAM-1-. Thus, most CLL cells and some non-Hodgkin's lymphoma cells express a functionally active LAM-1 molecule which may correlate with their capacity to migrate through the circulation and disseminate into peripheral LN. C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL, 44 BINNEY ST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA-34183, CA-36167]; NIAID NIH HHS [AI-26872] NR 43 TC 118 Z9 120 U1 1 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD APR PY 1991 VL 5 IS 4 BP 300 EP 308 PG 9 WC Oncology; Hematology SC Oncology; Hematology GA FN912 UT WOS:A1991FN91200005 PM 1709244 ER PT J AU NGUYEN, L DEWHIRST, FE HAUSCHKA, PV STASHENKO, P AF NGUYEN, L DEWHIRST, FE HAUSCHKA, PV STASHENKO, P TI INTERLEUKIN-1-BETA STIMULATES BONE-RESORPTION AND INHIBITS BONE-FORMATION INVIVO SO LYMPHOKINE AND CYTOKINE RESEARCH LA English DT Article ID PARATHYROID-HORMONE; NORMAL MICE; ACTIVATING FACTOR; FORMATION INVITRO; MYELOMA CELLS; GLA-PROTEIN; LYMPHOTOXIN; CALCIUM; PLASMA; HYPERCALCEMIA AB Interleukin-1-beta (IL-1-beta) and several other cytokines, including IL-1-alpha, tumor necrosis factor (TNF), and lymphotoxin, stimulate bone resorption and also inhibit bone formation in vitro. These effects are consistent with an uncoupling function for these mediators, although the effect of in vivo regulatory mechanism(s) that couple resorption and formation cannot be adequately evaluated in vitro. In the present studies, the effect of IL-1-beta on bone resorption and formation was determined in adult rats in vivo. Resorption was assessed by serum and urinary calcium levels, osteoclast number, and active resorption surface. Bone formation was determined by measurement of serum osteocalcin levels, and by quantitation of bone apposition rate using tetracycline labeling. A modest dose of IL-1-beta (1-mu-g/kg) was found to stimulate transient increases in serum calcium, and a persistent elevation of urinary calcium excretion. IL-1-beta treatment also resulted in decreases in serum iron levels and in the albumin/globulin ratio, well-established in vivo effects of IL-1. SGOT, SGPT, BUN, creatinine, and total protein were unaffected, indicating that IL-1-beta treatment did not compromise kidney or liver function, and that animals were systemically healthy. This was further evidenced by normal weight gain in IL-1-beta-treated animals. Low doses (50-mu-g/kg) of synthetic human parathyroid hormone (PTH 1-34) also stimulated resorption, as shown by a sustained increase in serum calcium without increased urinary excretion. Both IL-1-beta and parathyroid hormone (PTH) stimulated similar increases in osteoclast number (N.Oc) and active resorption surface [Oc.S(%)]. IL-1-beta caused a 20-30% decline in osteocalcin levels, and a 50% decrease in mineral apposition rate (MAR). These findings confirm and extend previous in vitro data, and are consistent with the interpretation that IL-1-beta, and probably other bone resorptive mediators, can act as uncouplers of the bone resorption-formation linkage in vivo. C1 FORSYTH RES INST,DEPT IMMUNOL,140 THE FENWAY,BOSTON,MA 02115. FORSYTH RES INST,DEPT PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT PROSTHET DENT,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT ORAL BIOL & PATHOPHYSIOL,BOSTON,MA 02115. FU NIDCR NIH HHS [DE-09018, DE-07378] NR 49 TC 131 Z9 131 U1 1 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0277-6766 J9 LYMPHOKINE CYTOK RES JI Lymphokine Cytokine Res. PD APR PY 1991 VL 10 IS 1-2 BP 15 EP 21 PG 7 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA FL932 UT WOS:A1991FL93200003 PM 1873357 ER PT J AU MEYER, JS AF MEYER, JS TI DOES DIASCHISIS HAVE CLINICAL CORRELATES SO MAYO CLINIC PROCEEDINGS LA English DT Editorial Material ID CEREBRAL BLOOD-FLOW; BEHAVIORAL ACTIVATION C1 BAYLOR UNIV,NEUROL,HOUSTON,TX 77030. RP MEYER, JS (reprint author), BAYLOR UNIV,DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,HOUSTON,TX 77030, USA. NR 9 TC 13 Z9 13 U1 0 U2 0 PU MAYO CLINIC PROCEEDINGS PI ROCHESTER PA 660 SIEBENS BLDG MAYO CLINIC, ROCHESTER, MN 55905 SN 0025-6196 J9 MAYO CLIN PROC JI Mayo Clin. Proc. PD APR PY 1991 VL 66 IS 4 BP 430 EP 432 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FH269 UT WOS:A1991FH26900011 PM 2013993 ER PT J AU DANDREA, AD YOSHIMURA, A YOUSSOUFIAN, H ZON, LI KOO, JW LODISH, HF AF DANDREA, AD YOSHIMURA, A YOUSSOUFIAN, H ZON, LI KOO, JW LODISH, HF TI THE CYTOPLASMIC REGION OF THE ERYTHROPOIETIN RECEPTOR CONTAINS NONOVERLAPPING POSITIVE AND NEGATIVE GROWTH-REGULATORY DOMAINS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID INFECTED ERYTHROID-CELLS; BETA-CHAIN; EXPRESSION CLONING; FRIEND-VIRUS; PROTEIN-KINASE; BINDING; FAMILY; IDENTIFICATION; HORMONE; PROLACTIN AB The erythropoietin (EPO) receptor (EPO-R), a member of a large cytokine receptor superfamily, has a 236-amino-acid cytoplasmic region which contains no obvious tyrosine kinase or other catalytic domain. In order to delineate the linear functional domains of the cytoplasmic tail, we generated truncated mutant cDNAs which were transfected into a murine interleukin-3-dependent cell line, Ba/F3, and the EPO-dependent growth characteristics of the stable transfectants were assayed. We identified two unique domains of the cytoplasmic tail. A membrane-proximal positive signal transduction domain of less-than-or-equal-to 103 amino acids, in a region highly similar to the interleukin-2 receptor beta-chain, was sufficient for EPO-mediated signal transduction. A carboxy-terminal negative-control domain, a serine-rich region of approximately 40 amino acids, increased the EPO requirement for the Ba/F3 transfectants without altering EPO-R cell surface expression, affinity for EPO, receptor oligosaccharide processing, or receptor endocytosis. Truncation of this negative-control domain allowed the Ba/F3 transfectants to grow maximally in only 1 pM EPO, 1/10 the concentration required for growth of cells expressing the wild-type EPO-R. All truncated EPO-R mutants which retained the transmembrane region of the EPO-R polypeptide bound to the gp55 envelope protein of Friend spleen focus-forming virus. Only the functional EPO-R mutants were activated by the gp55, however, suggesting that gp55- and EPO-mediated signaling occur via a similar mechanism. C1 MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP DANDREA, AD (reprint author), WHITEHEAD INST BIOMED RES,9 CAMBRIDGE CTR,CAMBRIDGE,MA 02142, USA. RI Yoshimura, Akihiko/K-5515-2013 FU NHLBI NIH HHS [HL02277-01, HL02347, HL32252] NR 43 TC 277 Z9 279 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1991 VL 11 IS 4 BP 1980 EP 1987 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FC852 UT WOS:A1991FC85200025 PM 1848667 ER PT J AU RUNGE, MS BODE, C HABER, E QUERTERMOUS, T AF RUNGE, MS BODE, C HABER, E QUERTERMOUS, T TI HYBRID MOLECULES - INSIGHTS INTO PLASMINOGEN-ACTIVATOR FUNCTION SO MOLECULAR BIOLOGY & MEDICINE LA English DT Article ID SINGLE-CHAIN UROKINASE; GROWTH-FACTOR DOMAIN; CROSS-LINKED FIBRIN; PHARMACOKINETIC PROPERTIES; THROMBOLYTIC PROPERTIES; MONOCLONAL-ANTIBODIES; TISSUE; VARIANTS; BINDING; MUTAGENESIS C1 UNIV HEIDELBERG,MED KLIN 3,W-6900 HEIDELBERG,GERMANY. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP RUNGE, MS (reprint author), EMORY UNIV,DIV CARDIOL,ATLANTA,GA 30322, USA. NR 41 TC 6 Z9 6 U1 0 U2 4 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0735-1313 J9 MOL BIOL MED PD APR PY 1991 VL 8 IS 2 BP 245 EP 255 PG 11 WC Biochemistry & Molecular Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Research & Experimental Medicine GA HG664 UT WOS:A1991HG66400009 PM 1806766 ER PT J AU BRENT, GA WILLIAMS, GR HARNEY, JW FORMAN, BM SAMUELS, HH MOORE, DD LARSEN, PR AF BRENT, GA WILLIAMS, GR HARNEY, JW FORMAN, BM SAMUELS, HH MOORE, DD LARSEN, PR TI EFFECTS OF VARYING THE POSITION OF THYROID-HORMONE RESPONSE ELEMENTS WITHIN THE RAT GROWTH-HORMONE PROMOTER - IMPLICATIONS FOR POSITIVE AND NEGATIVE REGULATION BY 3,5,3'-TRIIODOTHYRONINE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID THYROTROPIN-BETA GENE; RECEPTOR BINDS; PROLACTIN GENE; SUBUNIT GENE; EXPRESSION; SEQUENCES; INDUCTION; SITE; CDNA AB The thyroid hormone response element (T3RE) of the rat GH (rGH) promoter is located at -188 to -165 relative to the mRNA start site (TSS). Similar sites have been identified in other genes regulated by T3. We have investigated some of these T3REs in positions within the rGH promoter to assess the relative influences of DNA-binding site and position on positive and negative regulation by T3. Synthetic oligonucleotides were used with sequences from the rGH T3RE and proposed negative T3REs (nT3RE) from the rat and human alpha-subunit and rat BETA-TSH genes. The nT3REs were placed in the background of the wild-type rGH promoter in two positions, at -55 and down-stream of the TSS, with up- and down-mutations of the rGH T3RE. Rat GH T3RE elements were placed 700 basepairs up-stream of a basal rGH promoter and some also at the -55 and TSS positions. Constructions were tested in a transient transfection assay in rat pituitary tumor cells. Two copies of the rGHPAL (palindromic T3RE) placed 700 base-pairs up-stream of the rGH promoter conferred 10-fold T3 induction. In the -55 position, the rGHPAL increased T3 induction compared to that in controls, whereas a fragment from the rat and human alpha-subunit gene in the same position reduced induction. Negative T3REs from rat BETA-TSH and human alpha-subunit reduced T3 induction 50% when placed at the TSS position of a rGH promoter containing an up-mutant T3RE. The T3REPAL placed at the same site increased T3 induction. Gel mobility shift assays with pure T3R demonstrated binding to all of the elements studied. The rGH T3RE, therefore, functions as a T3-dependent enhancer across a wide range of positions. In the context of the rGH promoter, specific nT3REs reduced T3 induction. The magnitude of the increase or decrease in T3 induction, however, was influenced by the position of the T3RE or nT3RE. We conclude that positive and negative regulation by T3 is dependent on the nature of the binding site, but is influenced by promoter position. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NYU MED CTR,DEPT PHARMACOL,DIV MOLEC ENDOCRINOL,NEW YORK,NY 10016. NYU MED CTR,DEPT MED,NEW YORK,NY 10016. RP BRENT, GA (reprint author), BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,DIV THYROID,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIADDK NIH HHS [5-K12-AM-01401]; NIDDK NIH HHS [5-RO1-DK-36256, DK-16636] NR 36 TC 63 Z9 63 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1991 VL 5 IS 4 BP 542 EP 548 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FK114 UT WOS:A1991FK11400010 PM 1922086 ER PT J AU GERBING, DW TULEY, MR AF GERBING, DW TULEY, MR TI THE 16PF RELATED TO THE 5-FACTOR MODEL OF PERSONALITY - MULTIPLE-INDICATOR MEASUREMENT VERSUS THE A-PRIORI SCALES SO MULTIVARIATE BEHAVIORAL RESEARCH LA English DT Article ID NATURAL-LANGUAGE; QUESTIONNAIRES; GOODNESS; FIT AB This article examines the Sixteen Personality Factor Inventory (16PF; Cattell, Eber, & Tatsuoka, 1970) in terms of recent methodological and substantive developments: restricted (confirmatory) factor analysis and the five-factor model of personality as operationalized by the NEO-PI (NEO Personality Inventory). A multiple-indicator measurement model of the 16PF was constructed and analyzed with a restricted factor analysis and then cross-validated with a confirmatory analysis on a new sample. The relations of the a priori 16PF scales and the derived scales with the NEO-PI were investigated with comparative canonical correlation analyses. Both the a priori and derived 16PF scales demonstrated strong relationships to the NEO-PI scales, with the canonical correlations for the a priori scales slightly larger. These findings lead to the conclusion that the original 16PF remains robust in the context of these more recent developments. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. RP GERBING, DW (reprint author), PORTLAND STATE UNIV,SCH BUSINESS ADM,SBA MGMT,PORTLAND,OR 97207, USA. NR 36 TC 17 Z9 18 U1 3 U2 5 PU LAWRENCE ERLBAUM ASSOC INC PI MAHWAH PA 10 INDUSTRIAL AVE, MAHWAH, NJ 07430-2262 SN 0027-3171 J9 MULTIVAR BEHAV RES JI Multivariate Behav. Res. PD APR PY 1991 VL 26 IS 2 BP 271 EP 289 DI 10.1207/s15327906mbr2602_5 PG 19 WC Mathematics, Interdisciplinary Applications; Social Sciences, Mathematical Methods; Psychology, Experimental; Statistics & Probability SC Mathematics; Mathematical Methods In Social Sciences; Psychology GA GD732 UT WOS:A1991GD73200006 PM 26828255 ER PT J AU CANNON, SC BROWN, RH COREY, DP AF CANNON, SC BROWN, RH COREY, DP TI A SODIUM-CHANNEL DEFECT IN HYPERKALEMIC PERIODIC PARALYSIS - POTASSIUM-INDUCED FAILURE OF INACTIVATION SO NEURON LA English DT Article ID NEURO-BLASTOMA CELLS; SKELETAL-MUSCLE; ADYNAMIA EPISODICA; IDENTIFICATION; EXPRESSION; DYSTROPHY; MYOTONIA; CHLORIDE; AXONS; GENE AB Hyperkalemic periodic analysis (HPP) is an autosomal dominant disorder characterized by episodic weakness lasting minutes to days in association with a mild elevation in serum K+. In vitro measurements of whole-cell currents in HPP muscle have demonstrated a persistent, tetrodotoxin-sensitive Na+ current, and we have recently shown by linkage analysis that the Na+ channel alpha-subunit gene may contain the HPP mutation. In this study, we have made patch-clamp recordings from cultured HPP myotubes and found a defect in the normal voltage-dependent inactivation of Na+ channels. Moderate elevation of extracellular K+ favors an aberrant gating mode in a small fraction of the channels that is characterized by persistent reopenings and prolonged dwell times in the open state. The Na+ current, through noninactivating channels, may cause the skeletal muscle weakness in HPP by depolarizing the cell, thereby inactivating normal Na+ channels, which are then unable to generate an action potential. Thus the dominant expression of HPP is manifest by inactivation of the wild-type Na+ channel through the influence of the mutant gene product on membrane voltage. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. CHARLESTOWN NEUROSCI CTR,DAY NEUROMUSCULAR RES LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,PROGRAM NEUROSCI,BOSTON,MA 02115. RP CANNON, SC (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. OI Corey, David/0000-0003-4497-6016 NR 38 TC 153 Z9 153 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD APR PY 1991 VL 6 IS 4 BP 619 EP 626 DI 10.1016/0896-6273(91)90064-7 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FH802 UT WOS:A1991FH80200013 PM 1849724 ER PT J AU KALLAND, KH LANGHOFF, E BOS, HJ GOTTLINGER, H HASELTINE, WA AF KALLAND, KH LANGHOFF, E BOS, HJ GOTTLINGER, H HASELTINE, WA TI REX-DEPENDENT NUCLEOLAR ACCUMULATION OF HTLV-I MESSENGER-RNAS SO NEW BIOLOGIST LA English DT Article DE REX/NUCLEOLUS; MESSENGER RNA TRANSPORT; HTLV-I ID HUMAN IMMUNODEFICIENCY VIRUS; GENE-EXPRESSION; TRANS-ACTIVATOR; PROTEIN EXPRESSION; TARGET SEQUENCE; TYPE-1 AFFECTS; VIRAL-RNA; REPLICATION; LOCALIZATION; PRODUCT C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. RI Kalland, Karl-Henning/B-9445-2017 OI Kalland, Karl-Henning/0000-0003-4486-2334 FU NCI NIH HHS [CA36974] NR 46 TC 24 Z9 24 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD APR PY 1991 VL 3 IS 4 BP 389 EP 397 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK719 UT WOS:A1991GK71900012 PM 2065024 ER PT J AU GREENE, MF BENACERRAF, BR AF GREENE, MF BENACERRAF, BR TI PRENATAL-DIAGNOSIS IN DIABETIC GRAVIDAS - UTILITY OF ULTRASOUND AND MATERNAL SERUM ALPHA-FETOPROTEIN SCREENING SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID NEURAL-TUBE DEFECTS; AMNIOCENTESIS; MALFORMATION; SONOGRAPHY; RISK AB The differences in both the biology of pregnancy and the content of routine care between gravidas with and without diabetes mellitus lead to important differences in the potential utility of both ultrasound examination and maternal serum alpha-fetoprotein (MSAFP) screening. However, both diagnostic methods have become standards of care for these patients, without critical evaluation. This study examines the utility of both ultrasound and MSAFP in diabetic women. Four hundred thirty-two women with diabetes mellitus antedating pregnancy were examined sonographically between 12-23 weeks' gestation. Of these, 393 were also screened with MSAFP determinations. At delivery, 32 of these fetuses were found to have 38 major congenital malformations. All fatal or potentially life-threatening defects had been diagnosed in utero by sonography before 24 weeks' gestation. Ultrasound had a positive predictive value of 90% and a negative predictive value of 97% for identification of major birth defects before 24 weeks' gestation. There were 14 MSAFP values greater than 2.0 multiples of the median, and nine of these patients elected to undergo amniocentesis. Maternal serum alpha-fetoprotein screening had a positive predictive value of 17% and a negative predictive value of 94%. No malformations were detected through MSAFP screening that had not been diagnosed by sonography. No malformations missed sonographically were detected by MSAFP screening, and none of the amniocenteses were helpful diagnostically. We conclude that MSAFP screening is of minimal utility for diagnosing major congenital malformations in a high-risk population examined universally by an experienced sonographer. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN CLIN,BOSTON,MA 02115. RP GREENE, MF (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 15 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1991 VL 77 IS 4 BP 520 EP 524 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA FD561 UT WOS:A1991FD56100006 PM 1706079 ER PT J AU FONG, LP DELAMAZA, MS RICE, BA KUPFERMAN, AE FOSTER, CS AF FONG, LP DELAMAZA, MS RICE, BA KUPFERMAN, AE FOSTER, CS TI IMMUNOPATHOLOGY OF SCLERITIS SO OPHTHALMOLOGY LA English DT Article ID IMMUNE-COMPLEX FORMATION; NECROTIZING SCLERITIS; CELLS; ANTIGENS; DEPOSITION; ANTIBODY; DISEASE; EYE AB Conjunctival and scleral biopsies from 25 patients with necrotizing scleritis and 5 patients with recurrent nonnecrotizing scleritis were studied by histopathologic, immunofluorescence, and immunoperoxidase techniques. Vasculitis with fibrinoid necrosis and neutrophil invasion of the vessel wall was present in 75% of the scleral and 52% of the conjuctival specimens. Vascular immunodeposits were found in 93% of the scleral and 79% of the conjunctival tissue tested by immunofluorescence techniques. A dramatic increase in the number of inflammatory cells over normal controls was detected in both tissues by immunoperoxidase techniques. In the conjunctival epithelium, there were significantly more T-helpers, macrophages, and B cells. In the conjunctival substantia propria, there were significantly more T cells of all types, macrophages, and B cells. Likewise, scleral specimens showed an increase over controls of T cells of all types and macrophages. HLA-DR expression was dramatically increased in both tissues. Immune-complex-mediated vasculitis plays a pivotal role in the pathogenesis of necrotizing scleritis and recurrent nonnecrotizing scleritis. Induced HLA-DR expression on ocular nonimmune cells and T cell controlled responses also may participate. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,UVEITIS & IMMUNOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 21 TC 76 Z9 80 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1991 VL 98 IS 4 BP 472 EP 479 PG 8 WC Ophthalmology SC Ophthalmology GA FG123 UT WOS:A1991FG12300014 PM 1828871 ER PT J AU DUKER, JS NIELSEN, J VANDER, JF ROSENSTEIN, RB BENSON, WE AF DUKER, JS NIELSEN, J VANDER, JF ROSENSTEIN, RB BENSON, WE TI RETROBULBAR BUPIVACAINE IRRIGATION FOR POSTOPERATIVE PAIN AFTER SCLERAL BUCKLING SURGERY - A PROSPECTIVE-STUDY SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1990 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT-NOV -, 1990 CL ATLANTA, GA SP AMER ACAD OPHTHALMOL ID RETINAL-DETACHMENT SURGERY; ANESTHESIA AB The authors conducted a prospective, randomized, double-masked clinical trial to determine if retrobulbar irrigation with bupivacaine hydrochloride 0.75% (Marcaine) has an effect on postoperative pain after scleral buckling surgery. Fifty consecutive patients undergoing scleral buckling under general anesthesia were randomized to receive either bupivacaine or balanced salt solution as a retrobulbar irrigation at the end of their retinal detachment procedure. Of the 25 patients who received bupivacaine, only three (12%) required parenteral pain relief in the first 24 hours after surgery. This was statistically significant when compared with the 18 (72%) of 25 patients requiring parenteral pain relief in the placebo group (P < 0.0001). In addition, when questioned about their perception of the degree of postoperative pain, patients in the control group rated their level of pain as significantly more severe than did patients in the bupivacaine group. The authors conclude that retrobulbar irrigation with bupivacaine is a safe and effective way to achieve postoperative pain relief after surgery for scleral buckling. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. THOMAS JEFFERSON UNIV,WILLS EYE HOSP,RETINA SERV,PHILADELPHIA,PA 19107. RP DUKER, JS (reprint author), EYE RES INST,20 STANIFORD ST,BOSTON,MA 02114, USA. NR 7 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1991 VL 98 IS 4 BP 514 EP 518 PG 5 WC Ophthalmology SC Ophthalmology GA FG123 UT WOS:A1991FG12300020 PM 2052306 ER PT J AU DUKER, JS BELMONT, JB BENSON, WE BROOKS, HL BROWN, GC FEDERMAN, JL FISCHER, DH TASMAN, WS AF DUKER, JS BELMONT, JB BENSON, WE BROOKS, HL BROWN, GC FEDERMAN, JL FISCHER, DH TASMAN, WS TI INADVERTENT GLOBE PERFORATION DURING RETROBULBAR AND PERIBULBAR ANESTHESIA - PATIENT CHARACTERISTICS, SURGICAL-MANAGEMENT, AND VISUAL OUTCOME SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1990 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT-NOV -, 1990 CL ATLANTA, GA SP AMER ACAD OPHTHALMOL ID PERIOCULAR ANESTHESIA; INTRAOCULAR INJECTION; OCULAR PERFORATION; CATARACT-SURGERY AB The authors report a series of 20 eyes from 20 patients in whom inadvertent perforation of the globe occurred during local anesthesia for ocular surgery. Perforation resulted from retrobulbar anesthesia in 18 eyes and from peribulbar anesthesia in 2 eyes. Nine (45%) of 20 eyes had an axial length greater than or equal to 26.00 mm. Combining this figure with axial length data for the general population and estimates for the risk of globe perforation during local anesthesia yields an approximate incidence of perforation in eyes with axial length greater than or equal to 26.00 mm of 1 in 140 injections. Proliferative vitreoretinopathy (PVR) developed in 8 of the 20 eyes (40%) in this series. Overall, 15 (75%) of the 20 eyes were successfully repaired, and, in five eyes (25%), the final visual acuity was 20/70 or better. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,BOSTON,MA 02114. THOMAS JEFFERSON UNIV,WILLS EYE HOSP,RETINA SERV,PHILADELPHIA,PA 19107. RP DUKER, JS (reprint author), EYE RES INST LIB,20 STANIFORD ST,BOSTON,MA 02114, USA. NR 31 TC 179 Z9 189 U1 0 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1991 VL 98 IS 4 BP 519 EP 526 PG 8 WC Ophthalmology SC Ophthalmology GA FG123 UT WOS:A1991FG12300021 PM 2052307 ER PT J AU PITMAN, MB SHERMAN, ME BLACKSCHAFFER, WS AF PITMAN, MB SHERMAN, ME BLACKSCHAFFER, WS TI THE USE OF FINE-NEEDLE ASPIRATION IN THE DIAGNOSIS OF METASTATIC PULMONARY ADENOID CYSTIC CARCINOMA SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Article ID LUNG; EXPERIENCE; SURGERY; BIOPSY; CYLINDROMA; MANAGEMENT; SURVIVAL; CYTOLOGY; BREAST; GLAND AB Nine patients with a history of adenoid cystic carcinoma (ACC) arising in the head and neck and in whom transthoracic fine-needle aspiration (FNA) was performed to investigate pulmonary lesions are described. FNA yielded a definitive diagnosis of metastatic ACC in all cases. In six of the nine patients, the pulmonary metastases were asymptomatic. Lung lesions were discovered up to 19 years after primary tumor presentation, and in two, pulmonary spread was the only evidence of recurrent disease. On the basis of the FNA diagnosis, these two patients were treated surgically for their isolated pulmonary metastases, and are disease free at 107 and 139 months. Six of the nine patients received radiation or chemotherapy; one initially refused treatment. Thoracotomy was avoided in these patients on the basis of the FNA diagnosis. All are alive with disease at 25 to 246 months. The metastatic tumors were indistinguishable cytologically from two primary pulmonary ACCs that were available for comparsion. Our experience suggests FNA is a useful tool in the diagnosis of ACC in pulmonary material-one which obviates the need for thoracotomy with its associated morbidity. C1 JOHNS HOPKINS UNIV HOSP,DEPT PATHOL,BALTIMORE,MD 21205. RP PITMAN, MB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114, USA. NR 26 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD APR PY 1991 VL 104 IS 4 BP 441 EP 447 PG 7 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA FG001 UT WOS:A1991FG00100004 PM 1645465 ER PT J AU AMBROSINO, DM BLACK, CM PLIKAYTIS, BD REIMER, CB LEE, MC EVATT, BL CARLONE, GM AF AMBROSINO, DM BLACK, CM PLIKAYTIS, BD REIMER, CB LEE, MC EVATT, BL CARLONE, GM TI NORMAL IGG SUBCLASS VALUES DIFFER FOR BLACK-AND-WHITE CHILDREN SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CTR DIS CONTROL,ATLANTA,GA 30333. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A155 EP A155 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03800908 ER PT J AU BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF AF BOEPPLE, PA MANSFIELD, MJ CRAWFORD, JD CRIGLER, JF BLIZZARD, RM CROWLEY, WF TI FINAL HEIGHTS IN GIRLS WITH CENTRAL PRECOCIOUS PUBERTY (CPP) FOLLOWING GNRH AGONIST (GNRHA)-INDUCED PITUITARY-GONADAL SUPPRESSION SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,PEDIAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,PEDIAT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,REPROD ENDOCRINOL UNIT,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DIV ENDOCRINOL,BOSTON CH,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,DIV ADOLESCENT MED,BOSTON,MA 02115. UNIV VIRGINIA,HLTH SCI CTR,DIV ENDOCRINOL,CHARLOTTESVILLE,VA 22903. NR 0 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A74 EP A74 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03800431 ER PT J AU CASTILLO, L CHAPMAN, T YOUNG, V BURKE, J AF CASTILLO, L CHAPMAN, T YOUNG, V BURKE, J TI PHENYLALANINE AND TYROSINE KINETICS IN SEPTIC NEWBORNS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MIT,MASSACHUSETTS GEN HOSP,CAMBRIDGE,MA 02139. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A292 EP A292 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03801734 ER PT J AU CHANG, T CAPRARO, G KLEINMAN, RE ABBAS, AK AF CHANG, T CAPRARO, G KLEINMAN, RE ABBAS, AK TI NEONATAL-B CELL TOLERANCE IS REVERSED BY COGNATE-T HELP SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A274 EP A274 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03801623 ER PT J AU INGELFINGER, JR BOUVOUNES, B JUNG, FF TANG, SS AF INGELFINGER, JR BOUVOUNES, B JUNG, FF TANG, SS TI HIGH GLUCOSE DOWN-REGULATES EXPRESSION OF RENIN-ANGIOTENSIN SYSTEM (RAS) IN OPOSSUM KIDNEY-CELLS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. NR 0 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A344 EP A344 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03802043 ER PT J AU JUPPNER, H ABOUSAMRA, AB FREEMAN, MW KONG, X RICHARDS, J SCHIPANI, E HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV AF JUPPNER, H ABOUSAMRA, AB FREEMAN, MW KONG, X RICHARDS, J SCHIPANI, E HOCK, J POTTS, JT KRONENBERG, HM SEGRE, GV TI MOLECULAR-CLONING OF THE RENAL PTH/PTHRP RECEPTOR CDNA SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. TUFTS UNIV,SCH DENT,BOSTON,MA 02111. NR 0 TC 0 Z9 0 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A79 EP A79 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03800460 ER PT J AU LEVITSKY, LL EKWO, E GOSELINK, CA SOLOMON, IL ACETO, T AF LEVITSKY, LL EKWO, E GOSELINK, CA SOLOMON, IL ACETO, T TI DEATH FROM DIABETES (DM) IN HOSPITALIZED CHILDREN (1970-1988) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,BOSTON,MA 02114. UNIV CHICAGO,LA RABIDA CHILDRENS HOSP,CHICAGO,IL 60637. OAKLAND KAISER HOSP,DEPT PEDIAT,OAKLAND,MI. ST LOUIS UNIV,CARDINAL GLENNON CHILDRENS HOSP,SCH MED,ST LOUIS,MO. NR 0 TC 15 Z9 15 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A195 EP A195 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03801148 ER PT J AU LEVITSKY, LL STONESTREET, BS MINK, K ZHENG, QG AF LEVITSKY, LL STONESTREET, BS MINK, K ZHENG, QG TI GLUTAMINE FLUX AND GLYCOGENESIS IN THE FETUS OF THE FASTED EWE SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CHILD SERV,BOSTON,MA 02115. BROWN UNIV,WOMEN & INFANTS HOSP,DEPT PEDIAT,PROVIDENCE,RI 02908. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A299 EP A299 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03801775 ER PT J AU LEVITSKY, LL PATON, JB CILETTI, N FAN, J OGUNWOLE, JO SHANKARAO, R AF LEVITSKY, LL PATON, JB CILETTI, N FAN, J OGUNWOLE, JO SHANKARAO, R TI MECHANISM OF GLYCOGENESIS IN THE OVINE FETUS SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02115. UNIV CHICAGO,CHICAGO,IL 60637. MICHAEL REESE HOSP & MED CTR,DEPT PEDIAT,CHICAGO,IL 60616. MICHAEL REESE HOSP & MED CTR,DEPT LAB MED,CHICAGO,IL 60616. 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A46 EP A46 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03800261 ER PT J AU MATHIAS, RS HARMON, WH PARADES, A EMANS, J SEGRE, GV SALUSKY, IB GOODMAN, WG AF MATHIAS, RS HARMON, WH PARADES, A EMANS, J SEGRE, GV SALUSKY, IB GOODMAN, WG TI CHARACTERIZATION OF RENAL BONE-DISEASE IN PEDIATRIC-PATIENTS UNDERGOING CHRONIC-HEMODIALYSIS (HD) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DEPT ORTHOPAED,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,COLL MED,DEPT PEDIAT NEPHROL,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,DIV ENDOCRINOL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT NEPHROL,BOSTON,MA 02115. UNIV CALIF LOS ANGELES,SCH MED,DEPT PEDIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1991 VL 29 IS 4 BP A346 EP A346 PN 2 PG 1 WC Pediatrics SC Pediatrics GA FE038 UT WOS:A1991FE03802058 ER PT J AU KREBS, DE ELBAUM, L ORILEY, P HODGE, WA MANN, RW AF KREBS, DE ELBAUM, L ORILEY, P HODGE, WA MANN, RW TI EXERCISE AND GAIT EFFECTS ON INVIVO HIP CONTACT PRESSURES SO PHYSICAL THERAPY LA English DT Article DE EXERCISE; RANGE OF MOTION; HIP JOINT; HIP PROSTHESIS; KINESIOLOGY BIOMECHANICS; GAIT ANALYSIS AB Virtually all hip rehabilitation programs include exercise for muscle force development. The specific effects of various exercise modes on the hip joint itself are unknown. We will report on the effects of common exercise modalities on in vivo hip pressures. Four years prior to data collection, a pressure-instrumented Austin-Moore-type endoprosthesis was implanted in an otherwise healthy 73-year-old woman with a traumatic right hip fracture. Hip pressures during various experimental maneuvers were recorded periodically over a 5-year period. We compared measurements of peak pressure and rate of pressure rise obtained during gait with those obtained during isokinetic, isometric, and isotonic lower-limb exercises. Maximal exercise generated greater peak pressures than did gait, and tripling the angular velocity during exercise roughly tripled the rate of pressure rise. Torque production and resultant in vivo hip pressures varied directly during all experiments. Peak pressures and rate of pressure rise apparently can be controlled by varying the subject's exertion. The results reported are from a single subject; therefore, little generalizability is possible for these data. We suggest, however, that articular pressures may be important to rehabilitation planning; these data provide a direct insight into this potentially important exercise prescription consideration. C1 MIT,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BIOMOTION LAB,BOSTON,MA 02114. MIT,DEPT MECH ENGN,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,ORTHOPAED,BOSTON,MA 02114. RP KREBS, DE (reprint author), MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,PROGRAM PHYS THERAPY,15 RIVER ST,BOSTON,MA 02108, USA. NR 28 TC 53 Z9 54 U1 1 U2 1 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD APR PY 1991 VL 71 IS 4 BP 301 EP 309 PG 9 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA FF142 UT WOS:A1991FF14200008 PM 2008453 ER PT J AU PATARCA, R WEI, FY IREGUI, MV CANTOR, H AF PATARCA, R WEI, FY IREGUI, MV CANTOR, H TI DIFFERENTIAL INDUCTION OF INTERFERON GAMMA GENE-EXPRESSION AFTER ACTIVATION OF CD4+ T-CELLS BY CONVENTIONAL ANTIGEN AND MLS SUPERANTIGEN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-HELPER SUBSETS; CYTOKINE GENE EXPRESSION; MLS RECOGNITION ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLONES; SPECIFICITY; TOLERANCE; RECEPTOR; ALLOREACTIVITY; DETERMINANTS; SECRETION; PRODUCTS AB We have analyzed cytokine gene expression by a murine CD4+ T-cell clone that expresses three forms of T-cell recognition. The clone employs a V-beta-6-containing T-cell receptor to recognize (i) a self class II major histocompatibility complex and an ovalbumin-derived peptide (OVA), (ii) an I-A(b) alloantigen, and (iii) Mls-1a. All three responses are accompanied by similar levels of cell proliferation. However, although interferon-gamma-gene expression is strongly induced during both physiological recognition of the OVA peptide and allogeneic major histocompatibility complex recognition, expression of this gene was not detected during the Mls response. These studies indicate that Mls recognition is functionally distinct from T-cell recognition of peptides and alloantigens and leads to an alternative pattern of cytokine gene expression. They also suggest the possibility that encounter with these two classes of T-cell antigen in vivo may generate subsets of T helper cells that display different patterns of cytokine gene expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,IMMUNOPATHOL LAB,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA26695]; NIAID NIH HHS [AI13600, AI12184] NR 29 TC 39 Z9 39 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR PY 1991 VL 88 IS 7 BP 2736 EP 2739 DI 10.1073/pnas.88.7.2736 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FE864 UT WOS:A1991FE86400026 PM 1707172 ER PT J AU LEE, SW TOMASETTO, C SAGER, R AF LEE, SW TOMASETTO, C SAGER, R TI POSITIVE SELECTION OF CANDIDATE TUMOR-SUPPRESSOR GENES BY SUBTRACTIVE HYBRIDIZATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE BREAST CANCER; GAP-JUNCTION PROTEIN; GLUTATHIONE-S-TRANSFERASE PI; S100 PROTEIN ID CALCIUM-BINDING PROTEINS; SV40-TRANSFORMED CELLS; CANCER-CELLS; GROWTH; COMMUNICATION; EXPRESSION; CDNA; AMPLIFICATION; ONCOGENES; PHENOTYPE AB A positive selection system designed to identify and recover candidate tumor-suppressor genes is described. The system compares mRNA expression of genes from normal and tumor-derived human mammary epithelial cells grown in a special medium that supports similar growth rates of the two cell types. mRNAs uniquely expressed in normal cells are recovered as cDNAs after subtraction with mRNA from tumor cells. Seven different clones, from 0.6 to 4.8 kilobases in transcript size and including both rare and abundant transcripts, were recovered in the first 23 clones analyzed. Among the isolated clones were genes encoding the gap-junction protein connexin 26, two different keratins, and glutathione-S-transferase-pi, as well as an unknown gene in the S100 family of small calcium-binding proteins. In principle, tumor-suppressor genes include two classes: class I, in which loss of function results from mutation or deletion of DNA and class II, in which loss of function is from a regulatory block to expression. A class II suppressor gene is assumed to be regulated by a different suppressor gene that lost its function by mutation or deletion. Both classes of tumor-suppressor genes may provide valuable proteins with clinical applications in cancer diagnosis or therapy. Class II suppressors may be especially useful because the normal genes are present and their reexpression may be inducible by drugs or other treatments. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC GENET,44 BINNEY ST,BOSTON,MA 02115. RI Tomasetto, Catherine/J-2783-2014 OI Tomasetto, Catherine/0000-0002-1811-5848 FU NCI NIH HHS [CA39814] NR 62 TC 298 Z9 322 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR PY 1991 VL 88 IS 7 BP 2825 EP 2829 DI 10.1073/pnas.88.7.2825 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FE864 UT WOS:A1991FE86400045 PM 1849277 ER PT J AU SEIZINGER, BR SMITH, DI FILLINGKATZ, MR NEUMANN, H GREEN, JS CHOYKE, PL ANDERSON, KM FREIMAN, RN KLAUCK, SM WHALEY, J DECKER, HJH HSIA, YE COLLINS, D HALPERIN, J LAMIELL, JM OOSTRA, B WAZIRI, MH GORIN, MB SCHERER, G DRABKIN, HA ARONIN, N SCHINZEL, A MARTUZA, RL GUSELLA, JF HAINES, JL AF SEIZINGER, BR SMITH, DI FILLINGKATZ, MR NEUMANN, H GREEN, JS CHOYKE, PL ANDERSON, KM FREIMAN, RN KLAUCK, SM WHALEY, J DECKER, HJH HSIA, YE COLLINS, D HALPERIN, J LAMIELL, JM OOSTRA, B WAZIRI, MH GORIN, MB SCHERER, G DRABKIN, HA ARONIN, N SCHINZEL, A MARTUZA, RL GUSELLA, JF HAINES, JL TI GENETIC FLANKING MARKERS REFINE DIAGNOSTIC-CRITERIA AND PROVIDE INSIGHTS INTO THE GENETICS OF VONHIPPEL LINDAU DISEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEREDITARY TUMOR SYNDROME; RENAL CELL CARCINOMA; PHEOCHROMOCYTOMA; BRAIN TUMORS; TUMOR SUPPRESSOR GENE ID RENAL-CELL CARCINOMA; TRANSLOCATION; LOCALIZATION; NEUROFIBROMATOSIS; CHROMOSOME-3; LINKAGE AB Von Hippel Lindau disease (VHL) is a hereditary syndrome, associated with tumors and cysts in multiple organ systems, whose expression and age of onset are highly variable. The availability of a genetic test for the early and reliable detection of individuals carrying the defective gene would be beneficial for VHL patients and their relatives, since many of the manifestations of VHL can be successfully treated if detected in their early stages, while the complications of undetected disease can be devastating. We have previously shown that the VHL gene maps to chromosome 3p. To provide genetic markers for the development of a reliable diagnostic test, and to further narrow and eventually clone the VHL defect, we have generated DNA markers for chromosome 3p. With these markers, we have performed a multipoint genetic linkage analysis in 28 VHL pedigrees, comprising 470 individuals, 164 of whom were affected with VHL. Here we report the identification of tightly linked markers, including flanking markers that bracket the VHL gene to a small region on chromosome 3p25-p26. This finding has several major implications. While visceral cysts of the kidney, pancreas, and epididymis are commonly found in VHL and are considered diagnostic criteria for this disorder, they also occur in the general population. The presence of cysts, unaccompanied by other more typical lesions such as retinal and cerebellar hemangioblastoma, may therefore represent a major diagnostic problem, leading to errors in the assessment of disease status. The application of flanking markers for the VHL gene for presymptomatic diagnostic testing confirms that epididymal cysts are indeed not suitable as a diagnostic criterion in this disorder. Pheochromocytomas occur nonuniformly in VHL families and may also be associated with other hereditary tumor syndromes; our genetic studies imply that the phenotype in VHL families with and without pheochromocytomas is caused by defects within the same gene. The absence or presence of this tumor type is therefore due to the pleiotropic expression of a single gene rather than to the existence of several different genes for VHL. The region on chromosome 3p13-p14 known to contain several chromosomal translocation breakpoints in families with "pure familial renal cell carcinoma" is quite proximal to the VHL locus in 3p25-p26 we have identified. Chromosome 3p may therefore contain two loci for renal cell carcinoma: one gene (or genes) in 3p13-p14 and the VHL gene in 3p25-p26, whose aberration is also associated with other typical manifestations of VHL. Since renal cell carcinoma, pheochromocytoma, and visceral cysts can occur sporadically even in young people and may also be associated with other tumor syndromes, the availability of flanking markers for the VHL gene will be useful in identifying VHL gene carriers, particularly among those individuals at risk in whom these are the only manifestations of disease. The isolation and characterization of the VHL gene, based on the identification of flanking markers, will have important implications for diagnosis and treatment of patients with VHL, as well as for a much larger number of individuals having the sporadic counterparts of VHL-associated tumor types. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. WAYNE STATE UNIV,DEPT MOLEC BIOL & GENET,DETROIT,MI 48202. UNIV LOUISVILLE,DEPT NEUROL,LOUISVILLE,KY 40202. UNIV FREIBURG,DEPT MED,W-7800 FREIBURG,GERMANY. UNIV FREIBURG,INST GENET,W-7800 FREIBURG,GERMANY. MEM UNIV NEWFOUNDLAND,DEPT COMMUNITY MED,ST JOHNS A1B 3V6,NEWFOUNDLAND,CANADA. UNIV PITTSBURGH,INST EYE & EAR,DEPT OPHTHALMOL,PITTSBURGH,PA 15213. UNIV KANSAS,MED CTR,DEPT MED,KANSAS CITY,KS 66103. UNIV HAWAII,DEPT GENET,HONOLULU,HI 96826. UNIV HAWAII,DEPT PEDIAT,HONOLULU,HI 96826. MT SINAI MED CTR,DEPT NEUROL,NEW YORK,NY 10029. BROOKE ARMY MED CTR,CRIT CARE SERV,FT SAM HOUSTON,TX 78234. ERASMUS UNIV,DEPT CLIN GENET,3000 DR ROTTERDAM,NETHERLANDS. UNIV IOWA HOSP & CLIN,DEPT PEDIAT,IOWA CITY,IA 52242. UNIV COLORADO,DEPT MED,DENVER,CO 80262. UNIV ZURICH,DEPT HUMAN GENET,CH-8006 ZURICH,SWITZERLAND. UNIV MASSACHUSETTS,DEPT MED,WORCESTER,MA 01655. RP SEIZINGER, BR (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114, USA. RI Haines, Jonathan/C-3374-2012 FU NCI NIH HHS [R0I-CA49455]; NINDS NIH HHS [R0I NS22224] NR 33 TC 118 Z9 119 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR PY 1991 VL 88 IS 7 BP 2864 EP 2868 DI 10.1073/pnas.88.7.2864 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FE864 UT WOS:A1991FE86400053 PM 2011596 ER PT J AU DANA, N FATHALLAH, DM ARNAOUT, MA AF DANA, N FATHALLAH, DM ARNAOUT, MA TI EXPRESSION OF A SOLUBLE AND FUNCTIONAL FORM OF THE HUMAN BETA-2 INTEGRIN CD11B/CD18 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RECOMBINANT BETA-2 INTEGRINS; COMPLEMENT RECEPTORS; LEUKOCYTE-ENDOTHELIAL ADHESION; INFLAMMATORY REACTIONS; REPERFUSION INJURY ID COMPLEMENT RECEPTOR TYPE-3; MONOCLONAL-ANTIBODIES; LEUKOCYTE ADHESION; SURFACE GLYCOPROTEIN; VASCULAR ENDOTHELIUM; FIBRONECTIN RECEPTOR; MEMBRANE-PROTEINS; ALPHA-SUBUNITS; ANTIGEN; LFA-1 AB Polymorphonuclear cells and monocytes (phagocytes) are a critical component of host defense against infections. However, these cells also play a significant role in host tissue damage in many noninfectious diseases, such as ischemia-reperfusion injury syndromes and rejection of transplanted organs. The leukocyte adhesion molecule family CD11/CD18 (beta-2 integrins) is critical to the function of polymorphonuclear cells and monocytes in inflammation and injury. Inherited deficiency of CD11/CD18 impairs phagocyte chemotaxis, adhesion and transmigration across endothelium, and clearance of invading microorganisms through phagocytosis and cell-mediated killing. Furthermore, murine monoclonal antibodies directed against the CD11b/CD18 (CR3) heterodimer have been shown to reduce, by 50%-80%, phagocyte-mediated ischemia-reperfusion injury in several organ systems, such as the myocardium, liver, and gastrointestinal tract and to inhibit development of insulin-dependent diabetes mellitus in nonobese diabetic (NOD) mice. Expression of CD11b/CD18 in a soluble and functional form might therefore be potentially useful as an anti-inflammatory agent. We have now expressed a recombinant soluble heterodimeric form of this human beta-2 integrin, normally expressed as two noncovalently associated membrane-bound subunits. The secreted receptor exhibited direct and specific binding to its ligand, iC3b, the major complement C3 opsonin, and inhibited binding of polymorphonuclear cells to recombinant interleukin 1-activated endothelium. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DANA, N (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114, USA. NR 52 TC 64 Z9 65 U1 1 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR PY 1991 VL 88 IS 8 BP 3106 EP 3110 DI 10.1073/pnas.88.8.3106 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FG913 UT WOS:A1991FG91300030 PM 1673028 ER PT J AU GOTTLINGER, HG DORFMAN, T SODROSKI, JG HASELTINE, WA AF GOTTLINGER, HG DORFMAN, T SODROSKI, JG HASELTINE, WA TI EFFECT OF MUTATIONS AFFECTING THE P6 GAG PROTEIN ON HUMAN-IMMUNODEFICIENCY-VIRUS PARTICLE RELEASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CAPSID ASSEMBLY; BUDDING; CELL SURFACE ATTACHMENT; INTERFERON-ALPHA ID HTLV-III; VIRAL INFECTIVITY; HIV EXPRESSION; GENE; SEQUENCE; TYPE-1; AIDS; CELLS AB Mutations in sequences at the C terminus of the capsid precursor protein of human immunodeficiency virus type 1 that affect the viral p6 protein prevent release of budded virus particles from the cell surface. The experiments reported here define an important step in the life cycle of the virus, the release of the budded particle from a tether that binds the assembled particle to the cell surface. Inhibition of the release of the viral capsid proteins by interferon-alpha indicates that this step of virus maturation may be sensitive to inhibition by antiviral drugs. RP GOTTLINGER, HG (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,DANA FARBER CANC INST,HUMAN RETROVIROL LAB,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI24845, AI29873]; NIGMS NIH HHS [GM39599] NR 26 TC 500 Z9 506 U1 0 U2 8 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR PY 1991 VL 88 IS 8 BP 3195 EP 3199 DI 10.1073/pnas.88.8.3195 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FG913 UT WOS:A1991FG91300048 PM 2014240 ER PT J AU TAMLER, B SOMMER, FG GLOVER, GH SCHNEIDER, E AF TAMLER, B SOMMER, FG GLOVER, GH SCHNEIDER, E TI PROSTATIC MR-IMAGING PERFORMED WITH THE 3-POINT DIXON TECHNIQUE - WORK IN PROGRESS SO RADIOLOGY LA English DT Article DE MAGNETIC RESONANCE (MR), CHEMICAL SHIFT; MAGNETIC RESONANCE (MR), PULSE SEQUENCES; PROSTATE, MR STUDIES; PROSTATE, NEOPLASMS; PROSTATE, HYPERTROPHY AB The three-point Dixon technique is an enhancement of the original Dixon method for the creation of water-and fat-proton magnetic resonance (MR) images. With the three-point Dixon technique, three measurements of phase shift at 0, pi, and -pi between the fat and water resonances are employed. Compensation for B0 inhomogeneity leads to an error-free decomposition into water-and fat-proton images; an accurate B0 map is also created. The lack of chemical shift artifact in the water-and fat-selective MR images permits the application of narrow receive bandwidth for the creation of T2-weighted images with a high signal-to-noise ratio. The technique was applied in vivo with four healthy subjects, seven patients with prostatic carcinoma, and one patient with benign prostatic hypertrophy and compared with conventional T2-weighted imaging. The three-point technique yielded images with improved definition of normal intraprostatic structures and zonal anatomy and, in some cases of prostatic carcinoma, provided better visualization of extraprostatic spread of tumor. C1 STANFORD UNIV,MED CTR,SCH MED,DEPT DIAGNOST RADIOL,RM H1307,300 PASTEUR DR,STANFORD,CA 94305. GE,MED SYST,MILWAUKEE,WI 53201. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. NR 11 TC 6 Z9 6 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 APR PY 1991 VL 179 IS 1 BP 43 EP 47 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC883 UT WOS:A1991FC88300010 PM 2006302 ER PT J AU LITTRUP, PJ WILLIAMS, CR EGGLIN, TK KANE, RA AF LITTRUP, PJ WILLIAMS, CR EGGLIN, TK KANE, RA TI DETERMINATION OF PROSTATE VOLUME WITH TRANSRECTAL US FOR CANCER SCREENING .2. ACCURACY OF INVITRO AND INVIVO TECHNIQUES SO RADIOLOGY LA English DT Article DE CANCER SCREENING; PROSTATE, NEOPLASMS; PROSTATE, US STUDIES ID TRANS-RECTAL ULTRASOUND; CANINE PROSTATE; ANTIGEN; SIZE AB Improved diagnostic information is obtained when prostate volume is correlated with results of prostate-specific antigen assays for early detection of prostate cancer. Three commonly used prostate volume measurement techniques were analyzed: planimetry, prolate ellipse volume calculation (HWL), and an ellipsoid volume measurement technique. For in vitro volume measurement, the declining order of accuracy was planimetry, HWL, and ellipsoid techniques. At the 95% confidence level, inverse prediction produced full-range values for a 40-cm3 model of 5.7, 16.0, 28.8, and 32.8 cm3 for planimetry, HWL, and the two ellipsoid techniques, respectively. Despite its superior accuracy, planimetry is not available on most ultrasound units, increases estimated clinical scanning time, requires additional equipment, and is difficult for a sole operator to perform. Although less accurate than planimetry, HWL is a rapid volume measurement technique that appears to be more accurate than ellipsoid software packages; its universal availability makes it practical for routine clinical use. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP LITTRUP, PJ (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT RADIOL,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 12 TC 135 Z9 135 U1 1 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1991 VL 179 IS 1 BP 49 EP 53 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FC883 UT WOS:A1991FC88300011 PM 2006303 ER PT J AU RABINOWE, SN NEMUNAITIS, J ARMITAGE, J NADLER, LM AF RABINOWE, SN NEMUNAITIS, J ARMITAGE, J NADLER, LM TI THE IMPACT OF MYELOID GROWTH-FACTORS ON ENGRAFTMENT FOLLOWING AUTOLOGOUS BONE-MARROW TRANSPLANTATION FOR MALIGNANT-LYMPHOMA SO SEMINARS IN HEMATOLOGY LA English DT Article; Proceedings Paper CT JOINT SYMP AT THE 23RD CONGRESS OF THE INTERNATIONAL SOC OF HEMATOLOGY / 32ND ANNUAL MEETING OF THE AMERICAN SOC OF HEMATOLOGY CY NOV 30, 1990 CL BOSTON, MA SP HOECHST ROUSSEL PHARM ID COLONY-STIMULATING FACTOR; HIGH-DOSE CHEMOTHERAPY; GM-CSF; NEUTROPHIL RECOVERY; HODGKINS-DISEASE C1 UNIV WASHINGTON,FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98195. DEPT VET AFFAIRS MED CTR,SEATTLE,WA. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. RP RABINOWE, SN (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,MAYER 730,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 40216-06, CA 36727-07] NR 27 TC 29 Z9 29 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD APR PY 1991 VL 28 IS 2 SU 2 BP 6 EP 16 PG 11 WC Hematology SC Hematology GA FK901 UT WOS:A1991FK90100002 PM 1712125 ER PT J AU DANDREA, AD JONES, SS AF DANDREA, AD JONES, SS TI ACTIVATION OF THE ERYTHROPOIETIN RECEPTOR IN STABLE LYMPHOID AND MYELOID TRANSFECTANTS SO SEMINARS IN HEMATOLOGY LA English DT Article ID BETA-CHAIN; EXPRESSION; BINDING; PROTEIN; CLONING; FAMILY; GROWTH C1 GENET INST,CAMBRIDGE,MA. RP DANDREA, AD (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 14 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD APR PY 1991 VL 28 IS 2 BP 152 EP 157 PG 6 WC Hematology SC Hematology GA FK639 UT WOS:A1991FK63900010 PM 1652158 ER PT J AU APPERLEY, JF LUSKEY, BD WILLIAMS, DA AF APPERLEY, JF LUSKEY, BD WILLIAMS, DA TI RETROVIRAL-MEDIATED GENE-TRANSFER OF HUMAN ADENOSINE-DEAMINASE INTO MURINE HEMATOPOIETIC-CELLS SO SEMINARS IN HEMATOLOGY LA English DT Article ID LONG-TERM EXPRESSION; BETA-GLOBIN GENE; STEM-CELLS; RECOMBINANT RETROVIRUSES; BONE-MARROW; MICE; CULTURE; PROGENITORS; VECTORS; INVIVO C1 CHILDRENS HOSP MED CTR,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [5PO1-NIH HL32262, 5KO8 HL01554-02] NR 28 TC 4 Z9 4 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD APR PY 1991 VL 28 IS 2 BP 170 EP 176 PG 7 WC Hematology SC Hematology GA FK639 UT WOS:A1991FK63900012 PM 1876864 ER PT J AU TEICHER, BA HOLDEN, SA HERMAN, TS FREI, E AF TEICHER, BA HOLDEN, SA HERMAN, TS FREI, E TI MODULATION OF ALKYLATING-AGENTS BY LONIDAMINE INVIVO SO SEMINARS IN ONCOLOGY LA English DT Article ID ASCITES TUMOR-CELLS; PHASE-II; FIBRO-SARCOMA; MURINE; INVITRO; RADIOSENSITIVITY; POTENTIATION; INHIBITION C1 JOINT CTR RADIAT THERAPY,BOSTON,MA. RP TEICHER, BA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1PO1-CA38493] NR 23 TC 11 Z9 11 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1991 VL 18 IS 2 SU 4 BP 7 EP 10 PG 4 WC Oncology SC Oncology GA FM162 UT WOS:A1991FM16200002 PM 1903216 ER PT J AU SILVA, JA LEONG, GB FERRARI, MM AF SILVA, JA LEONG, GB FERRARI, MM TI POSTTRAUMATIC-STRESS-DISORDER IN BURN PATIENTS SO SOUTHERN MEDICAL JOURNAL LA English DT Article C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90033. RP SILVA, JA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,PSYCHIAT SERV,B116A WARD 206A,LOS ANGELES,CA 90073, USA. NR 8 TC 9 Z9 9 U1 0 U2 0 PU SOUTHERN MEDICAL ASSN PI BIRMINGHAM PA 35 LAKESHORE DR PO BOX 190088, BIRMINGHAM, AL 35219 SN 0038-4348 J9 SOUTHERN MED J JI South.Med.J. PD APR PY 1991 VL 84 IS 4 BP 530 EP 531 DI 10.1097/00007611-199104000-00035 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FG629 UT WOS:A1991FG62900035 PM 2014448 ER PT J AU BREWSTER, DC FRANKLIN, DP CAMBRIA, RP DARLING, RC MONCURE, AC LAMURAGLIA, GM STONE, WM ABBOTT, WM AF BREWSTER, DC FRANKLIN, DP CAMBRIA, RP DARLING, RC MONCURE, AC LAMURAGLIA, GM STONE, WM ABBOTT, WM TI INTESTINAL ISCHEMIA COMPLICATING ABDOMINAL AORTIC-SURGERY SO SURGERY LA English DT Review ID DOPPLER ULTRASOUND; COLONIC ISCHEMIA; RISK-FACTORS; RECONSTRUCTION; COLITIS; VIABILITY; ANEURYSM; PREVENTION; REVASCULARIZATION; CIRCULATION AB A 9-year experience with 2137 patients undergoing infrarenal abdominal aortic reconstruction was reviewed to determine both the incidence of intestinal ischemia and the clinical, anatomic, and technical factors associated with this complication of aortic surgery. A total of 24 (1.1%) patients had overt intestinal ischemia, documented by reoperation or endoscopic findings. Of these, colon ischemia occurred in 19 (0.9%) and small bowel ischemia developed in 5 (0.2%) patients. The incidence after elective operation for aneurysmal or occlusive disease did not differ, but patients with ruptured aneurysms and those undergoing reoperative procedures for total graft replacement were at higher risk. Properative angiography was most helpful in ascertaining risk. Ligation of a patent inferior mesenteric artery was the most common (74%) feature in patients with colon ischemia. With preexisting inferior mesenteric artery occlusion, impairment of collateral circulation was attributable to superior mesenteric artery disease, dissection or retractor injury, prior colon resection, or exclusion of hypogastric perfusion. Bloody diarrhea was the most frequent postoperative symptom and colonoscopy the most reliable means of diagnosis. One half of patients with colon ischemia required resection after late recognition of perforation. All cases of small bowel ischemia were related to superior mesenteric artery disease or injury or use of suprarenal clamping. The overall mortality rate was 25% but rose to 50% if bowel resection was required. Intestinal ischemia remains an infrequent but serious complication of aortic surgery. Despite a multifactorial cause, identification of patients at increased risk can lead to operative strategies to reduce its occurrence. C1 MASSACHUSETTS GEN HOSP,GEN SURG SERV,DIV VASC SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 36 TC 122 Z9 125 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD APR PY 1991 VL 109 IS 4 BP 447 EP 454 PG 8 WC Surgery SC Surgery GA FF166 UT WOS:A1991FF16600001 PM 1844392 ER PT J AU MALT, RA AF MALT, RA TI PRACTICAL SURGEONS DOING BASIC RESEARCH SO SURGERY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP MALT, RA (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114, USA. NR 6 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 0039-6060 J9 SURGERY JI Surgery PD APR PY 1991 VL 109 IS 4 BP 563 EP 564 PG 2 WC Surgery SC Surgery GA FF166 UT WOS:A1991FF16600019 PM 2008662 ER PT J AU ANSON, JA GLICK, RP CROWELL, RM AF ANSON, JA GLICK, RP CROWELL, RM TI USE OF GADOLINIUM-ENHANCED MAGNETIC-RESONANCE-IMAGING IN THE DIAGNOSIS AND MANAGEMENT OF POSTERIOR-FOSSA HEMANGIOBLASTOMAS SO SURGICAL NEUROLOGY LA English DT Article DE CENTRAL NERVOUS SYSTEM NEOPLASMS; GADOLINIUM-DTPA; HEMANGIOBLASTOMA; MAGNETIC RESONANCE; VON HIPPEL-LINDAU SYNDROME ID CENTRAL NERVOUS-SYSTEM; MR AB The diagnosis of central nervous system hemangioblastoma as well as the surgical treatment requires the accurate radiologic visualization of both the cystic and solid components of the tumor. We report two cases of posterior fossa hemangioblastoma examined with gadolinium-diethylenetriaminepentaacetic acid-enhanced magnetic resonance imaging, which clearly defined the tumor nodule that was not visualized on noncontrast magnetic resonance imaging, contrast-enhanced computed tomography scans, or angiography. In both cases the operative findings precisely correlated with the gadolinium-enhanced magnetic resonance image. Gadolinium-enhanced magnetic resonance imaging is the examination of choice for preoperative evaluation of posterior fossa hemangioblastoma. In cases of von Hippel-Lindau syndrome, magnetic resonance imaging is a useful tool for clinical screening as well as follow-up. C1 COOK CTY HOSP,DIV NEUROSURG,1825 W HARRISON ST,CHICAGO,IL 60612. UNIV ILLINOIS HOSP,DEPT NEUROSURG,CHICAGO,IL 60612. HEKTOEN INST,CHICAGO,IL. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 12 TC 12 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0090-3019 J9 SURG NEUROL JI Surg. Neurol. PD APR PY 1991 VL 35 IS 4 BP 300 EP 304 DI 10.1016/0090-3019(91)90009-X PG 5 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FB987 UT WOS:A1991FB98700009 PM 2008647 ER PT J AU YUNIS, EJ YUNIS, I AF YUNIS, EJ YUNIS, I TI UPDATE OF THE HUMAN MAJOR HISTOCOMPATIBILITY COMPLEX SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 2ND PAN-AMERICAN CONGRESS FOR DIALYSIS AND TRANSPLANTATION CY NOV 16-19, 1989 CL SAN JUAN, PR ID DEPENDENT DIABETES-MELLITUS; HLA-B; SUSCEPTIBILITY; ANTIGEN; RECOGNITION; RESTRICTION; DISEASE C1 AMER RED CROSS,NE REG,DEEDHAM,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU PHS HHS [20531] NR 24 TC 2 Z9 2 U1 0 U2 0 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1991 VL 23 IS 2 BP 1734 EP 1737 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA FG566 UT WOS:A1991FG56600002 PM 2053138 ER PT J AU TAKAYAMA, K OLSEN, M DATTA, P HUNTER, RL AF TAKAYAMA, K OLSEN, M DATTA, P HUNTER, RL TI ADJUVANT ACTIVITY OF NONIONIC BLOCK COPOLYMERS .5. MODULATION OF ANTIBODY ISOTYPE BY LIPOPOLYSACCHARIDES, LIPID-A AND PRECURSORS SO VACCINE LA English DT Article DE ADJUVANT; LIPOPOLYSACCHARIDE; LIPID-A; COPOLYMER; ISOTYPE ID DELAYED-TYPE HYPERSENSITIVITY; T-CELL CLONE; SALMONELLA-TYPHIMURIUM; POLYMER SURFACTANTS; ESCHERICHIA-COLI; STRUCTURAL DETERMINATION; POLYSACCHARIDE CHAIN; SUBCLASS RESPONSES; IMMUNE-RESPONSES; DEFICIENT MUTANT AB Non-ionic block copolymers and lipopolysaccharides are both effective immunological adjuvants which are thought to act via distinct mechanisms. We hypothesized that they might produce synergistic effects when used together. We prepared a series of lipopolysaccharide (LPS) preparations ranging from the smallest precursor, lipid X through complete LPS with O-polysaccharide chains. Three preparations with reduced toxicity, monophosphoryl lipid A, partially hydrolysed Ra-LPS and LPS of Rhodopseudomonas sphaeroides were also utilized. All LPS preparations except the smallest were effective adjuvants for inducing early antibody responses to trinitrophenyl-conjugated hen egg albumin (TNP-HEA) when injected in squalane-in-water emulsions with copolymer L141. Only the larger LPS preparations induced sustained antibody responses. By itself, emulsions of copolymer L141 induced a predominant IgG1 antibody isotype response with lesser amounts of IgG2a and IgG2b. Surprisingly, all of the LPS preparations tested increased the proportion of IgG2 isotypes even though some had little effect on overall titres. The detoxified Ra-LPS (Ra-detox) was the most effective preparation for both increasing antibody titres and inducing the desirable IgG2a and IgG2b isotypes. These results demonstrate that the combination of LPS and block polymer adjuvants can produce synergistic effects without unacceptable toxicities. C1 EMORY UNIV,DEPT PATHOL,762 WMB,ATLANTA,GA 30322. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIAID NIH HHS [AI-25856]; NIGMS NIH HHS [GM-36054] NR 55 TC 54 Z9 54 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0264-410X J9 VACCINE JI Vaccine PD APR PY 1991 VL 9 IS 4 BP 257 EP 265 DI 10.1016/0264-410X(91)90109-J PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FF564 UT WOS:A1991FF56400008 PM 2058268 ER PT J AU CHAN, BMC MATSUURA, N TAKADA, Y ZETTER, BR HEMLER, ME AF CHAN, BMC MATSUURA, N TAKADA, Y ZETTER, BR HEMLER, ME TI INVITRO AND INVIVO CONSEQUENCES OF VLA-2 EXPRESSION ON RHABDOMYOSARCOMA CELLS SO SCIENCE LA English DT Article ID INHIBITS EXPERIMENTAL METASTASIS; MELANOMA-CELLS; MONOCLONAL-ANTIBODY; INTEGRIN RECEPTORS; DEPENDENT ADHESION; SURFACE RECEPTORS; COLLAGEN RECEPTOR; LAMININ RECEPTOR; T-CELLS; FIBRONECTIN AB Cloned integrin alpha-2 subunit complementary DNA was expressed on human rhabdomyosarcoma (RD) cells to give a functional VLA-2 (alpha-2-beta-1) adhesion receptor. The VLA-2-positive RDA2 cells not only showed increased adhesion to collagen and laminin in vitro, but also formed substantially more metastatic tumor colonies in nude mice after either intravenous or subcutaneous injection. These results show that a specific adhesion receptor (VLA-2) can markedly enhance both experimental and spontaneous metastasis. In contrast to the metastasis results, there was no difference in either the in vitro growth rate or apparent in vivo tumorigenicity of RD and RDA2 cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. OI takada, yoshikazu/0000-0001-5481-9589 FU NCI NIH HHS [CA 37393]; NIGMS NIH HHS [GM 38903] NR 49 TC 302 Z9 305 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 MAR 29 PY 1991 VL 251 IS 5001 BP 1600 EP 1602 DI 10.1126/science.2011740 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FD890 UT WOS:A1991FD89000034 PM 2011740 ER PT J AU DOUDNA, JA COUTURE, S SZOSTAK, JW AF DOUDNA, JA COUTURE, S SZOSTAK, JW TI A MULTISUBUNIT RIBOZYME THAT IS A CATALYST OF AND TEMPLATE FOR COMPLEMENTARY STRAND RNA-SYNTHESIS SO SCIENCE LA English DT Article ID GROUP-I INTRONS; DIRECTED SYNTHESIS; POLYMERASE; CONSERVATION; TETRAHYMENA; EVOLUTION AB Derivatives of the sunY self-splicing intron efficiently catalyzed the synthesis of complementary strand RNA by template-directed assembly of oligonucleotides. These ribozymes were separated into three short RNA fragments that formed active catalytic complexes. One of the multisubunit sunY derivatives catalyzed the synthesis of a strand of RNA complementary to one of its own subunits. These results suggest that prebiotically synthesized oligonucleotides might have been able to assemble into a complex capable of self-replication. RP DOUDNA, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 21 TC 86 Z9 86 U1 2 U2 9 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 29 PY 1991 VL 251 IS 5001 BP 1605 EP 1608 DI 10.1126/science.1707185 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FD890 UT WOS:A1991FD89000036 PM 1707185 ER PT J AU HIBBS, ML XU, H STACKER, SA SPRINGER, TA AF HIBBS, ML XU, H STACKER, SA SPRINGER, TA TI REGULATION OF ADHESION TO ICAM-1 BY THE CYTOPLASMIC DOMAIN OF LFA-1 INTEGRIN BETA-SUBUNIT SO SCIENCE LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; COMPLEMENT RECEPTOR TYPE-3; AMINO-ACID SEQUENCE; ALPHA-SUBUNIT; VONWILLEBRAND-FACTOR; CLONING; CD2; HOMOLOGY; FAMILY; CHAIN AB Interactions between cytotoxic lymphocytes and their targets require the T cell antigen receptor (TCR) and the integrin lymphocyte function-associated molecule-1 (LFA-1, CD11a/CD18). LFA-1 is not constitutively avid for its counterreceptors, intercellular adhesion molecules (ICAMs)-1 and -2. Cross-linking of the TCR transiently converts LFA-1 to a high avidity state and thus provides a mechanism for regulating cellular adhesion and de-adhesion in an antigen-specific manner. Truncation of the cytoplasmic domain of the beta, but not the alpha, subunit of LFA-1 eliminated binding to ICAM-1 and sensitivity to phorbol esters. Thus, LFA-1 binding to ICAM-1 was found to be regulated by the cytoplasmic domain of the beta-subunit of LFA-1. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. RI Hibbs, Margaret/D-7013-2011 FU NCI NIH HHS [CA31798] NR 25 TC 252 Z9 252 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 MAR 29 PY 1991 VL 251 IS 5001 BP 1611 EP 1613 DI 10.1126/science.1672776 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FD890 UT WOS:A1991FD89000038 PM 1672776 ER PT J AU EMANUEL, LL BARRY, MJ STOECKLE, JD ETTELSON, LM EMANUEL, EJ AF EMANUEL, LL BARRY, MJ STOECKLE, JD ETTELSON, LM EMANUEL, EJ TI ADVANCE DIRECTIVES FOR MEDICAL-CARE - A CASE FOR GREATER USE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID LIFE-SUSTAINING TREATMENT; CARDIOPULMONARY RESUSCITATION; ELDERLY OUTPATIENTS; PHYSICIANS; DECISIONS; PREFERENCES; ATTITUDES; CHOICES; END AB Background. Advance directives for medical care and the designation of proxy decision makers to guide medical care after a patient has become incompetent have been widely advocated but little studied. We investigated the attitudes of patients toward planning, perceived barriers to such planning, treatment preferences in four hypothetical scenarios, and the feasibility of using a particular document (the Medical Directive) in the outpatient setting to specify advance directives. Methods. We surveyed 405 outpatients of 30 primary care physicians at Massachusetts General Hospital and 102 members of the general public in Boston and asked them as part of the survey to complete the Medical Directive. Results. Advance directives were desired by 93 percent of the outpatients and 89 percent of the members of the general public (P > 0.2). Both the young and the healthy subgroups expressed at least as much interest in planning as those older than 65 and those in fair-to-poor health. Of the perceived barriers to issuing advance directives, the lack of physician initiative was among the most frequently mentioned, and the disturbing nature of the topic was among the least. The outpatients refused life-sustaining treatments in 71 percent of their responses to options in the four scenarios (coma with chance of recovery, 57 percent; persistent vegetative state, 85 percent; dementia, 79 percent; and dementia with a terminal illness, 87 percent), with small differences between widely differing types of treatments. Specific treatment preferences could not be usefully predicted according to age, self-rated state of health, or other demographic features. Completing the Medical Directive took a median of 14 minutes. Conclusions. When people are asked to imagine themselves incompetent with a poor prognosis, they decide against life-sustaining treatments about 70 percent of the time. Health, age, or other demographic features cannot be used, however, to predict specific preferences. Advance directives as part of a comprehensive approach such as that provided by the Medical Directive are desired by most people, require physician initiative, and can be achieved during a regular office visit. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,PROGRAM ETH & PROFESS,CAMBRIDGE,MA 02138. RP EMANUEL, LL (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114, USA. FU AHRQ HHS [R01 HS06120] NR 26 TC 534 Z9 537 U1 1 U2 22 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 28 PY 1991 VL 324 IS 13 BP 889 EP 895 DI 10.1056/NEJM199103283241305 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA FD111 UT WOS:A1991FD11100005 PM 2000111 ER PT J AU THOMPSON, BT SOUTHERN, JF MCCLOUD, TC SCULLY, RE HUANG, PL BLAND, EF AF THOMPSON, BT SOUTHERN, JF MCCLOUD, TC SCULLY, RE HUANG, PL BLAND, EF TI A 63-YEAR-OLD WOMAN WITH CORONARY-ARTERY DISEASE, A PULMONARY INFILTRATE, AND SUDDEN-DEATH - PULMONARY EMBOLI, MULTIPLE, RIGHT LUNG, WITH PULMONARY INFARCT, CAVITATED, RIGHT LOWER LOBE - CORONARY-ARTERY DISEASE, SEVERE - MYOCARDIAL INFARCT, OLD POSTERIOR, WITH LEFT-VENTRICULAR ANEURYSM - PULMONARY-EMPHYSEMA, SEVERE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID CIRCULATORY FAILURE; VENOUS THROMBOSIS; AUTOPSY; AUDIT; SENSITIVITY; HYPOXEMIA; DIAGNOSIS; PRESSURE; ACCURACY; DECADES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP THOMPSON, BT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 48 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 MAR 28 PY 1991 VL 324 IS 13 BP 900 EP 909 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA FD111 UT WOS:A1991FD11100007 ER PT J AU PRINCE, MR AF PRINCE, MR TI BETA-CAROTENE TO PREVENT SKIN-CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP PRINCE, MR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. RI Prince, Martin/S-6850-2016 NR 2 TC 3 Z9 3 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 MAR 28 PY 1991 VL 324 IS 13 BP 924 EP 924 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FD111 UT WOS:A1991FD11100022 ER PT J AU SUN, H TRECO, D SZOSTAK, JW AF SUN, H TRECO, D SZOSTAK, JW TI EXTENSIVE 3'-OVERHANGING, SINGLE-STRANDED-DNA ASSOCIATED WITH THE MEIOSIS-SPECIFIC DOUBLE-STRAND BREAKS AT THE ARG4 RECOMBINATION INITIATION SITE SO CELL LA English DT Article ID MEIOTIC GENE CONVERSION; SACCHAROMYCES-CEREVISIAE; YEAST; CHROMOSOME; SYNAPSIS; EXCHANGE AB Meiosis-specific double-strand breaks occur at the initiation site for meiotic gene conversion in the yeast ARG4 gene. Here we show that the break fragments end in extensive 3'-overhanging, single-stranded tails. The single-stranded tails vary in length, generating a gradient of single-strandedness that parallels the gradient of gene conversion frequencies in ARG4. In strains carrying a rad50S mutation, which blocks meiotic recombination, the extensive single-stranded tails do not form, suggesting that their generation is an obligatory step in meiotic recombination. Using the rad50S mutant, we have mapped the site of the ARG4 break to a small region within the genetically defined recombination initiation site. These results strongly support the double-strand break model of meiotic recombination. RP SUN, H (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 32 TC 433 Z9 438 U1 2 U2 13 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 22 PY 1991 VL 64 IS 6 BP 1155 EP 1161 DI 10.1016/0092-8674(91)90270-9 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FD558 UT WOS:A1991FD55800013 PM 2004421 ER PT J AU LEHRER, RI ROSENMAN, M HARWIG, SSSL JACKSON, R EISENHAUER, P AF LEHRER, RI ROSENMAN, M HARWIG, SSSL JACKSON, R EISENHAUER, P TI ULTRASENSITIVE ASSAYS FOR ENDOGENOUS ANTIMICROBIAL POLYPEPTIDES SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE ANTIBIOTIC; RADIAL DIFFUSION ASSAY; POLYACRYLAMIDE; ESCHERICHIA; FUNGI; SALMONELLA ID PURIFICATION; NEUTROPHILS; DEFENSINS AB We developed two sensitive methods for identifying antimicrobial molecules in leukocytes and other tissues. One method uses a gel overlay technique and was designed to identify antimicrobial polypeptides in samples subjected to polyacrylamide gel electrophoresis. The other, a radial diffusion assay, allows multiple fractions obtained by chromatographic procedures to be tested for antimicrobial activity conveniently. When we used E. coli ML-35p or Salmonella typhimurium 14028S as test organisms in the radial diffusion assay, we routinely detected 5-10 ng of rabbit defensin NP-1 in 5-mu-l of sample. With minor modifications, both methods can be applied to other organisms, including Gram-positive bacteria, several Candida species and Cryptococcus neoformans. C1 W LOS ANGELES VET ADM HOSP,LOS ANGELES,CA 90073. RP LEHRER, RI (reprint author), UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,CHS 37-062,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [AI 22839, AI 25693, AI 29595] NR 11 TC 488 Z9 544 U1 2 U2 30 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-1759 J9 J IMMUNOL METHODS JI J. Immunol. Methods PD MAR 21 PY 1991 VL 137 IS 2 BP 167 EP 173 DI 10.1016/0022-1759(91)90021-7 PG 7 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA FD419 UT WOS:A1991FD41900003 PM 1901580 ER PT J AU LIPSHULTZ, SE COLAN, SD GELBER, RD PEREZATAYDE, AR SALLAN, SE SANDERS, SP AF LIPSHULTZ, SE COLAN, SD GELBER, RD PEREZATAYDE, AR SALLAN, SE SANDERS, SP TI LATE CARDIAC EFFECTS OF DOXORUBICIN THERAPY FOR ACUTE LYMPHOBLASTIC-LEUKEMIA IN CHILDHOOD SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ANTHRACYCLINE CARDIOTOXICITY; INTENSIVE ASPARAGINASE; BICYCLE EXERCISE; CHILDREN; ADRIAMYCIN; GROWTH; INDUCTION; TREADMILL; FAILURE; HEART AB Background. Cardiotoxicity is a recognized complication of doxorubicin therapy, but the long-term effects of doxorubicin are not well documented. We therefore-assessed the cardiac status of 115 children who had been treated for acute lymphoblastic leukemia with doxorubicin 1 to 15 years earlier in whom the disease was in continuous remission. Methods. Eighteen patients received one dose of doxorubicin (45 mg per square meter of body-surface area), and 97 received multiple doses totaling 228 to 550 mg per square meter (median, 360). The median interval between the end of treatment and the cardiac evaluation was 6.4 years. Our evaluation consisted of a history, 24-hour ambulatory electrocardiographic recording, exercise testing, and echocardiography. Results. Fifty-seven percent of the patients had abnormalities of left ventricular afterload (measured as end-systolic wall stress) or contractility (measured as the stress-velocity index). The cumulative dose of doxorubicin was the most significant predictor of abnormal cardiac function (P < 0.002). Seventeen percent of patients who received one dose of doxorubicin had slightly elevated-age-adjusted afterload, and none had decreased contractility. In contrast, 65 percent of patients who received at least 228 mg of doxorubicin per square meter had increased afterload (59 percent of patients), decreased contractility (23 percent), or both. Increased afterload was due to reduced ventricular wall thickness, not to hypertension or ventricular dilatation. In multivariate analyses restricted to patients who received at least 228 mg of doxorubicin per square meter, the only significant predictive factors were a higher cumulative dose (P = 0.01), which predicted decreased contractility, and an age of less than four years at treatment (P = 0.003), which predicted increased afterload. Afterload increased progressively in 24 of 34 patients evaluated serially (71 percent). Reported symptoms correlated poorly with indexes of exercise tolerance or ventricular function. Eleven patients had congestive heart failure within one year of treatment with doxorubicin; five of them had recurrent heart failure 3.7 to 10.3 years after completing doxorubicin treatment, and two required heart transplantation. No patient had late heart failure as a new event. Conclusions. Doxorubicin therapy in childhood impairs myocardial growth in a dose-related fashion and results in a progressive increase in left ventricular afterload, sometimes accompanied by reduced contractility. We hypothesize that the loss of myocytes during doxorubicin therapy in childhood might result in inadequate left ventricular mass and clinically important heart disease in later years. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP LIPSHULTZ, SE (reprint author), CHILDRENS HOSP MED CTR,DEPT CARDIOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. OI Sanders, Stephen/0000-0003-3521-4044 FU NCI NIH HHS [CA06516, CA34183]; NHLBI NIH HHS [HL01816] NR 37 TC 886 Z9 896 U1 2 U2 18 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 21 PY 1991 VL 324 IS 12 BP 808 EP 815 DI 10.1056/NEJM199103213241205 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FC442 UT WOS:A1991FC44200005 PM 1997853 ER PT J AU KLIBANSKI, A ZERVAS, NT AF KLIBANSKI, A ZERVAS, NT TI SEMINARS IN MEDICINE OF THE BETH-ISRAEL-HOSPITAL, BOSTON - DIAGNOSIS AND MANAGEMENT OF HORMONE-SECRETING PITUITARY-ADENOMAS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID SOMATOSTATIN ANALOG SMS-201-995; LONG-TERM TREATMENT; GONADOTROPIN-RELEASING HORMONE; DEXAMETHASONE SUPPRESSION TEST; TRANS-SPHENOIDAL MICROSURGERY; GROWTH-HORMONE; ALPHA-SUBUNIT; CUSHINGS-DISEASE; SMS 201-995; ACROMEGALIC PATIENTS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KLIBANSKI, A (reprint author), MASSACHUSETTS GEN HOSP,CTR NEUROENDOCRINE CLIN,NEUROENDOCRINE UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR01066]; NIDDK NIH HHS [DK-40947] NR 100 TC 118 Z9 119 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 MAR 21 PY 1991 VL 324 IS 12 BP 822 EP 831 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA FC442 UT WOS:A1991FC44200007 PM 1997855 ER PT J AU SHUSTER, E AF SHUSTER, E TI NAZI SCIENCE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP SHUSTER, E (reprint author), VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104, USA. NR 2 TC 0 Z9 0 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 21 PY 1991 VL 324 IS 12 BP 845 EP 845 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FC442 UT WOS:A1991FC44200011 ER PT J AU BOYLE, LA PANDOLFI, F SCOTT, S KURNICK, JT AF BOYLE, LA PANDOLFI, F SCOTT, S KURNICK, JT TI FIBROBLAST-PRODUCED FACTORS PREVENT PHA-INDUCED APOPTOSIS OF PRIMED LYMPHOCYTES-T SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 1 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 MAR 19 PY 1991 VL 5 IS 6 BP A1697 EP A1697 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55701396 ER PT J AU CONLAY, LA KISCHKA, U WURTMAN, RJ AF CONLAY, LA KISCHKA, U WURTMAN, RJ TI CAFFEINES PROTECTIVE EFFECTS DURING HYPOTENSION REFLECT AN INTERACTION WITH ADENOSINE RECEPTORS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,NEUROENDOCRINE REGULAT LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,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 MAR 19 PY 1991 VL 5 IS 6 BP A1573 EP A1573 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700673 ER PT J AU FISHMAN, RS SYSTROM, DM FRAGOSO, CV KANAREK, DJ KAZEMI, H AF FISHMAN, RS SYSTROM, DM FRAGOSO, CV KANAREK, DJ KAZEMI, H TI THE EFFECT OF MONOSODIUM GLUTAMATE ON INTRAMUSCULAR PH DURING EXERCISE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM 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 MAR 19 PY 1991 VL 5 IS 6 BP A1726 EP A1726 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55701566 ER PT J AU GROVE, JR WOODGETT, J BANERJEE, P BALASUBRAMANYAM, A COFFER, PJ PRICE, DJ AVRUCH, J AF GROVE, JR WOODGETT, J BANERJEE, P BALASUBRAMANYAM, A COFFER, PJ PRICE, DJ AVRUCH, J TI CLONING AND EXPRESSION OF 2 HUMAN-P70 S6-KINASE POLYPEPTIDES DIFFERING ONLY AT THEIR AMINO TERMINI SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. LUDWIG INST CANC RES,LONDON W1P 8BT,ENGLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 19 PY 1991 VL 5 IS 6 BP A1537 EP A1537 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700460 ER PT J AU HOLLANDER, GA LUSKEY, BD WILLIAMS, DA BURAKOFF, SJ AF HOLLANDER, GA LUSKEY, BD WILLIAMS, DA BURAKOFF, SJ TI LONG-TERM EXPRESSION OF HUMAN CD4 AND HUMAN CD8 IN MICE BY RETROVIRAL GENE-TRANSFER SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. 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 MAR 19 PY 1991 VL 5 IS 6 BP A1698 EP A1698 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55701404 ER PT J AU PANDOLFI, F WILZ, SW HAWES, GE VANDENELSEN, PJ MCCLUSKEY, RT KURNICK, JT AF PANDOLFI, F WILZ, SW HAWES, GE VANDENELSEN, PJ MCCLUSKEY, RT KURNICK, JT TI CHARACTERIZATION OF A T-CELL CLONE WHICH LOSES CD3 AND TCR ALPHA-BETA-EXPRESSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 MAR 19 PY 1991 VL 5 IS 6 BP A1700 EP A1700 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55701415 ER PT J AU QUINN, DA HONEYMAN, TW THOMPSON, BT HALES, CA SCHEID, CR AF QUINN, DA HONEYMAN, TW THOMPSON, BT HALES, CA SCHEID, CR TI FACTORS AFFECTING PH MEASUREMENTS IN PULMONARY-ARTERY SMOOTH-MUSCLE CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV MASSACHUSETTS,SCH MED,WORCESTER,MA 01605. MASSACHUSETTS GEN HOSP,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 MAR 19 PY 1991 VL 5 IS 6 BP A1606 EP A1606 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700867 ER PT J AU REISS, CS GAPUD, CP CAO, BN KEIL, W AF REISS, CS GAPUD, CP CAO, BN KEIL, W TI NASCENT CLASS-II MHC CHAINS ARE REQUIRED FOR VSV GLYCOPROTEIN PRESENTATION TO CTL CLONES SO FASEB JOURNAL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DIV INFECT DIS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH 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 MAR 19 PY 1991 VL 5 IS 6 BP A1461 EP A1461 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700018 ER PT J AU STAUNTON, DE GAUR, A CARPEN, O CHAN, PY SPRINGER, TA AF STAUNTON, DE GAUR, A CARPEN, O CHAN, PY SPRINGER, TA TI IDENTIFICATION OF ICAM-1 SEQUENCES ESSENTIAL TO HUMAN RHINOVIRUS INTERNALIZATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,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 MAR 19 PY 1991 VL 5 IS 6 BP A1695 EP A1695 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55701387 ER PT J AU TOMERA, JF MARTYN, JAJ AF TOMERA, JF MARTYN, JAJ TI BURN TRAUMA-INDUCED INTERACTIONS OF ADENOSINE-3'-5' CYCLIC MONOPHOSPHATE (CAMP), INOSITOL TRISPHOSPHATE (IP3), AND MYOPLASMIC CA2+ IN SKELETAL-MUSCLE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. SHRINERS BURN INST,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 MAR 19 PY 1991 VL 5 IS 6 BP A1598 EP A1598 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700821 ER PT J AU VERMEULEN, MW MILLER, JT BAER, NR AF VERMEULEN, MW MILLER, JT BAER, NR TI TRANSLATIONAL REGULATION OF TUMOR-NECROSIS-FACTOR GENE-EXPRESSION SO FASEB JOURNAL 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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 19 PY 1991 VL 5 IS 6 BP A1601 EP A1601 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700840 ER PT J AU WANG, C MERCOLA, M STILES, CD AF WANG, C MERCOLA, M STILES, CD TI THE REGULATION OF PDGF AND PDGF RECEPTOR EXPRESSION IN F9 TERATOCARCINOMA CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH 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 MAR 19 PY 1991 VL 5 IS 6 BP A1623 EP A1623 PN 3 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FE557 UT WOS:A1991FE55700968 ER PT J AU CARLSON, LL WEAVER, DR REPPERT, SM AF CARLSON, LL WEAVER, DR REPPERT, SM TI MELATONIN RECEPTORS AND SIGNAL TRANSDUCTION DURING DEVELOPMENT IN SIBERIAN HAMSTERS (PHODOPUS-SUNGORUS) SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE REPRODUCTION; PHOTOPERIODISM; 2-[I-125]IODOMELATONIN; RECEPTOR AUTORADIOGRAPHY; G-PROTEIN COUPLED RECEPTOR ID PHOTOPERIODIC INFORMATION; REPRODUCTIVE DEVELOPMENT; DJUNGARIAN HAMSTERS; MATERNAL TRANSFER; PARS TUBERALIS; BINDING-SITES; BRAIN; LOCALIZATION; RESPONSES; DAYLENGTH AB Maternal melatonin communicates daylength information to the fetus in Siberian hamsters. Fetal sensitivity to melatonin declines near birth. In this report, we describe melatonin receptor distribution and a second messenger response to melatonin in Siberian hamsters during the perinatal period. The sites of high-affinity 2-[I-125]iodomelatonin ([I-125]MEL) binding were generally similar throughout the perinatal period. The non-hydrolyzable GTP analog, guanosine-5'-O-(3-thiotriphosphate) (100-mu-M) inhibited [I-125]MEL binding at each age, suggesting the melatonin receptors are associated with guanine nucleotide binding proteins (G proteins). Furthermore, melatonin (10 nM) inhibited forskolin-stimulated cAMP accumulation in median eminence/pars tuberalis (ME/PT) explants as early as 4 days before birth, when sensitivity to melatonin in vivo is high. The cAMP regulatory system appeared disrupted on the day of birth, in that forskolin (10-mu-M) stimulation of cAMP accumulation was reduced, and melatonin did not inhibit cAMP accumulation stimulated by forskolin. A higher forskolin dose (100-mu-M) elevated cAMP levels more clearly on the day of birth, and melatonin inhibited forskolin-stimulated cAMP accumulation. These results suggest that the decreased physiological responsiveness to melatonin at the end of gestation may be due to alterations in the cAMP regulatory system. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DEV CHRONOBIOL LAB,JACKSON 1226,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02114. NR 28 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-3806 J9 DEV BRAIN RES JI Dev. Brain Res. PD MAR 18 PY 1991 VL 59 IS 1 BP 83 EP 88 DI 10.1016/0165-3806(91)90032-E PG 6 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA FE414 UT WOS:A1991FE41400011 ER PT J AU BRANCH, WT ARKY, RA WOO, B STOECKLE, JD LEVY, DB TAYLOR, WC AF BRANCH, WT ARKY, RA WOO, B STOECKLE, JD LEVY, DB TAYLOR, WC TI TEACHING MEDICINE AS A HUMAN-EXPERIENCE - A PATIENT-DOCTOR RELATIONSHIP COURSE FOR FACULTY AND 1ST-YEAR MEDICAL-STUDENTS SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID CLINICAL CORRELATION COURSE; RESIDENT-MATCHING-PROGRAM; INTERNAL MEDICINE; LEARNING PROJECTS; HUMAN-VALUES; 1ST YEAR; EDUCATION; CURRICULUM; PHYSICIAN; ETHICS AB We developed a required, longitudinal course for first-year medical students that addressed the patient-doctor relationship. Our course linked understanding patients' experiences and perspectives on illness with listening to, talking with, and establishing a rapport with patients while obtaining their medical histories. Learning was enhanced by use of an interdisciplinary faculty and by small-group continuity and faculty mentoring. Our curriculum adapted problem-based, self-directed educational methods to convey medical humanism. We focused on bedside interviewing as the means for exploring patients' social, emotional, and ethical concerns. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MT AUBURN HOSP,CAMBRIDGE,MA 02138. RP BRANCH, WT (reprint author), BRIGHAM & WOMENS HOSP,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 91 TC 70 Z9 74 U1 1 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 15 PY 1991 VL 114 IS 6 BP 482 EP 489 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FB640 UT WOS:A1991FB64000009 PM 1994796 ER PT J AU RANKIN, AC MCGOVERN, BA AF RANKIN, AC MCGOVERN, BA TI ADENOSINE OR VERAPAMIL FOR THE ACUTE TREATMENT OF SUPRAVENTRICULAR TACHYCARDIA SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material ID VENTRICULAR-TACHYCARDIA; JUNCTIONAL TACHYCARDIA; INTRAVENOUS VERAPAMIL; THERAPEUTIC USE; TERMINATION; DIAGNOSIS; ARRHYTHMIAS; EFFICACY; CHILDREN; INFANTS RP RANKIN, AC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 21 TC 10 Z9 10 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 15 PY 1991 VL 114 IS 6 BP 513 EP 515 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FB640 UT WOS:A1991FB64000012 PM 1994798 ER PT J AU ELLIOTT, ME JONES, HM GOODFRIEND, TL AF ELLIOTT, ME JONES, HM GOODFRIEND, TL TI EFFECTS OF CALMIDAZOLIUM AND OTHER CALMODULIN ANTAGONISTS ON ADRENAL GLOMERULOSA CELLS SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID DEPENDENT PROTEIN-KINASE; ANGIOTENSIN-II; ALDOSTERONE SYNTHESIS; ZONA GLOMERULOSA; CALCIUM; STEROIDOGENESIS; INOSITOL; PHOSPHODIESTERASE; CYCLOHEXIMIDE; INHIBITION C1 UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT INTERNAL MED,MADISON,WI 53706. RP ELLIOTT, ME (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,HYPERTENS RES LAB,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 26 TC 4 Z9 4 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 15 PY 1991 VL 41 IS 6-7 BP 1083 EP 1086 DI 10.1016/0006-2952(91)90219-U PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FD172 UT WOS:A1991FD17200033 PM 2009077 ER PT J AU ALCANTARA, O JAVORS, M BOLDT, DH AF ALCANTARA, O JAVORS, M BOLDT, DH TI INDUCTION OF PROTEIN-KINASE-C MESSENGER-RNA IN CULTURED LYMPHOBLASTOID T-CELLS BY IRON-TRANSFERRIN BUT NOT BY SOLUBLE IRON SO BLOOD LA English DT Article ID LYMPHOCYTES-T; RECEPTOR EXPRESSION; GENE-EXPRESSION; PHORBOL ESTERS; ACTIVATION; PROLIFERATION; LINES; INTERLEUKIN-2; HETEROGENEITY; METABOLISM C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV HEMATOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. NR 36 TC 32 Z9 32 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1991 VL 77 IS 6 BP 1290 EP 1297 PG 8 WC Hematology SC Hematology GA FB731 UT WOS:A1991FB73100022 PM 2001452 ER PT J AU KRAMER, ZB BOROS, L WIERNIK, PH ANDERSEN, J BENNETT, JM CASSILETH, P OKEN, M AF KRAMER, ZB BOROS, L WIERNIK, PH ANDERSEN, J BENNETT, JM CASSILETH, P OKEN, M TI 13-CIS-RETINOIC ACID IN THE TREATMENT OF ELDERLY PATIENTS WITH ACUTE MYELOID-LEUKEMIA - A PHASE-II PILOT-STUDY OF THE EASTERN COOPERATIVE ONCOLOGY GROUP SO CANCER LA English DT Article ID ACUTE PROMYELOCYTIC LEUKEMIA; TUMOR NECROSIS FACTOR; TRANS-RETINOIC ACID; DIFFERENTIATION; INVITRO; CELLS; GROWTH; ACNE AB The management of acute myeloid leukemia in the elderly (65 years and older) is unsatisfactory because of poor patient tolerance of standard myeloablative chemotherapy. The authors conducted a Phase II study to evaluate the effectiveness and toxicity of 13-cis-retinoic acid (CRA) in the therapy of elderly patients with acute myeloid leukemia (AML). Patients presenting with leukocyte counts less than 20,000/mu-l were treated with CRA alone. Those with leukocyte counts of 20,000/mu-l or greater were pretreated with hydroxyurea, followed by CRA. Twelve of 18 patients received at least 4 weeks of CRA and were thus considered evaluable for toxicity and response. No objective responses were observed. Cis-retinoic acid administration was well tolerated; only modest dermatologic, musculoskeletal, and gastrointestinal toxicity was observed. Alternative therapeutic strategies should be investigated in this subpopulation of AML patients. C1 UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. FU NCI NIH HHS [CA 17145, CA 21115, CA 14144] NR 20 TC 11 Z9 11 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 MAR 15 PY 1991 VL 67 IS 6 BP 1484 EP 1486 DI 10.1002/1097-0142(19910315)67:6<1484::AID-CNCR2820670603>3.0.CO;2-3 PG 3 WC Oncology SC Oncology GA FC040 UT WOS:A1991FC04000002 PM 2001535 ER PT J AU PAUL, SR TARBELL, NJ KORF, B KRETSCHMAR, CS LAVALLY, B GRIER, HE AF PAUL, SR TARBELL, NJ KORF, B KRETSCHMAR, CS LAVALLY, B GRIER, HE TI STAGE-IV NEUROBLASTOMA IN INFANTS - LONG-TERM SURVIVAL SO CANCER LA English DT Article ID N-MYC ONCOGENE; NEURO-BLASTOMA; CHILDREN; CHEMOTHERAPY; PROGNOSIS; EXPERIENCE; HYPOTHESIS; CANCER AB Before the advent of multiagent chemotherapy, the prognosis for patients with Stage IV neuroblastoma of all ages was dismal. More recently, marked improvement in infants with Stage IV neuroblastoma has been reported. Twenty-four infants with Stage IV neuroblastoma have been treated at the Dana-Farber Cancer Institute/The Children's Hospital, and the Joint Center For Radiation Therapy, Boston, Massachusetts, between 1970 and 1988. Twenty-three of these patients were treated with multiagent chemotherapy and one with a single drug. In the initial report, ten of 11 patients were alive without evidence of disease after intensive therapy. In this report the authors update their initial series of patients and include 13 additional patients who subsequently presented to our institutions with Stage IV neuroblastoma younger than 1 year of age. The 5-year actuarial event-free survival for the 24 patients is 75%. No patient without bone metastases died from neuroblastoma, and 12 of 16 patients with bone metastases remained disease free. These results confirm that infants with Stage IV neuroblastoma have a very good prognosis when treated with intensive multiagent chemotherapy. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV GENET,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT THERAPY,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP PAUL, SR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA19589] NR 23 TC 30 Z9 31 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 MAR 15 PY 1991 VL 67 IS 6 BP 1493 EP 1497 DI 10.1002/1097-0142(19910315)67:6<1493::AID-CNCR2820670605>3.0.CO;2-# PG 5 WC Oncology SC Oncology GA FC040 UT WOS:A1991FC04000004 PM 2001536 ER PT J AU WILLETT, CG SHELLITO, PC TEPPER, JE ELISEO, R CONVERY, K WOOD, WC AF WILLETT, CG SHELLITO, PC TEPPER, JE ELISEO, R CONVERY, K WOOD, WC TI INTRAOPERATIVE ELECTRON-BEAM RADIATION-THERAPY FOR RECURRENT LOCALLY ADVANCED RECTAL OR RECTOSIGMOID CARCINOMA SO CANCER LA English DT Article ID COLORECTAL-CANCER; ADENOCARCINOMA; RADIOTHERAPY; IRRADIATION; RESECTION; COLON AB A multimodality approach of moderate-dose to high-dose preoperative radiation therapy, surgical resection, and intraoperative electron beam radiation therapy (IORT) has been used for patients with locally recurrent rectal or rectosigmoid carcinoma. The 5-year actuarial local control and disease-free survival for 30 patients undergoing this treatment program were 26% and 19%, respectively. The most important factor predicting a favorable outcome was complete resection with negative pathologic resection margins. The determinate local control and disease-free survival for 13 patients undergoing complete resection were 62% and 54%, respectively, whereas for 17 patients undergoing partial resection these figures were 18% and 6%, respectively. There did not appear to be a difference in local control or survival based on the original surgical resection (adbominoperineal resection versus low anterior resection). However, the likelihood of obtaining a complete resection after preoperative radiation therapy was higher in patients who had previously undergone a low anterior resection than patients undergoing prior abdominoperineal resection. For the 30 patients undergoing external beam irradiation, resection, and IORT, the most significant toxicities were soft tissue or sacral injury and pelvic neuropathy. Efforts to further improve local control are directed toward the concurrent use of chemotherapy (5-fluorouracil with and without leucovorin) as radiation dose modifiers during external beam irradiation and the use of additional postoperative radiation therapy. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. UNIV N CAROLINA,SCH MED,DEPT RADIAT ONCOL,CHAPEL HILL,NC 27514. RP WILLETT, CG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RADIAT MED SERV,BOSTON,MA 02114, USA. NR 20 TC 113 Z9 114 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 MAR 15 PY 1991 VL 67 IS 6 BP 1504 EP 1508 DI 10.1002/1097-0142(19910315)67:6<1504::AID-CNCR2820670607>3.0.CO;2-X PG 5 WC Oncology SC Oncology GA FC040 UT WOS:A1991FC04000006 PM 2001537 ER PT J AU WEINSTOCK, MA STRYKER, WS STAMPFER, MJ LEW, RA WILLETT, WC SOBER, AJ AF WEINSTOCK, MA STRYKER, WS STAMPFER, MJ LEW, RA WILLETT, WC SOBER, AJ TI SUNLIGHT AND DYSPLASTIC NEVUS RISK - RESULTS OF A CLINIC-BASED CASE-CONTROL STUDY SO CANCER LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; MELANOCYTIC NEVI; SUN EXPOSURE; NEVOCYTIC NEVI; NAEVI; PREVALENCE; POPULATION; PHENOTYPE; NUMBER; MOLES AB The dysplastic nevus (DN) is the most important risk factor and precursor for malignant melanoma. The authors compared the responses of 132 consecutive cases of DN, 186 consecutive cases of cutaneous melanoma, and 239 controls attending the same subspecialty clinic to questions regarding sun sensitivity, sun exposure, and other possible risk factors. Dysplastic nervus cases were younger than controls and were of a higher social class, as indicated by more years of formal education. Sun sensitivity (assessed by reported depth of tan after multiple exposures) was associated with both DN risk and melanoma risk after controlling for age and education in logistic regression analysis (P = 0.009 and 0.03, respectively), but for DN risk this association was nonlinear: the relative risks (versus deep tan) were 2.3 for average tanners, 2.8 for light tanners, and 1.6 for those who reported practically no tan. Sun exposure measures were not associated with DN risk after controlling for age and education, whether or not depth of tan was controlled in the analysis. These observations suggest a role for either sunlight or a trait linked with sun sensitivity in the development of dysplastic nevi. C1 ROGER WILLIAMS GEN HOSP,PROVIDENCE,RI 02908. BROWN UNIV,PROVIDENCE,RI 02912. BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. UNIV MASSACHUSETTS,DEPT PHARMACOL,WORCESTER,MA 01605. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP WEINSTOCK, MA (reprint author), VET ADM MED CTR,DEPT MED,DERMATOEPIDEMIOL UNIT 111,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. FU NCI NIH HHS [CA 35837, CA 49531] NR 40 TC 31 Z9 31 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 MAR 15 PY 1991 VL 67 IS 6 BP 1701 EP 1706 DI 10.1002/1097-0142(19910315)67:6<1701::AID-CNCR2820670637>3.0.CO;2-X PG 6 WC Oncology SC Oncology GA FC040 UT WOS:A1991FC04000036 PM 2001561 ER PT J AU SCHILLER, JH STORER, BE WITT, PL ALBERTI, D TOMBES, MB ARZOOMANIAN, R PROCTOR, RA MCCARTHY, D BROWN, RR VOSS, SD REMICK, SC GREM, JL BORDEN, EC TRUMP, DL AF SCHILLER, JH STORER, BE WITT, PL ALBERTI, D TOMBES, MB ARZOOMANIAN, R PROCTOR, RA MCCARTHY, D BROWN, RR VOSS, SD REMICK, SC GREM, JL BORDEN, EC TRUMP, DL TI BIOLOGICAL AND CLINICAL EFFECTS OF INTRAVENOUS TUMOR-NECROSIS-FACTOR-ALPHA ADMINISTERED 3 TIMES WEEKLY SO CANCER RESEARCH LA English DT Article ID INTERFERON-GAMMA; PHASE-I; CELL-LINES; TRANSFORMED-CELLS; HUMAN LYMPHOTOXIN; CANCER-PATIENTS; MURINE TUMORS; FACTOR TNF; MACROPHAGES; EXPRESSION AB Tumor necrosis factor (TNF) is a cytokine with pleiotropic biological and antitumor effects in vitro and in mouse models. The immunological effects of the molecule as a single agent, however, have not been well studied clinically. We conducted a Phase I trial of TNF in 53 patients with advanced malignancies in order to determine the biological and clinical effects of TNF when administered as a 30-min i.v. infusion three times/week. Dose levels of TNF ranged from 5 to 275-mu-g/m2; doses of TNF were escalated between patient groups. The most common clinical toxicities of TNF consisted of rigors, anorexia, headache, and fatigue. Dose-limiting toxicity consisted of hypotension, fatigue, and nausea. Four patients treated at the maximally tolerated dose of 225-mu-g/m2 received dexamethasone to determine whether the toxicities of TNF could be ameliorated. No significant differences in hypotension or subjective symptomatology were observed in those patients receiving dexamethasone and those who did not or between injections in which dexamethasone was administered and when it was not. One patient with colorectal carcinoma treated with 50-mu-g/m2 had a partial response lasting about 9 months. Biological responses were evaluated in 8 patients treated at the maximally tolerated dose before therapy and 24 h afterward. TNF significantly (P < 0.05 for all) enhanced serum beta-2-microglobulin, serum neopterin, and serum interleukin-2 receptor (Tac antigen) levels. Indoleamine 2,3-dioxygenase activity was also increased 24 h following the administration of TNF, although this increase was only of borderline statistical significance (P = 0.07). TNF did not enhance granulocyte bactericidal activity. The expression of cell surface proteins on monocytes, including HLA-DR, HLA-DQ, beta-2-microglobulin, and the Fc receptor, and serum interleukin-1 activity also were not significantly increased by the administration of TNF. Thus, in humans TNF caused biological response modulation with evidence of HLA Class I (beta-2-microglobulin) increase and T-cell (Tac antigen) and monocyte (neopterin) activation. C1 UNIV WISCONSIN,DEPT HUMAN ONCOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP SCHILLER, JH (reprint author), UNIV WISCONSIN,CTR CLIN CANC,ROOM K4 666 CSC,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [N01 CM57735, P30-CA14520]; NCRR NIH HHS [N01-RR03186] NR 47 TC 89 Z9 95 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1991 VL 51 IS 6 BP 1651 EP 1658 PG 8 WC Oncology SC Oncology GA FB576 UT WOS:A1991FB57600013 PM 1998956 ER PT J AU AITAOUANE, A BOYLAN, J GUDAS, LJ GOLD, JD GOLIGER, J HOSLER, BA HU, L LANGSTON, A ROGERS, MB ROSEN, D STONER, CM VASIOS, GW YELICK, P AF AITAOUANE, A BOYLAN, J GUDAS, LJ GOLD, JD GOLIGER, J HOSLER, BA HU, L LANGSTON, A ROGERS, MB ROSEN, D STONER, CM VASIOS, GW YELICK, P TI EMBRYONIC TERATOCARCINOMA CELL-DIFFERENTIATION AS A MODEL SYSTEM FOR THE MOLECULAR ANALYSIS OF RETINOIC ACID ACTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1433 EP A1433 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002991 ER PT J AU ANTONIADES, HN GALANOPOULOS, T NEVILLEGOLDEN, J MAXWELL, M AF ANTONIADES, HN GALANOPOULOS, T NEVILLEGOLDEN, J MAXWELL, M TI EXPRESSION OF IGF-I AND IGF-II GENES IN PRIMARY HUMAN ASTROCYTOMAS AND MENINGIOMAS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1184 EP A1184 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001547 ER PT J AU CLINTON, SK UNDERWOOD, R SHERMAN, ML KUFE, DW LIBBY, P AF CLINTON, SK UNDERWOOD, R SHERMAN, ML KUFE, DW LIBBY, P TI THE EXPRESSION OF MACROPHAGE-COLONY STIMULATING FACTOR (M-CSF) IN CULTURED VASCULAR CELLS AND DURING ATHEROGENESIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,VASC MED UNIT,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 MAR 15 PY 1991 VL 5 IS 5 BP A1438 EP A1438 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55003023 ER PT J AU COLLINS, TL SHIN, J STROMINGER, JL MITTLER, RS BURAKOFF, SJ AF COLLINS, TL SHIN, J STROMINGER, JL MITTLER, RS BURAKOFF, SJ TI P56LCK IS REQUIRED FOR ASSOCIATION BETWEEN CD4 AND THE TCR/CD3 COMPLEX DURING T-CELL ACTIVATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRISTOL MEYER,WALLINGFORD,CT. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A993 EP A993 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000444 ER PT J AU DAVID, V LECA, G CORVAIA, N BOUMSELL, L BENSUSSAN, A AF DAVID, V LECA, G CORVAIA, N BOUMSELL, L BENSUSSAN, A TI PROLIFERATION OF RESTING LYMPHOCYTES IS INDUCED BY TRIGGERING T-CELLS THROUGH AN EPITOPE COMMON TO THE 3 CD18/CD11 LEUKOCYTE ADHESION MOLECULES SO FASEB JOURNAL LA English DT Meeting Abstract C1 HOP ST LOUIS,INSERM,U93,F-75475 PARIS 10,FRANCE. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Bensussan, Armand/E-5434-2017 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1455 EP A1455 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55003119 ER PT J AU DENEKE, SM AF DENEKE, SM TI ARSENITE EFFECTIVE INDUCER OF CYSTINE TRANSPORT AND CELLULAR GLUTATHIONE (GSH) IN BOVINE PULMONARY-ARTERY ENDOTHELIAL-CELLS (BPAEC) SO FASEB JOURNAL LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1188 EP A1188 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001569 ER PT J AU FERRARA, JLM SAKAMOTO, H MICHAELSON, J GOLAN, D ABHYANKAR, S BURAKOFF, SJ AF FERRARA, JLM SAKAMOTO, H MICHAELSON, J GOLAN, D ABHYANKAR, S BURAKOFF, SJ TI LYMPHOCYTES-T WITH A NOVEL CD4+8-3- PHENOTYPE ARE EFFECTOR-CELLS OF EXPERIMENTAL CUTANEOUS GRAFT VS HOST-DISEASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,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 MAR 15 PY 1991 VL 5 IS 5 BP A972 EP A972 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000323 ER PT J AU FREYALDENHOVEN, AM KATZ, MS AF FREYALDENHOVEN, AM KATZ, MS TI PARATHYROID-HORMONE AND DIRECT ACTIVATORS OF PROTEIN-KINASE-C INDUCE PHOSPHORYLATION OF COMMON SUBSTRATES IN CLONAL OSTEOBLAST-LIKE CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GRECC,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1066 EP A1066 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000864 ER PT J AU HAHN, WC ROSENSTEIN, Y BURAKOFF, SJ BIERER, BE AF HAHN, WC ROSENSTEIN, Y BURAKOFF, SJ BIERER, BE TI TCR-CD3 STIMULATION INCREASES THE AVIDITY OF CD2 FOR ITS LIGAND LFA-3 SO FASEB JOURNAL LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,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 MAR 15 PY 1991 VL 5 IS 5 BP A1377 EP A1377 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002666 ER PT J AU IGRAS, V SLECKMAN, B SHIN, J AMREIN, KE BORN, P STROMINGER, JL BURAKOFF, SJ AF IGRAS, V SLECKMAN, B SHIN, J AMREIN, KE BORN, P STROMINGER, JL BURAKOFF, SJ TI THE PP56LCK PROTEIN-KINASE REGULATES THE INTERNALIZATION OF CD4 IN T-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOCHEM & MOLEC BIOL,BOSTON,MA 02115. F HOFFMANN LA ROCHE & CO LTD,CH-4002 BASEL,SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A993 EP A993 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000447 ER PT J AU KRADIN, R MARATHIAS, K CONWA, B PREFFER, F XIA, W PINTO, C AF KRADIN, R MARATHIAS, K CONWA, B PREFFER, F XIA, W PINTO, C TI PULMONARY INFILTRATING LYMPHOCYTES SHOW DIMINISHED EXPRESSION OF CD4 ANTIGENS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 MAR 15 PY 1991 VL 5 IS 5 BP A984 EP A984 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000390 ER PT J AU MARUIWA, M NARULA, N MOSCICKI, R BHAN, A AF MARUIWA, M NARULA, N MOSCICKI, R BHAN, A TI ANTI-KCA-3, A MONOCLONAL-ANTIBODY REACTIVE WITH A RAT COMPLEMENT RECEPTOR, DISTINGUISHES KUPFFER CELLS FROM OTHER MACROPHAGES SO FASEB JOURNAL 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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1351 EP A1351 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002516 ER PT J AU ORSON, FM THOMAS, DW MCSHAN, WM KESSLER, DM HOGAN, ME AF ORSON, FM THOMAS, DW MCSHAN, WM KESSLER, DM HOGAN, ME TI TRIPLEX FORMING OLIGONUCLEOTIDE MODULATION OF IL2R-ALPHA MESSENGER-RNA TRANSCRIPTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 BAYLOR UNIV,CTR BIOTECHNOL,DEPT VET AFFAIRS MED CTR,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A970 EP A970 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000312 ER PT J AU PARK, SS WALKER, W AOYAMA, T LAPENSON, D WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV AF PARK, SS WALKER, W AOYAMA, T LAPENSON, D WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV TI MONOCLONAL-ANTIBODIES THAT DETECT CYTOCHROME-B5 OF RAT AND RABBIT AND EXPRESSED FROM HUMAN CDNA SO FASEB JOURNAL LA English DT Meeting Abstract C1 NCI,BETHESDA,MD 20892. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1164 EP A1164 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001429 ER PT J AU POLANSKI, M VERMEULEN, MW KARNOVSKY, ML AF POLANSKI, M VERMEULEN, MW KARNOVSKY, ML TI MURAMYL DIPEPTIDE SEROTONIN MIMICRY IN THE ACTIVATION OF HUMAN PLATELETS AND MURINE MACROPHAGES SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PULM 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 MAR 15 PY 1991 VL 5 IS 5 BP A1386 EP A1386 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002717 ER PT J AU QVIST, J HURFORD, WE RADERMACHER, P GUYTON, G FALKE, KJ PARK, YS AHN, DW HONG, SK STANEK, K ZAPOL, WM AF QVIST, J HURFORD, WE RADERMACHER, P GUYTON, G FALKE, KJ PARK, YS AHN, DW HONG, SK STANEK, K ZAPOL, WM TI ARTERIAL BLOOD-GAS TENSIONS DURING BREATH-HOLD DIVING IN THE KOREAN AMA SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. FREE UNIV BERLIN,DEPT ANESTHESIA,W-1000 BERLIN 33,GERMANY. SUNY BUFFALO,DEPT ANESTHESIA,BUFFALO,NY 14260. KOSIN MED COLL,DEPT PHYSIOL,PUSAN,SOUTH KOREA. KEIO UNIV,DEPT PHYSIOL,TOKYO 108,JAPAN. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 0 TC 0 Z9 0 U1 1 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1127 EP A1127 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001215 ER PT J AU RADERMACHER, P FALKE, KJ PARK, YS AHN, DW QVIST, J HONG, SK ZAPOL, WM AF RADERMACHER, P FALKE, KJ PARK, YS AHN, DW QVIST, J HONG, SK ZAPOL, WM TI NITROGEN TENSIONS IN BRACHIAL VEIN BLOOD OF KOREAN DIVERS (AMA) SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV DUSSELDORF,DEPT PHYSIOL,W-4000 DUSSELDORF 1,GERMANY. UNIV DUSSELDORF,DEPT ANESTHESIA,W-4000 DUSSELDORF 1,GERMANY. FREE UNIV BERLIN,W-1000 BERLIN 33,GERMANY. KOSIN MED COLL,PUSAN,SOUTH KOREA. HERLEV HOSP,DK-2730 HERLEV,DENMARK. SUNY BUFFALO,BUFFALO,NY 14260. MASSACHUSETTS GEN HOSP,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 MAR 15 PY 1991 VL 5 IS 5 BP A1125 EP A1125 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001204 ER PT J AU RAM, PA WAXMAN, DJ AF RAM, PA WAXMAN, DJ TI THYROID-HORMONE DEPENDENCE OF NADPH P450 REDUCTASE EXPRESSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1165 EP A1165 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001436 ER PT J AU RIMM, IJ GHAYUR, T GASSER, DL ROSENKRANTZ, K BURAKOFF, SJ SEIDMAN, JG FERRARA, JLM AF RIMM, IJ GHAYUR, T GASSER, DL ROSENKRANTZ, K BURAKOFF, SJ SEIDMAN, JG FERRARA, JLM TI ALLOREACTIVE LYMPHOCYTES FROM TCR-BETA (T-CELL RECEPTOR - BETA-CHAIN) TRANSGENIC MICE DO NOT MEDIATE A GRAFT VS HOST-REACTION (GVHR) SO FASEB JOURNAL LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. UNIV PENN,DEPT HUMAN GENET,PHILADELPHIA,PA 19104. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HHMI,DEPT GENET,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 MAR 15 PY 1991 VL 5 IS 5 BP A972 EP A972 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000324 ER PT J AU ROSENSTEIN, Y PARK, JK BIERER, BE ROSEN, FS BURAKOFF, SJ AF ROSENSTEIN, Y PARK, JK BIERER, BE ROSEN, FS BURAKOFF, SJ TI CD43, THE MOLECULE DEFECTIVE IN WISCOTT-ALDRICH SYNDROME ENHANCES THE ACTIVATION OF T-CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,CTR BLOOD RES,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A962 EP A962 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000268 ER PT J AU SCHWABER, J AF SCHWABER, J TI FAILURE OF IG V(D)J RECOMBINATION IN BONE-MARROW PRE-B CELLS FROM X-LINKED AGAMMAGLOBULINEMIA SO FASEB JOURNAL LA English DT Meeting Abstract C1 CTR BLOOD RES,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 MAR 15 PY 1991 VL 5 IS 5 BP A1382 EP A1382 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002697 ER PT J AU SEN, J ABBAS, AK BURAKOFF, SJ AF SEN, J ABBAS, AK BURAKOFF, SJ TI MODEL SYSTEMS TO STUDY THE ROLE OF CD2 IN IMMUNE-RESPONSES SO FASEB JOURNAL LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1002 EP A1002 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000500 ER PT J AU SPERTINI, O KANSAS, GS MUNRO, JM GRIFFIN, JD TEDDER, TF AF SPERTINI, O KANSAS, GS MUNRO, JM GRIFFIN, JD TEDDER, TF TI LEUKOCYTE MIGRATION IS REGULATED BY ACTIVATION OF THE LEUKOCYTE ADHESION MOLECULE-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 MAR 15 PY 1991 VL 5 IS 5 BP A1335 EP A1335 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002422 ER PT J AU STANEK, KS GUYTON, GP HURFORD, WE PARK, YS AHN, DW QVIST, J FALKE, KJ HONG, SK KOBAYASHI, H KOBAYASHI, K ZAPOL, WM AF STANEK, KS GUYTON, GP HURFORD, WE PARK, YS AHN, DW QVIST, J FALKE, KJ HONG, SK KOBAYASHI, H KOBAYASHI, K ZAPOL, WM TI CONTINUOUS PULSE OXIMETRY IN THE BREATH-HOLD DIVING WOMEN OF KOREA AND JAPAN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HERLEV HOSP,DEPT ANESTHESIA,DK-2730 HERLEV,DENMARK. FREE UNIV BERLIN,DEPT ANESTHESIA,W-1000 BERLIN 33,GERMANY. KOSIN MED COLL,DEPT PHYSIOL,PUSAN,SOUTH KOREA. SUNY BUFFALO,DEPT PHYSIOL,BUFFALO,NY 14260. KEIO UNIV,DEPT SURG,TOKYO 108,JAPAN. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 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 MAR 15 PY 1991 VL 5 IS 5 BP A1127 EP A1127 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001213 ER PT J AU SUBRAMANIAN, R VOLOVSEK, A COURSIN, D HO, YS AF SUBRAMANIAN, R VOLOVSEK, A COURSIN, D HO, YS TI ENHANCED POSTISCHEMIC RECOVERY OF CARDIAC-FUNCTION IN HEARTS OF RATS EXPOSED TO 85-PERCENT 02 SO FASEB JOURNAL LA English DT Meeting Abstract C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI. UNIV WISCONSIN,SCH MED,DEPT ANESTHESIOL,MADISON,WI 53706. DUKE UNIV,MED CTR,DEPT PULM MED,DURHAM,NC 27710. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1283 EP A1283 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002125 ER PT J AU TELFER, J RUDD, CE AF TELFER, J RUDD, CE TI A 34KD GTP-BINDING PROTEIN IS ASSOCIATED WITH THE P561CK - CD4 CD8 T-CELL RECEPTOR COMPLEXES 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 MAR 15 PY 1991 VL 5 IS 5 BP A1457 EP A1457 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55003132 ER PT J AU THOMAS, LJ DEGASPERI, R SUGIYAMA, E CHANG, HM BECK, PJ ORLEAN, P ALBRIGHT, C SAMBROOK, JF WARREN, CD YEH, ETH AF THOMAS, LJ DEGASPERI, R SUGIYAMA, E CHANG, HM BECK, PJ ORLEAN, P ALBRIGHT, C SAMBROOK, JF WARREN, CD YEH, ETH TI DEFECTIVE ACTIVATION BY ANTIGEN, SUPERANTIGEN, AND LECTIN IN T-CELL GLYCOSYLATION MUTANTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,PAIN UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A993 EP A993 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000442 ER PT J AU THOMPSON, BT SPENCE, CR JANSSENS, SP JOSEPH, PM HALES, CA AF THOMPSON, BT SPENCE, CR JANSSENS, SP JOSEPH, PM HALES, CA TI INHIBITION OF HYPOXIC PULMONARY-HYPERTENSION IN THE GUINEA-PIG BY HEPARINS OF DIFFERING INVITRO ANTIPROLIFERATIVE POTENCY SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH 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 MAR 15 PY 1991 VL 5 IS 5 BP A1028 EP A1028 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000647 ER PT J AU TSUZAKI, K SIMON, BA STRIEDER, DJ HALES, CA VENEGAS, JG AF TSUZAKI, K SIMON, BA STRIEDER, DJ HALES, CA VENEGAS, JG TI RESPIRATORY SYSTEM IMPEDANCE MEASURED FROM THE AIRWAY OPENING (AO) AND THE CARINA (C) SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. 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 MAR 15 PY 1991 VL 5 IS 5 BP A1134 EP A1134 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001255 ER PT J AU VENEGAS, JG TSUZAKI, K STRIEDER, DJ HALES, CA AF VENEGAS, JG TSUZAKI, K STRIEDER, DJ HALES, CA TI EFFECTS OF ALVEOLAR PCO2 ON RESPIRATORY SYSTEM IMPEDANCE-(Z) SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1134 EP A1134 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55001258 ER PT J AU WAGNER, JA DEFRANCO, C HAWLEY, R SCHEIBE, R ENDOH, T FRAZIER, D DAMON, D CHO, K AF WAGNER, JA DEFRANCO, C HAWLEY, R SCHEIBE, R ENDOH, T FRAZIER, D DAMON, D CHO, K TI THE REGULATION OF GENE-EXPRESSION AND NEURAL DIFFERENTIATION BY PEPTIDE GROWTH-FACTORS 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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A1433 EP A1433 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002992 ER PT J AU WARNER, GL LUDLOW, JW SCOTT, DW AF WARNER, GL LUDLOW, JW SCOTT, DW TI ROLE OF TGF-BETA AND RETINOBLASTOMA PHOSPHORYLATION IN ANTI-IG MEDIATED GROWTH-INHIBITION OF MURINE B-LYMPHOMAS SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV ROCHESTER,CTR CANC,DIV IMMUNOL,ROCHESTER,NY 14642. 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 MAR 15 PY 1991 VL 5 IS 5 BP A969 EP A969 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000307 ER PT J AU WILZ, SW PANDOLFI, F MCCLUSKEY, RT RUBIN, RH KURNICK, JT AF WILZ, SW PANDOLFI, F MCCLUSKEY, RT RUBIN, RH KURNICK, JT TI T-CELLS FROM EXPERIMENTAL ACUTE PYELONEPHRITIS RECOGNIZE SOLUBLE ESCHERICHIA-COLI ANTIGENS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 MAR 15 PY 1991 VL 5 IS 5 BP A1366 EP A1366 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55002602 ER PT J AU WONG, JT BONVENTRE, J DUNN, S COLVIN, RB AF WONG, JT BONVENTRE, J DUNN, S COLVIN, RB TI ISOLATED CD3-CD8 BUT NOT CD3-CD4 PAIRING ENHANCES ACTIVATION SO FASEB JOURNAL 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 FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 15 PY 1991 VL 5 IS 5 BP A993 EP A993 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000443 ER PT J AU XIA, W KRADIN, R AF XIA, W KRADIN, R TI PULMONARY IA+ DENDRITIC CELLS EFFICIENTLY AND SPECIFICALLY SUPPORT IMMUNE T-CELL PROLIFERATION FOLLOWING BRIEF INVIVO EXPOSURE TO ANTIGEN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL 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 MAR 15 PY 1991 VL 5 IS 5 BP A966 EP A966 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC550 UT WOS:A1991FC55000291 ER PT J AU GARCIA, AR SOUKIASIAN, SH FOSTER, CS AF GARCIA, AR SOUKIASIAN, SH FOSTER, CS TI PROGNOSTIC VALUE OF PREOPERATIVE CONJUNCTIVAL BIOPSY IN CLINICALLY QUIESCENT JRA PATIENTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 673 EP 673 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200030 ER PT J AU BARNEY, NP RAIZMAN, MB FOSTER, CS AF BARNEY, NP RAIZMAN, MB FOSTER, CS TI HUMAN CHOROIDAL MAST-CELLS - ENUMERATION AND LOCALIZATION BY FLAT MOUNT PREPARATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 676 EP 676 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200044 ER PT J AU LEVIN, LA ALBERT, D JOHNSON, D AF LEVIN, LA ALBERT, D JOHNSON, D TI MAST-CELLS IN HUMAN OPTIC-NERVE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 676 EP 676 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200045 ER PT J AU MERCHANT, A SOUKIASIAN, SH ZHAO, TZ FOSTER, CS AF MERCHANT, A SOUKIASIAN, SH ZHAO, TZ FOSTER, CS TI AQUEOUS SOLUBLE INTERLEUKIN-2 RECEPTOR (SIL-2R) IN CLINICALLY QUIESCENT UVEITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 677 EP 677 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200049 ER PT J AU NAYAK, RC ATTAWIA, MA CHARLES, JB RANKIN, G AF NAYAK, RC ATTAWIA, MA CHARLES, JB RANKIN, G TI ANTIPERICYTE AUTOANTIBODIES IN DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 680 EP 680 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200071 ER PT J AU HUNTER, DG FOSTER, CS AF HUNTER, DG FOSTER, CS TI ISOLATED OCULAR SARCOIDOSIS - LATE DEVELOPMENT OF SYSTEMIC MANIFESTATIONS IN UVEITIS PATIENTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,IMMUNOL SERV,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 681 EP 681 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200073 ER PT J AU DELAMAZA, MS FOSTER, CS AF DELAMAZA, MS FOSTER, CS TI NECROTIZING SCLERITIS AFTER OCULAR SURGERY - AN IMMUNOHISTOCHEMICAL STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 682 EP 682 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200083 ER PT J AU GAUDIO, AR SANDBERG, MA MILLER, S KINI, MM BERSON, EL AF GAUDIO, AR SANDBERG, MA MILLER, S KINI, MM BERSON, EL TI COMPUTERIZED ACUITY MAPPING OF THE MACULA IN PATIENTS WITH MACULAR DISEASE - A FIXED-CRITERION TEST COMPLEMENTARY TO THE AMSLER GRID SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 690 EP 690 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200126 ER PT J AU SCHAEFER, EJ GONG, JX ROSNER, B REES, DG WEIGELDIFRANCO, CA BERSON, EL AF SCHAEFER, EJ GONG, JX ROSNER, B REES, DG WEIGELDIFRANCO, CA BERSON, EL TI PLASMA DOCOSAHEXAENOIC ACID LEVELS IN VARIOUS GENETIC FORMS OF RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,HUMAN NUTR RES CTR AGING,LIPID METAB LAB,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 703 EP 703 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200191 ER PT J AU PULIAFITO, CA GUYER, DR MONES, JM WEAVER, Y AF PULIAFITO, CA GUYER, DR MONES, JM WEAVER, Y TI INDOCYANINE-GREEN DIGITAL ANGIOGRAPHY AND DYE-ENHANCED DIODE-LASER PHOTOCOAGULATION OF CHOROIDAL NEOVASCULARIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,MORSE LASER CTR,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 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 MAR 15 PY 1991 VL 32 IS 4 BP 712 EP 712 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200236 ER PT J AU LEE, PP SCHUMAN, JS HARMON, J DEKATER, AW BELLOWS, AR AF LEE, PP SCHUMAN, JS HARMON, J DEKATER, AW BELLOWS, AR TI SINGLE DONOR VERSUS COMMERCIAL FIBRIN TISSUE ADHESIVE IN SEALING CONJUNCTIVAL WOUND LEAKS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BLOOD TRANSFUS SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 743 EP 743 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200382 ER PT J AU SHIBA, T BURSELL, SE CLERMONT, A SPORTSMAN, R HEATH, W KING, GL AF SHIBA, T BURSELL, SE CLERMONT, A SPORTSMAN, R HEATH, W KING, GL TI PROTEIN-KINASE-C (PKC) ACTIVATION IS A CAUSAL FACTOR FOR THE ALTERATION OF RETINAL BLOOD-FLOW IN DIABETES OF SHORT DURATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 6 Z9 6 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 MAR 15 PY 1991 VL 32 IS 4 BP 785 EP 785 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200582 ER PT J AU FELD, JR LIN, CP PULIAFITO, CA AF FELD, JR LIN, CP PULIAFITO, CA TI Q-SWITCHED ND-YAG LASER-INDUCED PLASMA FORMATION ON METAL-SURFACES IN WATER - POTENTIAL USE IN PHACOEMULSIFICATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,MORSE LASER CTR,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 797 EP 797 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200641 ER PT J AU HEFETZ, Y ROIDER, J PULIAFITO, CA FLOTTE, T BIRNGRUBER, R AF HEFETZ, Y ROIDER, J PULIAFITO, CA FLOTTE, T BIRNGRUBER, R TI LOW REPETITION RATE PICOSECOND PHOTODISRUPTION IN OCULAR STRUCTURES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,MORSE LASER CTR,BOSTON,MA 02114. RI Roider, Johann/E-4513-2010; Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 798 EP 798 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200642 ER PT J AU WU, HK JABBUR, NS FOSTER, CS AF WU, HK JABBUR, NS FOSTER, CS TI THE ROLE OF CD4+ AND CD8+ LYMPHOCYTE-T IN THE VON SZILY MODEL IN BALB/C NUDE-MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 802 EP 802 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200665 ER PT J AU KENYON, KR HANNINEN, LA FRANGIEH, G SHAMS, NBK CHAVES, HV AZAR, D AF KENYON, KR HANNINEN, LA FRANGIEH, G SHAMS, NBK CHAVES, HV AZAR, D TI EFFECT OF VITAMIN-A-DEFICIENCY ON CORNEAL EPITHELIAL-ADHESION COMPLEX SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 843 EP 843 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200863 ER PT J AU FOSTER, CS ZHAO, TZ DUTT, JE AF FOSTER, CS ZHAO, TZ DUTT, JE TI INVESTIGATION OF THE IGG SUBCLASS RESPONSE TO CORNEAL HERPES-VIRUS INFECTION IN MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 853 EP 853 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200913 ER PT J AU LATINA, MA MARCH, WF AF LATINA, MA MARCH, WF TI ABINTERNO SCLEROSTOMY USING A GONIOLENS AND PULSED DYE-LASER IN GLAUCOMA PATIENTS - A PRELIMINARY-STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,EYE RES INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,WELLMAN LABS,BOSTON,MA 02114. UNIV OKLAHOMA,HLTH SCI CTR,DEAN MCGEE EYE INST,OKLAHOMA CITY,OK 73190. NR 0 TC 2 Z9 2 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 MAR 15 PY 1991 VL 32 IS 4 BP 860 EP 860 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200938 ER PT J AU HOOSHMAND, LB EPSTEIN, DL AF HOOSHMAND, LB EPSTEIN, DL TI THIOL ADDUCTS OF ETHACRYNIC-ACID INCREASE OUTFLOW FACILITY IN ENUCLEATED CALF EYES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 MAR 15 PY 1991 VL 32 IS 4 BP 870 EP 870 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200991 ER PT J AU SCHROEDER, A TINGEY, DP CHEN, WY EPSTEIN, MPM EPSTEIN, DL AF SCHROEDER, A TINGEY, DP CHEN, WY EPSTEIN, MPM EPSTEIN, DL TI TOPICAL ETHACRYNIC-ACID LOWERS INTRAOCULAR-PRESSURE IN RABBITS AND MONKEYS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 870 EP 870 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200992 ER PT J AU NATHANSON, JA SCHUMAN, JS ERICKSONLAMY, K AF NATHANSON, JA SCHUMAN, JS ERICKSONLAMY, K TI INTRAOCULAR-PRESSURE AND OUTFLOW FACILITY EFFECTS OF HYDRALAZINE IN CYNOMOLGUS MONKEYS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPHARMACOL RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 871 EP 871 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200995 ER PT J AU SCHUMAN, JS NATHANSON, JA ERICKSONLAMY, K AF SCHUMAN, JS NATHANSON, JA ERICKSONLAMY, K TI NITROGLYCERIN LOWERS INTRAOCULAR-PRESSURE AND INCREASES OUTFLOW FACILITY IN CYNOMOLGUS MONKEYS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPHARMACOL RES LAB,BOSTON,MA 02114. NR 0 TC 2 Z9 2 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 MAR 15 PY 1991 VL 32 IS 4 BP 871 EP 871 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76200996 ER PT J AU REICHEL, E ADAMIAN, M LESSELL, S RIZZO, JF BERSON, EL AF REICHEL, E ADAMIAN, M LESSELL, S RIZZO, JF BERSON, EL TI PERIPAPILLARY CONE DENSITY IN THE NORMAL HUMAN RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 912 EP 912 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201201 ER PT J AU WEINER, A SANDBERG, MA AF WEINER, A SANDBERG, MA TI FOVEAL CONE ERG LIGHT ADAPTATION IN NORMAL SUBJECTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 927 EP 927 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201269 ER PT J AU KNISELY, TL NAZARENO, R GRANSTEIN, RD AF KNISELY, TL NAZARENO, R GRANSTEIN, RD TI CHARACTERIZATION OF SMALL MOLECULAR-WEIGHT INHIBITORY FACTORS IN AQUEOUS-HUMOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 936 EP 936 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201316 ER PT J AU KUPFERMAN, AE LEE, SJ RICE, BA FOSTER, CS AF KUPFERMAN, AE LEE, SJ RICE, BA FOSTER, CS TI HLA CLASS-II EXPRESSION IN CONJUNCTIVA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 937 EP 937 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201322 ER PT J AU SHERMAN, B FOSTER, CS IHLEY, T LEE, SJ AF SHERMAN, B FOSTER, CS IHLEY, T LEE, SJ TI ELEVATED SERUM LEVELS OF IL-2R AND SCD8 IN OCULAR CICATRICIAL PEMPHIGOID SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 938 EP 938 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201323 ER PT J AU RAIZMAN, MB AUSTEN, KF KATZ, HR AF RAIZMAN, MB AUSTEN, KF KATZ, HR TI CYTOKINE INDUCTION OF CLASS-II MHC EXPRESSION ON MAST-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 940 EP 940 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201336 ER PT J AU PARK, CH LATINA, MA AF PARK, CH LATINA, MA TI EFFECTS OF GAMMA-INTERFERON ON CULTURED BOVINE TRABECULAR MESHWORK PHAGOCYTOSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS,BOSTON,MA 02114. EYE RES INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 942 EP 942 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201343 ER PT J AU TINGEY, DP ANDERSON, PJ SCHROEDER, A AF TINGEY, DP ANDERSON, PJ SCHROEDER, A TI EFFECTS OF IRON ON ENDOTHELIAL-CELL SUSCEPTIBILITY TO INJURY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 942 EP 942 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201342 ER PT J AU GROSS, FJ SCHUMAN, JS AF GROSS, FJ SCHUMAN, JS TI REDUCED OCULAR HYPOTENSIVE EFFECT OF TOPICAL BETA-BLOCKER THERAPY IN PATIENTS TAKING ORAL BETA-BLOCKERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,GLAUCOMA CONSULTAT SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 945 EP 945 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201363 ER PT J AU TANAKA, GH CHENG, HM AF TANAKA, GH CHENG, HM TI EFFECT OF EGF ON HEXOSE-MONOPHOSPHATE SHUNT ACTIVITY IN SINGLE CORNEAS DEMONSTRATED BY DEUTERIUM NMR-SPECTROSCOPY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 954 EP 954 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201408 ER PT J AU CASEY, R STINSON, WG RUPNICK, M MILLER, JW FOLKMAN, J PULIAFITO, CA AF CASEY, R STINSON, WG RUPNICK, M MILLER, JW FOLKMAN, J PULIAFITO, CA TI CYCLODEXTRIN-ENHANCED FLUORESCENCE IN VASCULARIZED CORNEAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. KING DREW MED CTR,LOS ANGELES,CA. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 955 EP 955 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201411 ER PT J AU CLERMONT, AC YU, NT BURSELL, SE AF CLERMONT, AC YU, NT BURSELL, SE TI INVIVO SPECTRAL MEASUREMENTS FROM HUMAN LENSES - A SENSITIVE DISCRIMINATION OF LENS CHANGES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GEORGIA INST TECHNOL,ATLANTA,GA 30332. JOSLIN DIABET CTR,BEETHAM EYE INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 973 EP 973 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201503 ER PT J AU MUKAI, S MUNZENRIDER, JE GRAGOUDAS, ES AF MUKAI, S MUNZENRIDER, JE GRAGOUDAS, ES TI PROTON-BEAM TREATMENT OF RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 981 EP 981 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201539 ER PT J AU WU, G PENDERGAST, S ROH, SY GUTIERREZ, J BRODIE, SE AF WU, G PENDERGAST, S ROH, SY GUTIERREZ, J BRODIE, SE TI ERG CHANGES IN PATIENTS WITH LONG-STANDING DIABETES-MELLITUS AND EARLY DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN CLIN,CTR DIABET,BOSTON,MA 02215. MT SINAI MED CTR,NEW YORK,NY 10029. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1029 EP 1029 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201774 ER PT J AU HETH, CA MARESCALCHI, PA AF HETH, CA MARESCALCHI, PA TI INOSITOL TRIPHOSPHATE GENERATION DURING ROS PHAGOCYTOSIS IN CULTURED RAT RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1057 EP 1057 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201909 ER PT J AU JEDZINIAK, JA ANDRZEJEWSKI, W AF JEDZINIAK, JA ANDRZEJEWSKI, W TI PROPERTIES OF PYRUVATE-KINASE IN THE RAT AND HUMAN LENS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1060 EP 1060 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201923 ER PT J AU SHAMS, NBK HANNINEN, LA REDDY, CV KENYON, KR AF SHAMS, NBK HANNINEN, LA REDDY, CV KENYON, KR TI INCREASED ACTIVITY OF METALLOPROTEINASES AND INTERLEUKIN-6-INDUCING FACTOR IN THE VITAMIN-A-DEFICIENT CORNEA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1067 EP 1067 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201958 ER PT J AU ZIESKE, JD BUKUSOGLU, G YANKAUCKAS, MA KEUTMANN, HT AF ZIESKE, JD BUKUSOGLU, G YANKAUCKAS, MA KEUTMANN, HT TI A 50-KD PROTEIN PRESENT IN BASAL CELLS OF LIMBAL EPITHELIUM IS ENOLASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,EYE RES INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 2 Z9 2 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 MAR 15 PY 1991 VL 32 IS 4 BP 1073 EP 1073 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76201988 ER PT J AU JAKOBIEC, FA TO, KW AF JAKOBIEC, FA TO, KW TI CORNEAL EPITHELIAL DYSMATURATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,OPHTHALM ONCOL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1075 EP 1075 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202000 ER PT J AU NEUMANN, R FOSTER, CS AF NEUMANN, R FOSTER, CS TI LANGERHANS CELLS IN CORNEA AND CONJUNCTIVA OF DISPARATE (IGH-1) CONGENIC MICE COINCIDENT WITH DIFFERENTIAL PATHOLOGY TO HERPES-SIMPLEX VIRUS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1077 EP 1077 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202011 ER PT J AU ANDLEY, U WALSH, A KOCHEVAR, I REDDAN, J AF ANDLEY, U WALSH, A KOCHEVAR, I REDDAN, J TI DAMAGE TO CULTURED RABBIT LENS EPITHELIAL-CELLS BY UV-B RADIATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OAKLAND UNIV,ROCHESTER,MI 48063. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1098 EP 1098 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202100 ER PT J AU GRANSTEIN, RD NAZARENO, R KNISELY, TL AF GRANSTEIN, RD NAZARENO, R KNISELY, TL TI INHIBITION OF CYTOTOXIC LYMPHOCYTE (CTL) GENERATION INVITRO BY A SMALL FACTOR IN AQUEOUS-HUMOR (AH) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1118 EP 1118 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202199 ER PT J AU CHUN, LLY SWEARINGEN, B CHANG, Y AF CHUN, LLY SWEARINGEN, B CHANG, Y TI SURVIVAL REQUIREMENTS OF PURIFIED POSTNATAL RAT RETINAL GANGLION-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1133 EP 1133 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202277 ER PT J AU WIGGS, JL BERSON, EL DRYJA, TP AF WIGGS, JL BERSON, EL DRYJA, TP TI SEARCH FOR MUTATIONS IN THE GENE FOR THE ROD ALPHA SUBUNIT OF HUMAN TRANSDUCIN IN PATIENTS WITH RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. NR 2 TC 0 Z9 0 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 MAR 15 PY 1991 VL 32 IS 4 BP 1136 EP 1136 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202290 ER PT J AU MAGOVCEVIC, I HAHN, LB FISHMAN, GA FULTON, AE LIBERFARB, RM BERSON, EL DRYJA, TP AF MAGOVCEVIC, I HAHN, LB FISHMAN, GA FULTON, AE LIBERFARB, RM BERSON, EL DRYJA, TP TI SEARCH FOR MUTATIONS IN THE RHODOPSIN GENE IN PATIENTS WITH LEBERS CONGENITAL AMAUROSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. UNIV ILLINOIS,ILLINOIS EYE & EAR INFIRM,CHICAGO,IL 60680. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1139 EP 1139 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202309 ER PT J AU TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL AF TO, KW ADAMIAN, M JAKOBIEC, FA BERSON, EL TI OLIVOPONTOCEREBELLAR ATROPHY WITH RETINAL DEGENERATION - AN OPHTHALMOLOGIC INVESTIGATION OF 3 GENERATIONS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,OPHTHALM PATHOL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1139 EP 1139 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202308 ER PT J AU CHARLES, JB WU, G ROH, SY GUTIERREZ, J PENDERGAST, S WEITER, JJ AF CHARLES, JB WU, G ROH, SY GUTIERREZ, J PENDERGAST, S WEITER, JJ TI PRACTICE PATTERN IN THE TREATMENT OF DIABETIC-RETINOPATHY IN A REFERRAL POPULATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. EYE RES INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1142 EP 1142 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202318 ER PT J AU ROOF, D HAYES, A ADAMIAN, M MARESCALCHI, P HETH, C AF ROOF, D HAYES, A ADAMIAN, M MARESCALCHI, P HETH, C TI PHOTORECEPTOR DEVELOPMENT IN RAT NEURAL RETINA RETINAL-PIGMENT EPITHELIUM COCULTURES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1148 EP 1148 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202352 ER PT J AU OBRIEN, J MARCUS, D KIVELA, T VIRTANEN, I BRAUNER, E REESE, K BERNARDS, R ALBERT, DM AF OBRIEN, J MARCUS, D KIVELA, T VIRTANEN, I BRAUNER, E REESE, K BERNARDS, R ALBERT, DM TI CHARACTERIZATION OF TRANSGENIC MURINE RETINOBLASTOMA CELL-LINES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. UNIV HELSINKI,DEPT OPHTHALMOL,SF-00100 HELSINKI 10,FINLAND. UNIV HELSINKI,DEPT ANAT,SF-00100 HELSINKI 10,FINLAND. MASSACHUSETTS GEN HOSP,CANC RES CTR,BOSTON,MA 02114. RI Kivela, Tero/C-9241-2009 OI Kivela, Tero/0000-0003-1198-4394 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1198 EP 1198 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202595 ER PT J AU SEMBA, R MUHILAL SCOTT, A NATADISASTRA, G WIRASASMITA, S GRIFFIN, D WINGET, M WEST, K SOMMER, A AF SEMBA, R MUHILAL SCOTT, A NATADISASTRA, G WIRASASMITA, S GRIFFIN, D WINGET, M WEST, K SOMMER, A TI IMMUNE STATUS IN CHILDREN WITH MILD VITAMIN-A-DEFICIENCY IN INDONESIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NUTR RES & DEV CTR,BOGOR,INDONESIA. CICENDO EYE HOSP,BANDUNG,INDONESIA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. JOHNS HOPKINS MED INST,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1222 EP 1222 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202708 ER PT J AU WEAVER, YK LIN, CP FUJIMOTO, JG BIRNGRUBER, R PULIAFITO, CA AF WEAVER, YK LIN, CP FUJIMOTO, JG BIRNGRUBER, R PULIAFITO, CA TI INTRAOCULAR PHOTOABLATION BY A HIGH REPETITION RATE PICOSECOND ND-YAG LASER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,MORSE LASER CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. RI Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1224 EP 1224 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202720 ER PT J AU GIOVINAZZO, VJ SOBEL, RS PATALANO, VJ CINCOTTA, L FOLEY, J CINCOTTA, AH AF GIOVINAZZO, VJ SOBEL, RS PATALANO, VJ CINCOTTA, L FOLEY, J CINCOTTA, AH TI PHOTODYNAMIC THROMBOSIS OF CHOROIDAL VESSELS IN ALBINO RABBITS USING A BENZOPHENOXAZINIUM DYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MANHATTAN EYE EAR & THROAT HOSP LABS,LU ESTHER T MERTZ RES CTR,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. SUNY COLL OPTOMETRY,NEW YORK,NY 10010. ROWLAND INST SCI INC,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1232 EP 1232 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202763 ER PT J AU SEDDON, JM CHRISTEN, WG MANSON, JE BURING, JE HENNEKENS, CH AF SEDDON, JM CHRISTEN, WG MANSON, JE BURING, JE HENNEKENS, CH TI LOW-DOSE ASPIRIN AND RISKS OF CATARACT SUBTYPES FROM A RANDOMIZED TRIAL OF UNITED-STATES PHYSICIANS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1244 EP 1244 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202826 ER PT J AU TALAMO, JH LEE, K PULIAFITO, CA STEINERT, RF AF TALAMO, JH LEE, K PULIAFITO, CA STEINERT, RF TI CORNEAL WOUND-HEALING AFTER EXCIMER LASER PHOTOREFRACTIVE KERATECTOMY IN CATS - THE ROLE OF MITOMYCIN-C AND STEROIDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,MORSE LASER CTR,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1247 EP 1247 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76202840 ER PT J AU GUYER, DR MUKAI, S EGAN, KM WALSH, SM SEDDON, JM GRAGOUDAS, ES AF GUYER, DR MUKAI, S EGAN, KM WALSH, SM SEDDON, JM GRAGOUDAS, ES TI RADIATION MACULOPATHY AFTER PROTON-BEAM IRRADIATION FOR CHOROIDAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1290 EP 1290 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76203049 ER PT J AU DE BRITO SANCHEZ, GM OLIVERPOZO, J SHIBA, T KING, GL AF DE BRITO SANCHEZ, GM OLIVERPOZO, J SHIBA, T KING, GL TI MODULATION OF ENDOTHELIN-1 (ET-1) RECEPTOR ON RETINAL PERICYTES BY ELEVATED GLUCOSE-LEVELS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR, BOSTON, MA USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1991 VL 32 IS 4 BP 1302 EP 1302 PG 1 WC Ophthalmology SC Ophthalmology GA FC762 UT WOS:A1991FC76203110 ER PT J AU CSERMELY, P KAHN, CR AF CSERMELY, P KAHN, CR TI THE 90-KDA HEAT-SHOCK PROTEIN (HSP-90) POSSESSES AN ATP BINDING-SITE AND AUTOPHOSPHORYLATING ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ROUS-SARCOMA VIRUS; OVIDUCT PROGESTERONE-RECEPTOR; LIVER GLUCOCORTICOID RECEPTOR; 2 CELLULAR PHOSPHOPROTEINS; ESCHERICHIA-COLI; KINASE-ACTIVITY; TRANSFORMING PROTEINS; NUCLEOTIDE-BINDING; MAMMALIAN-CELLS; CHICKEN OVIDUCT AB The 90-kDa heat shock protein (hsp-90) is an abundant cytosolic protein believed to play a role in maintenance of protein trafficking and closely associated with several steroid hormone receptors. Incubation of highly purified hsp-90 with [gamma-P-32]ATP results in its autophosphorylation on serine residues. There are several lines of evidence which suggest that this activity is due to a kinase intrinsic to hsp-90 rather than some closely associated protein kinases: 1) the phosphorylation persists after the removal of casein kinase II by heparin chromatography and after immunoprecipitation of hsp-90 with anti-hsp-90 antibodies. 2) The approximate k(M) for ATP of the reaction is 0.16 mM, higher than that of many other protein kinases. 3) Phosphorylation is not affected by a number of activators and inhibitors of other known kinases which might associate with hsp-90. 4) The phosphorylation displays a unique cation dependence being most active in the presence of Ca2+ and practically inactive with Mg2+, although the autophosphorylation in the presence of Mg2+ is activated by histones and polyamines. 5) The activity is remarkably heat-stable; incubation of hsp-90 for 20 min at 95-degrees-C results in only a 60% decrease in autophosphorylation. 6) Finally, and most importantly, purified hsp-90 can be labeled with azido-ATP and it is able to bind to ATP-agarose. The binding shows similar cation dependence to the autophosphorylation. These data are in agreement with the presence of a consensus sequence for ATP binding sites in the primary structure of the protein similar to that observed in the 70-kDa heat-shock proteins. Our data suggest the 90-kDa heat shock protein possesses an enzymatic activity analogous in many respects to the similar activity of the 70-kDa heat shock proteins. This may represent an important, previously unrecognized function of hsp-90. C1 JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02215. FU FIC NIH HHS [1F05 TW04319-01 B1-5]; NIDDK NIH HHS [DK 33201, DK 36836] NR 59 TC 135 Z9 137 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1991 VL 266 IS 8 BP 4943 EP 4950 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FC217 UT WOS:A1991FC21700043 PM 2002041 ER PT J AU LIND, SE SMITH, CJ AF LIND, SE SMITH, CJ TI ACTIN IS A NONCOMPETITIVE PLASMIN INHIBITOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID D-BINDING-PROTEIN; AMINO-ACID-SEQUENCE; SKELETAL-MUSCLE ACTIN; FIBRIN CLOTS; STRUCTURAL PROTEINS; NATIVE PLASMINOGEN; LYSINE RESIDUES; GELSOLIN LEVELS; LUNG INJURY; ACTIVATOR AB Actin, one of the most abundant cellular proteins, circulates at micromolar concentrations in peripheral blood. Because actin released from dying cells may be trapped in fibrin clots that form at sites of tissue injury, we examined the effects of actin upon lysis of fibrin clots in vitro. Incorporation of native rabbit skeletal muscle actin into fibrin clots slowed their rates of lysis for periods of up to 24 h, an effect not seen when comparable concentrations of human IgG or bovine serum albumin were added instead. Actins isolated from a variety of sources inhibited plasmin's hydrolysis of the synthetic substrate S-2251 in a noncompetitive manner, with a K(i) of a 0.6-3.1-mu-M. Inhibition was rapid, but covalent actin-plasmin complexes were not formed. Both epsilon-aminocaproic acid and tranexamic acid prevented actin's inhibition of plasmin, suggesting that accessible lysine residues of actin interact with the kringle (lysine-binding) regions of plasmin. Neither of the high-affinity actin-binding proteins of plasma (plasma gelsolin and vitamin D-binding protein) prevented actin from inhibiting plasmin. These findings suggest that actin released into the extracellular space following cell death may modulate plasmin action, and hence a number of plasmin-dependent biological responses, at sites of inflammation and tissue injury. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. RP LIND, SE (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL UNIT,COX BLDG,6TH FLOOR,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL 42457] NR 52 TC 32 Z9 33 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1991 VL 266 IS 8 BP 5273 EP 5278 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FC217 UT WOS:A1991FC21700086 PM 1848244 ER PT J AU SPIRO, MJ SPIRO, RG AF SPIRO, MJ SPIRO, RG TI POTENTIAL REGULATION OF N-GLYCOSYLATION PRECURSOR THROUGH OLIGOSACCHARIDE-LIPID HYDROLASE ACTION AND GLUCOSYLTRANSFERASE-GLUCOSIDASE SHUTTLE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ASPARAGINE-LINKED OLIGOSACCHARIDES; THYROID ENDOPLASMIC-RETICULUM; GLYCOPROTEIN-BIOSYNTHESIS; CARBOHYDRATE UNITS; PROTEIN-SYNTHESIS; INHIBITORS; RELEASE; SLICES; CHAINS AB The potential role of degradative mechanisms in controlling the level of the dolichyl pyrophosphate-linked Glc3Man9GlcNAc2 required for protein N-glycosylation has been explored in thyroid slices and endoplasmic reticulum (ER) vesicles, focusing on cleavage of the oligosaccharide from its lipid attachment and on the enzymatic removal of peripheral monosaccharide residues. Vesicle incubations demonstrated a substantial release of free Glc3Man9GlcNAc2 (at 30 min approximately 35% of that transferred to protein) which was inhibited in the presence of exogenous peptide acceptor and was sensitive to disruption of membrane integrity by detergent. In thyroid slices glucosylated oligosaccharides terminating in the di-N-acetylchitobiose sequence were also noted and these continued to be formed even during inhibition by puromycin of both protein synthesis and the attendant N-glycosylation. These observations indicated that the oligosaccharide originated from the lipid donor and suggested, together with previously reported similarities in substrate specificity and cofactor requirements, that the oligosaccharyltransferase can carry out in vivo both the hydrolytic and transfer functions. In addition to the release of the intact Glc3Man9GlcNAc2, we also obtained evidence that the lipid-linked oligosaccharide can be modified by the in vivo action of ER glycosidases. Since radiolabeling of the oligosaccharide-lipid in thyroid slices indicated a preferential turnover of the glucose residues, the possible existence of a glucosyltransferase-glucosidase shuttle was explored with the use of castanospermine. In the presence of this glucosidase inhibitor, the formation of underglucosylated and nonglucosylated oligosaccharides was not observed, even under conditions of energy deprivation in which they accumulate. Glucosidase inhibition in ER vesicle incubations likewise prevented the appearance of incompletely glucosylated oligosaccharide-lipids. Studies employing the mannosidase inhibitor 1-deoxymannojirimycin in thyroid slices furthermore indicated that in vivo removal of at least one mannose residue from the dolichyl pyrophosphate-linked oligosaccharide can occur. C1 ELLIOTT P JOSLIN RES LAB, 1 JOSLIN PL, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK 17477] NR 19 TC 62 Z9 62 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1991 VL 266 IS 8 BP 5311 EP 5317 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FC217 UT WOS:A1991FC21700092 PM 1825831 ER PT J AU RAKE, JB QUINONES, MA FALLER, DV AF RAKE, JB QUINONES, MA FALLER, DV TI INHIBITION OF PLATELET-DERIVED GROWTH FACTOR-MEDIATED SIGNAL TRANSDUCTION BY TRANSFORMING RAS - SUPPRESSION OF RECEPTOR AUTOPHOSPHORYLATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PROTEIN KINASE-C; TYROSINE PHOSPHORYLATION; PDGF RECEPTOR; ONCOGENE; PHOSPHOTYROSINE; PURIFICATION; ACTIVATION; ANTIBODY; BINDING; FAMILY AB The function of ras protein and its relationship to growth-factor mediated signal transduction remain unclear. The demonstration that the expression of transforming ras (v-ras) can block the stimulation of growth-related gene expression and cell division mediated by the platelet-derived growth factor (PDGF) may provide a model for the functional interation of ras with growth factor receptors. In the current studies, we have demonstrated that this blockade by v-ras of PDGF-BB signal transduction occurs very early in signal transduction, at the level of PDGF receptor autophosphorylation. Although the expression of PDGF receptor as detected by Western blot with anti-PDGF receptor antibody was not diminished in v-ras-transformed murine Balb/c 3T3 fibroblasts, the autophosphorylation of PDGF receptor in response to ligand (recombinant PDGF-BB homodimer) stimulation was profoundly suppressed. This same phenomenon of v-ras-mediated PDGF receptor autophosphorylation inhibition was also demonstrated in normal rat kidney fibroblasts. Further, factor(s) present in v-ras-expressing fibroblasts found in the membrane fractions of these cells can dominantly inhibit the autophosphorylation of the PDGF receptor obtained from normal fibroblasts. These findings suggest a role for ras in one of the earliest steps of the signal transduction pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 26 TC 38 Z9 38 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1991 VL 266 IS 8 BP 5348 EP 5352 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FC217 UT WOS:A1991FC21700097 PM 1848245 ER PT J AU THOMAS, JD OSHEA, JP RODRIGUEZ, L POPOVIC, AD SVIZERRO, T WEYMAN, AE AF THOMAS, JD OSHEA, JP RODRIGUEZ, L POPOVIC, AD SVIZERRO, T WEYMAN, AE TI IMPACT OF ORIFICE GEOMETRY ON THE SHAPE OF JETS - AN INVITRO DOPPLER COLOR FLOW STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID MITRAL REGURGITATION; REAL-TIME; ECHOCARDIOGRAPHY; VISUALIZATION; SYSTEM; MODEL AB To investigate the influence of orifice geometry on the three-dimensional shape of jets, an in vitro Doppler color flow study was performed. Jets were formed by discharging blood through round orifices and through orifices with major/minor axis ratios of 2:1, 3:1 and 5:1. These were repeated with orifice areas of 0.1, 0.3 and 0.5 cm2. For turbulent and laminar jets formed by these orifices, Doppler color flow images were obtained from two orthogonal scanning planes aligned with the major and minor orifice axes. Jet width was measured at 1 cm intervals from 0 to 5 cm from the orifice and used to calculate jet eccentricity (ratio of major to minor axis widths) and the rate of divergence of the jet walls. Jets were observed to diverge more rapidly along walls aligned with the orifice minor axis rather than along the major axis. This differential spreading led to the development of circular symmetry at a short distance from the orifice. Jet divergence (theta) occurred more rapidly for turublent jets and for jets formed by larger orifices: [GRAPHICS] where A is orifice area (cm2); T is 0 for laminar jets, 1 for turbulent jets and E-OR combines orifice eccentricity and scanning orientation, ranging from -5 for 5:1 orifices imaged along the major axis, 0 for circular orifices to 5 for 5:1 orifices imaged along the minor axis. Within the jet, eccentricity decayed approximately exponentially with distance from the orifice, more rapidly for turbulent jets, more slowly for the larger and more eccentric orifices. A nonlinear regression model of jet turbulence and orifice eccentricity and size was able to predict jet eccentricity with r = 0.95. Turbulent jets lost approximately 90% of their eccentricity within three orifice diameters of the jet origin. The cause of this circularization appears to be higher shear rates across the jet minor axis profile than across the major axis, leading to a more rapid lateral spread of momentum along the minor axis. These results demonstrate that the details of orifice geometry are obliterated within the proximal jet and support the use of quantitative techniques that assume axial symmetry. RP THOMAS, JD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,ZERO EMERSON PL,SUITE 2F,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-07535] NR 28 TC 13 Z9 13 U1 0 U2 3 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 MAR 15 PY 1991 VL 17 IS 4 BP 901 EP 908 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FB474 UT WOS:A1991FB47400011 PM 1999627 ER PT J AU BEILMANN, A PFITZNER, AJP GOODMAN, HM PFITZNER, UM AF BEILMANN, A PFITZNER, AJP GOODMAN, HM PFITZNER, UM TI FUNCTIONAL-ANALYSIS OF THE PATHOGENESIS-RELATED 1A PROTEIN GENE MINIMAL PROMOTER REGION - COMPARISON OF REPORTER GENE-EXPRESSION IN TRANSIENT AND IN STABLE TRANSFECTIONS SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article ID TOBACCO MOSAIC-VIRUS; FIREFLY LUCIFERASE GENE; BETA-GLUCURONIDASE; NICOTIANA-TABACUM; XANTHI-NC; TRANSGENIC PLANTS; FUSION MARKER; ACID; RESISTANCE; PROTOPLASTS AB Pathogenesis-related (PR) proteins are a heterogeneous group of host encoded, low-molecular-mass proteins that are induced in plants by various external stimuli, such as pathogen attack or exposure of the plants to certain chemicals. To examine the regulation of these genes, the 5'-flanking region of the tobacco PR-la gene [Pfitzner U. M., Pfitzner, A. J. P. & Goodman, H. M. (1988) Mol. Gen. Genet. 211, 290-295] was joined by a transcriptional fusion to the Escherichia coli beta-glucuronidase (GUS) gene. Expression of the reporter gene was monitored in transient expression assays as well as in stable transformants. The PR-la 5'-flanking sequences from -335, -149 or -71 to +28 are functional promoter elements in tobacco and carrot protoplasts, as determined by transient expression. These constructs direct correct initiation at the normal transcription-start site of the PR-la gene. The level of gene expression was about twofold less than that obtained with the cauliflower mosaic virus 35S RNA promoter. Regulation of gene expression by acetylsalicylic acid, however, could not be detected in the transient assays. When the same constructs were stably integrated into the tobacco genome, neither constitutive nor induced beta-glucuronidase activity was observed. A comparison of the results from the transient and the stable transfection experiments suggests that expression of the reporter gene may be due to a constitutive transcriptional activity of the PR-la 5'-flanking regions under the conditions of the transient assays and that the PR-la promoter may contain at least two functional domains. C1 UNIV MUNICH,INST BOT,MENZINGER STR 67,W-8000 MUNICH 19,GERMANY. GENZENTRUM MUNCHEN,MUNICH,GERMANY. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 42 TC 16 Z9 17 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD MAR 14 PY 1991 VL 196 IS 2 BP 415 EP 421 DI 10.1111/j.1432-1033.1991.tb15832.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FL584 UT WOS:A1991FL58400021 PM 2007405 ER PT J AU BALDESSARINI, RJ FRANKENBURG, FR AF BALDESSARINI, RJ FRANKENBURG, FR TI DRUG-THERAPY - CLOZAPINE - A NOVEL ANTIPSYCHOTIC AGENT SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID NEUROLEPTIC MALIGNANT SYNDROME; LONG-TERM TREATMENT; SCHIZOPHRENIC-PATIENTS; TARDIVE-DYSKINESIA; INDUCED AGRANULOCYTOSIS; PSYCHOTROPIC-DRUGS; CENTRAL DOPAMINE; RAT STRIATUM; D2 DOPAMINE; HUMAN-BRAIN C1 HARVARD UNIV, SCH MED, NEUROSCI PROGRAM, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, MCLEAN DIV, PSYCHOT DISORDERS PROGRAM, BELMONT, MA USA. MASSACHUSETTS GEN HOSP, MCLEAN DIV, PSYCHIAT RES LABS, BELMONT, MA USA. RP BALDESSARINI, RJ (reprint author), HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02115 USA. FU NIMH NIH HHS [MH-36420, MH-31154, MH-47370] NR 100 TC 640 Z9 641 U1 1 U2 19 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 EI 1533-4406 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 14 PY 1991 VL 324 IS 11 BP 746 EP 754 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA FB556 UT WOS:A1991FB55600007 PM 1671793 ER PT J AU ZIETMAN, AL SUGIYAMA, E RAMSAY, JR SILOBRCIC, V YEH, ETH SEDLACEK, RS SUIT, HD AF ZIETMAN, AL SUGIYAMA, E RAMSAY, JR SILOBRCIC, V YEH, ETH SEDLACEK, RS SUIT, HD TI A COMPARATIVE-STUDY ON THE XENOTRANSPLANTABILITY OF HUMAN SOLID TUMORS INTO MICE WITH DIFFERENT GENETIC IMMUNE DEFICIENCIES SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID CYTOLYTIC LYMPHOCYTE-T; NATURAL-KILLER CELLS; NUDE-MICE; CANCER-CELLS; GROWTH; IDENTIFICATION; PHENOTYPE; MURINE AB These experiments set out to assess the role of NK and B cells in the resistance of nude mice to human tumor xenotransplantation. The transplantability of 9 fresh and 8 cultured human tumors was compared in 2 strains of mice with different genetic immune deficiencies: athymic NCr/Sed (nu/nu) nude mice, and nude-beige-xid (N:NIH-nu-bg-xid/Sed mice). Flow cytometric studies showed both strains to be deficient in Thy. 1.2 (T) cells and unresponsive to stimulation by Concanavalin A (Con A) or direct T-cell-receptor triggering with anti-CD3. The number of B cells was similar in the 2 strains, but the response to lipopolysaccharide (LPS) was markedly reduced in the nude-beige-xid animals. The number of asialoGM1-positive cells (predominantly NK) detected by flow cytometry was also reduced in the nude-beige-xid mice. The transplantability of the human tumors was found to be equivalent in the 2 strains. Quantitative cell-transplantation assays performed for 2 of the tumor cell lines did not reveal any subtle transplantation advantage for the more broadly immune-deficient animals. No evidence could, therefore, be found to suggest that NK or B cells were major determinants of human tumor xenotransplantability in these strains of mice. C1 HARVARD UNIV,SCH MED,DEPT PULM MED,EDWIN L STEELE LAB,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ARTHRIT UNIT,BOSTON,MA 02114. RI Ramsay, Jonathan/F-7009-2013 FU NCI NIH HHS [CA 13311]; NIAMS NIH HHS [AR 03564] NR 25 TC 20 Z9 20 U1 1 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD MAR 12 PY 1991 VL 47 IS 5 BP 755 EP 759 DI 10.1002/ijc.2910470522 PG 5 WC Oncology SC Oncology GA FC757 UT WOS:A1991FC75700021 PM 2004856 ER PT J AU BRADBURY, L KANSAS, G LEVY, S EVANS, RL TEDDER, TF AF BRADBURY, L KANSAS, G LEVY, S EVANS, RL TEDDER, TF TI CD19 IS A COMPONENT OF A SIGNAL TRANSDUCING COMPLEX ON THE SURFACE OF B-CELLS THAT INCLUDES CD21, TAPA-1 AND LEU-13 SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. STANFORD UNIV,MED CTR,STANFORD,CA 94305. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. NR 0 TC 9 Z9 9 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A611 EP A611 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701397 ER PT J AU BUYSKE, J AUCHINCLOSS, H AF BUYSKE, J AUCHINCLOSS, H TI RECOGNITION OF XENOGENEIC MHC AND GENERATION OF CYTOTOXIC T-CELLS IN A XENOGENEIC SYSTEM SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 MAR 11 PY 1991 VL 5 IS 4 BP A731 EP A731 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20702094 ER PT J AU CALDERWOOD, S RODMAN, L HUNT, C AF CALDERWOOD, S RODMAN, L HUNT, C TI INTERACTIONS BETWEEN THE ATP BINDING AND PEPTIDE BINDING DOMAINS OF MURINE-HSP70 SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,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 MAR 11 PY 1991 VL 5 IS 4 BP A472 EP A472 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700589 ER PT J AU CANTIELLO, HF STOW, JL AUSIELLO, DA AF CANTIELLO, HF STOW, JL AUSIELLO, DA TI CORTICAL ACTIN-FILAMENTS CO-LOCALIZE WITH AND REGULATE APICAL EPITHELIAL NA+ CHANNELS IN A6 CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A690 EP A690 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701858 ER PT J AU CASTILLO, L YU, YM HOERR, RA WARNER, C BRANCH, S BURKE, JF YOUNG, VR AF CASTILLO, L YU, YM HOERR, RA WARNER, C BRANCH, S BURKE, JF YOUNG, VR TI ARGININE AND ORNITHINE KINETICS IN YOUNG MEN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SHRINERS BURN INST,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 MAR 11 PY 1991 VL 5 IS 4 BP A564 EP A564 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701125 ER PT J AU CHUNG, CK YEE, JA AF CHUNG, CK YEE, JA TI MACROMINERAL METABOLISM IN BONE REGULATED BY PARATHYROID-HORMONE (PTH) SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. CLAYTON UNIV,OMAHA,NE 68178. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A560 EP A560 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701097 ER PT J AU HUTCHISON, WG SPENCE, C JANSSENS, SP HALES, CA AF HUTCHISON, WG SPENCE, C JANSSENS, SP HALES, CA TI DUAL CYCLOOXYGENASE AND LIPOXYGENASE INHIBITION PREVENTS RISE IN LUNG WATER IF GIVEN AFTER SYNTHETIC SMOKE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A537 EP A537 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700964 ER PT J AU KANSAS, GS SPERTINI, O TEDDER, TF AF KANSAS, GS SPERTINI, O TEDDER, TF TI MOLECULAR MAPPING OF FUNCTIONAL DOMAINS OF LAM-1 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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A620 EP A620 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701448 ER PT J AU KOLACZYNSKI, JW MOSCICKI, RA AXELROD, L AF KOLACZYNSKI, JW MOSCICKI, RA AXELROD, L TI KUPFFER CELLS SPECIFICALLY BIND INSULIN IN THE RAT - EVIDENCE FOR A ROLE IN HEPATIC-CLEARANCE OF INSULIN SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,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 MAR 11 PY 1991 VL 5 IS 4 BP A756 EP A756 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20702239 ER PT J AU LAWRENCE, M CHAN, PY DUSTIN, ML FERGUSON, L GOLAN, D SPRINGER, TA AF LAWRENCE, M CHAN, PY DUSTIN, ML FERGUSON, L GOLAN, D SPRINGER, TA TI ROLE OF RECEPTOR MOBILITY IN CELL-ADHESION STRENGTHENING SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. CTR BLOOD RES,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 MAR 11 PY 1991 VL 5 IS 4 BP A652 EP A652 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701636 ER PT J AU LUKACOVA, D REED, GL HABER, E MATSUEDA, GR AF LUKACOVA, D REED, GL HABER, E MATSUEDA, GR TI FUNCTIONAL-CHARACTERISTICS OF A MONOCLONAL-ANTIBODY DIRECTED TO THE THROMBIN ACTIVATION SITE OF FACTOR-XIII SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. PRINCETON UNIV,PRINCETON,NJ 08544. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,PRINCETON,NJ 08543. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A515 EP A515 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700836 ER PT J AU PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH YOUNG, AJ SAWKA, MN AF PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH YOUNG, AJ SAWKA, MN TI HUMAN THERMOREGULATORY RESPONSES DURING COLD-WATER IMMERSION AFTER ARTIFICIALLY-INDUCED SUNBURN SO FASEB JOURNAL LA English DT Meeting Abstract C1 USA,INST ENVIRONM MED,NATICK,MA 01760. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,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 MAR 11 PY 1991 VL 5 IS 4 BP A393 EP A393 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700133 ER PT J AU PATTON, WF CHUNGWELCH, N SKEA, WM UTTERBACK, BL CAMBRIA, RP AF PATTON, WF CHUNGWELCH, N SKEA, WM UTTERBACK, BL CAMBRIA, RP TI ANALYSIS OF PROTEIN SECONDARY STRUCTURAL MOTIFS THAT PERSIST IN REDUCING, DENATURING 2-DIMENSIONAL GEL-ELECTROPHORESIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MILLIPORE INC,CORP RES & DEV,BEDFORD,MA 01730. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A371 EP A371 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700004 ER PT J AU PRAT, AG AUSIELLO, DA CANTIELLO, HF AF PRAT, AG AUSIELLO, DA CANTIELLO, HF TI ACTIN FILAMENT ORGANIZATION CONTROLS NA+ CHANNEL ACTIVITY IN A6 EPITHELIAL-CELLS 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 5 Z9 5 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A690 EP A690 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701860 ER PT J AU RIEK, P HANDSHUMACHER, M SUNG, SS NOVOTNY, J GRAHAM, RM AF RIEK, P HANDSHUMACHER, M SUNG, SS NOVOTNY, J GRAHAM, RM TI AN ALGORITHM FOR DETERMINING THE BOUNDARIES OF MEMBRANE-SPANNING ALPHA-HELICAL DOMAINS OF POLYTOPIC PROTEINS SO FASEB JOURNAL LA English DT Meeting Abstract C1 CLEVELAND CLIN FDN,RES INST,CLEVELAND,OH 44195. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SQUIBB INST MED RES,PRINCETON,NJ 08543. NR 1 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 MAR 11 PY 1991 VL 5 IS 4 BP A396 EP A396 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20700150 ER PT J AU SANDERSON, IR OUELLETTE, AJ CARTER, EA HARMATZ, PR AF SANDERSON, IR OUELLETTE, AJ CARTER, EA HARMATZ, PR TI ONTOGENY OF MESSENGER-RNA FOR INVARIANT CHAIN IN THE MOUSE ENTEROCYTE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT & SURG,BOSTON,MA 02114. SHRINERS BURN INST,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 MAR 11 PY 1991 VL 5 IS 4 BP A617 EP A617 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701430 ER PT J AU SUNG, SS RIEK, P HANDSHUMACHER, M NOVOTNY, J GRAHAM, RM AF SUNG, SS RIEK, P HANDSHUMACHER, M NOVOTNY, J GRAHAM, RM TI A MODEL FOR THE 3-DIMENSIONAL STRUCTURE OF THE ALPHA-1B-ADRENERGIC RECEPTOR SO FASEB JOURNAL LA English DT Meeting Abstract C1 CLEVELAND CLIN EDUC FDN,RES INST,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SQUIBB INST MED RES,PRINCETON,NJ 08540. NR 0 TC 6 Z9 6 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A804 EP A804 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20702517 ER PT J AU TONNER, PH DEARMENDI, AJ BUGGE, B MILLER, KW AF TONNER, PH DEARMENDI, AJ BUGGE, B MILLER, KW TI BARBITURATE INDUCED-INHIBITION OF AN ACETYLCHOLINE GATED ION CHANNEL SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH 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 MAR 11 PY 1991 VL 5 IS 4 BP A867 EP A867 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20702888 ER PT J AU TURJMINA, O CONLAY, L MEDVEDEV, O AF TURJMINA, O CONLAY, L MEDVEDEV, O TI PROPOFOL INCREASES, AND THEN REDUCES SYMPATHETIC-NERVE ACTIVITY SO FASEB JOURNAL LA English DT Meeting Abstract C1 MOSCOW CARDIOVASC SURG RES INST,INST EXPTL CARDIOL,MOSCOW,USSR. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,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 MAR 11 PY 1991 VL 5 IS 4 BP A867 EP A867 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20702886 ER PT J AU WELLER, PF RAND, TH FINBERG, RW AF WELLER, PF RAND, TH FINBERG, RW TI HUMAN EOSINOPHILS FUNCTION AS HLA-DR DEPENDENT, MHC-RESTRICTED ANTIGEN-PRESENTING CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 8 Z9 8 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A640 EP A640 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701562 ER PT J AU ZHOU, LJ ORD, DC TEDDER, TF AF ZHOU, LJ ORD, DC TEDDER, TF TI CD19 OF HUMAN, MOUSE, AND GUINEA-PIG B-CELLS - CONSERVATION OF THE EXTENSIVE CYTOPLASMIC DOMAIN 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. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 11 PY 1991 VL 5 IS 4 BP A611 EP A611 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC207 UT WOS:A1991FC20701394 ER PT J AU PACE, U SZOSTAK, JW AF PACE, U SZOSTAK, JW TI MUTATIONS IN A SEMICONSERVED REGION OF THE TETRAHYMENA INTRON SO FEBS LETTERS LA English DT Article DE GROUP-I SELF-SPLICING INTRON; RIBOZYME; P5 EXTENSION ID GROUP-I INTRONS; RIBOZYME; SITE; CORE AB The A-rich bulge in paired region P5a of the Tetrahymena intron is a structural feature that is conserved in the sub-group Ib self-splicing introns. We have constructed a series of substitution and deletion mutations in this region of the intron. Kinetic analysis has shown that some of the mutants have a reduced maximal extent of splicing, while others have a reduced V(max). These mutations could be reactivated to a great extent by spermidine and high Mg2+ concentrations. These data are consistent with the hypothesis that the A-rich bulge of P5a has a role in stabilizing the higher-level structure of the ribozyme. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 9 TC 11 Z9 11 U1 1 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 MAR 11 PY 1991 VL 280 IS 1 BP 171 EP 174 DI 10.1016/0014-5793(91)80230-Z PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FD286 UT WOS:A1991FD28600041 PM 2009960 ER PT J AU ROMEO, C SEED, B AF ROMEO, C SEED, B TI CELLULAR-IMMUNITY TO HIV ACTIVATED BY CD4 FUSED TO T-CELL OR FC RECEPTOR POLYPEPTIDES SO CELL LA English DT Article ID NATURAL-KILLER CELLS; RECOMBINANT SOLUBLE CD4; CLASS-II MHC; ANTIGEN RECEPTOR; ZETA-CHAIN; SURFACE EXPRESSION; MOLECULAR-CLONING; IMMUNODEFICIENCY VIRUS; TRANSFECTED CELLS; TRANS-ACTIVATOR AB We describe functional simplified T cell and Fc receptor chimeras that are capable of directing CD8+ cytotoxic T lymphocytes (CTLs) to specifically recognize and lyse cells expressing HIV envelope proteins. Target cells bearing HLA-DR molecules are not recognized by CTL armed with the chimeras. The variety of cell types in which the native receptors are active suggests multiple possibilities for antiviral intervention through genetic means. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP ROMEO, C (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. NR 69 TC 301 Z9 303 U1 2 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 8 PY 1991 VL 64 IS 5 BP 1037 EP 1046 DI 10.1016/0092-8674(91)90327-U PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FA940 UT WOS:A1991FA94000020 PM 1900456 ER PT J AU ROOF, D ADAMIAN, M JACOBS, D HAYES, A AF ROOF, D ADAMIAN, M JACOBS, D HAYES, A TI CYTOSKELETAL SPECIALIZATIONS AT THE ROD PHOTORECEPTOR DISTAL TIP SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE RODS AND CONES; MICROTUBULES; RETINA; CILIUM; ELECTRON MICROSCOPY ID OUTER SEGMENT MEMBRANES; CAENORHABDITIS-ELEGANS; ALPHA-TUBULIN; IMMUNOCYTOCHEMICAL LOCALIZATION; PIGMENT EPITHELIUM; CONNECTING CILIUM; BETA-TUBULIN; FROG RETINA; MICROTUBULES; PROTEIN AB We have examined microtubules and microtubule-like elements within the toad rod photoreceptor outer segment in order to define regional specializations of the photoreceptor cytoskeleton. "Ciliary" microtubules were localized within the rod outer segment (ROS) by using thin section electron microscopy, immunofluorescence, and rapid-freeze deep-etch microscopy. All three methods showed that ciliary microtubules stop short of the extreme ROS distal tip, although abundant microtubule-like structures distinct from the ciliary microtubules were found within the distal 10-15-mu-m of the ROS tip. These heretofore undescribed "distal ROS tubules" are clustered at the clefts or incisures of the disk membrane stack and resemble microtubules in overall size and shape, although they are not closely related antigenically to tubulin. The distal ROS tubules are more abundant in green rods than red rods and vary in number during the daily light/dark cycle. Quantitation of these tubules at two time points during the light/dark cycle suggests that there are three- to fourfold more tubules in the ROS tip one hour after light onset than one hour before light onset. Retinas prevented from normal disk membrane shedding by separation of the retina from the adjacent pigment epithelium, failed to develop increased numbers of tubules after light onset. This suggests that the newly described distal ROS tubules may modulate or be modulated by light-induced interactions between the photoreceptors and pigment epithelium, such as those that occur during the disk shedding phase of membrane turnover. RP ROOF, D (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY 06514] NR 53 TC 27 Z9 27 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 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD MAR 8 PY 1991 VL 305 IS 2 BP 289 EP 303 DI 10.1002/cne.903050210 PG 15 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA FA347 UT WOS:A1991FA34700009 PM 1902849 ER PT J AU CUNNINGHAM, CC STOSSEL, TP KWIATKOWSKI, DJ AF CUNNINGHAM, CC STOSSEL, TP KWIATKOWSKI, DJ TI ENHANCED MOTILITY IN NIH-3T3 FIBROBLASTS THAT OVEREXPRESS GELSOLIN SO SCIENCE LA English DT Article ID MYOSIN HEAVY-CHAIN; ACTIN-FILAMENTS; CA-2+ CONTROL; DICTYOSTELIUM; BINDING; GENE; INACTIVATION; EXPRESSION; PROTEIN; CELLS AB Increasing the content of the actin-binding protein gelsolin in cultured mouse fibroblasts by up to 125 percent by gene transfection proportionally enhanced the rate at which the cells migrated through porous filters toward a gradient of serum and closed a wound made on a confluent monolayer of cells in a tissue culture dish. These results provide direct evidence that gelsolin, which promotes both actin assembly and disassembly in vitro, is an important element in fibroblast locomotion and demonstrate that the manipulation of intracellular machinery can increase cell motility. RP CUNNINGHAM, CC (reprint author), MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. FU NHLBI NIH HHS [HL19429, HL07680]; NIAID NIH HHS [AI28465] NR 27 TC 263 Z9 270 U1 2 U2 11 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 8 PY 1991 VL 251 IS 4998 BP 1233 EP 1236 DI 10.1126/science.1848726 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FA691 UT WOS:A1991FA69100042 PM 1848726 ER PT J AU HASELTINE, WA AF HASELTINE, WA TI APART FROM THAT SO NATURE LA English DT Letter RP HASELTINE, WA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 7 PY 1991 VL 350 IS 6313 BP 10 EP 10 DI 10.1038/350010b0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FA693 UT WOS:A1991FA69300021 PM 2002833 ER PT J AU FERRARA, JLM DEEG, HJ AF FERRARA, JLM DEEG, HJ TI GRAFT-VERSUS-HOST DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID BONE-MARROW TRANSPLANTATION; T-CELL DEPLETION; LYMPHOCYTES-T; CYCLOSPORINE; ACTIVATION; CLONES; MOUSE C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. FRED HUTCHINSON CANC RES CTR,DIV CLIN RES,SEATTLE,WA 98104. RP FERRARA, JLM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NCI NIH HHS [CA18221, CA31787, CA39542] NR 56 TC 1048 Z9 1065 U1 3 U2 14 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 7 PY 1991 VL 324 IS 10 BP 667 EP 674 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FA144 UT WOS:A1991FA14400005 PM 1994250 ER PT J AU RIGOTTI, NA NEER, RM SKATES, SJ HERZOG, DB NUSSBAUM, SR AF RIGOTTI, NA NEER, RM SKATES, SJ HERZOG, DB NUSSBAUM, SR TI THE CLINICAL COURSE OF OSTEOPOROSIS IN ANOREXIA-NERVOSA - A LONGITUDINAL-STUDY OF CORTICAL BONE MASS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PRIMARY HYPERPARATHYROIDISM; GROWTH-HORMONE; FRACTURE RISK; SOMATOMEDIN-C; WOMEN; OSTEOPENIA; DENSITY; AMENORRHEA; PREDICTION; CALCIUM AB Women with anorexia nervosa have reduced bone mass and may develop fractures. Neither the pathophysiology of this osteoporosis nor its natural history is known. To study the clinical course of osteoporosis, we followed up 27 women with anorexia nervosa for a median of 25 months (range, 9 to 53 months). At study entry, cortical bone density, measured by single-photon absorptiometry of the radial shaft, was low (mean +/- SD, 0.63 +/- 0.07 g/cm2) and inversely related to the duration of amenorrhea (r = -0.49). During follow-up, most patients gained weight (n = 19), took calcium supplements (n = 16), and exercised regularly (n = 22), but fewer than half reached 80% or more of ideal body weight (n = 11), resumed menses (n = 6), or received estrogen (n = 4). Cortical bone density was stable during follow-up for the group as a whole; the mean annual change (+/-SD) was +0.005 (+/- .015) g/cm2 (95% confidence interval, -0.0009 to +0.0109). There was no significant difference in the mean change in bone density between women who attained 80% of ideal weight and those who did not or between groups who did or did not regain menses, take estrogen or calcium, or exercise vigorously. Four fractures were clinically observed in three women during follow-up. The rate of 0.05 nonspine fractures per person-year (95% confidence interval, 0.02 to 0.13) exceeds that of normal women in this age range (relative risk, 7.1; 95% confidence interval, 2.3 to 18.5). We conclude that reductions in cortical bone density appear not to be rapidly reversed recovery from anorexia nervosa and that anorectic women may have an increased risk of fracture. C1 MASSACHUSETTS GEN HOSP,MED SERV,ENDOCRINE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,EATING DISORDERS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP RIGOTTI, NA (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,GEN INTERNAL MED UNIT,BULFINCH 1,FRUIT ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [RR-1066] NR 46 TC 243 Z9 244 U1 1 U2 5 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 MAR 6 PY 1991 VL 265 IS 9 BP 1133 EP 1138 DI 10.1001/jama.265.9.1133 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA EZ474 UT WOS:A1991EZ47400030 PM 1995999 ER PT J AU FORCE, T HYMAN, G HAJJAR, R SELLMAYER, A BONVENTRE, JV AF FORCE, T HYMAN, G HAJJAR, R SELLMAYER, A BONVENTRE, JV TI NONCYCLOOXYGENASE METABOLITES OF ARACHIDONIC-ACID AMPLIFY THE VASOPRESSIN-INDUCED CA2+ SIGNAL IN GLOMERULAR MESANGIAL CELLS BY RELEASING CA2+ FROM INTRACELLULAR STORES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STIMULATES PHOSPHOLIPASE-C; FREE CALCIUM-CONCENTRATION; INOSITOL PHOSPHATES; CYTOSOLIC CA-2+; K+-CHANNEL; LIPOXYGENASE; INHIBITORS; IDENTIFICATION; MOBILIZATION; ACTIVATION AB Noncyclooxygenase metabolites of arachidonic acid may be potent modulators of the mitogenic response of renal mesangial cells to the mitogenic vasoactive peptide arginine vasopressin (AVP). Since Ca2+ is a critical second messenger in the response of mesangial cells to AVP, and Ca2+ has been implicated in the regulation of growth, we determined whether noncyclooxygenase metabolites altered the phospholipase C-Ca2+ signalling cascade which is activated by AVP. Pretreatment of mesangial cells for 10 min with lipoxygenase and cytochrome P450 monooxygenase inhibitors, nordihydroguaiaretic acid (NDGA, 10(-5) M) or SKF-525A (2.5 x 10(-5) M), but not the cyclooxygenase inhibitor indomethacin (2 x 10(-5) M), reduced the magnitude of the AVP (10(-8) and 10(-7) M)-induced increase in cytosolic free Ca2+ concentration ([Ca2+]i) without affecting inositol trisphosphate production. With 10(-8) M AVP, [Ca2+]i increased to 250 +/- 47 nM in NDGA-treated cells versus 401 +/- 59 nM in control cells (p < 0.01). [Ca2+]i, measured 2 min after exposure to AVP, was also lower with NDGA (152 +/- 21 nM) when compared with AVP alone (220 +/- 22 nM, p < 0.01). 14,15-epoxyeicosatrienoic acid (EET) (10(-8) M), which had no effect on inositol trisphosphate production, completely reversed the NDGA-induced inhibition of the [Ca2+]i transient, whereas 5-hydroperoxyeicosatetraenoic acid (HPETE) (5 x 10(-7) M) did not. Pretreatment with higher concentrations of 14,15-EET (10(-7)-10(-6) M) markedly potentiated the AVP-induced increase in [Ca2+]i. NDGA-induced inhibition of the AVP-generated [Ca2+]i transient was also observed when cells were incubated in low Ca2+ media ([Ca2+] < 5 x 10(-8) M), suggesting that NDGA pretreatment impaired intracellular release of Ca2+. Since NDGA had no direct effect on inositol 1,4,5-trisphosphate-induced Ca2+ release, we postulated that NDGA blocked production of a metabolite that releases Ca2+ from intracellular stores. 14,15-EET and 15-HPETE, but not 15-hydroxyeicosatetraenoic acid (each at 3 x 10(-7) M), raised [Ca2+]i when added directly to cells in low Ca2+ media. In permeabilized cells 14,15-EET and 15-HPETE (10(-7) M) potently released Ca2+ from intracellular stores. In summary, noncyclooxygenase metabolites of arachidonic acid, and in particular P450 metabolites, are potent endogenous amplifiers of the AVP-induced [Ca2+]i signal by mechanisms not directly involving phospholipase C activation. This effect is mediated, at least in part, by enhanced release of Ca2+ from intracellular storage sites by an inositol 1,4,5-trisphosphate-independent mechanism. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FORCE, T (reprint author), MASSACHUSETTS GEN HOSP,DEPT PREVENT MED,BOSTON,MA 02114, USA. OI Force, Thomas/0000-0002-0450-8659 FU NIDDK NIH HHS [DK-38165, DK-38452, DK-39773] NR 46 TC 71 Z9 72 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 MAR 5 PY 1991 VL 266 IS 7 BP 4295 EP 4302 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA694 UT WOS:A1991FA69400045 PM 1900289 ER PT J AU WILEMAN, T KANE, LP CARSON, GR TERHORST, C AF WILEMAN, T KANE, LP CARSON, GR TERHORST, C TI DEPLETION OF CELLULAR CALCIUM ACCELERATES PROTEIN-DEGRADATION IN THE ENDOPLASMIC-RETICULUM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ANTIGEN RECEPTOR CHAINS; INTRACELLULAR-TRANSPORT; BREFELDIN-A; INFLUENZA HEMAGGLUTININ; RAPID REDISTRIBUTION; BINDING-PROTEIN; GOLGI PROTEINS; COMPLEX; CELLS; ER AB In this study the effects of A23187 and thapsigargin on the degradation of T-cell antigen receptor-beta (TCR-beta) and CD3-delta in the endoplasmic reticulum have been studied. Preliminary experiments showed that these drugs had different effects on the secretory pathway. Depletion of cellular calcium pools by incubation of cells with A23187 in calcium-free medium blocked transport between the endoplasmic reticulum and the Golgi apparatus whereas thapsigargin caused a modest increase in transport. When added to cells transfected with TCR-beta or CD3-delta the drugs caused an immediate stimulation of proteolysis of presynthesized protein and at maximum effective concentrations caused a 3-fold increase in the rate of degradation. They did not affect the lag period of 1 h which precedes degradation of newly synthesized proteins. Chelation of cytosolic calcium also accelerated degradation, suggesting that depletion of calcium from the endoplasmic reticulum was the main stimulus of proteolysis and that increased degradation was not caused by a transient increase in cytosolic calcium levels. The selectivity of degradation in the endoplasmic reticulum was maintained. A23187 had no effect on the stability of CD3-gamma nor co-transfected epsilon-beta-dimers. Calcium depletion increased the overall rate of degradation in the endoplasmic reticulum and increased the rate of proteolysis of an "anchor minus" beta-chain. The results suggested that proteolysis within the endoplasmic reticulum may be regulated by the high concentrations of Ca2+ which are stored in the organelle. Ca2+ may be required for protein folding. Calcium depletion may have caused the beta and delta-chains to adopt a conformation that was more susceptible to proteolysis. Alternatively, calcium depletion may have disrupted the lumenal content of the endoplasmic reticulum and increased the access of proteases to potential substrates. C1 T CELL SCI INC,PROT EXPRESS GRP,CAMBRIDGE,MA 02139. RP WILEMAN, T (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,RM 309 JFB,44 BINNEY ST,BOSTON,MA 02115, USA. OI Kane, Lawrence/0000-0001-5198-516X FU NIAID NIH HHS [AI-15066] NR 39 TC 89 Z9 89 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 MAR 5 PY 1991 VL 266 IS 7 BP 4500 EP 4507 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA694 UT WOS:A1991FA69400075 PM 1825655 ER PT J AU SCHILDBACH, JF PANKA, DJ PARKS, DR JAGER, GC NOVOTNY, J HERZENBERG, LA MUDGETTHUNTER, M BRUCCOLERI, RE HABER, E MARGOLIES, MN AF SCHILDBACH, JF PANKA, DJ PARKS, DR JAGER, GC NOVOTNY, J HERZENBERG, LA MUDGETTHUNTER, M BRUCCOLERI, RE HABER, E MARGOLIES, MN TI ALTERED HAPTEN RECOGNITION BY 2 ANTIDIGOXIN HYBRIDOMA VARIANTS DUE TO VARIABLE REGION POINT MUTATIONS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HEAVY-CHAIN; 3-DIMENSIONAL STRUCTURE; BINDING-SPECIFICITY; HIGH-AFFINITY; SOMATIC HYPERMUTATION; ARSONATE IDIOTYPE; GENIN ACTIVITY; ANTIBODIES; COMPLEX; RECOMBINATION AB Two spontaneous variants of the murine anti-digoxin antibody-producing hybridoma cell line 26-10 were isolated by two-color fluorescence-activated cell sorting on the basis of altered hapten binding. The variable region sequences of the antibodies produced by the mutant lines revealed that each contains a single amino acid change in the heavy chain second complementarity determining region. A Tyr to His change at position 50 leads to a 40-fold reduction in affinity for digoxin. A Ser to Phe mutation at position 52 results in a 300-fold reduction in affinity for digoxin. A competition assay involving 33 digoxin analogues was used to examine the specificity of hapten binding of 26-10 and the two mutant antibodies. The position 50 mutant has a distinct specificity change; it exhibits a preference for digoxin congeners containing a hydroxyl group at the steroid 12 position, whereas the 26-10 parent does not. The affinities of all three antibodies for hapten are progressively lowered by substitutions of increasing size at the digoxin steroid D ring 16 position. Although 26-10 binds digoxin and its genin form equally, 12 and 16 steroid position substitutions which lower affinity also confer a preference for a sugar at the steroid 3 position. These results suggest that position 50 contributes to specificity of the antibody and that alterations of the hapten can lead to differences in recognition, possibly through a shift in hapten orientation within the binding site. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. STANFORD UNIV,DEPT GENET,STANFORD,CA 94305. BRISTOL MYERS CO,SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. FU NHLBI NIH HHS [P01-HL19259] NR 57 TC 37 Z9 37 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 MAR 5 PY 1991 VL 266 IS 7 BP 4640 EP 4647 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FA694 UT WOS:A1991FA69400094 PM 1999439 ER PT J AU ARRIAGADA, PV LOUIS, DN HEDLEYWHYTE, ET HYMAN, BT AF ARRIAGADA, PV LOUIS, DN HEDLEYWHYTE, ET HYMAN, BT TI NEUROFIBRILLARY TANGLES AND OLFACTORY DYSGENESIS SO LANCET LA English DT Letter ID ALZHEIMERS-DISEASE; PATHOLOGICAL-CHANGES; DOWNS-SYNDROME; PLAQUES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP ARRIAGADA, PV (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL & NEUROL,BOSTON,MA 02114, USA. FU NIA NIH HHS [AG08487, P50 AG05134] NR 9 TC 9 Z9 10 U1 0 U2 0 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAR 2 PY 1991 VL 337 IS 8740 BP 559 EP 559 DI 10.1016/0140-6736(91)91351-T PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA EZ874 UT WOS:A1991EZ87400052 PM 1671925 ER PT J AU DICHEK, HL MACLAUGHLIN, DT BRINGHURST, FR KEUTMANN, HT RICHARDSON, GS AF DICHEK, HL MACLAUGHLIN, DT BRINGHURST, FR KEUTMANN, HT RICHARDSON, GS TI PARTIAL PRIMARY SEQUENCE OF A HUMAN ENDOMETRIAL EPITHELIAL PROGESTERONE DEPENDENT PROTEIN SECRETED INVITRO SO ACTA ENDOCRINOLOGICA LA English DT Article ID TRIMESTER PREGNANCY ENDOMETRIUM; PLACENTAL PROTEIN-14; BETA-LACTOGLOBULINS; MENSTRUAL-CYCLE; LUTEAL PHASE; PROLACTIN; FLUID; ALPHA-2-GLOBULIN; ELECTROPHORESIS; CULTURE AB We have recently identified a uterine progesterone-dependent 25 kD protein (protein #27) secreted by endometrial epithelial cells but not stroma. Protein #27 was originally isolated from human luteal phase uterine fluids and partially purified by two-dimensional gel-electrophoresis and electroelution. It could not be detected in serum. We here report the further purification and amino terminal sequence of this protein, obtained from in vitro luteal phase endometrial tissue incubation media. Protein #27 was purified by a one-step method using reverse-phase high performance liquid chromatography. Amino acid compositional analysis confirms a high content of nonpolar and hydrophobic residues (40 mol%) and reveals a preponderance of acidic amino acids, consistent with its isoelectric point (5.9-6.3 pH). The amino terminal sequence obtained from a single individual reveals 85% homology with that of pregnancy-associated alpha-2-globulin from pooled cytosolic fractions from pregnancy endometria. We propose that protein #27, secreted by the endometrial epithelium, is an excellent candidate for a marker to be used to study pathological processes of the endometrium such as endometriosis and invasive carcinoma. C1 MASSACHUSETTS GEN HOSP,VINCENT RES LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT GYNECOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NCI NIH HHS [CA 30687] NR 24 TC 0 Z9 0 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-5598 J9 ACTA ENDOCRINOL-COP JI Acta Endocrinol. PD MAR PY 1991 VL 124 IS 3 BP 338 EP 345 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FE480 UT WOS:A1991FE48000017 PM 2011922 ER PT J AU WILEMAN, TE AF WILEMAN, TE TI PROPERTIES OF ASPARAGINASE-DEXTRAN CONJUGATES SO ADVANCED DRUG DELIVERY REVIEWS LA English DT Review DE PROTEIN MODIFICATION; CANCER; ENZYME CONJUGATE; THERAPEUTIC PROTEIN ID SOYBEAN TRYPSIN-INHIBITOR; PHARMACEUTICAL PROPERTIES; PLASMA PERSISTENCE; COVALENT LINKAGE; SOLUBLE DEXTRANS; ESCHERICHIA-COLI; CARBOXYPEPTIDASE-G2; LEUKEMIA; ENZYMES; INVIVO AB Asparaginases isolated from Escherichia coli and Erwinia carotovora are used in the treatment of acute lymphoblastic leukemia. Unfortunately, their use has been limited by their relatively short circulatory half-lives and by immune reactions that develop in response to repeated injections of the enzymes. This review describes studies that have used dextran to improve the therapeutic potential Of L-asparaginase. Dextran, a biocompatible polymer of D-glucose, is bound covalently to the surface of asparaginase. The resulting soluble dextran-asparaginase conjugates show increased circulatory persistence and markedly reduced antigen reactivity. These studies have shown that it is possible to use dextran to create a steric barrier around asparaginase that not only protects the enzyme from degradation in vivo but also slows its inactivation by the immune system. Soluble-dextran conjugates provide a means of avoiding the biological limitations to the use of microbial enzymes in therapy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. NR 40 TC 17 Z9 17 U1 1 U2 7 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-409X J9 ADV DRUG DELIVER REV JI Adv. Drug Deliv. Rev. PD MAR-APR PY 1991 VL 6 IS 2 BP 167 EP 180 DI 10.1016/0169-409X(91)90039-F PG 14 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA GF477 UT WOS:A1991GF47700005 ER PT J AU WARPINSKI, JR FOLGERT, J COHEN, M BUSH, RK AF WARPINSKI, JR FOLGERT, J COHEN, M BUSH, RK TI ALLERGIC REACTION TO LATEX - A RISK FACTOR FOR UNSUSPECTED ANAPHYLAXIS SO ALLERGY PROCEEDINGS LA English DT Article AB Allergic reactions to latex, including anaphylaxis may be a problem in certain individuals exposed to latex. Four atopic patients with symptoms of rhinitis, asthma, anaphylaxis, and/or urticaria upon contact with latex products were studied. The patients showed IgE binding to latex RAST disks ranging from 1.0 to 27.3 times the negative control. Latex products (gloves, balloons, and condoms) directly bound IgE from all four patients. Eluted proteins from the latex products inhibited IgE binding to commercial latex RAST disks. SDS-PAGE demonstrated multiple latex protein bands by Coomassie Blue staining between 14 and 66 kD. Immunoblotting showed specific IgE binding to latex proteins at 30 and 66 kD. These results indicate that latex-allergic patients have IgE directed against specific latex proteins. Allergy to latex can pose a substantial health risk to susceptible individuals. RP WARPINSKI, JR (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705, USA. NR 0 TC 46 Z9 46 U1 0 U2 0 PU OCEAN SIDE PUBLICATIONS INC PI PROVIDENCE PA 95 PITMAN ST, PROVIDENCE, RI 02906 SN 1046-9354 J9 ALLERGY PROC JI Allergy Proc. PD MAR-APR PY 1991 VL 12 IS 2 BP 95 EP 102 DI 10.2500/108854191779011846 PG 8 WC Allergy SC Allergy GA FK469 UT WOS:A1991FK46900006 PM 2060787 ER PT J AU PICARD, MH WILKINS, GT GILLAM, LD THOMAS, JD WEYMAN, AE AF PICARD, MH WILKINS, GT GILLAM, LD THOMAS, JD WEYMAN, AE TI IMMEDIATE REGIONAL ENDOCARDIAL SURFACE EXPANSION FOLLOWING CORONARY-OCCLUSION IN THE CANINE LEFT-VENTRICLE - DISPROPORTIONATE EFFECTS OF ANTERIOR VERSUS INFERIOR ISCHEMIA SO AMERICAN HEART JOURNAL LA English DT Article ID TRANSMURAL MYOCARDIAL-INFARCTION; ANEURYSM FORMATION; CONSCIOUS DOGS; BLOOD-FLOW; SIZE; ECHOCARDIOGRAPHY; DILATION; ENLARGEMENT; GEOMETRY; ARTERY AB The exact time of onset of functional expansion after acute myocardial infarction/ischemia remains unclear in spite of its potential link to chronic pathologic infarct expansion and its potential implications for therapy. To examine this early change in ventricular morphology, 14 open-chest dogs were studied with two-dimensional echocardiography before and after occlusion (10 minutes) of the left anterior descending coronary artery (LAD, n = 7) or circumflex artery (CIRC, n = 7). The endocardial surface area (ESA) and the area of abnormal wall motion (AWM) were reconstructed from the echocardiographic data using a previously reported technique for quantitatively mapping the ESA and extent of AWM. For the total group (N = 14), the mean ESA before occlusion was 48.9 +/- 9.8 cm2, increasing to 65.7 +/- 18.9 cm2 at 10 minutes occlusion (rho < 0.001). For the LAD subgroup, the mean ESA before occlusion was 50.7 +/- 9.3 cm2, increasing to 79.1 +/- 14.1 cm2 at 10 minutes following occlusion (p < 0.001). For the CIRC subgroup, the mean ESA before occlusion was 47.1 +/- 10.8 cm2, increasing to 52.3 +/- 12.6 cm2 at 10 minutes after occlusion (p < 0.001). The ESA increase for the LAD subgroup was significantly larger than that of the CIRC subgroup (LAD range 14.5 to 49.9 cm2 versus CIRC range 1.5 to 9 cm2, p < 0.0001). Coronary occlusion resulted in similarly sized regions of AWM for both subgroups (LAD, 31.3 +/- 12.2 cm2 versus CIRC, 25.9 +/- 10.3 cm2, p = n.s.). For the LAD group, the largest increase in endocardial circumference occurred within the zone of AWM at the apex (39.9 +/- 12%). The endocardial surface area therefore expands immediately after coronary occlusion and the magnitude of this process is primarily related to the site (anteroapical) rather than to the extent of AWM. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PICARD, MH (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,CARDIAC NON INVASIVE LAB,PHILLIPS 8,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 FU NHLBI NIH HHS [HL-07535, HL-26215] NR 45 TC 25 Z9 25 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD MAR PY 1991 VL 121 IS 3 BP 753 EP 762 DI 10.1016/0002-8703(91)90185-K PN 1 PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FA655 UT WOS:A1991FA65500004 PM 2000741 ER PT J AU FRIEDENBERG, WR KYLE, RA KNOSPE, WH BENNETT, JM TSIATIS, AA OKEN, MM AF FRIEDENBERG, WR KYLE, RA KNOSPE, WH BENNETT, JM TSIATIS, AA OKEN, MM TI HIGH-DOSE DEXAMETHASONE FOR REFRACTORY OR RELAPSING MULTIPLE-MYELOMA SO AMERICAN JOURNAL OF HEMATOLOGY LA English DT Article DE TOXICITY; EFFICACY; SUBJECTIVE RESPONSE ID THERAPY AB In order to assess the efficacy and toxicity of dexamethasone as a single agent without the concomitant infusion of Adriamycin and vincristine (VAD), an ECOG pilot study was initiated using 40 mg by mouth daily for 4 days every week for 8 weeks. Patients who responded were then maintained on the same treatment, but at 2 week intervals. Of the 32 patients evaluable for response, three were completely refractory to all prior therapy. All patients had advanced disease and 26 had received multiple prior treatments. There were 13/32 (40%) objective responses by ECOG criteria. Of the 28 patients evaluable for subjective response, i.e., significant decrease in performance status and/or bone pain, eight (28.5%) responded. Of the 34 patients evaluable for toxicity, 19 patients (55%) had moderate to severe side effects, including nine who had central nervous system effects, three who had gastrointestinal bleeding, two who had pulmonary emboil, one with psychosis, and four who had serious infections with one death. Median survival for the entire group was 19 weeks, with 31 weeks in the responders and 9 weeks in the non-responders. Although high-dose dexamethasone is capable of producing a significant number of partial responses (40%), it is associated with excessive toxicity. Less frequent administration of the dexamethasone at 2 week intervals was well tolerated in the maintenance of partial response, but has not been studied for efficacy in induction of remission. C1 MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV ROCHESTER,ROCHESTER,NY 14627. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MINNESOTA,VET ADM MED CTR,MINNEAPOLIS,MN 55455. RP FRIEDENBERG, WR (reprint author), MARSHFIELD CLIN FDN MED RES & EDUC,DEPT HEMATOL,1000 N OAK AVE,MARSHFIELD,WI 54449, USA. NR 14 TC 39 Z9 39 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 0361-8609 J9 AM J HEMATOL JI Am. J. Hematol. PD MAR PY 1991 VL 36 IS 3 BP 171 EP 175 DI 10.1002/ajh.2830360303 PG 5 WC Hematology SC Hematology GA EY678 UT WOS:A1991EY67800002 PM 1996557 ER PT J AU OLIVER, LC SPRINCE, NL GREENE, R AF OLIVER, LC SPRINCE, NL GREENE, R TI ASBESTOS-RELATED DISEASE IN PUBLIC-SCHOOL CUSTODIANS SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE ASBESTOS-CONTAINING MATERIAL (ACM); BUILDING EXPOSURE; NO OUTSIDE EXPOSURE (NOE); PLEURAL PLAQUES; PULMONARY RESTRICTION ID PLEURAL MESOTHELIOMA; EXPOSURE; WORKERS; PREVALENCE; POPULATION; MORTALITY; FIBROSIS; PLAQUES; VALUES AB A cross-sectional prevalence study of 120 public school custodians was carried out. The purposes were 1) to investigate the prevalence of asbestos-related disease in a group of custodians at risk for asbestos exposure in public schools and 2) to determine the proportion with disease attributable to exposures in school buildings. Medical and occupational histories, flow-volume loops, and posterior-anterior, lateral, and anterior oblique (AO) chest radiographs were obtained. Single breath DLCO was measured and chest auscultation performed. Mean age of subjects was 57 years and mean duration of work as a custodian, 27 years. Fifty-seven (47.5%) had no known or likely exposure to asbestos outside of their work as a school custodian (NOE). Pleural plaques (PP) occurred in 40 (33%) of the total group and 12 (21%) of the group with NOE. Pulmonary restriction (FVC < 80% predicted, FEV1/FVC% greater-than-or-equal-to 70) occurred in 22 (18%) of the total group and 10 (17%) of those with NOE. DLCO was lower in the group with restriction. Multivariate analysis revealed significant associations (p < 0.05) between both PP and restriction and duration of asbestos exposure. AO radiographs increased PP detection by a factor of 1.9. Our results reveal PP prevalence in excess of background and pulmonary restriction in the study population, and indicate that PP are attributable to asbestos in schools. Findings with regard to pulmonary restriction need further investigation. Prudent management of asbestos in buildings is indicated for the prevention of related disease. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP OLIVER, LC (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,55 FRUIT ST,BOSTON,MA 02114, USA. NR 41 TC 28 Z9 28 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD MAR PY 1991 VL 19 IS 3 BP 303 EP 316 DI 10.1002/ajim.4700190305 PG 14 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EX263 UT WOS:A1991EX26300004 PM 2008920 ER PT J AU ZWERLING, C RYAN, J ORAV, EJ AF ZWERLING, C RYAN, J ORAV, EJ TI WORKERS COMPENSATION COST SHIFTING - AN EMPIRICAL-STUDY SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE OCCUPATIONAL ILLNESS COSTS; MEDICAL COST CONTAINMENT; HMOS; FEE-FOR-SERVICE PLANS AB It has been suggested that health maintenance organizations (HMOs) overdiagnose work-related injuries and illnesses to increase their income. This study compared the Workers' Compensation experience of 2,176 Boston postal employees enrolled in a large HMO with that of 3,473 employees enrolled in a large fee-for-service health insurance plan. It controlled for the potential confounders of age, gender, job classification, type of injury, and duration of employment. It found no difference in the incidence of injuries: 5.93% for HMO enrollees and 6.25% for fee-for-service plan enrollees. Medical costs averaged $475 for HMO enrollees and $838 for fee-for-service plan enrollees (p = 0.018). Total costs averaged $909 for HMO enrollees and $1388 for fee-for-service plan enrollees (p = 0.063). In our cohort, there was no evidence of cost shifting. It appeared that the HMO provided less expensive medical care for injured postal workers. C1 BOSTON POSTAL SERV,MED UNIT,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM SCI & PHYSIOL,OCCUPAT MED PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,OCCUPAT MED CLIN,BOSTON,MA 02114. TUFTS UNIV,SCH MED,DEPT COMMUNITY MED,BOSTON,MA 02111. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. NR 8 TC 11 Z9 11 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 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD MAR PY 1991 VL 19 IS 3 BP 317 EP 325 DI 10.1002/ajim.4700190306 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA EX263 UT WOS:A1991EX26300005 PM 1826190 ER PT J AU ROZICH, JD SMITH, B THOMAS, JD ZILE, MR KAISER, J MANN, DL AF ROZICH, JD SMITH, B THOMAS, JD ZILE, MR KAISER, J MANN, DL TI DIALYSIS-INDUCED ALTERATIONS IN LEFT-VENTRICULAR FILLING - MECHANISMS AND CLINICAL-SIGNIFICANCE SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE DOPPLER ECHOCARDIOGRAPHY; HEMODIALYSIS; HYPOTENSION ID NON-INVASIVE ASSESSMENT; DOPPLER ECHOCARDIOGRAPHY; IONIZED CALCIUM; TIME INTERVALS; RENAL-FAILURE; REAL-TIME; HEMODIALYSIS; FLOW; CONTRACTILITY; RELAXATION C1 VET ADM MED CTR,CARDIOL SECT,CHARLESTON,SC 29403. VET ADM MED CTR,NEPHROL SECT,CHARLESTON,SC 29403. MED UNIV S CAROLINA,CHARLESTON,SC 29425. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. OI Mann, Douglas /0000-0002-2516-0145 NR 31 TC 35 Z9 36 U1 0 U2 2 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 MAR PY 1991 VL 17 IS 3 BP 277 EP 285 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA FA643 UT WOS:A1991FA64300006 PM 1996569 ER PT J AU FLESCHER, E TALAL, N AF FLESCHER, E TALAL, N TI DO VIRUSES CONTRIBUTE TO THE DEVELOPMENT OF SJOGREN SYNDROME SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID EPSTEIN-BARR VIRUS; SYSTEMIC LUPUS-ERYTHEMATOSUS; SALIVARY-GLAND BIOPSIES; INFECTION; COMPLEX; MICE; DNA C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. NR 24 TC 58 Z9 59 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD MAR PY 1991 VL 90 IS 3 BP 283 EP 285 DI 10.1016/0002-9343(91)90566-G PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FC488 UT WOS:A1991FC48800001 PM 1848393 ER PT J AU POLLOCK, SG ABBOTT, RD BOUCHER, CA WATSON, DD KAUL, S AF POLLOCK, SG ABBOTT, RD BOUCHER, CA WATSON, DD KAUL, S TI A MODEL TO PREDICT MULTIVESSEL CORONARY-ARTERY DISEASE FROM THE EXERCISE TL-201 STRESS TEST SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID ISCHEMIC-HEART-DISEASE; CARDIAC-CATHETERIZATION; AMBULATORY PATIENTS; NATURAL-HISTORY; CHEST PAIN; TL-201; VARIABLES; EXTENT AB Purpose: The aim of this study was to (1) determine whether nonimaging variables add to the diagnostic information available from exercise thallium-201 images for the detection of multivessel coronary artery disease; and (2) to develop a model based on the exercise thallium-201 stress test to predict the presence of multivessel disease. Patients and Methods: The study populations included 383 patients referred to the University of Virginia and 325 patients referred to the Massachusetts General Hospital for evaluation of chest pain. All patients underwent both cardiac catheterization and exercise thallium-201 stress testing between 1978 and 1981. Results: In the University of Virginia cohort, at each level of thallium-201 abnormality (no defects, one defect, more than one defect), ST depression and patient age added significantly in the detection of multivessel disease. Logistic regression analysis using data from these patients identified three independent predictors of multivessel disease: initial thallium-201 defects, ST depression, and age. A model was developed to predict multivessel disease based on these variables. As might be expected, the risk of multivessel disease predicted by the model was similar to that actually observed in the University of Virginia population. More importantly, however, the model was accurate in predicting the occurrence of multivessel disease in the unrelated population studied at the Massachusetts General Hospital. Conclusion: It is, therefore, concluded that (1) nonimaging variables (age and exercise-induced ST depression) add independent information to thallium-201 imaging data in the detection of multivessel disease; and (2) a model has been developed based on the exercise thallium-201 stress test that can accurately predict the probability of multivessel disease in other populations. C1 UNIV VIRGINIA,SCH MED,DEPT MED,DIV CARDIOL,BOX 158,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,SCH MED,DEPT MED,DIV BIOSTAT,CHARLOTTESVILLE,VA 22908. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [K08-HL-01833, R01-HL26215, R01-HL-26205] NR 33 TC 17 Z9 17 U1 1 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 MAR PY 1991 VL 90 IS 3 BP 345 EP 352 DI 10.1016/0002-9343(91)90575-I PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA FC488 UT WOS:A1991FC48800010 PM 2003517 ER PT J AU FLETCHER, JA GIBAS, Z DONOVAN, K PEREZATAYDE, A GENEST, D MORTON, CC LAGE, JM AF FLETCHER, JA GIBAS, Z DONOVAN, K PEREZATAYDE, A GENEST, D MORTON, CC LAGE, JM TI OVARIAN GRANULOSA STROMAL CELL TUMORS ARE CHARACTERIZED BY TRISOMY-12 SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID ABNORMALITIES; CHROMOSOMES AB Eleven ovarian granulosa-stromal cell tumors, including 1 thecoma, 2 fibromas, 6 fibrothecomas, and 2 granulosa cell tumors, were karyotyped after direct harvests and/or short-term tissue culture. Bilateral fibrothecomas from one patient appeared to lack cytogenetic aberrations; the remaining nine tumors were characterized by trisomy for chromosome 12. Cytogenetic aberrations in the two granulosa cell tumors were much less complex than those described previously in undifferentiated carcinomas; accordingly cytogenetic analyses might be useful in distinguishing these categories. The consistent occurrence of trisomy 12 in different varieties of granulosa-stromal cell tumors suggests a common mechanism of oncogenesis within this diverse group of neoplasms. That mechanism probably involves promotion of low-grade, orderly cell proliferation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. THOMAS JEFFERSON UNIV,DIV MED GENET,PHILADELPHIA,PA 19107. CHILDRENS HOSP MED CTR,DEPT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1K11CA01498-01] NR 22 TC 65 Z9 66 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAR PY 1991 VL 138 IS 3 BP 515 EP 520 PG 6 WC Pathology SC Pathology GA FA838 UT WOS:A1991FA83800001 PM 2000932 ER PT J AU GREENSPAN, SL KLIBANSKI, A ROWE, JW ELAHI, D AF GREENSPAN, SL KLIBANSKI, A ROWE, JW ELAHI, D TI AGE-RELATED ALTERATIONS IN PULSATILE SECRETION OF TSH - ROLE OF DOPAMINERGIC REGULATION SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CLUSTER ANALYSIS; THYROTROPIN; METOCLOPRAMIDE ID THYROTROPIN-RELEASING-HORMONE; PITUITARY CELL-CULTURE; PROLACTIN SECRETION; ELDERLY MEN; METOCLOPRAMIDE; BASAL; RESPONSES; SUBUNIT AB To investigate the influence of aging on dopaminergic modulation of pulsatile thyrotropin (TSH) secretion, we examined changes in circulating TSH levels during the day and night with and without a dopamine antagonist metoclopramide, in healthy young (20-35 yr old) and old (69-83 yr old) subjects, with the use of cluster analysis. Baseline thyroid function tests including serum thyroxine, 3,5,3' -triiodothyronine (T3), T3 resin uptake, and TSH and the response of TSH to thyrotropin-releasing hormone were within normal limits in young and old subjects, and antimicrosomal and anti-thyrogloublin antibodies were absent in all participants. Pulsatile TSH secretion was indentified in all subjects, and as a group there were significant increases in nocturnal peak height (P < 0.01), amplitude (P < 0.01), and mean TSH (P < 0.001). TSH pulse amplitude increased 160% (P < 0.05) at night compared with day in the young but was unchanged at night in the old. After the administration of metoclopramide there was a significant increase in peak height (P < 0.01), amplitude (P < 0.01), and mean TSH (P < 0.01). However, the effect of metoclopramide was different in young and old subjects. In the young, daytime administration of metoclopramide increased TSH pulse height (P < 0.02) and mean TSH (P < 0.05); pulse parameters remained unchanged at night. In comparison, in old subjects after metoclopramide, pulse parameters were unchanged during the day but pulse amplitude significantly (P < 0.01) increased at night. TSH pulse frequency remained stable with age and was unaltered after metoclopramide. We conclude that TSH pulsatile secretion is preserved in elderly men but blunted at night. The mechanisms for this alteration in pulsatile TSH secretion may be due to age-associated changes in day-night dopaminergic regulation. C1 BETH ISRAEL HOSP,DIV ENDOCRINOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROENDOCRINE UNIT,BOSTON,MA 02114. CUNY MT SINAI SCH MED,DEPT MED & GERIATR,NEW YORK,NY 10029. RP GREENSPAN, SL (reprint author), BETH ISRAEL HOSP,DIV GERONTOL,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NCRR NIH HHS [RR-01032]; NIA NIH HHS [AG-00599, K12AG00294] NR 27 TC 28 Z9 29 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1991 VL 260 IS 3 BP E486 EP E491 PN 1 PG 6 WC Physiology SC Physiology GA FC250 UT WOS:A1991FC25000057 PM 1900670 ER PT J AU KRADIN, RL MCCARTHY, KM XIA, WJ LAZARUS, D SCHNEEBERGER, EE AF KRADIN, RL MCCARTHY, KM XIA, WJ LAZARUS, D SCHNEEBERGER, EE TI ACCESSORY CELLS OF THE LUNG .1. INTERFERON-GAMMA INCREASES IA+ DENDRITIC CELLS IN THE LUNG WITHOUT AUGMENTING THEIR ACCESSORY ACTIVITIES SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID LYMPHOCYTE-T PROLIFERATION; ANTIGEN-PRESENTING CELLS; MIXED LEUKOCYTE REACTION; RAT; MACROPHAGES; IDENTIFICATION; MONOCYTES; INVIVO; MICE; STIMULATORS AB Dendritic cells are specifically adapted to provide accessory signals for the growth of T lymphocytes. Ia+ dendritic cells are present within the normal lung; however, little is known concerning their regulation in vivo. Interferon-gamma (IFN-gamma) is a proinflammatory lymphokine that augments the expression of Ia antigens and promotes the accessory activities of a variety of cells. In order to determine whether IFN-gamma regulates pulmonary dendritic cells in vivo, Lewis rats were injected intraperitoneally with recombinant murine IFN-gamma (2 x 10(5) U/rat/day) or with buffered saline for 5 consecutive days. Following sacrifice, the lungs were excised, and the distribution and number of Ia (OX-6)+ cells was determined in situ. Dendritic cells were localized in the mucosal lining of the tracheobronchial tree, in pulmonary capillaries, as well as in the alveolar septal interstitium and subjacent to the pleural surfaces. IFN-gamma yielded a specific increase in Ia+ dendritic cells in alveolar septa and in pulmonary airways. Purified Ia+ dendritic cells from enzymatic digests of lung were excellent accessory cells for the proliferative responses of both antigen-primed and naive T lymphocytes. IFN-gamma did not, however, further augment the expression of Ia antigens or the accessory activities of pulmonary dendritic cells. These results suggest that IFN-gamma may promote pulmonary T cell-mediated inflammatory responses in vivo by increasing the number of Ia+ dendritic accessory cells in the lung. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,COX BLDG 5,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-36781] NR 46 TC 47 Z9 47 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD MAR PY 1991 VL 4 IS 3 BP 210 EP 218 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA FA840 UT WOS:A1991FA84000004 PM 1900424 ER PT J AU BUCKLEY, KM SCHAEFER, CM GREENE, R AGATSTON, S FAY, J LLEWELLYN, HJ MROSE, HE RUBENS, JR AF BUCKLEY, KM SCHAEFER, CM GREENE, R AGATSTON, S FAY, J LLEWELLYN, HJ MROSE, HE RUBENS, JR TI DETECTION OF BULLOUS LUNG-DISEASE - CONVENTIONAL RADIOGRAPHY VS DIGITAL STORAGE PHOSPHOR RADIOGRAPHY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID EDGE ENHANCEMENT; CHEST RADIOGRAPHY; ROC; RESOLUTION AB The detection of fine linear contours and altered aeration are requirements for the radiologic diagnosis of bullous lung disease and are severe measures of the spatial and contrast resolution of chest imaging systems. We compared plain film radiography with five postprocessing algorithms of storage phosphor digital radiography (2144 x 1744 x 10 bit matrix with 0.2-mm pixel size) in the detection of CT-proved bullous lung disease (35 patients and 25 normal control subjects). Receiver-operating-characteristic analysis of 2160 observations by six interpreters was done to evaluate the observers' performance. By analysis of variance (p < .05), we found that the default digital algorithm and the three edge-enhancing algorithms of high and medium frequencies performed less well than plain films did, but the differences fell short of statistical significance. Gray-scale reversal was the only digital algorithm that performed significantly less well than plain films did. We conclude that any difference between digital algorithms and plain films in the detection of bullous lung disease were too small to be detected in this study. Any difference between the two methods in providing clinically important, diagnostic information is likely to be insignificant. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. HANOVER MED SCH,DEPT RADIOL,W-3000 HANNOVER 61,GERMANY. NR 20 TC 14 Z9 14 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 MAR PY 1991 VL 156 IS 3 BP 467 EP 470 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY478 UT WOS:A1991EY47800004 PM 1899739 ER PT J AU CHEW, FS SMITH, PL BARBORIAK, D AF CHEW, FS SMITH, PL BARBORIAK, D TI CANDIDAL SPLENIC ABSCESSES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 3 TC 10 Z9 10 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 MAR PY 1991 VL 156 IS 3 BP 474 EP 474 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY478 UT WOS:A1991EY47800006 PM 1899741 ER PT J AU CHEW, FS AF CHEW, FS TI FATE OF MANUSCRIPTS REJECTED FOR PUBLICATION IN THE AJR SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID ABSTRACT FORM; RADIOLOGY; CITATIONS; JOURNALS AB The fate of rejected manuscripts that were originally submitted to the American Journal of Roentgenology (AJR) during the first 5 months of 1986 was investigated to learn whether, when, and where they had been published. AJR, a peer-reviewed journal of diagnostic radiology with a circulation of over 21,000, annually publishes about 500 papers and receives over 11,500 citations. MEDLINE searches conducted 45 to 54 months after the dates of rejection by AJR located 162 (64%) published papers out of a consecutive series of 254 manuscripts rejected by AJR, including 69% of the rejected major papers and 62% of the rejected case reports. The papers had been published in 30 different radiologic and 27 different nonradiologic journals. Most of these journals published fewer papers, had smaller circulations, and had lower impact factors (a ratio of citations received to papers published) than AJR does. The mean time lapse between rejection by AJR and publication in other journals was 15 months. The delay in publication was greater for papers published in nonradiologic and foreign journals than for papers published in radiologic and American journals. The results of this study indicate that rejection of a manuscript by a peer-reviewed journal such as AJR delays but by no means precludes publication. At least 82% of the major papers and 70% of the case reports that are submitted to AJR are eventually published, either in AJR or elsewhere. Because a scientific paper represents not only many hours of writing and manuscript preparation but also a great investment of research time and resources, authors are reluctant to abandon rejected manuscripts. In the majority of cases, submission to other journals gains acceptance and publication. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. OI Chew, Felix/0000-0003-2711-2013 NR 22 TC 41 Z9 41 U1 0 U2 2 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 MAR PY 1991 VL 156 IS 3 BP 627 EP 632 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA EY478 UT WOS:A1991EY47800038 PM 1899764 ER PT J AU BELL, DA AF BELL, DA TI MUCINOUS ADENOFIBROMAS OF THE OVARY - A REPORT OF 10 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; MUCINOUS; ADENOFIBROMA ID BORDERLINE; BENIGN; TUMORS AB Mucinous epithelium is the most uncommon type identified in ovarian adenofibromas. Because of the rarity of mucinous adenofibromas and the presence of cytologic atypia in some, these neoplasms may be mistaken for low-grade metastatic adenocarcinoma. The clinicopathologic features of 10 mucinous adenofibromas are reviewed. They occurred in women 24 to 76 (mean, 51) years of age, were unilateral, and ranged in diameter from 1 to 25 cm. Seven tumors were classified as benign, containing glands lined by a single layer of mucin-containing columnar cells. Three tumors that contained crowded glands lined by mucin-containing cells with mild to moderate nuclear atypia, nuclear stratification of up to three cells in thickness, and focal tufting were classified as benign with epithelial atypia. Most women had a hysterectomy and bilatal salpingo-oophorectomy. Follow-up information was available on six women, who were alive and well from 6 to 126 (mean 41) months after diagnosis. The identification of mucinous glands in typical fibromatous stroma should allow the distinction of these benign neoplasms from metastatic carcinomas. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BELL, DA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 13 TC 11 Z9 12 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 MAR PY 1991 VL 15 IS 3 BP 227 EP 232 DI 10.1097/00000478-199103000-00003 PG 6 WC Pathology; Surgery SC Pathology; Surgery GA EY998 UT WOS:A1991EY99800003 PM 1996729 ER PT J AU FERRY, JA SKLAR, J ZUKERBERG, LR HARRIS, NL AF FERRY, JA SKLAR, J ZUKERBERG, LR HARRIS, NL TI NASAL LYMPHOMA - A CLINCO-PATHOLOGICAL STUDY WITH IMMUNOPHENOTYPIC AND GENOTYPIC ANALYSIS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE NOSE; MALIGNANT LYMPHOMA; GENE REARRANGEMENT; NASAL LYMPHOMA; ANGIOCENTRIC LYMPHOMA ID LETHAL MIDLINE GRANULOMA; T-CELL LYMPHOMA; NON-HODGKINS LYMPHOMA; MALIGNANT-LYMPHOMAS; POLYMORPHIC RETICULOSIS; HEMOPHAGOCYTIC SYNDROME; GENE REARRANGEMENTS; WALDEYERS RING; SINUSES; CAVITY AB We studied 13 cases of malignant lymphoma involving the nasal cavity, in six men and seven women, from 27 to 92 years of age (mean, 56 years; median, 55 years). All lymphomas had a diffuse pattern, with 10 of large-cell type (six immunoblastic polymorphous, one immunoblastic, three large cleaved cell), one of mixed small- and large-cell type and one of small cleaved-cell type. One case could not be subclassified. Angioinvasion and prominent necrosis were seen in 10 cases. Pseudoepitheliomatous hyperplasia of the overlying epithelium was present in five cases. Immunohistochemical studies on frozen or paraffin sections in nine cases revealed that the atypical cells were T cells in four cases (CD8+ in two cases) and B cells with monotypic immunoglobulin in two cases. In three cases, the findings were suggestive but not diagnostic of T lineage. Genotypic analysis in one of two cases of T-cell lymphoma revealed clonal rearrangement of the genes for beta and gamma chains of the T-cell receptor. Patients were treated initially with local radiation therapy (10 cases) or with radiation and chemotherapy (three cases). Eight patients (62%) had no relapse and were free of disease between 9 months and 23 years (mean, 6 years 5 months; median 2 years 1 month) after diagnosis. Five patients developed recurrent disease, three of whom were successfully salvaged. One patient was alive with tumor at the time of last follow-up and one died with tumor. Among cases of malignant lymphoma presenting with involvement of the nasal cavity, we find a high proportion of angioinvasive, diffuse large-cell lymphomas, with a predominance of T-cell type, and a relatively good prognosis when treated with radiation therapy. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 45 TC 100 Z9 102 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 MAR PY 1991 VL 15 IS 3 BP 268 EP 279 DI 10.1097/00000478-199103000-00007 PG 12 WC Pathology; Surgery SC Pathology; Surgery GA EY998 UT WOS:A1991EY99800007 PM 1996731 ER PT J AU BARNHILL, RL AF BARNHILL, RL TI CELLULAR NEUROTHEKEOMA - REPLY SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Letter RP BARNHILL, RL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV DERMATOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1991 VL 15 IS 3 BP 311 EP 311 DI 10.1097/00000478-199103000-00015 PG 1 WC Pathology; Surgery SC Pathology; Surgery GA EY998 UT WOS:A1991EY99800015 ER PT J AU FLETCHER, EC GOODNIGHTWHITE, S MUNAFO, D MILLER, CC LUCKETT, R QIAN, W AF FLETCHER, EC GOODNIGHTWHITE, S MUNAFO, D MILLER, CC LUCKETT, R QIAN, W TI RATE OF OXYHEMOGLOBIN DESATURATION IN OBSTRUCTIVE VERSUS NONOBSTRUCTIVE APNEA SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID SATURATION; SLEEP AB Preapneic thoracic gas volume (Vtg), arterial saturation (Sa(O2)), and mixed venous oxygen saturation (SvBAR(O2)), have been shown to influence the rate of Sa(O2) fall (dSa(O2)/dt) during apnea. We asked the following question: does tissue oxygen consumption (tV(O2)) affect the dSa(O2)/dt during apnea? We attempted to answer this question by comparing dSa(O2)/dt during obstructive apneas (high tVO2) with dSa(O2)/dt during nonobstructive apneas (low tVO2) in six adult baboons. Fiberoptic central venous and arterial catheters were used for continuous monitoring of SvBAR(O2), Sa(O2), and cardiac output. A sapphire-bearing turbine monitored minute ventilation and airflow cessation. A Respitrace(R) and esophageal pressures were used to assess relative differences in Vtg. Obstructive apneas (30, 45, and 60-s) were created by clamping an indwelling cuffed endotracheal tube at end-expiration. Nonobstructive apneas were created by paralyzing the animals with atracurium and interrupting ventillation for periods equivalent to those of the obstructed apneas. The ventillator was adjusted to duplicate the respiratory rate, tidal volume, and relative Vtg of the spontaneously breathing animal. Mean tVO2 during spontaneous breathing was 110 ml/min (Fick method) and decreased to 90 ml/min during paralysis (p < 0.05). The dSa(O2)/dt for the three apnea durations (mean, all animals), obstructive versus nonobstructed were: 0.85 and 0.74%/s (n = 6), 0.87 and 0.75%/s (n = 6), and 0.60 and 0.48%/s (n = 4), respectively. The dSa(O2)/dt was significantly lower during the nonobstructive apneas. We conclude that differences in VO2 during apnea may affect the dSa(O2)/dt and that for the same duration apnea, central apneas may show less desaturation than obstructive apneas where vigorous muscular efforts at overcoming obstruction are common. C1 BAYLOR UNIV,HOUSTON,TX 77030. RP FLETCHER, EC (reprint author), HOUSTON VET AFFAIRS MED CTR,DEPT MED 3I,PULM DIS SECT,UAMC,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 10 TC 8 Z9 9 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD MAR PY 1991 VL 143 IS 3 BP 657 EP 660 PG 4 WC Respiratory System SC Respiratory System GA FA931 UT WOS:A1991FA93100034 PM 2001079 ER PT J AU BEHRINGER, EC AF BEHRINGER, EC TI THE CARE AND CLEANING OF THE FLEXIBLE FIBEROPTIC BRONCHOSCOPE SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP BEHRINGER, EC (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02115, USA. 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 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 35 EP 42 PG 8 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200005 ER PT J AU KRAFT, M AF KRAFT, M TI ANCILLARY FIBEROPTIC EQUIPMENT SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP KRAFT, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 43 EP 51 PG 9 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200006 ER PT J AU ROBERTS, JT AF ROBERTS, JT TI ANATOMY AND PATIENT POSITIONING FOR FIBEROPTIC LARYNGOSCOPY SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP ROBERTS, JT (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. 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 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 53 EP 61 PG 9 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200007 ER PT J AU SHORTEN, GD ROBERTS, JT AF SHORTEN, GD ROBERTS, JT TI THE PREDICTION OF DIFFICULT INTUBATION SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP SHORTEN, GD (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. 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 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 63 EP 67 PG 5 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200008 ER PT J AU HURFORD, WE AF HURFORD, WE TI FIBEROPTIC ENDOBRONCHIAL INTUBATION SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP HURFORD, WE (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 97 EP 109 PG 13 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200011 ER PT J AU NOVISKI, N TODRES, ID AF NOVISKI, N TODRES, ID TI FIBEROPTIC BRONCHOSCOPY IN THE PEDIATRIC-PATIENT SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP NOVISKI, N (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 163 EP 174 PG 12 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200014 ER PT J AU SHORTEN, GD ROBERTS, JT AF SHORTEN, GD ROBERTS, JT TI SOME APPLICATIONS OF FIBEROPTICS IN ANESTHESIA SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Article RP SHORTEN, GD (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 7 Z9 7 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP 187 EP 193 PG 7 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200016 ER PT J AU ROBERTS, JT AF ROBERTS, JT TI FIBEROPTICS IN ANESTHESIA - PREFACE SO ANESTHESIOLOGY CLINICS OF NORTH AMERICA LA English DT Editorial Material RP ROBERTS, JT (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8537 J9 ANESTHESIOL CLIN N A JI Anesthesiol. Clin. N. Am. PD MAR PY 1991 VL 9 IS 1 BP UR13 EP UR14 PG 2 WC Anesthesiology SC Anesthesiology GA FH032 UT WOS:A1991FH03200002 ER PT J AU TRUCKSIS, M HOOPER, DC WOLFSON, JS AF TRUCKSIS, M HOOPER, DC WOLFSON, JS TI EMERGING RESISTANCE TO FLUOROQUINOLONES IN STAPHYLOCOCCI - AN ALERT SO ANNALS OF INTERNAL MEDICINE LA English DT Editorial Material DE CIPROFLOXACIN; NORFLOXACIN; STAPHYLOCOCCUS-AUREUS; DRUG RESISTANCE, MICROBIAL; FLUOROQUINOLONES ID ANTIMICROBIAL AGENTS; AUREUS ENDOCARDITIS; INVITRO ACTIVITY; CIPROFLOXACIN; INFECTIONS; QUINOLONES; THERAPY AB The use of fluoroquinolones as oral therapeutic agents for staphylococcal infections, problems with bacterial resistance, and approaches to suppression of resistance are discussed. Although they are particularly effective for treatment of gram-negative bacillary infections, quinolones, including ciprofloxacin and pefloxacin in limited experience, have been effective in treating staphylococcal infections. Clinical failures have occurred, however, in association with emergence of resistance or poor delivery of drug to the infected site. Recent surveys of drug susceptibility reveal substantial increases in resistance among methicillin-resistant and to a lesser extent methicillin-susceptible Staphylococcus aureus. Some strains were isolated from patients not receiving quinolone therapy. Resistance occurs by mutation in chromosomal genes, by mechanisms not yet defined, but probably involving either alteration of the target enzyme DNA gyrase or changes in drug accumulation, or both. Strategies to suppress emergence of fluoroquinolone resistance should be evaluated, including prudent drug use, use of combination drug therapy, and development of fluoroquinolone derivatives that have a higher therapeutic index and are less prone to select resistant organisms. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,32 FRUIT ST,BOSTON,MA 02114. FU NIAID NIH HHS [AI07061, R01 AI23988] NR 26 TC 86 Z9 86 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 1 PY 1991 VL 114 IS 5 BP 424 EP 426 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA EZ174 UT WOS:A1991EZ17400012 PM 1992885 ER PT J AU LUQUE, FA FURNEAUX, HM FERZIGER, R ROSENBLUM, MK WRAY, SH SCHOLD, SC GLANTZ, MJ JAECKLE, KA BIRAN, H LESSER, M PAULSEN, WA RIVER, ME POSNER, JB AF LUQUE, FA FURNEAUX, HM FERZIGER, R ROSENBLUM, MK WRAY, SH SCHOLD, SC GLANTZ, MJ JAECKLE, KA BIRAN, H LESSER, M PAULSEN, WA RIVER, ME POSNER, JB TI ANTI-RI - AN ANTIBODY ASSOCIATED WITH PARANEOPLASTIC OPSOCLONUS AND BREAST-CANCER SO ANNALS OF NEUROLOGY LA English DT Article ID NEOPLASTIC CEREBELLAR DEGENERATION; EATON MYASTHENIC SYNDROME; CELL LUNG-CANCER; MYOCLONUS SYNDROME; CARCINOMA; AUTOANTIBODIES; INDIVIDUALS; DISORDERS; PROTEINS; NERVE AB The serum and cerebrospinal fluid (CSF) of 8 women with ataxia, 6 of whom also had eye movement abnormalities believed to be opsoclonus, were found to contain a highly specific antineuronal antibody we call anti-Ri. Seven of the 8 women also had or developed cancer: carcinoma of the breast in 5, adenocarcinoma in an axillary lymph node in 1, and carcinoma of the fallopian tube in 1. Four patients presented with the neurological disorder; the cancer was diagnosed first in the other 4. Immunohistochemical studies using serum or CSF from all 8 patients revealed a highly specific antibody interaction with central nervous system neuronal nuclei but not with glial or other cells; the titer ranged from 1:5,000 to 1:320,000 in serum and from 1:2,000 to 1:16,000 in CSF. Biotinylated IgG from the patients' serum reacted with the tumors of 3 of 4 patients with anti-Ri antibody but not with breast cancers from patients without anti-Ri antibody. Immunoblots against cerebral cortex neuronal extracts identified protein antigens of 55-kd and 80-kd relative molecular mass. Serum titers by immunoblot ranged from 1:500 to more than 1:40,000 and CSF titers, from 1:10 to 1:2,000. The relative amount of anti-Ri was always higher in CSF than in serum. The antibody was not present in sera from normal individuals; patients with breast cancer without opsoclonus; other patients with opsoclonus; or patients with other paraneoplastic syndromes related to breast, ovarian, or small-cell lung cancer. We conclude that the presence of anti-Ri antibody identifies a subset of patients with paraneoplastic ataxia and eye movement disorders (opsoclonus) who usually suffer from breast or other gynecological cancer; the antibody when present is a useful marker for an underlying malignancy. C1 MEM SLOAN KETTERING CANC CTR,GEORGE C COTZIAS LAB NEUROONCOL,NEW YORK,NY 10021. SOROKA MED CTR,DEPT ONCOL,IL-84101 BEER SHEVA,ISRAEL. CORNELL UNIV,MED CTR,COLL MED,DEPT NEUROL & NEUROSCI,NEW YORK,NY 10021. E TENNESSEE NEUROL ASSOCIATES,KNOXVILLE,TN. SALIA MED CLIN INC,VISALIA,CA. DUKE UNIV,MED CTR,DEPT NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MEM SLOAN KETTERING CANC CTR,DEPT NEUROL,NEW YORK,NY 10021. UNIV UTAH,DEPT NEUROL,SALT LAKE CITY,UT 84112. MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,NEW YORK,NY 10021. FU NINDS NIH HHS [NS26064] NR 44 TC 272 Z9 274 U1 1 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 1991 VL 29 IS 3 BP 241 EP 251 DI 10.1002/ana.410290303 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FB415 UT WOS:A1991FB41500002 PM 2042940 ER PT J AU FRISOLI, JK HEFETZ, Y DEUTSCH, TF AF FRISOLI, JK HEFETZ, Y DEUTSCH, TF TI TIME-RESOLVED UV ABSORPTION OF POLYIMIDE - IMPLICATIONS FOR LASER ABLATION SO APPLIED PHYSICS B-PHOTOPHYSICS AND LASER CHEMISTRY LA English DT Article ID POLYMERS AB The 355-nm transient absorption of polyimide thin films has been measured following excitation with subablative, 24-ps long, 355-nm laser pulses. The 355-nm absorption increases by 25% following 355-nm, 20 mJ/cm2 excitation and recovers with a fast time constant almost-equal-to 34 ps, and a slow time constant which is much longer than 6ns. The data are fitted by a three-level rate equation model incorporating the temperature dependence of the ground state absorption coefficient. The fast component is attributed to the decay of S1 and the slow component results from increased ground state absorption caused by a laser-induced temperature rise. The nonlinear intensity dependence is attributed to excited state (S1) absorption. These results indicate the importance of considering the dynamic absorption in modelling ablation. RP FRISOLI, JK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 13 TC 43 Z9 43 U1 0 U2 3 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-7269 J9 APPL PHYS B-PHOTO PD MAR PY 1991 VL 52 IS 3 BP 168 EP 172 PG 5 WC Physics, Applied SC Physics GA EZ745 UT WOS:A1991EZ74500004 ER PT J AU WALSH, JT DEUTSCH, TF AF WALSH, JT DEUTSCH, TF TI MEASUREMENT OF ER - YAG LASER ABLATION PLUME DYNAMICS SO APPLIED PHYSICS B-PHOTOPHYSICS AND LASER CHEMISTRY LA English DT Article ID TISSUE; SURGERY; CORNEA AB The dynamics of tissue ablation using an Er:YAG laser were studied using flash photography and optical pump-probe techniques. Both normal-spiking-mode and Q-switched Er:YAG laser radiation were used to study the ablation of skin and bone. Time-resolved photographs of the ablation plume were obtained using a microscope-mounted camera together with pulsed illumination from an excimer-pumped dye laser. The velocity of the plume front, obtained from the photographs, was approximately 1400 m/s. The same velocity was also measured using an optical pump-probe technique. Both techniques indicate that material removal occurred after the end of the 90-ns-long Q-switched laser pulse and that each micropulse in the normal-spiking-mode pulse train was capable of ablating and rapidly ejecting tissue. C1 NORTHWESTERN UNIV,DEPT BIOMED ENGN,2145 SHERIDAN RD,EVANSTON,IL 60208. RP WALSH, JT (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA 02114, USA. RI Walsh, Joseph/B-7636-2009 NR 31 TC 40 Z9 41 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0721-7269 J9 APPL PHYS B-PHOTO PD MAR PY 1991 VL 52 IS 3 BP 217 EP 224 PG 8 WC Physics, Applied SC Physics GA EZ745 UT WOS:A1991EZ74500012 ER PT J AU HUSAIN, SS AF HUSAIN, SS TI A SINGLE-STEP SEPARATION OF THE ONE-CHAIN AND 2-CHAIN FORMS OF TISSUE PLASMINOGEN-ACTIVATOR SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Note ID N-GLYCOSYLATION; PURIFICATION; MELANOMA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP HUSAIN, SS (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL38178] NR 19 TC 11 Z9 11 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD MAR PY 1991 VL 285 IS 2 BP 373 EP 376 DI 10.1016/0003-9861(91)90375-S PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FA647 UT WOS:A1991FA64700027 PM 1910280 ER PT J AU STERN, RS LANGE, R AF STERN, RS LANGE, R TI OUTCOMES OF PREGNANCIES AMONG WOMEN AND PARTNERS OF MEN WITH A HISTORY OF EXPOSURE TO METHOXSALEN PHOTOCHEMOTHERAPY (PUVA) FOR THE TREATMENT OF PSORIASIS SO ARCHIVES OF DERMATOLOGY LA English DT Article ID LONGWAVE ULTRAVIOLET-LIGHT; CYCLOSPORIN-A; 8-METHOXYPSORALEN; MALFORMATIONS; RAT AB Because oral methoxsalen and UV-A radiation (PUVA) therapy is mutagenic, concern exists about the potential for teratogenic effects resulting from the use of this therapy at the time of conception and during pregnancy. After 12.8 years of prospective study, we documented the pregnancy outcomes among 1380 patients (892 men and 488 women) who received PUVA treatments. Ninety-four men reported 167 pregnancies in their partners, and 93 women reported 159 pregnancies. For 34% of pregnancies among partners of male patients, the man received PUVA therapy near the time of conception. Nineteen percent of female patients reported exposure to PUVA at the time of conception or during pregnancy. Induced and spontaneous abortions were reported as the outcome of pregnancy more often by female than by male patients (12% vs 30%). Two congenital malformations and two stillbirths occurred, an incidence not significantly different from that expected for the general population. Although the power of our study to detect an increase in the risk of specific defects is limited, our data show no evidence to suggest that PUVA is a potent teratogen. Still, because PUVA is mutagenic, we believe it prudent for patients to avoid PUVA treatment during pregnancy whenever practical. C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. BETH ISRAEL HOSP, CHARLES A DANA RES INST, BOSTON, MA 02215 USA. HARVARD UNIV, SCH PUBL HLTH, CTR ANAL HLTH PRACTICE, BOSTON, MA 02115 USA. RP STERN, RS (reprint author), BETH ISRAEL HOSP, DEPT DERMATOL, 330 BROOKLINE AVE, BOSTON, MA 02215 USA. NR 20 TC 12 Z9 13 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-987X EI 1538-3652 J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1991 VL 127 IS 3 BP 347 EP 350 DI 10.1001/archderm.127.3.347 PG 4 WC Dermatology SC Dermatology GA FA772 UT WOS:A1991FA77200006 ER PT J AU KAYE, ET LEVIN, JA BLANK, IH ARNDT, KA ANDERSON, RR AF KAYE, ET LEVIN, JA BLANK, IH ARNDT, KA ANDERSON, RR TI EFFICIENCY OF OPAQUE PHOTOPROTECTIVE AGENTS IN THE VISIBLE-LIGHT RANGE SO ARCHIVES OF DERMATOLOGY LA English DT Article ID PHOTORADIATION THERAPY; HUMAN-SKIN; PROTECTION; TUMORS; CANCER AB "Opaque" physical sunscreens are important for photoprotection of individuals with visible light and UV-A photosensitivity such as those with porphyria, drug photoallergy, and polymorphous light eruption. Diffuse spectral transmittance of various thicknesses of opaque sunscreen formulations were measured from 350- to 800-nm range using a spectrophotometer equipped with an integrating sphere. Transmission through 20% zinc oxide paste was high and decreased minimally despite large increases in the sunscreen layer thickness. Adding a visible light absorber such as iron oxide to scattering sunscreens, however, substantially lowered transmittance below that predicted by the product of the transmittances for each component alone. Opaque sunscreens protected against hematoporphyrin derivative photosensitization of albino guinea pig skin; these results were quantitatively consistent with the in vitro findings. Poor photoprotection against visible light is obtained with white paste sunscreens, even if thick layers are applied. The addition of pigments to such sunscreens, however, greatly enhances photoprotection and cosmetic acceptability. C1 MASSACHUSETTS GEN HOSP,WELLMAN LAB PHOTOMED,DEPT DERMATOL,WELLMAN-2,BOSTON,MA 02114. BETH ISRAEL HOSP,DEPT DERMATOL,BOSTON,MA 02215. FU NIAMS NIH HHS [R01-AR25395] NR 17 TC 23 Z9 23 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1991 VL 127 IS 3 BP 351 EP 355 DI 10.1001/archderm.127.3.351 PG 5 WC Dermatology SC Dermatology GA FA772 UT WOS:A1991FA77200007 PM 1998365 ER PT J AU MURPHY, JM OLIVIER, DC MONSON, RR SOBOL, AM FEDERMAN, EB LEIGHTON, AH AF MURPHY, JM OLIVIER, DC MONSON, RR SOBOL, AM FEDERMAN, EB LEIGHTON, AH TI DEPRESSION AND ANXIETY IN RELATION TO SOCIAL-STATUS - A PROSPECTIVE EPIDEMIOLOGIC-STUDY SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID STIRLING COUNTY; AFFECTIVE-DISORDERS; GENERAL-POPULATION; SCHIZOPHRENIA; MORTALITY; RISK; DIAGNOSIS; SURVIVAL AB Longitudinal research in Stirling County, Atlantic Canada, indicated that during the 1950s and 1960s the prevalence of depression was significantly and persistently higher in the "low" socioeconomic status population than at other socioeconomic status levels. Anxiety was found to show a less clear picture. Incidence of depression after the study started was also higher among those who were initially in the low socioeconomic status group, supporting the view that the stress of poverty may be causally related to depression. There was also a trend for prior depression to be associated with subsequent downward social mobility, supporting the view that the concentration of depressed people at the lower end of the social hierarchy may result from handicapping aspects of the illness. Neither of these trends was statistically significant. More striking was evidence that, irrespective of socioeconomic status, depression carried a substantial risk for poor clinical course and outcome. Both depression and poverty tended to be chronic, and, accordingly, their association at the end of the study was influenced by their association at its beginning. The stability of the relationship between poverty and depression warrants the attention of caregivers and policymakers and raises new questions about strategies for the study of causal sequences. C1 HARVARD UNIV,SCH PUBL HLTH,INSTRUCTIONAL COMP FACIL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. DALHOUSIE UNIV,DEPT PSYCHIAT,HALIFAX B3H 4H2,NS,CANADA. DALHOUSIE UNIV,DEPT COMMUNITY HLTH & EPIDEMIOL,HALIFAX B3H 4H2,NS,CANADA. RP MURPHY, JM (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PSYCHIAT EPIDEMIOL UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NCRR NIH HHS [S 07 RR05486 27]; NIMH NIH HHS [MH39576] NR 47 TC 140 Z9 144 U1 1 U2 14 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 MAR PY 1991 VL 48 IS 3 BP 223 EP 229 PG 7 WC Psychiatry SC Psychiatry GA FA690 UT WOS:A1991FA69000003 PM 1996918 ER PT J AU AUSTIN, CP LESSELL, S AF AUSTIN, CP LESSELL, S TI HORNERS SYNDROME FROM HYPOTHALAMIC INFARCTION SO ARCHIVES OF NEUROLOGY LA English DT Article AB We report a case of Horner's syndrome due to ipsilateral posterior hypothalamic infarction, occurring in the absence of other signs of hypothalamic dysfunction. Associated symptoms of contralateral faciobrachial weakness and dysarthria correlated with the extension of the infarct into the posterior limb of the internal capsule seen by magnetic resonance imaging. The likely vascular anatomy of this lesion is discussed. C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 14 TC 7 Z9 7 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 MAR PY 1991 VL 48 IS 3 BP 332 EP 334 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA FA667 UT WOS:A1991FA66700019 PM 2001193 ER PT J AU DUKER, JS SIVALINGAM, A BROWN, GC REBER, R AF DUKER, JS SIVALINGAM, A BROWN, GC REBER, R TI A PROSPECTIVE-STUDY OF ACUTE CENTRAL RETINAL ARTERY OBSTRUCTION - THE INCIDENCE OF SECONDARY OCULAR NEOVASCULARIZATION SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID OPTIC DISK; IRIS AB We conducted a prospective study to determine the incidence of ocular neovascularization following acute central retinal artery obstruction. Only patients initially evaluated within 7 days of visual loss were eligible. Any patient with preexisting ocular neovascularization or clinical evidence of the ocular ischemic syndrome noted at the initial evaluation was excluded. During the 18-month study, 33 consecutive patients were enrolled. Six patients subsequently developed neovascularization of the iris, an incidence of 18.2%. In these six patients, neovascularization of the iris appeared as early as 12 days to as late as 15 weeks following the artery obstructions. Five of the six patients (15.2% of the total) later developed neovascular glaucoma. Another patient in this series developed neovascularization of the optic disc without neovascularization of the iris, an incidence of 3.0%. Only two of the seven patients with ocular neovascularization had ipsilateral hemodynamically significant carotid artery disease as determined by noninvasive carotid artery testing. This study confirms results of previous retrospective studies that the incidence of ocular neovascularization after central retinal artery obstruction is higher than commonly thought. It also shows that, in the majority of cases, carotid artery disease is not responsible for the neovascularization seen after central retinal artery obstruction. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA ASSOCIATES,EYE RES INST,BOSTON,MA 02114. THOMAS JEFFERSON UNIV,WILLS EYE HOSP,RETINA VASC UNIT,PHILADELPHIA,PA 19107. NR 15 TC 44 Z9 45 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1991 VL 109 IS 3 BP 339 EP 342 PG 4 WC Ophthalmology SC Ophthalmology GA FB463 UT WOS:A1991FB46300030 PM 1706177 ER PT J AU PHAN, TM FOSTER, CS SHAW, CD ZAGACHIN, LM COLVIN, RB AF PHAN, TM FOSTER, CS SHAW, CD ZAGACHIN, LM COLVIN, RB TI TOPICAL FIBRONECTIN IN AN ALKALI BURN MODEL OF CORNEAL ULCERATION IN RABBITS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; CONJUNCTIVAL TRANSPLANTATION; PREVENTION; SURFACE; WOUNDS; PERFORATION; DEGRADATION; MIGRATION; ULCERS; BLOOD AB We studied the effect of topical fibronectin on epithelial wound healing and ulceration in alkali-burned rabbit corneas. After the first 56 hours, fibronectin accelerated complete surface reepithelialization to 4.3 +/- 2.3 days. Control alkali-burned corneas treated with phosphate-buffered saline or albumin did not resurface for 6.7 +/- 3.7 days and 6.2 +/- 2.5 days, respectively. When recurrent epithelial defects occurred, the time required for healing was also significantly accelerated by fibronectin treatment. Corneal ulceration developed in 25 of 28 and 15 of 18 saline and albumin-treated control eyes, respectively; only nine of 18 fibronectin-treated eyes ultimately ulcerated. Immunohistologic studies showed that the initially deposited fibronectin-fibrinogen matrix on the surface of burned corneas had disintegrated by 72 to 96 hours after wounding, corresponding clinically to the time of secondary epithelial breakdown. A prominent fibronectin-fibrinogen matrix remained on the surface of fibronectin-treated corneas, presumably aiding surface reepithelialization and decreasing corneal ulceration. C1 MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,COX 5,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,HILLES IMMUNOL LAB,BOSTON,MA 02114. FU NCI NIH HHS [R37-CA-20822] NR 43 TC 16 Z9 18 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAR PY 1991 VL 109 IS 3 BP 414 EP 419 PG 6 WC Ophthalmology SC Ophthalmology GA FB463 UT WOS:A1991FB46300046 PM 2003805 ER PT J AU MOSKOWITZ, MA MACFARLANE, R TASDEMIROGLU, E WEI, EP KONTOS, HA AF MOSKOWITZ, MA MACFARLANE, R TASDEMIROGLU, E WEI, EP KONTOS, HA TI NEUROEFFECTOR FUNCTIONS OF SENSORY NERVE-FIBERS IN THE CEREBRAL-CIRCULATION AFTER GLOBAL CEREBRAL-ISCHEMIA SO ARZNEIMITTEL-FORSCHUNG/DRUG RESEARCH LA English DT Article; Proceedings Paper CT 24TH DEIDESHEIMER COLLOQUIUM ON ACUTE CEREBRAL ISCHEMIA : PATHOGENESIS AND THERAPY CY APR 28-29, 1990 CL DEIDESHEIM, FED REP GER DE CAPSAICIN; CEREBRAL BLOOD FLOW, POSTISCHEMIC; CORTICAL HYPEREMIA; ISCHEMIA, CEREBRAL, NEUROEFFECTOR MECHANISMS; TRIGEMINAL NERVE ID SUBSTANCE-P; CAROTID ENDARTERECTOMY; VASCULAR HEADACHES; BLOOD-FLOW; MECHANISMS; HYPERTENSION; ADENOSINE; SEIZURES; BRAIN; CATS AB The importance of trigeminal neuroeffector mechanisms in the regulation of postischemic cerebral blood flow (CBF) was evaluated in cats subjected to chronic unilateral denervation of cortical sensory nerve fibers by trigeminal ganglionectomy or by the topical application of capsaicin to a cortical branch of the middle cerebral artery. CBF was determined using isotopically labeled microspheres before and at intervals after reperfusion following 10 min of global cerebral ischemia induced by four vessel occlusion combined with systemic hypotension. Postocclusive hyperemia 30 min after reperfusion in cortical gray matter ipsilateral to the side of denervation was attenuated by up to 58 % (176 vs. 91 ml/100 g per min; p < 0.05), but resting CBF, the duration of hyperemia, and the cerebrovascular response to hypercapnia were unaffected. These data underline the influence of neurogenic mechanisms in the regulation of postischemic CBF. Blockade of this axon reflex-like mechanism may reduce the morbidity associated with several hyperperfusion syndromes. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROSURG SERV,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV CARDIOL,RICHMOND,VA 23298. RP MOSKOWITZ, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 26361, NS 21558] NR 26 TC 2 Z9 2 U1 0 U2 0 PU ECV-EDITIO CANTOR VERLAG MEDIZIN NATURWISSENSCHAFTEN PI AULENDORF PA BANDELSTOCKWEG 20, POSTFACH 1255, D-88322 AULENDORF, GERMANY SN 0004-4172 J9 ARZNEIMITTEL-FORSCH JI Arzneimittelforschung PD MAR PY 1991 VL 41-1 IS 3A BP 315 EP 318 PG 4 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA FH709 UT WOS:A1991FH70900009 PM 1859501 ER PT J AU MANSCHRECK, TC MAHER, BA AF MANSCHRECK, TC MAHER, BA TI APPROXIMATIONS TO A NEUROPSYCHOLOGICAL MODEL OF SCHIZOPHRENIA SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HARVARD UNIV,DEPT PSYCHOL,CAMBRIDGE,MA 02193. RP MANSCHRECK, TC (reprint author), DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HANOVER,NH 03756, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD MAR PY 1991 VL 14 IS 1 BP 36 EP 36 PG 1 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA FC750 UT WOS:A1991FC75000020 ER PT J AU STRITTMATTER, SM FISHMAN, MC AF STRITTMATTER, SM FISHMAN, MC TI THE NEURONAL GROWTH CONE AS A SPECIALIZED TRANSDUCTION SYSTEM SO BIOESSAYS LA English DT Review ID CELL-ADHESION MOLECULES; PROTEIN-KINASE-C; FETAL-RAT-BRAIN; EXTRACELLULAR-MATRIX PROTEIN; CALMODULIN-BINDING PROTEIN; GAP-43 GENE-EXPRESSION; CENTRAL NERVOUS-SYSTEM; IMMUNOGLOBULIN SUPERFAMILY; NEURITE EXTENSION; DEVELOPMENTAL REGULATION AB Neuronal growth and remodelling are guided by both intracellular gene programs and extracellular stimuli. The growth cone is one site where the effects of these extrinsic and intrinsic factors converge upon the mechanical determinants of cell shape. We review the growth cone as a transduction device, converting extracellular signals into mechanical forces. A variety of soluble, extracellular matrix and membrane bound molecules control growth cone behavior. In addition, GAP-43 is discussed as a possible component of the intraneuronal gene program which modulates growth cone activity. The GTP-binding protein, G0, is a major growth cone membrane protein that may transduce signals not only from outside the cell, but from within as well. This may provide a molecular site in the growth cone for the coordination of a genetic growth program with environmental signals. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STRITTMATTER, SM (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,DEV BIOL LAB,BOSTON,MA 02114, USA. OI Strittmatter, Stephen/0000-0001-8188-3092 NR 127 TC 69 Z9 69 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD MAR PY 1991 VL 13 IS 3 BP 127 EP 134 DI 10.1002/bies.950130306 PG 8 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA FD385 UT WOS:A1991FD38500005 PM 1831353 ER PT J AU KANAKURA, Y CANNISTRA, SA BROWN, CB NAKAMURA, M SEELIG, GF PROSISE, WW HAWKINS, JC KAUSHANSKY, K GRIFFIN, JD AF KANAKURA, Y CANNISTRA, SA BROWN, CB NAKAMURA, M SEELIG, GF PROSISE, WW HAWKINS, JC KAUSHANSKY, K GRIFFIN, JD TI IDENTIFICATION OF FUNCTIONALLY DISTINCT DOMAINS OF HUMAN GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR USING MONOCLONAL-ANTIBODIES SO BLOOD LA English DT Article ID GROWTH-FACTORS; EXPRESSION; CELLS; RESIDUES; MOLECULE; REGIONS; CLONING; MOUSE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. SCHERING PLOUGH CORP,BLOOMFIELD,NJ. UNIV WASHINGTON,DIV HEMATOL,SEATTLE,WA 98195. FU NCI NIH HHS [CA34183, CA36167] NR 28 TC 44 Z9 46 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1991 VL 77 IS 5 BP 1033 EP 1043 PG 11 WC Hematology SC Hematology GA EZ330 UT WOS:A1991EZ33000017 PM 1704802 ER PT J AU UEMURA, Y KOWALL, NW BEAL, MF AF UEMURA, Y KOWALL, NW BEAL, MF TI GLOBAL-ISCHEMIA INDUCES NMDA RECEPTOR-MEDIATED C-FOS EXPRESSION IN NEURONS RESISTANT TO INJURY IN GERBIL HIPPOCAMPUS SO BRAIN RESEARCH LA English DT Note DE C-FOS; N-METHYL-D-ASPARTATE RECEPTOR; DELAYED NEURONAL DEATH; GLOBAL ISCHEMIA; GERBIL ID EPIDERMAL GROWTH-FACTOR; BRAIN-DAMAGE; INDUCTION; CELLS; PROTEIN; TRANSCRIPTION; ANTAGONISTS; STIMULATION; CORTEX; NERVE AB The induction of c-fos protein-like immunoreactivity (CFPLI) was examined in the hippocampus of gerbils at several time points after transient global ischemia. c-Fos protein induction was largely confined to the dentate gyrus, CA3 and CA4 regions from 2 to 8 h after transient bilateral carotid occlusion. Little CFPLI was seen in the CA1 subfield, which is disproportionately sensitive to injury after global ischemia. c-Fos induction was completely blocked by pretreatment with MK-801 (3 mg/kg). Our results show that c-fos expression after global ischemia is NMDA receptor mediated, and mainly found in hippocampal neurons resistant to ischemic injury. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NINDS NIH HHS [NS 10828-14A1] NR 36 TC 95 Z9 96 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 1 PY 1991 VL 542 IS 2 BP 343 EP 347 DI 10.1016/0006-8993(91)91589-S PG 5 WC Neurosciences SC Neurosciences & Neurology GA FB829 UT WOS:A1991FB82900026 PM 1827611 ER PT J AU BURKE, E LI, FP JANOV, AJ BATTER, S GRIER, H GOORIN, A AF BURKE, E LI, FP JANOV, AJ BATTER, S GRIER, H GOORIN, A TI CANCER IN RELATIVES OF SURVIVORS OF CHILDHOOD SARCOMA SO CANCER LA English DT Article ID RISK AB Relatives of 88 long-term survivors of childhood sarcoma were examined for the familial cancer syndrome of sarcoma, breast cancer, and other neoplasms (Li-Fraumeni syndrome). Twenty-six of 402 close relatives developed cancer (expected, 23.8), including breast cancer in four mothers (expected, 3.1). Two sarcoma probands who developed second malignant tumors have multiple relatives with cancer and might have an inherited predisposition. An increased cancer risk and exceptional requirement for disease screening appear to be confined to first-degree relatives of a small fraction of children with sarcoma, notably probands with second cancer. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT & EPIDEMIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NCI,CLIN EPIDEMIOL BRANCH,CLIN STUDIES SECT,BETHESDA,MD 20892. NR 12 TC 13 Z9 13 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 MAR 1 PY 1991 VL 67 IS 5 BP 1467 EP 1469 DI 10.1002/1097-0142(19910301)67:5<1467::AID-CNCR2820670535>3.0.CO;2-4 PG 3 WC Oncology SC Oncology GA EX815 UT WOS:A1991EX81500034 PM 1991315 ER PT J AU HENDERSON, IC SHAPIRO, CL AF HENDERSON, IC SHAPIRO, CL TI HEXAMETHYLMELAMINE USE IN THE TREATMENT OF METASTATIC BREAST-CANCER SO CANCER TREATMENT REVIEWS LA English DT Article ID PHASE-II; CIS-DDP; TRIAL; CISPLATIN; CARCINOMA; SCHEDULES; THERAPY RP HENDERSON, IC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,BOSTON,MA 02115, USA. NR 24 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7372 J9 CANCER TREAT REV JI Cancer Treat. Rev. PD MAR PY 1991 VL 18 SU A BP 91 EP 98 DI 10.1016/0305-7372(91)90029-Y PG 8 WC Oncology SC Oncology GA GQ522 UT WOS:A1991GQ52200012 PM 1904313 ER PT J AU BONVENTRE, JV SUKHATME, VP BAMBERGER, M OUELLETTE, AJ BROWN, D AF BONVENTRE, JV SUKHATME, VP BAMBERGER, M OUELLETTE, AJ BROWN, D TI LOCALIZATION OF THE PROTEIN PRODUCT OF THE IMMEDIATE EARLY GROWTH-RESPONSE GENE, EGR-1, IN THE KIDNEY AFTER ISCHEMIA AND REPERFUSION SO CELL REGULATION LA English DT Article ID THICK ASCENDING LIMB; ACUTE RENAL-FAILURE; RAT-KIDNEY; CELLS; EXPRESSION; IDENTIFICATION; SEQUENCES; NEURONS; ENCODES; TUBULE AB Egr-1 is an "immediate early" gene that is induced by growth factors and agents that induce differentiation and encodes a protein with a "zinc-finger" motif. This protein is believed to be involved in transcriptional regulation. Because the fate of the kidney, and hence the organism, after an ischemic insult is dependent upon cellular repair, differentiation, and proliferation, we examined whether there was expression of the Egr-1 protein after an ischemic insult to the rat kidney. We have previously reported that Egr-1 mRNA accumulates to high levels in mouse kidneys after 30 min of ischemia and 1 h of reperfusion. In the present study, performed in rats, we show that Egr-1 mRNA transiently accumulates to very high levels after 40 min of ischemia and 1 h of reperfusion, is decreased by 3 h, and is nondetectable by 24 h of reperfusion. Reperfusion is required for Egr-1 protein accumulation to occur. The Egr-1 protein was localized by immunohistochemical techniques primarily to the nuclei of the thick ascending limbs and principal cells of the collecting ducts in the cortex and medulla. The subcellular localization was exclusively nuclear. There was some staining of the glomerular tuft and staining was particularly prominent in the parietal epithelial cells. In parallel to the accumulation of Egr-1 mRNA, the expression of the protein was transient and was no longer apparent after 5 h of reperfusion. The Egr-1 protein may play an important role in regulation of the response to ischemia of those segments of the nephron that are highly susceptible to oxygen deprivation and have a high level of intrinsic plasticity. It is possible that this protein may modulate cellular processes important for the ultimate ability of these critical nephron segments to recover from an ischemic insult. C1 UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MED,CHICAGO,IL 60637. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA 02114. UNIV CHICAGO,HOWARD HUGHES MED INST,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. RP BONVENTRE, JV (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-38452, DK-39249, DK-39773] NR 35 TC 56 Z9 56 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1044-2030 J9 CELL REGUL PD MAR PY 1991 VL 2 IS 3 BP 251 EP 260 PG 10 WC Cell Biology SC Cell Biology GA FF114 UT WOS:A1991FF11400008 PM 1859855 ER PT J AU DAVIDOFF, R PALACIOS, I SOUTHERN, J FALLON, JT NEWELL, J DEC, GW AF DAVIDOFF, R PALACIOS, I SOUTHERN, J FALLON, JT NEWELL, J DEC, GW TI GIANT-CELL VERSUS LYMPHOCYTIC MYOCARDITIS - A COMPARISON OF THEIR CLINICAL-FEATURES AND LONG-TERM OUTCOMES SO CIRCULATION LA English DT Article DE GIANT CELL MYOCARDITIS; ENDOMYOCARDIAL BIOPSY; DILATED CARDIOMYOPATHY; CLINICAL TRIALS ID ENDOMYOCARDIAL BIOPSY; GRANULOMATOUS MYOCARDITIS; VENTRICULAR-FUNCTION; CARDIAC SARCOIDOSIS; NECROPSY PATIENTS; HEART; CARDIOMYOPATHIES; CORTICOSTEROIDS; DIAGNOSIS AB Background. Giant cell myocarditis has rarely been diagnosed premortem, and little is known about its natural history. In addition, no comparative studies with lymphocytic myocarditis exist. Methods and Results. The clinical features, serial change in left ventricular fraction (LVEF), and outcomes of all patients with histologically verified myocarditis were retrospectively evaluated. Ten patients (22%) were found to have giant cell myocarditis (group 1), whereas the remaining 36 (78%) had lymphocytic myocarditis (group 2). Age at presentation, gender distribution, duration of symptoms, initial LVEF, and resting hemodynamics did not differ between groups. Ventricular tachycardia was detected in 90% of group 1 patients compared with only 25% of group 2 (p = 0.0007). Atrioventricular block that required pacemaker insertion was also more common in group 1 (60%) than in group 2 (8.3%) (p = 0.001). Left ventricular systolic function declined during follow-up in group 1 patients (LVEF, 0.43 +/- 0.07-0.26 +/- 0.05, p = 0.11) but increased in group 2 patients (LVEF, 0.33 +/- 0.03-0.41 +/- 0.03, p = 0.02). When the net change between initial and final LVEF was assessed, a significant difference was evident (giant cell group, -0.17 +/- 0.06; lymphocytic group, +0.07 +/- 0.03; p = 0.0008). Although a greater proportion of patients in group 1 died or required transplantation (seven of 10 versus 11 of 36, p = 0.03), actuarial survival over 4 years was not different for the giant cell group (50%) than for the lymphocytic group (62%). Conclusion. Giant cell myocarditis was more prevalent than previously recognized and highly associated with both ventricular tachycardia and pacemaker requirement. The likelihood of an adverse event, either cardiovascular mortality or cardiac transplantation, was significantly greater for patients with giant cell myocarditis than for those with lymphocytic myocarditis, perhaps because of the progressive decline in left ventricular systolic function that was observed in those with giant cell myocarditis. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. BOSTON UNIV,MED CTR,EVANS MEM DEPT CLIN RES,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DIV PATHOL,BOSTON,MA 02114. BOSTON UNIV,MED CTR,DEPT MED,DIV CARDIOL,BOSTON,MA 02215. NR 33 TC 87 Z9 92 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 MAR PY 1991 VL 83 IS 3 BP 953 EP 961 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FA141 UT WOS:A1991FA14100024 PM 1999043 ER PT J AU YASUDA, T GOLD, HK LEINBACH, RC YAOITA, H FALLON, JT GUERRERO, L NAPIER, MA BUNTING, S COLLEN, D AF YASUDA, T GOLD, HK LEINBACH, RC YAOITA, H FALLON, JT GUERRERO, L NAPIER, MA BUNTING, S COLLEN, D TI KISTRIN, A POLYPEPTIDE PLATELET GPIIB/IIIA RECEPTOR ANTAGONIST, ENHANCES AND SUSTAINS CORONARY ARTERIAL THROMBOLYSIS WITH RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN A CANINE PREPARATION SO CIRCULATION LA English DT Article DE GLYCOPROTEIN-IIB/IIIA; ANTIPLATELET AGENT; THROMBOLYTIC THERAPY; REOCCLUSION ID ACUTE MYOCARDIAL-INFARCTION; GLYCOPROTEIN-IIB/IIIA RECEPTOR; ARG-GLY-ASP; MONOCLONAL-ANTIBODY; INTRACORONARY STREPTOKINASE; FACTOR BINDING; INHIBITION; REOCCLUSION; THROMBOSIS; FIBRINOGEN AB Background. Kistrin is a 68-amino acid polypeptide from the venom of the Malayan pit viper Agkistrodon rhodostoma, which inhibits the platelet GPIIb/IIIa receptor. Its effect on thrombolysis, reocclusion, and bleeding associated with administration of recombinant tissue-type plasminogen activator (rt-PA) was studied in a canine model of coronary artery thrombosis. Methods and Results. Coronary patency was monitored for 2 hours by ultrasonic flow probe and repeated coronary angiography. The rt-PA was given as 0.45-mg/kg bolus injections at 15-minute intervals until recanalization or to a maximum of four boluses. Four groups of four or five dogs were studied: a control group that received intravenous heparin (4,000-unit bolus and 1,000 units each hour) and three groups that received heparin and 0.48, 0.24, or 0.12 mg/kg kistrin, administered as a 10% bolus injection and an infusion during a 60-minute period. In the control group, reflow occurred in four of five dogs within 37 +/- 47 minutes but was followed by cyclic reflow and reocclusion. Kistrin at a dose of 0.48 and 0.24 mg/kg reduced the time to reflow to 6 +/- 5 and 10 +/- 3 minutes, respectively, and abolished reocclusion. With 0.12 mg/kg kistrin, reflow occurred in all four animals, within 27 +/- 23 minutes, and reocclusion occurred in two animals. Kistrin induced a dose-related prolongation of the template bleeding time: with 0.48 mg/kg kistrin, the bleeding time was prolonged from 3.8 +/- 1.3 minutes before infusion to 29 +/- 2 minutes during infusion, but it was shortened to 8.3 +/- 2.6 minutes at 90 minutes after the end of infusion. Kistrin also caused a dose-related inhibition of platelet aggregation with ADP and collagen: with 0.48 mg/kg kistrin, platelet aggregation was abolished during the infusion but had partially recovered toward the end of the observation period. Pathological examination of recanalized coronary arterial segments of dogs given 0.48 or 0.24 mg/kg kistrin revealed widely patent arteries with some platelets layered on the damaged intimal surface. Conclusions. Kistrin increases the rate and extent of thrombolysis with a reduced dose of rt-PA, and it prevents reocclusion. At an effective dose, it is associated with a transient prolongation of the bleeding time and inhibition of platelet aggregation. Kistrin may offer promise as adjunctive treatment to thrombolytic agents in patients with acute myocardial infarction. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 4,ROOM 480,15 PARKMAN ST,BOSTON,MA 02114. GENENTECH INC,SAN FRANCISCO,CA 94080. UNIV VERMONT,COLL MED,DEPT BIOCHEM,BURLINGTON,VT 05405. UNIV VERMONT,COLL MED,DEPT MED,BURLINGTON,VT 05405. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-35058, HL-26205] NR 58 TC 101 Z9 101 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 MAR PY 1991 VL 83 IS 3 BP 1038 EP 1047 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FA141 UT WOS:A1991FA14100033 PM 1900221 ER PT J AU GELBERMAN, RH NUNLEY, JA OSTERMAN, AL BREEN, TF DIMICK, MP WOO, SLY AF GELBERMAN, RH NUNLEY, JA OSTERMAN, AL BREEN, TF DIMICK, MP WOO, SLY TI INFLUENCES OF THE PROTECTED PASSIVE MOBILIZATION INTERVAL ON FLEXOR TENDON HEALING - A PROSPECTIVE RANDOMIZED CLINICAL-STUDY SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID ARTICULAR-CARTILAGE; REPAIR; MOTION; SHEATH; RABBIT AB A prospective multicenter clinical study was carried out to determine whether improved tendon gliding could be achieved with greater durations of daily passive-motion rehabilitation after flexor tendon repair. Fifty-one patients were placed randomly into two controlled passive-motion protocols. Group 1 patients received greater intervals of passive-motion rehabilitation using a continuous passive-motion device. Group 2 patients were treated with a traditional early passive-motion protocol for tendon rehabilitation. For Group 1 patients, the mean interval of controlled motion rehabilitation was 75 hours a week, and the mean number of cycles was 12,000. For Group 2 patients the mean interval of controlled passive motion was four hours a week, and the mean number of cycles was 1000. The minimum follow-up time was six months (mean, 10.8 months). Using Strickland and Glogovac's formula, the mean active motion for digits in Group 1 was 138-degrees +/- 6-degrees. Mean motion for tendons in Group 2 was 119-degrees +/- 8-degrees. The difference between Groups 1 and 2 was statistically significant. The effect of the number of tendons injured per digit within each group was not significant. The data from this experiment indicate that the duration of the daily controlled motion interval is a significant variable insofar as postrepair flexor tendon function is concerned. C1 DUKE UNIV,MED CTR,DURHAM,NC 27710. HOSP UNIV PENN,DEPT ORTHOPAED SURG,PHILADELPHIA,PA 19104. UNIV MASSACHUSETTS,MED CTR,DEPT ORTHOPAED SURG,WORCESTER,MA 01605. UNIV CALIF SAN DIEGO,SCH MED,LA JOLLA,CA 92093. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC-527,BOSTON,MA 02114, USA. NR 31 TC 43 Z9 43 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0009-921X J9 CLIN ORTHOP RELAT R JI Clin. Orthop. Rel. Res. PD MAR PY 1991 IS 264 BP 189 EP 196 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FA393 UT WOS:A1991FA39300021 PM 1997235 ER PT J AU BISHOP, SJ MURPHY, JM JELLINEK, MS DUSSEAULT, K AF BISHOP, SJ MURPHY, JM JELLINEK, MS DUSSEAULT, K TI PSYCHOSOCIAL SCREENING IN PEDIATRIC PRACTICE - A SURVEY OF INTERESTED PHYSICIANS SO CLINICAL PEDIATRICS LA English DT Article ID SYMPTOM CHECKLIST; CHILDREN; DYSFUNCTION AB This study followed up on 201 pediatricians and family practitioners who had requested information about the Pediatric Symptom Checklist (PSC), a parent-completed questionnaire which screens for psychosocial dysfunction in school-aged children. The physicians were sent a postcard survey asking whether they had used the PSC in their practices. Of the 157 (78%) who responded to the postcard survey, 36 (23%) reported that they had used the PSC. On a follow-up questionnaire, all of these physicians rated the PSC as useful, and nearly 80% reported that it led to increased case-finding and/or referrals. Ninety-six percent stated that they will continue to use the PSC; more than half of them routinely or frequently. The findings indicate a widespread interest in psychosocial screening, and suggest that additional educational efforts may be necessary to support the acceptance of the PSC in pediatric practice. C1 MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,ACC 725,BOSTON,MA 02114. NR 16 TC 11 Z9 11 U1 1 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 MAR PY 1991 VL 30 IS 3 BP 142 EP 147 DI 10.1177/000992289103000301 PG 6 WC Pediatrics SC Pediatrics GA FF830 UT WOS:A1991FF83000001 PM 2009718 ER PT J AU SHEPARD, JAO MCLOUD, TC AF SHEPARD, JAO MCLOUD, TC TI IMAGING THE AIRWAYS - COMPUTED-TOMOGRAPHY AND MAGNETIC-RESONANCE-IMAGING SO CLINICS IN CHEST MEDICINE LA English DT Article ID THIN-SECTION CT; RELAPSING POLYCHONDRITIS; LOBAR COLLAPSE; ENDOBRONCHIAL OBSTRUCTION; FIBEROPTIC BRONCHOSCOPY; WEGENER GRANULOMATOSIS; BRONCHIAL INVOLVEMENT; BRONCHIECTASIS; TRACHEAL; DIAGNOSIS C1 HARVARD UNIV,SCH MED,RADIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,THORAC RADIOL,BOSTON,MA 02114. NR 80 TC 16 Z9 17 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-5231 J9 CLIN CHEST MED JI Clin. Chest Med. PD MAR PY 1991 VL 12 IS 1 BP 151 EP 168 PG 18 WC Respiratory System SC Respiratory System GA EZ563 UT WOS:A1991EZ56300010 PM 2009742 ER PT J AU DELTITO, JA ARGYLE, N BULLER, R NUTZINGER, D OTTOSSON, JO BRANDON, S MELLERGARD, M SHERA, D AF DELTITO, JA ARGYLE, N BULLER, R NUTZINGER, D OTTOSSON, JO BRANDON, S MELLERGARD, M SHERA, D TI THE SEQUENCE OF IMPROVEMENT OF THE SYMPTOMS ENCOUNTERED IN PATIENTS WITH PANIC DISORDER SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID AGORAPHOBIA C1 CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. UNIV MAINZ,PSYCHIAT KLIN & POLIKLIN,W-6500 MAINZ,GERMANY. UNIV VIENNA,PSYCHIAT KLIN,A-1010 VIENNA,AUSTRIA. GOTHENBURG UNIV,DEPT PSYCHIAT,S-41124 GOTHENBURG,SWEDEN. UNIV LEICESTER,DEPT PSYCHIAT,LEICESTER LE1 7RH,ENGLAND. NORDVANG HOSP,KOBENHAUNS AMT,GLOSTRUP,DENMARK. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BIOSTAT UNIT,BOSTON,MA 02114. NR 20 TC 9 Z9 10 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD MAR-APR PY 1991 VL 32 IS 2 BP 120 EP 129 DI 10.1016/0010-440X(91)90003-U PG 10 WC Psychiatry SC Psychiatry GA FA954 UT WOS:A1991FA95400003 PM 2022110 ER PT J AU SCHALL, R GONIN, R AF SCHALL, R GONIN, R TI DIAGNOSTICS FOR NONLINEAR LP-NORM ESTIMATION SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE COOK DISTANCE; HAT-MATRIX; INFLUENCE; LEVERAGE; OUTLIER; PERTURBATION; RESIDUAL ID NUMERICAL ALGORITHMS; REGRESSION; MODEL AB In this paper we propose diagnostics for nonlinear L(p)-norm estimation. The basic idea is to replace the notion of likelihood displacement (Cook and Weisberg, 1982; Cook, 1986) by that of L(p)-norm displacement. The general methods and diagnostics developed by Cook (1986) and Schall and Dunne (1988a, b, 1989) for the case of maximum likelihood estimation can then be extended to L(p)-norm estimation. C1 MRC,INST BIOSTAT,CAPE TOWN,SOUTH AFRICA. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RI Schall, Robert/A-9174-2012 NR 17 TC 2 Z9 2 U1 1 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD MAR PY 1991 VL 11 IS 2 BP 189 EP 198 DI 10.1016/0167-9473(91)90069-E PG 10 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA FG187 UT WOS:A1991FG18700004 ER PT J AU SHEPHERD, KE LEITER, JC AF SHEPHERD, KE LEITER, JC TI ACUTE HISTOLOGIC EFFECTS OF SUCRALFATE IN RATS - REPLY SO CRITICAL CARE MEDICINE LA English DT Letter ID ASPIRATION C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,HANOVER,NH 03756. RP SHEPHERD, KE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 7 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 MAR PY 1991 VL 19 IS 3 BP 449 EP 449 DI 10.1097/00003246-199103000-00039 PG 1 WC Critical Care Medicine SC General & Internal Medicine GA FC034 UT WOS:A1991FC03400037 ER PT J AU LERNER, UH LJUNGGREN, O DEWHIRST, FE BORASCHI, D AF LERNER, UH LJUNGGREN, O DEWHIRST, FE BORASCHI, D TI COMPARISON OF HUMAN INTERLEUKIN-1-BETA AND ITS 163-171 PEPTIDE IN BONE-RESORPTION AND THE IMMUNE-RESPONSE SO CYTOKINE LA English DT Article DE INTERLEUKIN-1; BONE; BONE RESORPTION; PROSTAGLANDINS ID CULTURED MOUSE CALVARIA; RECOMBINANT INTERLEUKIN-1; PROSTAGLANDIN PRODUCTION; PARATHYROID-HORMONE; POTENTIAL MEDIATOR; ORGAN-CULTURE; CELLS; STIMULATION; INVITRO; SEQUENCE C1 UMEA UNIV,DEPT ORAL PATHOL,S-90187 UMEA,SWEDEN. FORSYTH DENT CTR,DEPT PHARMACOL,BOSTON,MA 02115. SCLAVO RES CTR,I-53100 SIENA,ITALY. NR 38 TC 27 Z9 27 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4666 J9 CYTOKINE JI Cytokine PD MAR PY 1991 VL 3 IS 2 BP 141 EP 148 DI 10.1016/1043-4666(91)90035-C PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Immunology SC Biochemistry & Molecular Biology; Cell Biology; Immunology GA FZ153 UT WOS:A1991FZ15300009 PM 1888884 ER PT J AU SHAHANI, BT AF SHAHANI, BT TI THE UTILITY OF PROXIMAL NERVE-CONDUCTION IN RADICULOPATHIES - THE PROS SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article ID SOMATOSENSORY-EVOKED-POTENTIALS; LUMBOSACRAL RADICULOPATHY; STIMULATION; DIAGNOSIS; ELECTROMYOGRAPHY RP SHAHANI, BT (reprint author), MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,BOSTON,MA 02114, USA. NR 16 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD MAR PY 1991 VL 78 IS 3 BP 168 EP 170 DI 10.1016/0013-4694(91)90029-4 PG 3 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA FD866 UT WOS:A1991FD86600002 PM 1707787 ER PT J AU MIKATI, MA TREVATHAN, E KRISHNAMOORTHY, KS LOMBROSO, CT AF MIKATI, MA TREVATHAN, E KRISHNAMOORTHY, KS LOMBROSO, CT TI PYRIDOXINE-DEPENDENT EPILEPSY - EEG INVESTIGATIONS AND LONG-TERM FOLLOW-UP SO ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY LA English DT Article DE EPILEPSY; PYRIDOXINE-DEPENDENT EPILEPSY; EEG FEATURES; B6 ID SEIZURES; INFANTS AB The EEG features and clinical correlates were investigated before, directly after, and on long-term follow-up after initiation of pyridoxine therapy in 6 patients with B6-dependent epilepsy. At each phase, the EEG provided important diagnostic and prognostic information. Pre-B6 3 neonates manifested a unique EEG pattern of generalized bursts of 1-4 Hz sharp and slow activity. This pattern has not been previously described in neonates with B6 dependency and in this age group appears to be highly suggestive of the diagnosis. Five patients experienced an apparent initial response to traditional antiepileptics. The parenteral pyridoxine test, performed in all 5, and repeated in 3, proved to be a highly reliable and reproducible diagnostic test. After 50-100 mg of B6 there was cessation of clinical seizures within minutes and of paroxysmal discharges within hours. On long-term follow-up (3-28 years) all 6 patients were seizure free on B6 (10-100 mg/day) monotherapy. Recurrences of seizures and of specific sequential EEG changes (background slowing, photoparoxysmal response, spontaneous discharges, stimulus-induced myoclonus, generalized seizures) occurred upon B6 withdrawal. Long-term prognosis correlated with the EEG. Two patients had persistently abnormal EEG backgrounds and were moderately to severely retarded, while 4 had normal EEGs with normal or near normal development. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. SCOTTISH RITE CHILDRENS HOSP,NEUROPHYSIOL LABS,ATLANTA,GA. EMORY UNIV,SCH MED,DEPT PEDIAT,ATLANTA,GA 30322. EMORY UNIV,SCH MED,DEPT EPIDEMIOL,ATLANTA,GA 30322. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 36 TC 70 Z9 70 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0013-4694 J9 ELECTROEN CLIN NEURO JI Electroencephalogr. Clin. Neurophysiol. PD MAR PY 1991 VL 78 IS 3 BP 215 EP 221 DI 10.1016/0013-4694(91)90035-3 PG 7 WC Engineering, Biomedical; Clinical Neurology SC Engineering; Neurosciences & Neurology GA FD866 UT WOS:A1991FD86600008 PM 1707793 ER PT J AU MOINGEON, PE LUCICH, JL STEBBINS, CC RECNY, MA WALLNER, BP KOYASU, S REINHERZ, EL AF MOINGEON, PE LUCICH, JL STEBBINS, CC RECNY, MA WALLNER, BP KOYASU, S REINHERZ, EL TI COMPLEMENTARY ROLES FOR CD2 AND LFA-1 ADHESION PATHWAYS DURING T-CELL ACTIVATION SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN LYMPHOCYTES-T; B-CELLS; RECEPTOR; MEMBRANE; LIGAND; EXPRESSION; MOLECULE; CLONING; PROTEIN; COMPLEX AB The influence of T cell receptor (TcR) triggering on T cell adhesion function has been systematically investigated in the present studies; we show that the adhesion function of LFA-1 is minimal in non-activated T cells but is augmented within minutes following TcR-mediated activation. In contrast, CD2 function is essentially optimal in non-activated T cells and undergoes no detectable modification within 12 h of TcR stimulation. Protein kinase C activation augments LFA-1 but not CD2 adhesion function and cyclic AMP reduces LFA-1 adhesion without affecting CD2-LFA-3 interactions. Up-regulation of this pathway occurs in the absence of any detectable surface redistribution of this molecule, suggesting an activation dependent modification leading to a high-affinity ICAM-1 binding state. The TcR independence of CD2 adhesion function implies a critical role of the CD2 pathway in initiating cell-cell interactions prior to TcR engagement and LFA-1-ICAM-1 binding and underscores the complementary nature of the CD2 and LFA-1 adhesion pathways during the immune response. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BIOGEN RES CORP,CAMBRIDGE,MA. RP MOINGEON, PE (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] NR 32 TC 80 Z9 80 U1 0 U2 5 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 MAR PY 1991 VL 21 IS 3 BP 605 EP 610 DI 10.1002/eji.1830210311 PG 6 WC Immunology SC Immunology GA FF293 UT WOS:A1991FF29300010 PM 1672642 ER PT J AU CHENG, HM KWONG, KK DIXON, S TANAKA, G XIONG, J MOORE, G CHESLER, DA AF CHENG, HM KWONG, KK DIXON, S TANAKA, G XIONG, J MOORE, G CHESLER, DA TI WATER-MOVEMENT IN THE RABBIT EYE SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE DEUTERIUM NMR SPECTROSCOPY; D2O FLOW; WATER MOVEMENT; RABBIT EYE; ANTERIOR SEGMENT C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP CHENG, HM (reprint author), HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. RI Moore, Gregory/E-7184-2010 OI Moore, Gregory/0000-0001-8541-3194 FU NCRR NIH HHS [RR03264, RR00995] NR 7 TC 3 Z9 3 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 MAR PY 1991 VL 52 IS 3 BP 337 EP 339 DI 10.1016/0014-4835(91)90098-Y PG 3 WC Ophthalmology SC Ophthalmology GA FE076 UT WOS:A1991FE07600013 PM 2015863 ER PT J AU WAKABAYASHI, GO GELFAND, JA BURKE, JF THOMPSON, RC DINARELLO, CA AF WAKABAYASHI, GO GELFAND, JA BURKE, JF THOMPSON, RC DINARELLO, CA TI A SPECIFIC RECEPTOR ANTAGONIST FOR INTERLEUKIN-1 PREVENTS ESCHERICHIA-COLI-INDUCED SHOCK IN RABBITS SO FASEB JOURNAL LA English DT Note DE INTERLEUKIN-1; TUMOR NECROSIS FACTOR; SEPTIC SHOCK; NEUTROPHILS; INTERLEUKIN-1 RECEPTOR ANTAGONIST ID TUMOR NECROSIS FACTOR; LETHAL BACTEREMIA; CACHECTIN; HYPOTENSION; ENDOTOXEMIA; ANTIBODIES; APPEARANCE; INHIBITOR; INJURY AB Despite antibiotic therapy, the septic shock syndrome continues to have a high mortality. Tumor necrosis factor (TNF) and interleukin 1 (IL 1), two polypeptide cytokines produced during sepsis, are thought to mediate the hypotension and tissue damage of shock. In the present studies, rabbits were infused with Escherichia coli organisms to produce shock. The IL 1 receptor antagonist (IL 1ra), which competes with IL 1 for occupancy of the IL 1 cell-surface receptors without agonist properties, was given 15 min before the bacterial infusion and during the subsequent 4 h. In saline-treated controls, hypotension was sustained for 4 h and death occurred for two of five rabbits; in rabbits treated with the IL 1ra, however, blood pressure was only transiently decreased, returned to pre-E. coli levels, and no deaths occurred. The associated leukopenia was also reduced by treatment with the antagonist (P < 0.05). Histological examination of lung tissues showed reduced infiltrating neutrophils in the IL 1ra treatment group. Despite the attenuated responses in animals treated with the IL 1ra, circulating TNF and IL 1 levels were nearly identical in both groups. We conclude that specific blockade of IL 1 at the receptor level demonstrates an essential role for this cytokine in the pathogenesis of septic shock. C1 NEW ENGLAND MED CTR HOSP,750 WASHINGTON ST,BOSTON,MA 02111. TUFTS UNIV,DEPT MED,DIV GEOG MED & INFECT DIS,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SYNERGEN INC,BOULDER,CO 80301. FU NIAID NIH HHS [AI15614]; NIGMS NIH HHS [GM21700] NR 34 TC 408 Z9 412 U1 2 U2 5 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 1 PY 1991 VL 5 IS 3 BP 338 EP 343 PG 6 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FC556 UT WOS:A1991FC55600013 PM 1825816 ER PT J AU SUMMERGRAD, P AF SUMMERGRAD, P TI GENERAL-HOSPITAL INPATIENT PSYCHIATRY IN THE 1990S - PROBLEMS AND POSSIBILITIES SO GENERAL HOSPITAL PSYCHIATRY LA English DT Editorial Material ID UNITS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SUMMERGRAD, P (reprint author), MASSACHUSETTS GEN HOSP,INPATIENT PSYCHIAT SERV,BOSTON,MA 02114, USA. NR 15 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0163-8343 J9 GEN HOSP PSYCHIAT JI Gen. Hosp. Psych. PD MAR PY 1991 VL 13 IS 2 BP 79 EP 82 DI 10.1016/0163-8343(91)90017-Q PG 4 WC Psychiatry SC Psychiatry GA FB979 UT WOS:A1991FB97900001 PM 2037245 ER PT J AU GRAVES, RA TONTONOZ, P ROSS, SR SPIEGELMAN, BM AF GRAVES, RA TONTONOZ, P ROSS, SR SPIEGELMAN, BM TI IDENTIFICATION OF A POTENT ADIPOCYTE-SPECIFIC ENHANCER - INVOLVEMENT OF AN NF-1-LIKE FACTOR SO GENES & DEVELOPMENT LA English DT Article DE ADIPOCYTE P2 GENE; ADIPOCYTE TRANSCRIPTION FACTOR; DIFFERENTIATION-DEPENDENT ENHANCER; NUCLEAR FACTOR 1; TISSUE-SPECIFIC ENHANCER ID DNA-BINDING PROTEIN; MAMMARY-TUMOR VIRUS; FATTY ACID-BINDING; NUCLEAR FACTOR-I; ADIPOSE CONVERSION; GENE-EXPRESSION; MESSENGER-RNAS; 3T3 CELLS; GEL-ELECTROPHORESIS; ADENOVIRUS ORIGIN AB The molecular basis for adipocyte-specific gene expression is not known. We have demonstrated that while short (-168) segments of the 5'-flanking sequence of the adipocyte P2 gene containing AP-1- and C/EBP-binding sites can direct expression of a heterologous gene in cultured adipocytes, they cannot support tissue-specific expression in a transgenic mouse. We have therefore analyzed larger segments of the aP2 5'-flanking region by transfection into adipocytes and have found an enhancer at -5.4 kb. This 500-bp enhancer directs expression of the bacterial chloramphenicol acetyltransferase (CAT) gene in a differentiation-dependent fashion when linked to its own minimal promoter or to an enhancerless SV40 promoter. Moreover, this enhancer stimulates very strong and highly specific expression from the CAT gene in the adipose tissues of transgenic mice. A smaller fragment (190 bp) having enhancer activity in adipocytes was defined and demonstrated to contain a binding site for an abundant nuclear protein. This factor has the binding specificity and several other properties characteristic of the nuclear factor 1 (NF-1) transcription/replication factor family, and mutation of this NF-1-binding site greatly reduces the function of the 500-bp enhancer. These results identify and characterize the first functional enhancer with specificity for adipose cells and also demonstrate that a member(s) of the NF-1 family is involved in adipocyte-specific gene expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV ILLINOIS,SCH MED,DEPT BIOCHEM,CHICAGO,IL 60680. FU NIDDK NIH HHS [DK31405] NR 62 TC 137 Z9 138 U1 0 U2 1 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 MAR PY 1991 VL 5 IS 3 BP 428 EP 437 DI 10.1101/gad.5.3.428 PG 10 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA FB280 UT WOS:A1991FB28000009 PM 2001842 ER PT J AU MUNTZ, HG TARRAZA, HM GOFF, BA OGRANAI, C RICE, LW NIKRUI, N FULLER, AF AF MUNTZ, HG TARRAZA, HM GOFF, BA OGRANAI, C RICE, LW NIKRUI, N FULLER, AF TI COMBINATION CHEMOTHERAPY IN ADVANCED ADENOCARCINOMA OF THE FALLOPIAN-TUBE SO GYNECOLOGIC ONCOLOGY LA English DT Article ID PRIMARY-CARCINOMA; OVARIAN-CANCER; MANAGEMENT; CYCLOPHOSPHAMIDE; CISPLATIN C1 MASSACHUSETTS GEN HOSP,DEPT GYNECOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV GYNECOL ONCOL,BOSTON,MA 02114. RP MUNTZ, HG (reprint author), HARVARD UNIV,SCH MED,DEPT OBSTET GYNECOL & REPROD BIOL,BOSTON,MA 02115, USA. NR 26 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD MAR PY 1991 VL 40 IS 3 BP 268 EP 273 PG 6 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA FF762 UT WOS:A1991FF76200014 PM 2013452 ER PT J AU BARNHILL, RL MIHM, MC MAGRO, CM AF BARNHILL, RL MIHM, MC MAGRO, CM TI PLEXIFORM SPINDLE CELL NEVUS - A DISTINCTIVE VARIANT OF PLEXIFORM MELANOCYTIC NEVUS SO HISTOPATHOLOGY LA English DT Article DE MELANOCYTIC NEVUS; PLEXIFORM PATTERN; BENIGN NEVUS; MALIGNANT MELANOMA ID NEVUS AB Twelve cases of a unique plexform melanocytic naevus that we have termed plexiform spindle cell naevus are reported. The lesions affected young individuals (mean age 22.5 years) of both sexes and were most frequently located on the shoulders and back. The lesions clinically were slightly raised and blue or darkly pigmented, suggesting blue naevus. Histologically these tumours had a symmetrical wedge-shaped configuration, as seen in typical Spitz naevus, with the apex directed toward the deep reticular dermis or subcutis. The pigmented spindle cells were disposed in fascicles in association with neurovascular bundles and adnexal structures, imparting a plexiform architecture to the lesion. The predominant cell type consisted of spindle cells containing granular melanin and elongated nuclei. Low-grade cellular atypia was commonly noted. Varying numbers of epithelioid cells were observed in most of the cases. In two cases studied, the naevus cells showed S-100 protein and HMB-45 immunoreactivity. The differential diagnosis of plexiform spindle cell naevus includes malignant melanoma, and spindle and epithelioid cell (Splitz) naevus, blue naevus and combined naevus. Plexiform spindle cell naevus is a distinctive type of pigmented spindle naevus distinguished from the above entities by its striking plexiform architecture, predominance of melanin-containing spindle cells and lack of significant cellular atypia. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BARNHILL, RL (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,DIV DERMATOPATHOL,WARREN 827,BOSTON,MA 02114, USA. NR 14 TC 47 Z9 47 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0309-0167 J9 HISTOPATHOLOGY JI Histopathology PD MAR PY 1991 VL 18 IS 3 BP 243 EP 247 DI 10.1111/j.1365-2559.1991.tb00832.x PG 5 WC Cell Biology; Pathology SC Cell Biology; Pathology GA FC101 UT WOS:A1991FC10100007 PM 2045075 ER PT J AU COYNE, JD WILSON, G SANDHU, D YOUNG, RH AF COYNE, JD WILSON, G SANDHU, D YOUNG, RH TI INFLAMMATORY PSEUDOTUMOR OF THE URINARY-BLADDER SO HISTOPATHOLOGY LA English DT Article DE URINARY BLADDER; INFLAMMATORY PSEUDOTUMOR; MYOFIBROBLASTS ID FIBROMYXOID TUMOR AB An inflammatory pseudotumour that arose in the urinary bladder of a 33-year-old woman is reported. This is the twelfth reported example of this unusual non-neoplastic lesion that may be mistaken for a sarcoma. The lesion was composed predominantly of spindle cells that by routine light microscopical, ultrastructural and immunohistochemical examination had features consistent with myofibroblasts. Awareness of this unusual lesion is important to prevent its misinterpretation. C1 WITHINGTON HOSP,DEPT UROL,MANCHESTER M20 8LR,LANCS,ENGLAND. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP COYNE, JD (reprint author), WITHINGTON HOSP,DEPT HISTOPATHOL,NELL LANE,MANCHESTER M20 8LR,LANCS,ENGLAND. NR 16 TC 32 Z9 32 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0309-0167 J9 HISTOPATHOLOGY JI Histopathology PD MAR PY 1991 VL 18 IS 3 BP 261 EP 264 DI 10.1111/j.1365-2559.1991.tb00835.x PG 4 WC Cell Biology; Pathology SC Cell Biology; Pathology GA FC101 UT WOS:A1991FC10100010 PM 2045077 ER PT J AU POLLACK, MH SACHS, GS TESAR, GE SHUSHTARI, J HERMAN, JB OTTO, MW ROSENBAUM, JF AF POLLACK, MH SACHS, GS TESAR, GE SHUSHTARI, J HERMAN, JB OTTO, MW ROSENBAUM, JF TI PILOT OUTREACH SERVICES TO HOMEBOUND AGORAPHOBIC PATIENTS SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Note ID THERAPY RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,ANXIETY CLIN RES PROGRAM,ACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 7 TC 1 Z9 1 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD MAR PY 1991 VL 42 IS 3 BP 315 EP 317 PG 3 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA EZ386 UT WOS:A1991EZ38600019 PM 2030018 ER PT J AU DICKERSIN, GR ROSENBERG, AE AF DICKERSIN, GR ROSENBERG, AE TI THE ULTRASTRUCTURE OF SMALL-CELL OSTEOSARCOMA, WITH A REVIEW OF THE LIGHT-MICROSCOPY AND DIFFERENTIAL-DIAGNOSIS SO HUMAN PATHOLOGY LA English DT Review DE ULTRASTRUCTURE; SMALL-CELL OSTEOSARCOMA ID OSTEO-SARCOMA; EWINGS-SARCOMA; BONE C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP DICKERSIN, GR (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114, USA. NR 14 TC 22 Z9 22 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 MAR PY 1991 VL 22 IS 3 BP 267 EP 275 PG 9 WC Pathology SC Pathology GA FB287 UT WOS:A1991FB28700011 PM 2004750 ER PT J AU ALFILLE, PH ROSOW, CE AF ALFILLE, PH ROSOW, CE TI OPIOID ANTAGONISTS SO INTERNATIONAL ANESTHESIOLOGY CLINICS LA English DT Article ID INDUCED RESPIRATORY DEPRESSION; MORPHINE ANESTHESIA; NALOXONE REVERSAL; EPIDURAL MORPHINE; FENTANYL; NALBUPHINE; ANALGESIA; INFUSION; DOGS RP ALFILLE, PH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 31 TC 0 Z9 0 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-5907 J9 INT ANESTHESIOL CLIN JI Int. Anesthesiol. Clin. PD SPR PY 1991 VL 29 IS 2 BP 83 EP 92 DI 10.1097/00004311-199121000-00009 PG 10 WC Anesthesiology SC Anesthesiology GA FP123 UT WOS:A1991FP12300008 PM 1676987 ER PT J AU HELD, KD AWAD, S AF HELD, KD AWAD, S TI EFFECTS OF POLYAMINES AND THIOLS ON THE RADIATION SENSITIVITY OF BACTERIAL TRANSFORMING DNA SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article ID SULFYDRYL-CONTAINING COMPOUNDS; BIOLOGICALLY-ACTIVE DNA; INDUCED PHENYLALANINE RADICALS; EQUILIBRIUM DIALYSIS; PHI-X174 DNA; BINDING; OXYGEN; DAMAGE; INACTIVATION; GLUTATHIONE AB The effects of polyamines on the loss of biological activity of bacterial transforming DNA irradiated in the absence and presence of sulphydryl-containing compounds has been investigated. In both oxygenated and hypoxic conditions the polyamines (spermine, spermidine, putrescine and cadaverine) are radioprotectors with the degree of protection increasing with increasing polyamine concentration. When O2-saturated DNA solutions are irradiated, the degree of radioprotection by polyamines generally correlates with the efficiency of scavenging of OH. radicals. In N2 the protection does not show that correlation; several possible reasons are discussed. With the exception of spermine, the polyamines are slightly more protective of oxygenated DNA than of hypoxic DNA. When DNA is irradiated in the presence of both polyamines and thiols, the combined protection is usually greater than that exhibited by either agent alone. When irradiation is in oxygen, the combined agents appear to operate by the same mechanism, namely OH. radical scavenging. In N2-saturated solutions, polyamines and dithiothreitol appear to act by different, non-interacting mechanisms; however WR1065 and polyamines may radioprotect by the same mechanism. Also, the results suggest that polyamines may reduce the ability of some thiols to radioprotect DNA. RP HELD, KD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA42152] NR 32 TC 42 Z9 43 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0955-3002 J9 INT J RADIAT BIOL JI Int. J. Radiat. Biol. PD MAR PY 1991 VL 59 IS 3 BP 699 EP 710 DI 10.1080/09553009114550611 PG 12 WC Biology; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA FB700 UT WOS:A1991FB70000009 PM 1672358 ER PT J AU NISHIZAWA, K OKUNIEFF, P ELMALEH, D MCKUSICK, KA STRAUSS, HW SUIT, HD AF NISHIZAWA, K OKUNIEFF, P ELMALEH, D MCKUSICK, KA STRAUSS, HW SUIT, HD TI BLOOD-FLOW OF HUMAN SOFT-TISSUE SARCOMAS MEASURED BY TL-201 SCANNING - PREDICTION OF TUMOR RESPONSE TO RADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE RADIATION THERAPY; TUMOR BLOOD FLOW; SARCOMA; METASTASIS ID MYOCARDIAL PERFUSION; HYPERTHERMIA; TL-201; OXYGEN AB Thallium-201 chloride (Tl-201) has been used to determine regional perfusion in the myocardium and in tumors. This study was done to determine the potential prognostic importance of lesion tracer uptake to regression, local control, and rate of distant metastasis in 14 patients with neoplasms of soft tissue. Most patients had planned resections following preoperative radiation therapy. Minimum follow-up was 4 years. The ratio of nuclide uptake in the tumor to surrounding normal tissue was used as an estimate of relative blood flow. Tumors with acute volume responses (greater-than-or-equal-to 50% at the completion of X irradiation) had lower Tl-201 uptake indicating lower relative blood flow than tumors that failed to have a volume reduction [1.63 +/- 0.30 (n = 9) vs 3.49 +/- 0.41 (n = 5) Tl-201]. All patients had local tumor control. Patients with high uptake tumors tended to develop metastases at a higher frequency, although this was not statistically significant (p = 0.10). We conclude that Tl-201 scans are a safe, non-invasive method of estimating tumor perfusion which can be useful to predict acute response to radiation, and may help to identify patients who will ultimately develop distant metastases. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. FU NCI NIH HHS [CA13311] NR 23 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. PD MAR PY 1991 VL 20 IS 3 BP 593 EP 597 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA EZ900 UT WOS:A1991EZ90000029 PM 1995546 ER PT J AU ROOF, D HAYES, A HARDENBERGH, G ADAMIAN, M AF ROOF, D HAYES, A HARDENBERGH, G ADAMIAN, M TI A 52 KD CYTOSKELETAL PROTEIN FROM RETINAL ROD PHOTORECEPTORS IS RELATED TO ERYTHROCYTE DEMATIN SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE BAND-4.9; CYTOSKELETON; DEMATIN; DISK ADDITION; RETINAL DEGENERATION ID OUTER SEGMENT; POLYACRYLAMIDE GELS; VERTEBRATE RETINAS; CONNECTING CILIUM; CYTOCHALASIN-D; MOUSE RETINA; F-ACTIN; PHOSPHORYLATION; LOCALIZATION; IMMUNOFLUORESCENCE AB A novel cytoskeletal antigen, RET52, has been identified in the mouse retina. This 52 kD polypeptide is antigenically related to dematin (band 4.9), an actin-bundling phosphoprotein component of the erythrocyte membrane skeleton. Like dematin, RET52 is also a substrate for cAMP-dependent protein kinase. Within the retina, RET52 is primarily concentrated in two regions-the rod inner segment and the outer synaptic layers-although the developmental expression of RET52 differs in these areas. RET52 is present at birth in the inner segment, but appears about the time of initial synapse formation (postnatal day 4-6) in the outer plexiform layer. No differences in RET52 expression have been detected in early-stage mouse retians with the retinal degeneration (rd) phenotype. RET52 localization, developmental expression, homologies to dematin, and in vitro phosphorylation pattern suggest a possible role for cytoskeleton-associated proteins in the initiation or control of disk membrane assembly and/or synapse formation in the rod photoreceptor. RP HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, BERMAN GUND LAB, 243 CHARLES ST, BOSTON, MA 02114 USA. FU NEI NIH HHS [EY07131, EY06514] NR 55 TC 12 Z9 12 U1 0 U2 0 PU ASSOC RESEARCH VISION OPHTHALMOLOGY INC PI ROCKVILLE PA 12300 TWINBROOK PARKWAY, ROCKVILLE, MD 20852-1606 USA SN 0146-0404 EI 1552-5783 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR PY 1991 VL 32 IS 3 BP 582 EP 593 PG 12 WC Ophthalmology SC Ophthalmology GA FB726 UT WOS:A1991FB72600020 PM 2001933 ER PT J AU BUCKNER, CK RO, J BRENDEL, J FISHLEDER, RI WILL, JA CONKLIN, R GRAZIANO, FM AF BUCKNER, CK RO, J BRENDEL, J FISHLEDER, RI WILL, JA CONKLIN, R GRAZIANO, FM TI STUDIES OF DESENSITIZATION AND CROSS-DESENSITIZATION TO IMMUNOLOGICAL AND NONIMMUNOLOGIC STIMULI THAT EVOKE CONTRACTION AND HISTAMINE-RELEASE IN SUPERFUSED GUINEA-PIG TRACHEA SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID HUMAN BASOPHILS; MEDIATOR RELEASE; SMOOTH-MUSCLE; MAST-CELLS; ANTIGEN; ACTIVATION; SECRETION AB This study examined the possibility that there is cross-desensitization between immunologic and nonimmunologic stimuli that evoke contraction and histamine release (HR) in the isolated guinea pig trachea. Compound 48/80 and D-tubocurarine were found to cause homologous and heterologous desensitization for both contraction and HR from superfused trachea. Specific antigen challenge of trachea obtained from animals sensitized with either IgG1 (ovalbumin [OA]) or IgE (oxazolone-human serum albumin [OX-HSA]) also resulted in homologous desensitization for both contraction and HR. However, in experiments with animals sensitized with both IgGl and IgE antibodies, prechallenge with OA resulted in cross-desensitization to OX-HSA, whereas the reverse sequence was ineffective in eliciting this phenomenon. This may be related to the type of desensitization produced by each antigen (specific versus nonspecific) or to heterogeneity of mast cells in the tissue. Prechallenge of the trachea with compound 48/80 or D-tubocurarine failed to alter subsequent effects of antigen after active sensitization with OA or passive sensitization with either IgGl or IgE antibodies. Small but statistically significant decreases in tracheal responses to D-tubocurarine were observed after antigen prechallenge to activate both IgGl and IgE antibodies. This is the first study to demonstrate a cross-desensitization between compound 48/80 and D-tubocurarine and the first to examine cross-desensitization with IgGl and IgE antibodies in the guinea pig trachea. The overall conclusion is that there is no major overlap in the desensitization mechanisms between immunologic and nonimmunologic stimuli in the guinea pig trachea. C1 UNIV WISCONSIN HOSP & CLIN,SCH MED,600 HIGHLAND AVE,MADISON,WI 53792. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. UNIV WISCONSIN,DEPT VET SCI,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NHLBI NIH HHS [HL33237] NR 24 TC 1 Z9 1 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD MAR PY 1991 VL 87 IS 3 BP 655 EP 661 DI 10.1016/0091-6749(91)90384-Z PG 7 WC Allergy; Immunology SC Allergy; Immunology GA FB801 UT WOS:A1991FB80100008 PM 1706369 ER PT J AU JENKINSON, SG ROBERTS, RJ DELEMOS, RA LAWRENCE, RA COALSON, JJ KING, RJ NULL, DM GERSTMANN, DR AF JENKINSON, SG ROBERTS, RJ DELEMOS, RA LAWRENCE, RA COALSON, JJ KING, RJ NULL, DM GERSTMANN, DR TI ALLOPURINOL-INDUCED EFFECTS IN PREMATURE BABOONS WITH RESPIRATORY-DISTRESS SYNDROME SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GLUTATHIONE; OXYGEN TOXICITY ID LUNG INJURY; OXYGEN-TOXICITY; TISSUE-INJURY; FREE-RADICALS; RAT LUNGS; SURFACTANT; REPERFUSION; OXYPURINOL; INHIBITOR; HYPEROXIA AB To test the hypothesis that administration of allopurinol could modify the response to prolonged hyperoxia in premature baboons (140 days gestation) with respiratory distress syndrome, we evaluated physiological, pathological, and lung biochemical parameters in groups of premature baboons treated with mechanical ventilation and exposed to various amounts of oxygen for 6 days. Three groups of experimental animals were studied, including animals that received oxygen as needed to maintain arterial oxygen between 60 and 80 Torr [inspiratory O2 concentration- (FI(o2)) PRN], animals that received 100% oxygen continuously but also received allopurinol intravenously at a dose of 10 mg.kg-1.day-1 (FI(o2) -1.0 + allopurinol), and animals that received 100% oxygen continuously and the vehicle for allopurinol administration (FI(o2) -1.0). Pathological examinations of the experimental animals showed evidence of lung injury in both 100% oxygen-exposed groups, but the allopurinol-treated animals had findings more compatible with the FI(o2) - PRN group, with relatively few macrophages or polymorphonuclear lymphocytes being present in lung tissue. Lungs of animals treated with allopurinol were also more distensible and had a trend toward decreased lung water compared with the FI(o2) -1.0 group. Allopurinol-treated animals were able to induce lung glutathione concentrations and glutathione-related and antioxidant enzyme activities compared with the normoxic control (FI(o2) - PRN) group. Ventilator pressure requirements were also decreased in the allopurinol-treated animals compared with the FI(o2) -1.0 controls after 42 h. These data suggest that treatment of hyperoxia-exposed premature baboons with allopurinol for the first 6 days of life results in significant changes in lung responses and antioxidant defenses compared with vehicle-treated baboons exposed to 100% oxygen for the same time period. C1 SW FDN BIOMED RES,SAN ANTONIO,TX 78284. UNIV VIRGINIA,HLTH SCI CTR,CHARLOTTESVILLE,VA 22908. RP JENKINSON, SG (reprint author), UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY VET ADM HOSP,DEPT MED,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. RI Vinnikova, Lydmila/P-5860-2015; Pshenishnyuk, George /E-8554-2016; Ignatenkov, Oleksandr/J-1429-2016 OI Vinnikova, Lydmila/0000-0002-6106-1785; Pshenishnyuk, George /0000-0002-9915-5576; Ignatenkov, Oleksandr/0000-0002-0770-3847 FU NHLBI NIH HHS [HL-30556, HL-36536] NR 33 TC 19 Z9 19 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD MAR PY 1991 VL 70 IS 3 BP 1160 EP 1167 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA FA971 UT WOS:A1991FA97100027 PM 2032982 ER PT J AU MEGERMAN, J REDDY, E LITALIEN, GJ WARNOCK, DF ABBOTT, WM AF MEGERMAN, J REDDY, E LITALIEN, GJ WARNOCK, DF ABBOTT, WM TI A LABORATORY MODEL TO QUANTITATE THE RESISTANCE OF COLLAGEN VASCULAR GRAFTS TO BIODEGRADATION SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID CARDIAC-VALVE BIOPROSTHESES; BOVINE ARTERIAL GRAFT; GRANULATION-TISSUE; ANEURYSM FORMATION; SOLCOGRAFT-P; VEIN GRAFT; CALCIFICATION; EXPERIENCE; RECONSTRUCTION; FORMALDEHYDE AB Recent reports have shown that despite extensive preclinical testing, vascular grafts of biological origin undergo severe biodegradation and aneurysm formation after two or more years of implantation in man. The purpose of this study was to develop a laboratory model to quantitate and correlate the stability of crosslinked collagen grafts in vitro and in vivo. This resistance to biodegradation was assessed by measuring changes in suture pullout force and sample weight in response to controlled digestion with bacterial collagenase, in 0.5-cm-long cylindrical graft segments (chemically processed bovine carotid artery and human umbilical cord vein) that were implanted in the rat subcutis for 2 to 12 weeks. Scar tissue was removed from the explants by brief enzymatic digestion, a process that was inhibited when graft segments had become infected. Changes in dry weight were more consistent than were changes in wet weight; drying the graft segments had no effect on their degradation in vivo or in vitro. Intact cylindrical rings suffered somewhat less damage than did opened, flattened cylinders. Graft degradation increased markedly with implantation time, and was detected after only 3 weeks. We conclude that the rat subcutis model, when combined with controlled enzymatic digestion, first to remove scar tissue and then to challenge structural integrity, provides an accelerated assay by which to predict the stability of collagen vascular grafts. C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. UNIV NATAL,FAC MED,DEPT SURG,CONGELLA 4013,SOUTH AFRICA. RP MEGERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,VASC RES LAB,ACC 458,BOSTON,MA 02114, USA. NR 43 TC 4 Z9 4 U1 0 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD MAR PY 1991 VL 25 IS 3 BP 295 EP 313 DI 10.1002/jbm.820250303 PG 19 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA EY016 UT WOS:A1991EY01600002 PM 1851178 ER PT J AU JUPITER, JB AF JUPITER, JB TI FRACTURES OF THE DISTAL END OF THE RADIUS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Review ID COLLES FRACTURE; EXTERNAL FIXATION; COMPLICATIONS; PLASTER; ADULTS; JOINT RP JUPITER, JB (reprint author), MASSACHUSETTS GEN HOSP,SUITE 102,5 WHITTIER PL,BOSTON,MA 02114, USA. NR 100 TC 147 Z9 156 U1 0 U2 5 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 MAR PY 1991 VL 73A IS 3 BP 461 EP 469 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FD859 UT WOS:A1991FD85900019 PM 2002085 ER PT J AU KURIHARA, N CIVIN, C ROODMAN, GD AF KURIHARA, N CIVIN, C ROODMAN, GD TI OSTEOTROPIC FACTOR RESPONSIVENESS OF HIGHLY PURIFIED POPULATIONS OF EARLY AND LATE PRECURSORS FOR HUMAN MULTINUCLEATED CELLS EXPRESSING THE OSTEOCLAST PHENOTYPE SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID BONE-MARROW CULTURES; PARATHYROID-HORMONE; 1,25-DIHYDROXYVITAMIN-D3 CAUSES; PROGENITOR CELLS; INVITRO; GENERATION; RESORPTION; BLOOD AB Recently we have adapted human long-term bone marrow cultures to form multinucleated cells (MNC) that express the osteoclast phenotype and used semisolid culture techniques to identify early (bipotent) and late (unipotent) mononuclear precursors for these MNC. The early precursor can form both osteoclast-like MNC and macrophage polykaryons; the late precursor forms only osteoclast-like MNC. In this study we examined the effects of osteotropic hormones and cytokines of MNC formation from highly purified populations of these early or late mononuclear precursor cells. MNC expressing the osteoclast phenotype were identified by their cross-reactivity with the 23c6 monoclonal antibody, which preferentially identifies osteoclasts. 1,25-(OH)2D3 (10(-8) M), IL-1-beta (10 u/ml), and IL-6 (100 pg/ml) stimulated formation of 23c6-positive MNC from highly purified populations of early or late precursor cells. In contrast, PTH (50 ng/ml) did not act directly on late precursor cells but only stimulated 23c6-positive MNC formation from early precursors. These results show that (1) 1,25-(OH)2D3, IL-1-beta, and IL-6 can stimulate 23c6-positive MNC formation from a highly enriched population of early and late precursors, and (2) PTH does not act on late precursors but may act indirectly on the late precursors. C1 AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. JOHNS HOPKINS UNIV,CTR ONCOL,BALTIMORE,MD 21218. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM 35188] NR 24 TC 105 Z9 105 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD MAR PY 1991 VL 6 IS 3 BP 257 EP 261 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA GN785 UT WOS:A1991GN78500006 PM 2035352 ER PT J AU BOYLAN, JF GUDAS, LJ AF BOYLAN, JF GUDAS, LJ TI OVEREXPRESSION OF THE CELLULAR RETINOIC ACID BINDING PROTEIN-I (CRABP-I) RESULTS IN A REDUCTION IN DIFFERENTIATION-SPECIFIC GENE-EXPRESSION IN F9 TERATOCARCINOMA CELLS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID DIBUTYRYL CYCLIC-AMP; CHICK LIMB BUD; C-MYC; SPATIAL-DISTRIBUTION; MOLECULAR-CLONING; VITAMIN-A; MOUSE; RECEPTOR; DNA; IDENTIFICATION AB Treatment of F9 teratocarcinoma stem cells with retinoic acid (RA) causes their irreversible differentiation into extraembryonic endoderm. To elucidate the role of the cellular retinoic acid binding protein-I (CRABP-I) in this differentiation process, we have generated several different stably transfected F9 stem cell lines expressing either elevated or reduced levels of functional CRABP-I protein. Stably transfected lines expressing elevated levels of CRABP-I exhibit an 80-90% reduction in the RA induced expression of retinoic acid receptor (RAR) beta, laminin B1, and collagen type IV (alpha-1) mRNAs at low exogenous RA concentrations, but this reduction is eliminated at higher RA concentrations. Thus, greater expression of CRABP-I reduces the potency of RA in this differentiation system. Moreover, transfection of a CRABP-I expression vector into F9 cells resulted in five- and threefold decreases in the activation of the laminin B1 RARE (retinoic acid response element) and the RAR-beta-RARE, respectively, as measured from RARE/CAT expression vectors in transient transfection assays. These results support the idea that CRABP-I sequesters RA within the cell and thereby prevents RA from acting to regulate differentiation specific gene expression. Our data suggest a mechanism whereby the level of CRABP-I can regulate responsiveness to RA during development. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,BOSTON,MA 02115. RP BOYLAN, JF (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA-43796] NR 53 TC 323 Z9 327 U1 0 U2 1 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 MAR PY 1991 VL 112 IS 5 BP 965 EP 979 DI 10.1083/jcb.112.5.965 PG 15 WC Cell Biology SC Cell Biology GA EZ876 UT WOS:A1991EZ87600017 PM 1847931 ER PT J AU MACFARLANE, R TASDEMIROGLU, E MOSKOWITZ, MA UEMURA, Y WEI, EP KONTOS, HA AF MACFARLANE, R TASDEMIROGLU, E MOSKOWITZ, MA UEMURA, Y WEI, EP KONTOS, HA TI CHRONIC TRIGEMINAL GANGLIONECTOMY OR TOPICAL CAPSAICIN APPLICATION TO PIAL VESSELS ATTENUATES POSTOCCLUSIVE CORTICAL HYPEREMIA BUT DOES NOT INFLUENCE POSTISCHEMIC HYPOPERFUSION SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE TRIGEMINAL NERVE; SUBSTANCE-P; CAPSAICIN; CALCITONIN GENE-RELATED PEPTIDE; CEREBRAL ISCHEMIA; HYPEREMIA ID CEREBRAL BLOOD-FLOW; VASOACTIVE INTESTINAL POLYPEPTIDE; TRANSIENT FOREBRAIN ISCHEMIA; CEREBROVASCULAR NERVE-FIBERS; GENE-RELATED PEPTIDE; SUBSTANCE-P; REACTIVE HYPEREMIA; VASCULAR HEADACHES; CEPHALIC ARTERIES; POSSIBLE ORIGINS AB Marked hyperemia accompanies reperfusion after ischemia in the brain, and may account for the propensity of cerebral hemorrhage to follow embolic stroke or carotid endarterectomy, and for the morbidity that follows head injury or the ligation of large arteriovenous malformations. To evaluate the contribution of trigeminal sensory fibers to the hyperemic response, CBF was determined in 12 symmetrical brain regions, using microspheres with up to five different isotopic labels, in four groups of cats. Measurements were made at 15-min intervals for up to 2 h of reperfusion after global cerebral ischemia induced by four-vessel occlusion combined with systemic hypotension of either 10- or 20-min duration. In normal animals, hyperemia in cortical gray matter 30 min after reperfusion was significantly greater after 20 min (n = 10) than after 10 min (n = 7) of ischemia (312 ml/100 g/min versus 245 ml/100 g/min; p < 0.01). CBF returned to preischemic levels approximately 45 min after reperfusion and was reduced to approximately 65% of basal CBF for the remaining 75 min. In cat subjected to chronic trigeminal ganglionectomy (n = 15), postocclusive hyperemia in cortical gray matter was attenuated by up to 48% on the denervated side (249 versus 150 ml/100 g/min; p < 0.01) after 10 min of ischemia. This effect was maximal in the middle cerebral artery (MCA) territory, and was confined to regions known to receive a trigeminal innervation. In these animals, substance P (SP) levels in the MCA were reduced by 64% (p < 0.01), and the density of nerve fibers containing calcitonin gene-related peptide (but not vasoactive intestinal polypeptide or neuropeptide Y) was decreased markedly on the lesioned side. Topical application of capsaicin (100 nM; 50-mu-l) to the middle or posterior temporal branch of the MCA 10-14 days before ischemia decreased SP levels by 36%. Postocclusive hyperemia in cortical gray matter was attenuated throughout the ipsilateral hemisphere by up to 58%, but the cerebral vascular response to hypercapnia (P(a)CO2 = 60 mm Hg) was unimpaired. The duration of hyperemia and the severity of the delayed hypoperfusion were not influenced by trigeminalectomy, capsaicin application, or the intravenous administration of ATP. These data demonstrate the importance of neurogenic mechanisms in the development of postischemic hyperperfusion, and suggest the potential utility of strategies aimed at blocking axon reflex-like mechanisms to reduce severe cortical hyperemia. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,STROKE RES LAB,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,DIV CARDIOL,RICHMOND,VA 23298. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS21558, NS26361] NR 62 TC 57 Z9 57 U1 1 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD MAR PY 1991 VL 11 IS 2 BP 261 EP 271 PG 11 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EZ346 UT WOS:A1991EZ34600009 PM 1705254 ER PT J AU ALPERT, NM BARKER, WC GELMAN, A WEISE, S SENDA, M CORREIA, JA AF ALPERT, NM BARKER, WC GELMAN, A WEISE, S SENDA, M CORREIA, JA TI THE PRECISION OF POSITRON EMISSION TOMOGRAPHY - THEORY AND MEASUREMENT SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article; Proceedings Paper CT WORKSHOP ON PET ( POSITRON EMISSION TOMOGRAPHY ) DATA ANALYSIS CY MAY 01-02, 1989 CL NEW YORK, NY DE POSITRON EMISSION TOMOGRAPHY; RANDOM ERROR; STATISTICAL ERROR ID COMPUTED-TOMOGRAPHY; PROJECTIONS; CAMERA; NOISE AB The limits of quantitation with positron emission tomography (PET) are examined with respect to the noise propagation resulting from radioactive decay and other sources of random error. Theoretical methods for evaluating the statistical error have been devised but seldom applied to experimental data obtained on human subjects. This paper extends the analysis in several ways: (1) A Monte Carlo method is described for tracking the propagation of statistical error through the analysis of in vivo measurements; (2) Experimental data, obtained in phantoms, validating the Monte Carlo method and other methods are presented; (3) A difference in activation paradigm, performed on regional CBF (rCBF) data from five human subjects, was analyzed on 1.6-cm diameter regions of interest to determine the mean fractional statistical error in PET tissue concentration and in rCBF before and after stereotactic transformation; and (4) A linear statistical model and calculations of the various statistical errors were used to estimate the magnitude of the subject-specific fluctuations under various conditions. In this specific example, the root mean squared (RMS) noise in flow measurements was about three times higher than the RMS noise in the concentration measurements. In addition, the total random error was almost equally partitioned between statistical error and random fluctuations due to all other sources. C1 HARVARD UNIV,DEPT STAT,CAMBRIDGE,MA 02138. RP ALPERT, NM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA09362]; NIMH NIH HHS [MH31154]; NINDS NIH HHS [NS10828] NR 14 TC 18 Z9 18 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD MAR PY 1991 VL 11 IS 2 BP A26 EP A30 PG 5 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA EZ346 UT WOS:A1991EZ34600025 PM 1997483 ER PT J AU LANDY, H BOEPPLE, PA MANSFIELD, MJ WHITCOMB, RW SCHNEYER, AL CRAWFORD, JD CRIGLER, JF CROWLEY, WF AF LANDY, H BOEPPLE, PA MANSFIELD, MJ WHITCOMB, RW SCHNEYER, AL CRAWFORD, JD CRIGLER, JF CROWLEY, WF TI ALTERED PATTERNS OF PITUITARY SECRETION AND RENAL EXCRETION OF FREE ALPHA-SUBUNIT DURING GONADOTROPIN-RELEASING-HORMONE AGONIST-INDUCED PITUITARY DESENSITIZATION SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; FOLLICLE-STIMULATING HORMONE; LUTEINIZING-HORMONE; METABOLIC-CLEARANCE; BETA-SUBUNIT; ANTERIOR-PITUITARY; PRECOCIOUS PUBERTY; RATES; LH; WOMEN AB Intact LH and free alpha-subunit (FAS) are differentially regulated during GnRH agonist (GnRHa)-induced pituitary desensitization; circulating levels of FAS rise, while LH levels decline. Increased steady state alpha and decreased LH-beta mRNA levels in desensitized rat pituitaries suggest that differential regulation occurs at the level of subunit transcription. We assessed a renal contribution to these changes in serum hormone concentrations by studying LH and FAS levels in serum and urine in 15 pubertal children before and during long term GnRHa administration. Before GnRHa, serum LH and FAS were secreted in concordant pulses, and both responded briskly to exogenous GnRH. During GnRHa-induced pituitary desensitization, mean (+/- SEM) serum and urinary LH levels fell [11 +/- 3 vs. 2 +/- 0.2 IU/L (P < 0.01) and 39 +/- 15 vs. 5 +/- 1 IU/g creatinine (P < 0.05), respectively), and the LH response to exogenous GnRH was ablated (117 +/- 20 vs. 1 +/- 0.3 IU/L; P < 0.01). In contrast, despite suppression of FAS pulsatility, mean serum FAS levels rose during GnRHa treatment (204 +/- 23 vs. 405 +/- 50 ng/L; P < 0.01), and responsiveness to exogenous GnRH was maintained. Paradoxically, urinary FAS levels fell (3.2 +/- 0.9 vs. 1.7 +/- 0.4-mu-g/g creatinine; P < 0.05) as did it renal clearance (3.1 +/- 0.5 vs. 1.3 +/- 0.1 mL/min.m2; P < 0.05). We conclude that during GnRHa-induced pituitary desensitization, the gonadotrope maintains the ability to respond to GnRH with FAS release, and the rise in serum FAS is due in part to its diminished renal clearance. C1 MASSACHUSETTS GEN HOSP, DEPT MED, VINCENT MEM RES LABS, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CHILDRENS SERV, PEDIAT ENDOCRINOL UNIT, BOSTON, MA 02114 USA. CHILDRENS HOSP MED CTR, DEPT MED, DIV ENDOCRINOL, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, DIV ADOLESCENT & YOUNG ADULT MED, BOSTON, MA 02115 USA. RP LANDY, H (reprint author), MASSACHUSETTS GEN HOSP, REPROD ENDOCRINE UNIT, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR-01066]; NICHD NIH HHS [P30 HD028138, U01 HD044417, HD-07277, HD-18169, U54 HD029164, U54 HD028138] NR 45 TC 10 Z9 10 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 MAR PY 1991 VL 72 IS 3 BP 711 EP 717 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FA523 UT WOS:A1991FA52300029 PM 1997524 ER EF