FN Thomson Reuters Web of Science™ VR 1.0 PT J AU HARRITY, P PATEL, A BIANCO, J SUBRAMANIAN, R AF HARRITY, P PATEL, A BIANCO, J SUBRAMANIAN, R TI IMPROVED DIAGNOSIS AND CHARACTERIZATION OF POSTINFARCTION LEFT-VENTRICULAR PSEUDOANEURYSM BY CARDIAC MAGNETIC-RESONANCE-IMAGING SO CLINICAL CARDIOLOGY LA English DT Article DE MAGNETIC RESONANCE IMAGING; PSEUDOANEURYSM; LEFT VENTRICLE; MYOCARDIAL INFARCTION ID ACUTE MYOCARDIAL-INFARCTION; ANEURYSMS; RUPTURE AB A patient with a ruptured left ventricular pseudoaneurysm complicating an acute posteroinferior myocardial infarction is described. Left ventricular pseudoaneurysms are a rare complication of acute myocardial infarction, usually occurring with inferior and/or posterior infarction. In contrast to true aneurysms, pseudoaneurysms are much more likely to rupture, regardless of size, causing hemopericardium and death. Therefore, once the diagnosis has been confirmed, prompt surgical resection is the current accepted treatment. The most accurate noninvasive diagnostic method has been echocardiography, with recent reports suggesting improved diagnosis with color flow Doppler echocardiography. Ventriculography confirms the diagnosis with more accurate anatomic detail, but is an invasive procedure. In our patient, two-dimensional and color Doppler echocardiography could not demonstrate the suspected pseudoaneurysm, which was demonstrated by ventriculography. However, magnetic resonance imaging (MRI) demonstrated the pseudoaneurysm, showing detailed anatomy not obvious on ventriculography. Before surgery could be performed, the patient died and was autopsied. Heart sections corresponding to MRI planes confirmed the MRI findings. A review of the literature has revealed no similar reports using MRI in the diagnosis of postinfarction pseudoaneurysms. Major advantages of MRI are generation of three-dimensional soft tissue images noninvasively, and generation of tissue contrast by rapid imaging sequences, obviating the need for contrast injection. Major disadvantages of MRI are the high cost of instrumentation, nonportability, and a requirement for patient immobility during the study. In cases of suspected pseudoaneurysm with equivocal echocardiography findings, MRI could provide early diagnosis, leading to early surgical intervention and increased patient survival. C1 UNIV WISCONSIN HOSP,DEPT RADIOL,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT PATHOL,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT CARDIOL,MADISON,WI 53705. NR 11 TC 23 Z9 24 U1 0 U2 0 PU CLINICAL CARDIOLOGY PUBL CO PI MAHWAH PA PO BOX 832, MAHWAH, NJ 07430-0832 SN 0160-9289 J9 CLIN CARDIOL JI Clin. Cardiol. PD JUL PY 1991 VL 14 IS 7 BP 603 EP 606 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FV022 UT WOS:A1991FV02200012 PM 1747971 ER PT J AU PUOPOLO, PR FLOOD, JG AF PUOPOLO, PR FLOOD, JG TI FLUOXETINE (PROZAC) INTERFERENCE IN CN COLUMN LIQUID-CHROMATOGRAPHIC ASSAYS OF TRICYCLIC ANTIDEPRESSANTS AND METABOLITES SO CLINICAL CHEMISTRY LA English DT Letter ID ULTRAVIOLET DETECTION; NORFLUOXETINE RP PUOPOLO, PR (reprint author), MASSACHUSETTS GEN HOSP,CHEM LAB,BOSTON,MA 02114, USA. NR 7 TC 14 Z9 14 U1 0 U2 1 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 JUL PY 1991 VL 37 IS 7 BP 1304 EP 1305 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FX182 UT WOS:A1991FX18200040 PM 1855312 ER PT J AU TRUHAN, AP AF TRUHAN, AP TI SUN PROTECTION IN CHILDHOOD SO CLINICAL PEDIATRICS LA English DT Article ID SKIN-CANCER; CUTANEOUS MELANOMA; MALIGNANT-MELANOMA; EXPOSURE HABITS; SUNSCREEN USE; SUNLIGHT; PHOTOPROTECTION; CHILDREN; AGE AB There is compelling evidence that childhood is a particularly vulnerable time for the photocarcinogenic effects of sun exposure on the skin. Studies indicate that excessive sun exposure during the first 10-20 years of life greatly increases the risk of skin cancer. Nonmelanoma skin cancer (basal cell and squamous cell carcinoma) has been associated with cumulative sun exposure, whereas melanoma has been associated with short, intense sun exposure or blistering sunburn. Under normal circumstances, children receive three times the annual sun exposure of adults; most of one's lifetime sun exposure occurs in childhood. Depletion of the earth's protective ozone layer adds to the photodamage problem. It is clear that sun protection is most vital in the early years. Those with fair skin are at highest risk. Photoprotective measures including sunscreen, clothing, and sun avoidance in childhood may significantly reduce the occurrence of melanoma and other skin cancer in later life. Regular use of sunscreen with a sun protection factor of 15 during the first 18 years of life could reduce the lifetime incidence of nonmelanoma skin cancer by 78%. Pediatricians can play a major role in educating parents and children. RP TRUHAN, AP (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,ACC 715,BOSTON,MA 02114, USA. NR 28 TC 7 Z9 7 U1 0 U2 0 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 JUL PY 1991 VL 30 IS 7 BP 412 EP 421 DI 10.1177/000992289103000702 PG 10 WC Pediatrics SC Pediatrics GA GD196 UT WOS:A1991GD19600002 ER PT J AU YUNIS, JJ AHMED, AR AF YUNIS, JJ AHMED, AR TI IMMUNOGENETICS OF DERMATITIS-HERPETIFORMIS SO CLINICS IN DERMATOLOGY LA English DT Article C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. NR 0 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0738-081X J9 CLIN DERMATOL JI Clin. Dermatol. PD JUL-SEP PY 1991 VL 9 IS 3 BP 341 EP 346 DI 10.1016/0738-081X(91)90025-G PG 6 WC Dermatology SC Dermatology GA HL572 UT WOS:A1991HL57200009 PM 1806221 ER PT J AU GUIGO, R JOHANSSON, A SMITH, TF AF GUIGO, R JOHANSSON, A SMITH, TF TI AUTOMATIC EVALUATION OF PROTEIN-SEQUENCE FUNCTIONAL PATTERNS SO COMPUTER APPLICATIONS IN THE BIOSCIENCES LA English DT Article ID MOLECULAR-BIOLOGY; IDENTIFICATION; GENERATION AB A procedure that automatically provides an evaluation of the diagnostic ability of a protein sequence functional pattern is described. The procedure relies on the identification of the closest definable set in terms of a (protein sequence) database functional annotation to the set of database instances containing a given pattern. Assuming annotation correctness and completeness in the protein sequence database, the degree of statistical association between these sets provides an appropriate measure of the diagnostic ability of the pattern. An experimental implementation of the procedure, using the NBRF/PIR protein database, has been applied to a diverse collection of published sequence patterns. Results obtained reveal that frequently it is not possible to define (in NBRF/PIR database terminology) the set of database instances containing a given pattern, suggesting either lack of pattern diagnostic ability or protein database annotation incompleteness and/or inconsistencies. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP GUIGO, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,LG-127,44 BINNEY ST,BOSTON,MA 02115, USA. RI sebastianovitsch, stepan/G-8507-2013; Guigo, Roderic/D-1303-2010 OI Guigo, Roderic/0000-0002-5738-4477 FU NCRR NIH HHS [RR02275] NR 15 TC 11 Z9 11 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0266-7061 J9 COMPUT APPL BIOSCI JI Comput. Appl. Biosci. PD JUL PY 1991 VL 7 IS 3 BP 309 EP 315 PG 7 WC Computer Science, Interdisciplinary Applications SC Computer Science GA FY071 UT WOS:A1991FY07100004 PM 1913211 ER PT J AU RAIZMAN, MB DELAMAZA, MS FOSTER, CS AF RAIZMAN, MB DELAMAZA, MS FOSTER, CS TI TECTONIC KERATOPLASTY FOR PERIPHERAL ULCERATIVE KERATITIS SO CORNEA LA English DT Article DE KERATOPLASTY; PERIPHERAL ULCERATIVE KERATITIS; IMMUNOSUPPRESSION; MOORENS ULCER; WEGENERS GRANULOMATOSIS; RHEUMATOID ARTHRITIS; VASCULITIS AB Peripheral ulcerative keratitis (PUK) is a destructive, inflammatory process that can lead to corneal perforation and visual loss. Successful control of PUK has been reported with conjunctival resection, cyanoacrylate adhesive, and systemic immunosuppression. Cases with impending or actual corneal performation may require more extensive surgery, including lamellar or penetrating keratoplasty, to maintain the integrity of the globe. We report on 17 eyes of 14 patients with PUK that required tectonic keratoplasty because of progressive ulceration. Surgery with concomitant immunosuppression preserved the eyes in all but two cases, and 8 of 17 eyes maintained or improved preoperative visual acuity. Six eyes had final visual acuities of 20/200 or better. This therapeutic strategy can preserve eyes that might otherwise be lost to progressive inflammation. RP RAIZMAN, MB (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD JUL PY 1991 VL 10 IS 4 BP 312 EP 316 DI 10.1097/00003226-199107000-00006 PG 5 WC Ophthalmology SC Ophthalmology GA FR921 UT WOS:A1991FR92100006 PM 1889217 ER PT J AU HOANGXUAN, T FOSTER, CS JAKOBIEC, FA TAUBER, J DELAMAZA, MS KREBS, W AF HOANGXUAN, T FOSTER, CS JAKOBIEC, FA TAUBER, J DELAMAZA, MS KREBS, W TI ROMBERGS PROGRESSIVE HEMIFACIAL ATROPHY - AN ASSOCIATION WITH SCLERAL MELTING SO CORNEA LA English DT Article DE PROGRESSIVE FACIAL HEMIATROPHY; ROMBERG DISEASE; SCLERAL LOSS; ULTRASTRUCTURE AB We report the unusual case of a 43-year-old woman who presented with Romberg's progressive facial hemiatrophy and spontaneous scleral perforation in the ipsilateral eye, for which scleral grafting was performed. Histologic and ultrastructural examination of the scleral specimen revealed a noninflammatory lytic process. The location of the scleral loss, exactly on the line of the "en coup de sabre" atrophy, as well as the light microscopy and ultrastructural histopathologic findings suggest that the scleral destruction was a late manifestation of Romberg's disease. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,243 CHARLES ST,BOSTON,MA 02114. NR 0 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD JUL PY 1991 VL 10 IS 4 BP 361 EP 366 DI 10.1097/00003226-199107000-00014 PG 6 WC Ophthalmology SC Ophthalmology GA FR921 UT WOS:A1991FR92100014 PM 1889224 ER PT J AU TAKAHASHI, LK TURNER, JG KALIN, NH AF TAKAHASHI, LK TURNER, JG KALIN, NH TI DEVELOPMENT OF STRESS-INDUCED RESPONSES IN PREWEANLING RATS SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article ID ULTRASONIC VOCALIZATIONS; RATTUS-NORVEGICUS; NEONATAL RAT; ALBINO-RATS; SHOCK; PUPS; CORTICOTROPIN; PITUITARY; BEHAVIOR; ONTOGENY AB This study examined in postnatal Days 7, 14, and 21 male rats the effects of social isolation and social isolation with administration of brief foot shocks on the development of stress-induced behavioral and pituitary-adrenal hormone responses. Day 21 rats appeared similar to adult rats in their responses to the two test conditions. That is, exposure to either isolation or to shock increased both pituitary-adrenal hormone secretion and tail-flick latencies but only administration of shock potentiated freezing and ultrasonic vocalizations. Younger rats differed from Day 21 rats in their responses to the two test conditions. In both tests, Day 7 rats produced the highest number of ultrasounds, which may be due to a significant decrease in body temperature. In contrast, in Day 14 pups, exposure to shock significantly reduced isolation-induced ultrasonic vocalizations. Additional age-dependent differences were found in the analgesic responses of Days 7 and 14 rats. Day 7 rats exposed to stress became consistently hyperalgesic whereas Day 14 rats showed only a short-lasting analgesic response. Although in Days 7 and 14 rats exposure to the two stress conditions produced significant elevations in pituitary-adrenal hormone concentrations, plasma levels were lower than those measured in Day 21 rats. To summarize, preweanling rats exhibit varied age-dependent responses when exposed to different stress environments. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,MADISON,WI 53706, USA. FU NIMH NIH HHS [MH-43986] NR 35 TC 22 Z9 22 U1 1 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0012-1630 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD JUL PY 1991 VL 24 IS 5 BP 341 EP 360 DI 10.1002/dev.420240504 PG 20 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA GM919 UT WOS:A1991GM91900003 PM 1661243 ER PT J AU JACOBSON, AM ADLER, AG DERBY, L ANDERSON, BJ WOLFSDORF, JI AF JACOBSON, AM ADLER, AG DERBY, L ANDERSON, BJ WOLFSDORF, JI TI CLINIC ATTENDANCE AND GLYCEMIC CONTROL - STUDY OF CONTRASTING GROUPS OF PATIENTS WITH IDDM SO DIABETES CARE LA English DT Note AB Objective: To assess factors associated with attendance at a specialized clinic for diabetes care. Research Design and Methods: Adults with insulin-dependent diabetes mellitus (IDDM) in poor (HbA1 greater-than-or-equal-to 12%) versus good (HbA1 less-than-or-equal-to 10%) control and with no known complications comprised the study group. Results: Infrequent attenders were in worse glycemic control than regular attenders (chi-2 = 6.60, P less-than-or-equal-to 0.01) and held health beliefs that downplayed the importance of getting advice from physicians (P less-than-or-equal-to 0.002) or providing opinions to physicians about what might be done to improve their health (P less-than-or-equal-to 0.001). Conclusions: Because infrequent attenders are more likely to be in poor glycemic control and thus at greater risk for diabetic complications, engaging them in regularly supervised treatment has important personal and public health implications. Additional studies are needed to understand why some diabetic patients limit their contact with medical providers and to develop more effective strategies for reversing this process. Initial findings from this study suggest that patient beliefs about the doctor-patient relationship may influence clinic attendance. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JACOBSON, AM (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-27845] NR 11 TC 42 Z9 42 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD JUL PY 1991 VL 14 IS 7 SU 3 BP 599 EP 601 DI 10.2337/diacare.14.7.599 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FU311 UT WOS:A1991FU31100013 PM 1914802 ER PT J AU NATOWICZ, M SHAW, L AF NATOWICZ, M SHAW, L TI DIGOXIN ASSAY ANOMALIES DUE TO DIGOXIN-SPECIFIC FAB IMMUNOTHERAPY SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Note ID ANTIBODY FRAGMENTS; SERUM AB We demonstrate that digoxin-specific Fab antibody fragments, used in the treatment of severe digitalis intoxication, cause a marked interference with both fluorescence excitation transfer immunoassays and radioimmunoassays for digoxin. In addition, we describe a rapid ultrafiltration method that avoids the Fab-induced interference and affords excellent accuracy and precision. This technique will provide a useful adjunct to the clinical evaluation of patients with digoxin toxicity who are recipients of antidigoxin immunotherapy by enabling a precise determination of their serum digoxin concentrations. By separating the free and protein-bound digoxin this technique also may be useful in evaluating serum digoxin concentrations in patients with abnormal plasma protein concentrations. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HOSP UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. RP NATOWICZ, M (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 11 TC 6 Z9 6 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD JUL-AUG PY 1991 VL 25 IS 7-8 BP 739 EP 741 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FX646 UT WOS:A1991FX64600007 PM 1949929 ER PT J AU BURGESS, KE ODYSSEOS, AD ZALVAN, C DRUKER, BJ ANDERSON, P SCHLOSSMAN, SF RUDD, CE AF BURGESS, KE ODYSSEOS, AD ZALVAN, C DRUKER, BJ ANDERSON, P SCHLOSSMAN, SF RUDD, CE TI BIOCHEMICAL-IDENTIFICATION OF A DIRECT PHYSICAL INTERACTION BETWEEN THE CD4 - P56LCK AND TI(TCR)/CD3 COMPLEXES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID PROTEIN-TYROSINE KINASE; T-CELL ACTIVATION; HUMAN LYMPHOCYTES-T; ANTIGEN RECEPTOR; CROSS-LINKING; MONOCLONAL-ANTIBODIES; ANTI-L3T4 ANTIBODIES; CYTOPLASMIC DOMAINS; NEGATIVE SIGNAL; MOLECULE AB The CD4 and CD8 antigens function in synergy with the TcR/CD3 complex in the generation of intracellular signals leading to T cell proliferation. The association of the protein-tyrosine kinase p56lck with CD4 and CD8 provides a potential mechanism in the generation of intracellular signals. Several studies have shown that CD4 can co-modulate with TcR/CD3 suggesting that these receptor complexes may associate on the surface of the T cell. Nevertheless, it has proven difficult to formally demonstrate a direct physical interaction between the CD4 and TcR/CD3 complexes using biochemical techniques. In this study, we have used the sensitivity of the in vitro kinase assay to show a direct physical linkage between the CD4:p56lck complex and various CD3 subunits. Immunoprecipitation of CD4 from cell lysates derived from the T lymphoblastoid line HPB-ALL results in the co-purification of p56lck with an additional polypeptide at 20 kDa. Re-precipitation analysis and isoelectric focusing demonstrated that this band corresponds to the CD3-epsilon chain. An alternative approach which involves the labeling of microsomal membranes with [gamma-P-32]ATP revealed the presence of CD3-epsilon and zeta-chains in anti-CD4 immunoprecipitates. By contrast, we were unable to demonstrate the association of the CD4:p56lck and TcR/CD3 complex in resting peripheral blood lymphocytes. These data indicate that the CD4:p56lck and TcR/CD3 complexes have the ability to form stable complexes on the surface of certain T cell lines. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIAID NIH HHS [AI 125505-01, AI 12069-16] NR 49 TC 83 Z9 83 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 JUL PY 1991 VL 21 IS 7 BP 1663 EP 1668 DI 10.1002/eji.1830210712 PG 6 WC Immunology SC Immunology GA FW387 UT WOS:A1991FW38700011 PM 1829412 ER PT J AU GREINER, JV WEIDMAN, TA AF GREINER, JV WEIDMAN, TA TI COMPARATIVE HISTOGENESIS OF BRUCHS MEMBRANE (COMPLEXUS BASALIS) SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE BRUCHS MEMBRANE (COMPLEXUS BASALIS); PHOTORECEPTORS; HISTOGENESIS; COMPARATIVE DEVELOPMENT; CAT; FERRET; RABBIT; VOLE; HAMSTER ID RETINA; RAT C1 BETH ISRAEL HOSP,DIV OPHTHALMOL,BOSTON,MA 02215. RETINA FDN,EYE RES INST,BOSTON,MA 02114. MED COLL GEORGIA,DEPT ANAT,AUGUSTA,GA 30912. RP GREINER, JV (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,20 STANIFORD ST,BOSTON,MA 02114, USA. NR 16 TC 9 Z9 9 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 JUL PY 1991 VL 53 IS 1 BP 47 EP 54 DI 10.1016/0014-4835(91)90143-3 PG 8 WC Ophthalmology SC Ophthalmology GA FX285 UT WOS:A1991FX28500007 PM 1879501 ER PT J AU LIANG, JN LI, XY AF LIANG, JN LI, XY TI INTERACTION AND AGGREGATION OF LENS CRYSTALLINS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE CRYSTALLIN; PROTEIN INTERACTION; HIGH MOLECULAR WEIGHT PROTEIN AGGREGATION; FLUORESCENCE ID AGE-RELATED-CHANGES; EYE LENS; ALPHA-CRYSTALLIN; CALF LENS; BOVINE; FLUORESCENCE; PROTEINS; MEMBRANE; ACCESSIBILITY; CONFORMATION RP LIANG, JN (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,HOWE LAB OPHTHALMOL,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY05803] NR 24 TC 61 Z9 62 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 JUL PY 1991 VL 53 IS 1 BP 61 EP 66 DI 10.1016/0014-4835(91)90145-5 PG 6 WC Ophthalmology SC Ophthalmology GA FX285 UT WOS:A1991FX28500009 PM 1879503 ER PT J AU WILLIAMS, DA AF WILLIAMS, DA TI MICROENVIRONMENT REGULATION OF HEMATOPOIESIS - THE ROLE OF STROMAL-DERIVED CYTOKINES IN BLOOD-CELL FORMATION SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUL PY 1991 VL 19 IS 6 BP 457 EP 457 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA FQ310 UT WOS:A1991FQ31000003 ER PT J AU GRIFFIN, JD OKUDA, K KANAKURA, Y DRUKER, B AF GRIFFIN, JD OKUDA, K KANAKURA, Y DRUKER, B TI GM-CSF AND IL-3 ACTIVATE MULTIPLE CELLULAR KINASES SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 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 CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUL PY 1991 VL 19 IS 6 BP 458 EP 458 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA FQ310 UT WOS:A1991FQ31000008 ER PT J AU TEIXIDO, J HEMMLER, M GREENBERGER, J ANKLESARIA, P AF TEIXIDO, J HEMMLER, M GREENBERGER, J ANKLESARIA, P TI ADHESION OF HUMAN HEMATOPOIETIC PROGENITORS TO MARROW STROMAL CELLS-INVITRO INVOLVES VLA-4 AND VCAM-1 SO EXPERIMENTAL HEMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MASSACHUSETTS,MED CTR,AMHERST,MA 01003. NR 0 TC 5 Z9 5 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD JUL PY 1991 VL 19 IS 6 BP 476 EP 476 PG 1 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA FQ310 UT WOS:A1991FQ31000073 ER PT J AU HASELTINE, WA AF HASELTINE, WA TI MOLECULAR-BIOLOGY OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO FASEB JOURNAL LA English DT Review DE AIDS; HIV-1 PATHOGENESIS; HIV-1 REPLICATION; GENE CONTROL OF HIV-1 ID LONG TERMINAL REPEAT; OPEN READING FRAME; T-CELL ACTIVATION; VIRION-ASSOCIATED PROTEIN; MURINE LEUKEMIA-VIRUS; VIRAL MESSENGER-RNA; REV TRANS-ACTIVATOR; III HTLV-III/LAV; TAT PROTEIN; ENVELOPE GLYCOPROTEIN AB The immunodeficiency virus type 1 is a complex retrovirus. In addition to genes that specify the proteins of the virus particle and the replicative enzymes common to all retroviruses, HIV-1 specifies at least six additional proteins that regulate the virus life cycle. Two of these regulatory genes, tat and rev, specify proteins essential for replication. These proteins bind to specific sequences of newly synthesized virus RNA and profoundly affect virus protein expression. Tat and rev appear to be prototypes of novel eukaryotic regulatory proteins. These two genes may play a central role in regulating the rate of virus replication. Three other viral genes, vif, vpu, and vpr, affect the assembly and replication capacity of newly made virus particles. These genes may play a critical role in spread of the virus from tissue to tissue and from person to person. Our understanding of the contribution of each of the virus structural proteins and regulatory genes to the complex life cycle of the virus in natural infections is incomplete. However, enough insight has been gained into the structure and function of each of these components to provide a firm basis for rational antiviral drug development. RP HASELTINE, WA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 120 TC 130 Z9 130 U1 1 U2 9 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 JUL PY 1991 VL 5 IS 10 BP 2349 EP 2360 PG 12 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA FW087 UT WOS:A1991FW08700005 PM 1829694 ER PT J AU BERG, M MURAKAWA, Y CAMERINI, D JAMES, SP AF BERG, M MURAKAWA, Y CAMERINI, D JAMES, SP TI LAMINA PROPRIA LYMPHOCYTES ARE DERIVED FROM CIRCULATING CELLS THAT LACK THE LEU-8 LYMPH-NODE HOMING RECEPTOR SO GASTROENTEROLOGY LA English DT Article ID HIGH-ENDOTHELIAL VENULES; NORMAL NONHUMAN-PRIMATES; SUPPRESSOR T-CELLS; DIFFERENTIATION ANTIGENS; ADHESION MOLECULE; SURFACE MOLECULE; HELPER-INDUCER; EXPRESSION; MUCOSAL; ACTIVATION C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. NR 47 TC 38 Z9 38 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD JUL PY 1991 VL 101 IS 1 BP 90 EP 99 PG 10 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FQ871 UT WOS:A1991FQ87100012 PM 2044931 ER PT J AU TAYLOR, ICA WORKMAN, JL SCHUETZ, TJ KINGSTON, RE AF TAYLOR, ICA WORKMAN, JL SCHUETZ, TJ KINGSTON, RE TI FACILITATED BINDING OF GAL4 AND HEAT-SHOCK FACTOR TO NUCLEOSOMAL TEMPLATES - DIFFERENTIAL FUNCTION OF DNA-BINDING DOMAINS SO GENES & DEVELOPMENT LA English DT Article DE HEAT SHOCK FACTOR; GAL4; TFIID; NUCLEOSOME BINDING; TRANSCRIPTIONAL REGULATION ID I HYPERSENSITIVE SITES; UPSTREAM ACTIVATING SEQUENCE; HUMAN HSP70 PROMOTER; CHROMATIN STRUCTURE; PROTEIN-BINDING; TRANSCRIPTIONAL REGULATION; POSITIONED NUCLEOSOMES; 5' ENDS; YEAST; GENE AB Regulatory factors must contend with chromatin structure to function. Although nucleosome structure and position on promoters can be important in determining factor access, the intrinsic ability of factors to bind to nucleosomal DNA might also play an essential regulatory role. We have used templates where nucleosomes were either randomly positioned or rotationally phased to demonstrate that two transcription factors, heat shock factor (HSF) and GAL4, differ significantly in their ability to bind to nucleosomes. GAL4 was able to bind to nucleosomal templates. Surprisingly, in contrast to its behavior on naked DNA, GAL4 bound better to multiple GAL4 sites than to a single GAL4 site on these templates. HSF alone was not able to bind to nucleosomal templates. HSF was able to bind to nucleosomal templates, however, when the TATA-binding factor TFIID was present. Consequently, binding to nucleosomal templates could be facilitated by adjacent binding of the same protein in the case of GAL4 but required binding of a second protein in the case of HSF. Taken together, these data demonstrate that regulatory factors differ in their inherent ability to bind to nucleosomal templates. These differences are likely to be important to the function of these factors in vivo. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 67 TC 220 Z9 220 U1 1 U2 2 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 JUL PY 1991 VL 5 IS 7 BP 1285 EP 1298 DI 10.1101/gad.5.7.1285 PG 14 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA FV521 UT WOS:A1991FV52100016 PM 2065977 ER PT J AU MAISONPIERRE, PC LEBEAU, MM ESPINOSA, R IP, NY BELLUSCIO, L DELAMONTE, SM SQUINTO, S FURTH, ME YANCOPOULOS, GD AF MAISONPIERRE, PC LEBEAU, MM ESPINOSA, R IP, NY BELLUSCIO, L DELAMONTE, SM SQUINTO, S FURTH, ME YANCOPOULOS, GD TI HUMAN AND RAT BRAIN-DERIVED NEUROTROPHIC FACTOR AND NEUROTROPHIN-3 - GENE STRUCTURES, DISTRIBUTIONS, AND CHROMOSOMAL LOCALIZATIONS SO GENOMICS LA English DT Article ID NERVE GROWTH-FACTOR; MOLECULAR-CLONING; ENZYMATIC AMPLIFICATION; NUCLEOTIDE-SEQUENCE; MESSENGER-RNA; FACTOR FAMILY; EXPRESSION; DNA; IDENTIFICATION; SYSTEM C1 REGENERON PHARMACEUT INC,777 OLD SAW MILL RIVER RD,TARRYTOWN,NY 10591. UNIV CHICAGO,DEPT MED,HEMATOL ONCOL SECT,CHICAGO,IL 60637. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MOLEC NEUROPATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA 42557, CA 40046] NR 38 TC 370 Z9 391 U1 0 U2 9 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD JUL PY 1991 VL 10 IS 3 BP 558 EP 568 DI 10.1016/0888-7543(91)90436-I PG 11 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FQ640 UT WOS:A1991FQ64000007 PM 1889806 ER PT J AU TURA, S CANELLOS, G GOLDSTONE, A LONGO, D MCMILLAN, A URBA, W ZINZANI, PL AF TURA, S CANELLOS, G GOLDSTONE, A LONGO, D MCMILLAN, A URBA, W ZINZANI, PL TI HODGKINS-DISEASE - CONTROVERSIES AND CHALLENGES FOR THE FUTURE SO HAEMATOLOGICA LA English DT Discussion ID BONE-MARROW TRANSPLANTATION; HIGH-DOSE CYCLOPHOSPHAMIDE; COMBINATION CHEMOTHERAPY; MALIGNANT NEOPLASMS; MOPP CHEMOTHERAPY; INCREASED RISK; FREE SURVIVAL; 1ST RELAPSE; FOLLOW-UP; LEUKEMIA C1 UNIV BOLOGNA,IST EMATOL LA SERAGNOLI,I-40126 BOLOGNA,ITALY. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. UNIV COLL HOSP LONDON,DEPT HEMATOL,WC1 LONDON,ENGLAND. NCI,FREDERICK,MD 21701. RI Zinzani, Pier Luigi/J-9182-2016 OI Zinzani, Pier Luigi/0000-0002-2112-2651 NR 72 TC 7 Z9 7 U1 0 U2 0 PU PENSIERO SCIENTIFICO EDITOR PI ROME PA VIA BRADANO 3/C, 00199 ROME, ITALY SN 0390-6078 J9 HAEMATOLOGICA JI Haematologica PD JUL-AUG PY 1991 VL 76 IS 4 BP 263 EP 279 PG 17 WC Hematology SC Hematology GA GC709 UT WOS:A1991GC70900001 PM 1724436 ER PT J AU HEATHER, DJ HOWELL, L MONTANA, M HOWELL, M HILL, R AF HEATHER, DJ HOWELL, L MONTANA, M HOWELL, M HILL, R TI EFFECT OF A BULK-FORMING CATHARTIC ON DIARRHEA IN TUBE-FED PATIENTS SO HEART & LUNG LA English DT Article AB Diarrhea is a significant complication for the patient being tube-fed. The purpose of this study was to observe whether giving a bulk-forming cathartic to patients receiving enteral nutrition via nasogastric or nasoduodenal tube would result in firmer stools for these patients. Forty-nine patients in a large medical center were randomly assigned to either a control or an experimental group. During the 6-day study period 1 teaspoon (5 ml) of psyllium preparation was administered through the feeding tube three times a day. Data were analyzed by using the Mann-Whitney U test for nonparametric data. The hypothesis that giving a bulk-forming cathartic would lead to firmer stools was supported at an alpha level of less than 0.01. The results of this study suggest that use of a bulk-forming cathartic in tube-fed patients will significantly reduce the diarrhea associated with this type of feeding. C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. NR 0 TC 17 Z9 17 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0147-9563 J9 HEART LUNG JI Heart Lung PD JUL PY 1991 VL 20 IS 4 BP 409 EP 413 PG 5 WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System SC Cardiovascular System & Cardiology; Nursing; Respiratory System GA FZ436 UT WOS:A1991FZ43600015 PM 1906447 ER PT J AU BLUM, HE LIANG, TJ GALUN, E WANDS, JR AF BLUM, HE LIANG, TJ GALUN, E WANDS, JR TI PERSISTENCE OF HEPATITIS-B VIRAL-DNA AFTER SEROLOGICAL RECOVERY FROM HEPATITIS-B VIRUS-INFECTION SO HEPATOLOGY LA English DT Article ID CHRONIC LIVER-DISEASE; PRE-C REGION; SURFACE-ANTIGEN; HEPATOCELLULAR-CARCINOMA; PRECORE REGION; CORE ANTIGEN; PLASMID DNA; NON-A; IDENTIFICATION; TRANSMISSION AB Chronic hepatitis B virus infection is a major medical problem worldwide. Apart from HBsAg carriers, hepatitis B virus has also been identified in some HBsAg- individuals with or without antibodies to viral antigens. The molecular mechanisms underlying hepatitis B virus persistence in HBsAg- individuals are unresolved, however. To identify a possible genetic basis for viral persistence, we cloned the viral genome from the liver of a patient serologically immune to hepatitis B virus infection. DNA sequence analysis of the complete viral genome identified numerous mutations in all viral genes. Analysis of the biological effects of these mutations revealed three major findings: a low level of HBsAg synthesis, absence of HBeAg production and a defect terminating viral replication. These data suggest that mutations accumulating during the natural course of hepatitis B virus infection may be a mechanism underlying viral persistence in HBsAg- individuals, presumably through escape from immune surveillance. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. RP BLUM, HE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,149 13TH ST,BOSTON,MA 02129, USA. FU NIAAA NIH HHS [AA-00048, AA-02666]; NIDDK NIH HHS [DK-01952] NR 51 TC 107 Z9 108 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD JUL PY 1991 VL 14 IS 1 BP 56 EP 62 DI 10.1002/hep.1840140110 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FW002 UT WOS:A1991FW00200009 PM 2066074 ER PT J AU MITLAK, BH HUTCHISON, JS KAUFMAN, SD NUSSBAUM, SR AF MITLAK, BH HUTCHISON, JS KAUFMAN, SD NUSSBAUM, SR TI PARATHYROID HORMONE-RELATED PEPTIDE MEDIATES HYPERCALCEMIA IN AN ISLET CELL TUMOR OF THE PANCREAS SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE HYPERCALCEMIA; ISLET CELL TUMOR; PARATHYROID HORMONE-RELATED PEPTIDE ID HUMORAL HYPERCALCEMIA; MALIGNANCY; PROTEIN; HYPERPARATHYROIDISM; CARCINOMA AB Hypercalcemia occurring in a patient with an islet cell carcinoma of the pancreas suggests the diagnosis of Multiple Endocrine Neoplasia Type I and associated hyperparathyroidism. We describe a patient with an islet cell carcinoma and hypercalcemia in whom low concentrations of PTH, the absence of skeletal metastases, hypophosphatemia, and elevated nephrogenous cAMP alternatively suggested the syndrome of humoral hypercalcemia of malignancy. The peptide PTHrP was measured in the patient's serum during the course of therapy by an immunoradiometric assay directed toward the midportion of the molecule. Hypercalcemia was treated with an investigational aminobisphosphonate. The concentration of PTHrP[56-86] increased over time and fell after the patient received chemotherapy directed toward the islet cell tumor. C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,WELLMAN 5,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NICHOLS INST DIAGNOST,SAN JUAN CAPISTRANO,CA. NR 13 TC 20 Z9 20 U1 0 U2 1 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD JUL PY 1991 VL 23 IS 7 BP 344 EP 346 DI 10.1055/s-2007-1003693 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FX986 UT WOS:A1991FX98600010 PM 1663481 ER PT J AU SULLIVAN, G WELLS, KB LEAKE, B AF SULLIVAN, G WELLS, KB LEAKE, B TI QUALITY-OF-LIFE OF SERIOUSLY MENTALLY-ILL PERSONS IN MISSISSIPPI SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Note C1 UNIV CALIF LOS ANGELES,DEPT GEN INTERNAL MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,ROBERT WOOD JOHNSON CLIN SCHOLARS PROGRAM,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT,BRENTWOOD,CA. RP SULLIVAN, G (reprint author), RAND CORP,1700 MAIN ST,SANTA MONICA,CA 90406, USA. NR 9 TC 64 Z9 64 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD JUL PY 1991 VL 42 IS 7 BP 752 EP 755 PG 4 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA FU493 UT WOS:A1991FU49300021 PM 1885191 ER PT J AU SCHUBACK, D KRAMER, P OZELIUS, L HOLMGREN, G FORSGREN, L KYLLERMAN, M WAHLSTROM, J CRAFT, CM NYGAARD, T BRIN, M DELEON, D BRESSMAN, S MOSKOWITZ, CB BURKE, RE SANNER, G DRUGGE, U GUSELLA, JF FAHN, S BREAKEFIELD, XO AF SCHUBACK, D KRAMER, P OZELIUS, L HOLMGREN, G FORSGREN, L KYLLERMAN, M WAHLSTROM, J CRAFT, CM NYGAARD, T BRIN, M DELEON, D BRESSMAN, S MOSKOWITZ, CB BURKE, RE SANNER, G DRUGGE, U GUSELLA, JF FAHN, S BREAKEFIELD, XO TI DOPAMINE BETA-HYDROXYLASE GENE EXCLUDED IN 4 SUBTYPES OF HEREDITARY DYSTONIA SO HUMAN GENETICS LA English DT Article ID AUTOSOMAL DOMINANT INHERITANCE; IDIOPATHIC TORSION DYSTONIA; SEGREGATION ANALYSIS; LINKAGE ANALYSIS; BRAIN NEUROTRANSMITTERS; ASHKENAZI JEWS; LOCALIZATION; REGIONS; COMPLEX; FAMILY AB The hereditary dystonias include a clinically heterogeneous group of movement disorders varying in symptoms, age of onset, and drug responsiveness. Dopamine beta-hydroxylase (DBH), the enzyme that converts dopamine to norepinephrine, has been implicated in dystonia because of increased serum levels of DBH in some patients, the influence of catecholaminergic drugs on the human phenotypes, and altered norepinephrine levels in several brain regions in dystonia patients and in genetically dystonic rodents. In addition, markers linked to the dystonia gene in two ethnic groups map close to the DBH locus on human chromosome 9q34. Here we evaluate the inheritance of restriction fragment length polymorphisms near the DBH gene in families with four subtypes of hereditary dystonia: Jewish and non-Jewish, early onset, generalized idiopathic torsion dystonia (ITD); dopa-responsive dystonia; and myoclonic dystonia. In all families, obligate recombination events were observed between the DBH and dystonia genes, thus excluding the DBH gene as the primary defect. C1 MASSACHUSETTS GEN HOSP,NEUROSCI CTR NEUROL,BOSTON,MA 02114. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UMEA UNIV HOSP,DEPT CLIN GENET,S-90185 UMEA,SWEDEN. UMEA UNIV HOSP,DEPT NEUROL,S-90185 UMEA,SWEDEN. GOTHENBURG UNIV,DEPT PEDIAT,S-41124 GOTHENBURG,SWEDEN. GOTHENBURG UNIV,DEPT CLIN GENET,S-41124 GOTHENBURG,SWEDEN. VET ADM MED CTR,DALLAS,TX 75216. COLUMBIA PRESBYTERIAN MED CTR,DEPT NEUROL,DYSTONIA CLIN RES CTR,NEW YORK,NY 10032. CENT HOSP KARLSTAD,CTR CHILD HABILITAT,KARLSTAD,SWEDEN. UMEA UNIV,DEPT SOCIOL,S-90187 UMEA,SWEDEN. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RI Burke, Robert/B-7226-2011 OI Burke, Robert/0000-0002-4760-8553 FU NINDS NIH HHS [NS26656] NR 48 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6717 J9 HUM GENET JI Hum. Genet. PD JUL PY 1991 VL 87 IS 3 BP 311 EP 316 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA FY516 UT WOS:A1991FY51600012 PM 1677923 ER PT J AU RUSSELL, GJ WINTER, HS FOX, VL BHAN, AK AF RUSSELL, GJ WINTER, HS FOX, VL BHAN, AK TI LYMPHOCYTES BEARING THE GAMMA-DELTA-T-CELL RECEPTOR IN NORMAL HUMAN INTESTINE AND CELIAC-DISEASE SO HUMAN PATHOLOGY LA English DT Article DE INTRAEPITHELIAL LYMPHOCYTES; MUCOSAL IMMUNOLOGY ID INTRAEPITHELIAL LYMPHOCYTES; MONOCLONAL-ANTIBODIES; EXPRESSION; SUBPOPULATION; HETERODIMER; THYMOCYTES; FORMS; THY-1 C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,COMBINED PROGRAM PEDIAT GASTROENTEROL,BOSTON,MA 02115. RP RUSSELL, GJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,IMMUNOPATHOL UNIT,COX 5,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL18646]; NIAID NIH HHS [AI27747]; PHS HHS [DR33506] NR 35 TC 19 Z9 21 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 JUL PY 1991 VL 22 IS 7 BP 690 EP 694 DI 10.1016/0046-8177(91)90291-V PG 5 WC Pathology SC Pathology GA GQ801 UT WOS:A1991GQ80100010 PM 1906424 ER PT J AU YOKOI, T MARK, EJ AF YOKOI, T MARK, EJ TI ATYPICAL MESOTHELIAL HYPERPLASIA ASSOCIATED WITH BRONCHOGENIC-CARCINOMA SO HUMAN PATHOLOGY LA English DT Article DE ATYPICAL MESOTHELIAL HYPERPLASIA; BRONCHOGENIC CARCINOMA ID PLEURISY; DIFFERENTIATION; PROLIFERATION; BIOPSIES; LESION C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 16 TC 9 Z9 9 U1 1 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 JUL PY 1991 VL 22 IS 7 BP 695 EP 699 DI 10.1016/0046-8177(91)90292-W PG 5 WC Pathology SC Pathology GA GQ801 UT WOS:A1991GQ80100011 PM 1712750 ER PT J AU FRASER, PA AWDEH, ZL RONCO, P SIMON, S MOORE, B FICI, D MARCUSBAGLEY, D YUNIS, EJ ALPER, CA AF FRASER, PA AWDEH, ZL RONCO, P SIMON, S MOORE, B FICI, D MARCUSBAGLEY, D YUNIS, EJ ALPER, CA TI C4B GENE POLYMORPHISMS AMONG AFRICAN AND AFRICAN-AMERICAN HLA-BW42-DRW18 HAPLOTYPES SO IMMUNOGENETICS LA English DT Note ID MAJOR HISTOCOMPATIBILITY COMPLEX; STEROID 21-HYDROXYLASE GENES; EXTENDED HAPLOTYPES; MHC HAPLOTYPES; C-4; HLA; SIZE; DETERMINANTS; C4-GENES; VARIANTS C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. RP FRASER, PA (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 20531]; NIAID NIH HHS [AI 14157]; NIAMS NIH HHS [AR 36308] NR 37 TC 8 Z9 8 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JUL PY 1991 VL 34 IS 1 BP 52 EP 56 DI 10.1007/BF00212312 PG 5 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA FW127 UT WOS:A1991FW12700008 PM 1677346 ER PT J AU LECHLER, R GALLAGHER, RB AUCHINCLOSS, H AF LECHLER, R GALLAGHER, RB AUCHINCLOSS, H TI HARD GRAFT - FUTURE CHALLENGES IN TRANSPLANTATION SO IMMUNOLOGY TODAY LA English DT Article ID CELLS; SPECIFICITY; ACTIVATION; TOLERANCE; CHIMERAS; INVITRO AB A small group of transplantation surgeons, immunologists and molecular biologists gathered in Vienna in early February to discuss the prospects for organ transplantation. Participants at the meeting were challenged with setting goals for transplantation research and with speculating on how this research might influence the practice of transplantation in the next two decades. Some goals were set, but the most vigorous discussion focused on the existing barriers that stand in the way of achieving these goals. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP LECHLER, R (reprint author), HAMMERSMITH HOSP,ROYAL POSTGRAD MED SCH,DEPT IMMUNOL,LONDON W12 0HS,ENGLAND. OI Gallagher, Richard/0000-0001-5639-2187 NR 13 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0167-5699 J9 IMMUNOL TODAY JI Immunol. Today PD JUL PY 1991 VL 12 IS 7 BP 214 EP 216 DI 10.1016/0167-5699(91)90030-W PG 3 WC Immunology SC Immunology GA FU065 UT WOS:A1991FU06500002 PM 1679634 ER PT J AU DUGGER, KO GALGIANI, JN AMPEL, NM SUN, SH MAGEE, DM HARRISON, J LAW, JH AF DUGGER, KO GALGIANI, JN AMPEL, NM SUN, SH MAGEE, DM HARRISON, J LAW, JH TI AN IMMUNOREACTIVE APOGLYCOPROTEIN PURIFIED FROM COCCIDIOIDES-IMMITIS SO INFECTION AND IMMUNITY LA English DT Article ID SUBMAXILLARY-GLAND APOMUCIN; TUBE PRECIPITIN; WALL FRACTION; ANTIGEN; ANTIBODY; PROTEIN; INFECTION; RESPONSES; PURIFICATION; RESISTANCE AB Deglycosylation of glycoproteins in a lysate of spherules of Coccidioides immitis has permitted purification and partial characterization of a proline-rich pronase-sensitive antigen. Moreover, soluble antigen specifically stimulated lymphocytes from persons with dermal delayed-type hypersensitivity to coccidiodial antigens. When related to reference coccidioidin by tandem two-dimensional immunoelectrophoresis, the antigen fused in the anodal region with a specific reference antigen (antigen 2). It did not show identity with coccidiodial antigens used in conventional serologic assays. Although immunoblots of the purified protein with monospecific rabbit and serum showed a single antigen at 33 kDa, the parent spherule lysate bound the same antibody in a broad band between 70 and > 200 kDa, which could be explained by microheterogeneity of glycosylation. Immunoelectron microscopy using affinity-purified human antibodies localized the antigen to the cell wall and internal septa of spherules. These findings suggest that the apoglycoprotein may be important in human immune responses to coccidioidal infection. C1 VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ 85723. VET AFFAIRS MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV ARIZONA,DEPT BIOCHEM,TUCSON,AZ 85724. VET AFFAIRS MED CTR,MED SERV,TUCSON,AZ 85723. UNIV ARIZONA,COLL MED,DEPT MED,TUCSON,AZ 85724. NR 48 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1991 VL 59 IS 7 BP 2245 EP 2251 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FT922 UT WOS:A1991FT92200004 PM 2050396 ER PT J AU MAGEE, DM WILLIAMS, DM WING, EJ BLEICKER, CA SCHACHTER, J AF MAGEE, DM WILLIAMS, DM WING, EJ BLEICKER, CA SCHACHTER, J TI PRODUCTION OF COLONY-STIMULATING FACTORS DURING PNEUMONIA CAUSED BY CHLAMYDIA-TRACHOMATIS SO INFECTION AND IMMUNITY LA English DT Article ID LISTERIA-MONOCYTOGENES; GAMMA INTERFERON; PROGENITOR CELLS; MICE; MOUSE; INFECTION; IMMUNITY; GROWTH; AGENT AB The colony-stimulating factors (CSFs) are cytokines involved in the production, differentiation, and activation of host phagocytes. During murine infection with Chlamydia trachomatis (MoPn), plasma CSF levels increased in euthymic (nu/+) and athymic (nu/nu) BALB/c mice. Levels declined later in infection, with the nu/+ mice resolving the infection but the nu/nu mice succumbing by day 16. Either live or heat-killed Chlamydia organisms could induce CSF increases on day 7 postchallenge in nu/+ mice; however, by day 14, only mice challenged with live organims maintained high plasma levels. CSFs were also produced by spleen cells of nu/+ and nu/nu mice in response to Chlamydia antigen. Spleen cell CSF production was detectable by days 3 to 5 postinfection. In nu/+ mice, spleen cell CSF production was elevated throughout the rest of the time course but in nu/nu mice fell significantly at day 14. Like the plasma CSF activity (CSA) production, spleen cell CSA production on day 7 was seen in mice challenged with either live or heat-killed Chlamydia organisms, but on day 14 only nu/+ mice challenged with live organisms maintained significant CSA production. To further characterize the T-cell dependence of CSA production, spleen cells of nu/+ mice were depleted of T cells or T-cell subsets before producing supernatants. On day 14 postinfection, the CD4+ lymphocyte was the major producer of CSFs. Additionally, there were different types of CSFs secreted by nu/+ and nu/nu mice as determined by the ability of spleen cell supernatants to support the granulocyte-macrophage CSF/interleukin 3-dependent cell line FDCP-1. Supernatants from nu/+ mice had 4 to 8 times the level of FDCP-1 CSF activity of the supernatants from nu/nu mice. These results support the evidence that nu/+ mice were producing some CSFs by T-cell-dependent mechanisms. This is the first report of CSF production in vivo during Chlamydia infection. Furthermore, we show that CSFs are produced by both T-cell-dependent and T-cell-independent mechanisms. The capacity of the CSFs to increase the production and effector function of phagocytes may be important to host defenses. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV INFECT DIS,SAN ANTONIO,TX 78284. UNIV PITTSBURGH,SCH MED,DEPT MED,PITTSBURGH,PA 15213. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94132. RP MAGEE, DM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284, USA. FU NIAID NIH HHS [AI 24141, AI 22380] NR 24 TC 13 Z9 13 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUL PY 1991 VL 59 IS 7 BP 2370 EP 2375 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FT922 UT WOS:A1991FT92200022 PM 1828791 ER PT J AU CARRERA, AC LI, P ROBERTS, TM AF CARRERA, AC LI, P ROBERTS, TM TI CHARACTERIZATION OF AN ACTIVE, NON-MYRISTYLATED, CYTOPLASMIC FORM OF THE LYMPHOID PROTEIN TYROSINE KINASE PP56LCK SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE ICK; SIGNALING; PHOSPHORYLATION; HETEROGENEITY ID T-CELL RECEPTOR; SIGNAL TRANSDUCTION; CD4 RECEPTOR; INSECT CELLS; PHOSPHORYLATION; P56LCK; ACTIVATION; PP60C-SRC; ANTIGEN; SITES AB pp56lck is a member of the src family of tyrosine kinases mainly expressed in T lymphocytes. Src tyrosine kinases have been implicated in the control of cell growth and differentiation in different cell types, but the mechanism of regulation of these enzymes is poorly understood. In order to characterize the distinct species of pp56lck, we have produced high yields of enzymatically active wild type pp56lck using the eukaryotic baculovirus expression system in Spodoptera frugiperda insect cells (Sf9). We find that the various species of baculoviral pp56lck are not only differentially phosphorylated (on serine and tyrosine residues) but also heterogeneously myristylated. Surprisingly a non-myristylated, very active form of bv-pp56lck is found in the cytoplasm of Sf9 cells. Fractionation of T cells reveals that cytoplasmic pp56lck exists in T lymphocytes as well. RP CARRERA, AC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,BOSTON,MA 02115, USA. OI Carrera, Ana/0000-0002-3999-5434 FU NCI NIH HHS [CA43803] NR 38 TC 13 Z9 13 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 JUL PY 1991 VL 3 IS 7 BP 673 EP 682 DI 10.1093/intimm/3.7.673 PG 10 WC Immunology SC Immunology GA FX137 UT WOS:A1991FX13700008 PM 1911540 ER PT J AU ROHRER, TE AHMED, AR AF ROHRER, TE AHMED, AR TI TOXIC EPIDERMAL NECROLYSIS SO INTERNATIONAL JOURNAL OF DERMATOLOGY LA English DT Review ID SCALDED-SKIN SYNDROME; STEVENS-JOHNSON SYNDROME; ANTI-INFLAMMATORY DRUGS; ERUPTIVE NEVOCYTIC NEVI; SEVERE BULLOUS DISEASE; LYELLS SYNDROME; ERYTHEMA MULTIFORME; CUTANEOUS REACTIONS; MUCOCUTANEOUS ERUPTIONS; MARROW TRANSPLANTATION C1 HARVARD UNIV,SCH DENT MED,CTR BLOOD RES,DEPT ORAL PATHOL,800 HUNTINGTON AVE,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT INTERNAL MED,NEW HAVEN,CT 06510. FU NIDCR NIH HHS [DE 07117] NR 147 TC 11 Z9 11 U1 0 U2 0 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0011-9059 J9 INT J DERMATOL JI Int. J. Dermatol. PD JUL PY 1991 VL 30 IS 7 BP 457 EP 466 DI 10.1111/j.1365-4362.1991.tb04861.x PG 10 WC Dermatology SC Dermatology GA FY340 UT WOS:A1991FY34000001 PM 1769764 ER PT J AU JONES, MA YOUNG, RH SCULLY, RE AF JONES, MA YOUNG, RH SCULLY, RE TI ENDOMETRIAL ADENOCARCINOMA WITH A COMPONENT OF GIANT-CELL CARCINOMA SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE ENDOMETRIAL CARCINOMA; GIANT CELL CARCINOMA; SARCOMATOID PATTERN ID TUMORS; LUNG; LIGHT AB We report six high-grade endometrial adenocarcinomas with a malignant giant cell component. The patients ranged in age from 43 to 85 years (mean 65); five were postmenopausal. All the patients presented with vaginal bleeding. The tumors all had a giant cell component that was composed of poorly cohesive sheets and nests of bizarre multinucleated giant cells admixed with an approximately equal number of mononucleate tumor cells. A sarcomatoid pattern and a marked inflammatory infiltrate were each present in three cases. All the tumors contained at least focal areas of endometrial adenocarcinoma of one of the usual types. Occasional malignant giant cells were positive for cytokeratins (AE1/AE3 or CAM 5.2) and epithelial membrane antigen in all three tumors tested. Three tumors were in stage I, one stage III and two stage IV. Two of the patients with stage I disease (each with superficial myometrial invasion) were alive and well 6 and 2 years later. Of the remaining four patients, three died of disease 2.5 years, 6 months, and 5 months after presentation, and one was alive with extensive abdominal disease after 1 year. Giant cell carcinoma of the endometrium is an aggressive tumor that should be distinguished from other endometrial tumors with a prominent giant cell component, including trophoblastic tumors, certain primary sarcomas, and malignant mixed mullerian tumors. It is imperative that malignant giant cells and non-neoplastic giant cells not be confused, as is possible in a curettage or biopsy specimen. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP JONES, MA (reprint author), MAINE MED CTR,DEPT PATHOL,PORTLAND,ME 04102, USA. NR 24 TC 16 Z9 16 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 JUL PY 1991 VL 10 IS 3 BP 260 EP 270 DI 10.1097/00004347-199107000-00005 PG 11 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA FT317 UT WOS:A1991FT31700005 PM 1917275 ER PT J AU HAFFNER, SM KATZ, MS DUNN, JF AF HAFFNER, SM KATZ, MS DUNN, JF TI INCREASED UPPER-BODY AND OVERALL ADIPOSITY IS ASSOCIATED WITH DECREASED SEX-HORMONE BINDING GLOBULIN IN POSTMENOPAUSAL WOMEN SO INTERNATIONAL JOURNAL OF OBESITY LA English DT Article DE SEX HORMONE BINDING GLOBULIN; BODY FAT DISTRIBUTION ID DEPENDENT DIABETES-MELLITUS; HIGH-DENSITY LIPOPROTEIN-2; FAT DISTRIBUTION; CARDIOVASCULAR-DISEASE; TISSUE DISTRIBUTION; INSULIN RESISTANCE; CENTRALIZED ADIPOSITY; POSTHEPARIN PLASMA; MEXICAN-AMERICANS; HDL-CHOLESTEROL AB An unfavorable body fat distribution is associated with many metabolic abnormalities including a high prevalence and incidence of noninsulin dependent diabetes mellitus and decreased high density lipoprotein cholesterol and increased triglyceride levels. One mechanism for the effect of body fat distribution on metabolic variables may be through sex hormones. We examined the relationship of body mass index (BMI), ratio of subscapular-to-triceps skinfold ratio (centrality index) and ratio of waist-to-hip ratio (WHR) to sex hormone binding globulin (SHBG) (an in vivo measure of androgenicity) in 101 postmenopausal Mexican-American and non-Hispanic white women from the San Antonio Heart Study,a population based study of diabetes and cardiovascular disease. SHBG was significantly correlated with BMI (r = -0.440,P < 0.001), WHR (r = -0.255, P < 0.01) and centrality index (r = -0.210,P < 0.05). In a multiple linear regression analysis, SHBG remained significantly associated with BMI (P < 0.001) and WHR (P < 0.05) but not with age, ethnicity or centrality index. This work suggests that in postmenopausal women overall adiposity and an unfavorable body fat distribution are associated with increased androgenicity as measured by a lower SHBG concentration. Our finding may help to explain the association of body fat distribution with diabetes and cardiovascular risk factors in older women. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GERIATR & GERONTOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV ENDOCRINOL & METAB,SAN ANTONIO,TX 78284. RP HAFFNER, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN EPIDEMIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Perez , Claudio Alejandro/F-8310-2010 OI Perez , Claudio Alejandro/0000-0001-9688-184X FU NCRR NIH HHS [RR-01346]; NHLBI NIH HHS [HL-24799] NR 54 TC 101 Z9 101 U1 1 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0307-0565 J9 INT J OBESITY JI Int. J. Obes. PD JUL PY 1991 VL 15 IS 7 BP 471 EP 478 PG 8 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA FV207 UT WOS:A1991FV20700005 PM 1894424 ER PT J AU SCHULTZHECTOR, S KUMMERMEHR, J SUIT, HD AF SCHULTZHECTOR, S KUMMERMEHR, J SUIT, HD TI VASCULAR ARCHITECTURE OF EXPERIMENTAL-TUMORS - INFLUENCE OF TUMOR VOLUME AND TRANSPLANTATION SITE SO INTERNATIONAL JOURNAL OF RADIATION BIOLOGY LA English DT Article; Proceedings Paper CT 16TH L H GRAY CONF ON VASCULATURE AS A TARGET FOR ANTI-CANCER THERAPY CY SEP 17-21, 1990 CL UNIV MANCHESTER, INST SCI & TECHNOL, MANCHESTER, ENGLAND SP L LT GRAY MEM TRUST, SIR SAMUEL SCOTT YEWS TRUST, CANC RES CAMPAIGN, INT ASSOC RADIAT RES, EDINBURG E A R CONGRESS EDUC TRUST, CLATTERBRIDGE CANC RES TRUST, HOECHST UK, LIPHA PHARM, GLAXO GRP RES, WELLCOME FDN HO UNIV MANCHESTER, INST SCI & TECHNOL ID ATHYMIC NUDE-MICE; CARCINOMA; CELLS; PROLIFERATION C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. RP SCHULTZHECTOR, S (reprint author), GESELL STRAHLEN & UMWELTFORSCH MBH,INST STRAHLENBIOL,W-8042 NEUHERBERG,GERMANY. FU NCI NIH HHS [CA-13311] NR 15 TC 8 Z9 8 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 JUL-AUG PY 1991 VL 60 IS 1-2 BP 101 EP 107 DI 10.1080/09553009114551631 PG 7 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 GA969 UT WOS:A1991GA96900017 PM 1677955 ER PT J AU ABNER, AL RECHT, A VICINI, FA SILVER, B HAYES, D COME, S HARRIS, JR AF ABNER, AL RECHT, A VICINI, FA SILVER, B HAYES, D COME, S HARRIS, JR TI COSMETIC RESULTS AFTER SURGERY, CHEMOTHERAPY, AND RADIATION-THERAPY FOR EARLY BREAST-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE BREAST CANCER; CONSERVATIVE SURGERY AND RADIOTHERAPY; CHEMOTHERAPY; COSMESIS ID ADJUVANT CHEMOTHERAPY; CONSERVATIVE SURGERY; RADIOTHERAPY; COMPLICATIONS; IRRADIATION AB Adjuvant chemotherapy (CT) is increasingly being used in conjunction with radiation therapy (RT) in the treatment of early stage breast cancer. To assess the effect of CT on the cosmetic outcome of the irradiated breast, we retrospectively reviewed the cosmetic results of patients who received either cyclophosphamide-methotrexate-fluorouracil (CMF) or doxorubicin-based chemotherapy in conjunction with breast irradiation between 1968 and 1985. The overall cosmetic results were evaluated by the physician as "excellent," "good," "fair," or "poor" using a standardized scale. The CT group consisted of 170 patients treated with CT and RT administered either concurrently or sequentially (CT before RT, after RT, or both) with a minimum of 24 months of cosmetic follow-up. These were compared to an RT alone control group of 170 patients who did not receive CT and were matched by tumor size, radiation technique, and year of treatment. At 36 months, the cosmetic scores for the CT group compared to RT alone were 47% versus 71% excellent (p < 0.01), 36% versus 19% good, and 17% versus 9% fair or poor. For the 50 patients treated with concurrent CMF and RT, the scores were 31% excellent, 45% good, and 24% fair/poor, whereas for the 118 patients treated with sequential RT and CT they were 54%, 31%, and 14%, respectively. There was no difference between those patients who received sequential CMF and those treated with doxorubicin. We conclude that adjuvant chemotherapy adversely affects the cosmetic outcome of breast irradiation, but that this effect is not clinically significant unless CMF is administered concurrently with RT. Patients treated with either sequential CMF or doxorubicin-based CT had only a slight decrement in their cosmetic result compared to patients treated without CT. C1 BETH ISRAEL HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02215. WILLIAM BEAUMONT HOSP,DEPT RADIAT ONCOL,ROYAL OAK,MI 48072. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,BOSTON,MA 02115. RP ABNER, AL (reprint author), HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,50 BINNEY ST,BOSTON,MA 02115, USA. NR 19 TC 95 Z9 97 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JUL PY 1991 VL 21 IS 2 BP 331 EP 338 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FV885 UT WOS:A1991FV88500009 PM 2061109 ER PT J AU WEINBERG, DV KOLODNY, NH KOHLER, SJ BURR, TA CELI, A DAMICO, DJ GRAGOUDAS, ES AF WEINBERG, DV KOLODNY, NH KOHLER, SJ BURR, TA CELI, A DAMICO, DJ GRAGOUDAS, ES TI DYNAMIC SODIUM CHEMICAL-SHIFT IMAGING FOR THE STUDY OF AQUEOUS-HUMOR FLOW SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE ANTERIOR CHAMBER; AQUEOUS HUMOR; CHEMICAL SHIFT IMAGING; SHIFT REAGENT; TM(DOTP)5- AB Ocular images were obtained using sodium chemical shift imaging (CSI) and 1,4,7,10-tetraazacyclododecane-N,N',N",N"'-tetramethylenephosphonate thulium (III) [Tm(DOTP)5-], a paramagnetic chemical shift reagent. After injecting the shift reagent into the anterior chamber of rabbits, serial imaging was done, monitoring the change in chemical shift with time. Sodium CSI produced images of the eye in three dimensions, quantitatively depicting the spatial and temporal changes in the concentration of a paramagnetic tracer substance. The Tm(DOTP)5- is eliminated from the anterior chamber by first-order kinetics with a half-life of 49 min. These data suggest that this substance is eliminated from the anterior chamber at the same rate as aqueous humor is replaced. Sodium CSI shows promise as a valuable technique for monitoring fluid dynamics in the living eye. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114. MIT,MAGNET RESONANCE IMAGING FACIL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,NUCL MAGNET RESONANCE LAB,BOSTON,MA 02115. WELLESLEY COLL,DEPT MED,WELLESLEY,MA 02181. FU NCRR NIH HHS [RR00995] NR 15 TC 3 Z9 3 U1 0 U2 3 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 JUL PY 1991 VL 32 IS 8 BP 2212 EP 2218 PG 7 WC Ophthalmology SC Ophthalmology GA FX406 UT WOS:A1991FX40600006 PM 2071335 ER PT J AU KNISELY, TL ANDERSON, TM SHERWOOD, ME FLOTTE, TJ ALBERT, DM GRANSTEIN, RD AF KNISELY, TL ANDERSON, TM SHERWOOD, ME FLOTTE, TJ ALBERT, DM GRANSTEIN, RD TI MORPHOLOGICAL AND ULTRASTRUCTURAL EXAMINATION OF I-A+ CELLS IN THE MURINE IRIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE IRIS; CLASS-II MHC; IMMUNOPEROXIDASE; ELECTRON MICROSCOPY; MOUSE ID FOLLICULAR DENDRITIC CELLS; ENDOTOXIN-INDUCED UVEITIS; ANTIGEN-PRESENTING CELLS; INTERFERON-GAMMA; TUMORICIDAL ACTIVITY; MACROPHAGE FUNCTION; OCULAR-TISSUES; EXPRESSION; PROLIFERATION; NEUROPEPTIDES AB The surface membrane expression of major histocompatibility (MHC) class II antigens is an important prerequisite for presentation of foreign antigens to the immune system. Because particular antigens that are placed within the anterior chamber of the eye elicit a deviant form of immunity in which effector delayed-type hypersensitivity responses are suppressed, it has been proposed that novel MHC class II antigen-bearing cells exist in the tissues that line the anterior chamber. Class II MHC antigen expression has been identified within the iris, but the detailed morphologic description of these cells is incomplete. With the use of in situ immunoperoxidase and immunoelectron microscopic techniques, we examined the morphologic and ultrastructural characteristics of resident MHC-positive class II (I-A+) cells in murine irises. A significant number of these cells was found in the connective tissue of BALB/c irises. The majority showed extensive dendritic morphologic characteristics and formed a network throughout the iris that did not overlap. Ultrastructurally, I-A+ cells had an indented nucleus, some vacuoles, lysosomes, mitochondria, and an occasional phagosome within their cytoplasm and an absence of desmosomes or other intercellular junctions. Based on these features, it is unlikely that these cells are epithelial or endothelial in origin, but rather are similar to cells of the monocyte/macrophage/dendritic cell lineage. These results show the presence of an I-A+ dendritic cell population, within the murine iris, distributed in a pattern that is similar to that of Langerhans cells in the skin. Due to their compartmentalization within the eye, this cell population may represent a novel antigen-presenting cell that contributes to the immunologic privilege of the anterior chamber. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NEI NIH HHS [EY07782] NR 39 TC 41 Z9 41 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 JUL PY 1991 VL 32 IS 8 BP 2423 EP 2431 PG 9 WC Ophthalmology SC Ophthalmology GA FX406 UT WOS:A1991FX40600029 PM 2071354 ER PT J AU REITER, SR OTTO, MW POLLACK, MH ROSENBAUM, JF AF REITER, SR OTTO, MW POLLACK, MH ROSENBAUM, JF TI MAJOR DEPRESSION IN PANIC DISORDER PATIENTS WITH COMORBID SOCIAL PHOBIA SO JOURNAL OF AFFECTIVE DISORDERS LA English DT Article DE PANIC DISORDER; DEPRESSION; SOCIAL PHOBIA; DYSFUNCTIONAL ATTITUDES; ASSERTIVENESS ID DYSFUNCTIONAL ATTITUDES; AGORAPHOBIA; SYMPTOMS; ANXIETY AB Rates of depression among panic disorder patients are particularly elevated in patients with comorbid social phobia. However, it is unclear whether this association is specific to social phobia, or whether any comorbid anxiety disorder increases the risk of depression. We assessed 100 panic disorder patients and found a significantly higher incidence of lifetime major depression for panic patients with comorbid social phobia or generalized anxiety disorder (GAD). Panic patients with comorbid social phobia had significantly higher scores on measures of dysfunctional attitudes and lower scores on measures of assertiveness; these variables may mediate the link between social phobia and depression in this population. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC-815,15 PARKMAN ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 27 TC 21 Z9 21 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-0327 J9 J AFFECT DISORDERS JI J. Affect. Disord. PD JUL PY 1991 VL 22 IS 3 BP 171 EP 177 DI 10.1016/0165-0327(91)90051-S PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FZ668 UT WOS:A1991FZ66800009 PM 1918660 ER PT J AU KOMADINA, KH DUNCAN, CA BRYAN, CL JENKINSON, SG AF KOMADINA, KH DUNCAN, CA BRYAN, CL JENKINSON, SG TI PROTECTION FROM HYPERBARIC OXIDANT STRESS BY ADMINISTRATION OF BUTHIONINE SULFOXIMINE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE GLUTATHIONE; GAMMA GLUTAMYL CYSTEINE SYNTHASE; HYPERBARIC OXYGEN TOXICITY ID OXYGEN-TOXICITY; GLUTATHIONE DEPLETION; REDUCED GLUTATHIONE; HYPEROXIA; INHIBITION; METABOLISM; INVIVO; CELLS; RATS AB To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold. C1 AUDIE L MURPHY MEM VET ADM MED CTR,PULM DIS SECT,111E,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,LUNG METAB UNIT,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [HL-30556] NR 29 TC 10 Z9 10 U1 0 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD JUL PY 1991 VL 71 IS 1 BP 352 EP 358 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA FV262 UT WOS:A1991FV26200051 PM 1680846 ER PT J AU GELBERMAN, RH KHABIE, V CAHILL, CJ AF GELBERMAN, RH KHABIE, V CAHILL, CJ TI THE REVASCULARIZATION OF HEALING FLEXOR TENDONS IN THE DIGITAL SHEATH - A VASCULAR INJECTION STUDY IN DOGS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID PASSIVE MOBILIZATION; SYNOVIAL ENVIRONMENT; CELLULAR MECHANISMS; NUTRIENT PATHWAYS; BLOOD-FLOW; REPAIR AB The role of revascularization in the nutritional support of repair of the flexor tendons is not completely understood. To explore the extent to which intrasynovial flexor tendons revascularize after transection and suture, a vascular injection study was carried out in a canine model. The tendons to the second and fifth digits of the forepaw in twelve adult mongrel dogs were transected and repaired. There were twenty-four experimental tendons and twenty-four normal tendons. The limb was placed in a polyurethane shoulder-spica cast, and the paw was treated with immediate protected passive mobilization. At three, seven, ten, seventeen, and twenty-eight days, the animals were killed and the major arteries supplying both the paw that had been operated on (left) and the contralateral normal paw (right) were injected with 200 milliliters of India ink. Segments of repaired and normal tendons were then clarified by a modified Spalteholz technique. The normal tendons demonstrated a well developed mesotenon that provided vascularization of the proximal portion of the flexor digitorum profundus tendon. A consistent three-cubic-millimeter avascular intrasynovial portion of tendon was noted. Distally, vessels arose from the vinculum breve, supplying the terminal twenty millimeters of tendon substance. In the experimental tendons, longitudinal and transverse clarified sections showed consistent revascularization of the site of repair by proximal vessels in the absence of ingrowth of peripheral adhesions. Vessels in the epitenon progressively extended for a distance of ten millimeters, through normally avascular regions, to reach the site of repair by the seventeenth postoperative day. Intratendinous vessels about the site of repair consistently originated from surface vessels, rather than from extensions of pre-existing intratendinous vessels. New vessels penetrated all areas, including the normally avascular volar segments of tendon, irrespective of previous topical zones of avascularity. Proximal vascular plexi were characterized by large tortuous vessels with frequent circuitous branches. More distal vessels had a longitudinally oriented, feathery appearance. CLINICAL RELEVANCE: The occurrence of neovascularization of once-avascular tissue suggests a major role for new vessels in the healing of intrasynovial dense tendinous connective tissue. The timing of revascularization at the site of repair corresponds well with the findings of previous experimental studies, which demonstrated increases in strength at the site of repair beginning on the sixteenth to twenty-first postoperative day. Conditions that may have stimulated revascularization in this model include the early reinstitution of function by alternation of flexion and extension, achieved by controlled passive mobilization that was initiated immediately after repair. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC 527,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5R01-AR33097] NR 53 TC 67 Z9 68 U1 2 U2 4 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 JUL PY 1991 VL 73A IS 6 BP 868 EP 881 PG 14 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FY784 UT WOS:A1991FY78400009 PM 1712787 ER PT J AU JASTY, M MALONEY, WJ BRAGDON, CR OCONNOR, DO HAIRE, T HARRIS, WH AF JASTY, M MALONEY, WJ BRAGDON, CR OCONNOR, DO HAIRE, T HARRIS, WH TI THE INITIATION OF FAILURE IN CEMENTED FEMORAL COMPONENTS OF HIP ARTHROPLASTIES SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID 10-YEAR FOLLOW-UP; REPLACEMENT AB We studied 16 femora retrieved at post-mortem from symptomless patients who had a satisfactory cemented total hip arthroplasty from two weeks to 17 years earlier, with the aim of delineating the initial mechanisms involved in loosening. Only one specimen showed radiographic evidence of loosening; the other 15 were stable to mechanical testing at 17.0 Nm of torque. In all 16 specimens, the cement-bone interface was intact with little fibrous tissue formation. By contrast, separation at the cement-prosthesis interface and fractures in the cement mantle were frequent. The most common early feature was debonding of the cement from the metal, seen at the proximal and distal ends of the prosthesis. Specimens which had been in place for longer also showed circumferential fractures in the cement, near the cement-metal interface, and radial fractures extending from this interface into the cement and sometimes to the bony interface. The most extensive cement fractures appeared to have started at or near sharp corners in the metal, or where the cement mantle was thin or incomplete. Fractures were also related to voids in the cement. The time relationship in this series suggested that long-term failure of the fixation of cemented femoral components was primarily mechanical, starting with debonding at the interface between the cement and the prosthesis, and continuing as slowly developing fractures in the cement mantle. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,HIP & IMPLANT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,ORTHOPAED BIOMECH LABS,BOSTON,MA 02114. RP JASTY, M (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 23 TC 448 Z9 453 U1 1 U2 13 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JUL PY 1991 VL 73 IS 4 BP 551 EP 558 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FZ059 UT WOS:A1991FZ05900005 PM 2071634 ER PT J AU POWER, RA WOOD, DJ TOMFORD, WW MANKIN, HJ AF POWER, RA WOOD, DJ TOMFORD, WW MANKIN, HJ TI REVISION OSTEOARTICULAR ALLOGRAFT TRANSPLANTATION IN WEIGHT-BEARING JOINTS - A CLINICAL REVIEW SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Review ID BONE-TUMORS; MANAGEMENT AB The early results of revision osteoarticular allografts in weight-bearing joints are reported. Sixteen consecutive patients underwent surgery over a six-year period between 1982 and 1988. At the time of review eight patients (50%) had surviving second allografts with an average follow-up time of 48 months (range 12 to 87). Five patients were graded excellent according to the Mankin scale, one good and two fair. Eight patients (50%) required further surgery, but only two patients came to amputation. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED ONCOL UNIT,BOSTON,MA 02114. NR 13 TC 6 Z9 6 U1 0 U2 1 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD JUL PY 1991 VL 73 IS 4 BP 595 EP 599 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FZ059 UT WOS:A1991FZ05900014 PM 2071641 ER PT J AU KANSAS, GS SPERTINI, O STOOLMAN, LM TEDDER, TF AF KANSAS, GS SPERTINI, O STOOLMAN, LM TEDDER, TF TI MOLECULAR MAPPING OF FUNCTIONAL DOMAINS OF THE LEUKOCYTE RECEPTOR FOR ENDOTHELIUM, LAM-1 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID NODE HOMING RECEPTOR; CELL-SURFACE MOLECULE; ACTIVATED PLATELETS; ADHESION MOLECULE; LYMPHOCYTE RECIRCULATION; MEMBRANE-PROTEIN; LECTIN DOMAIN; SIALIC-ACID; NEUTROPHILS; BINDING AB The human lymphocyte homing receptor LAM-1, like its murine counterpart MEL-14, functions as a mammalian lectin, and mediates the binding of leukocytes to specialized high endothelial cells in lymphoid organs (HEV). LAM-1 is a member of a new family of cell adhesion molecules, termed selectins or LEC-CAMs, which also includes ELAM-1 and PADGEM (GMP-140/CD62). To localize the regions of LAM-1 that are involved in cell adhesion, we developed chimeric selectins, in which various domains of PADGEM were substituted into LAM-1, and used these chimeric proteins to define the domain requirements for carbohydrate binding, and to localize the regions recognized by several mAb which inhibit the adhesion of lymphocytes to lymph node HEV. The binding of PPME or fucoidin, soluble complex carbohydrates that specifically define the lectin activity of LAM-1 and MEL-14, required only the lectin domain of LAM-1. The LAM1-1, LAM1-3, and LAM1-6 mAb each strongly inhibit the binding of lymphocytes to HEV in the in vitro frozen section assay, and defined three independent epitopes on LAM-1. Blocking of PPME or fucoidin binding by LAM1-3 indicated that this site is identical, or in close proximity, to the carbohydrate binding site, and analysis of the binding of LAM1-3 to chimeric selectins showed that the epitope detected by LAM1-3 is located within the lectin domain. Although the LAM1-6 epitope is also located in the lectin domain, LAM1-6 did not affect the binding of PPME or function. The LAM1-1 epitope was located in, or required, the EGF domain, and, importantly, binding of LAM1-1 significantly enhanced the binding of both PPME and fucoidin. These results suggest that adhesion mediated by LAM-1 may involve cooperativity between functionally and spatially distinct sites, and support previous data suggesting a role for the EGF domain of LAM-1 in lymphocyte adhesion to HEV. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. RP KANSAS, GS (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-26872] NR 50 TC 97 Z9 99 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JUL PY 1991 VL 114 IS 2 BP 351 EP 358 DI 10.1083/jcb.114.2.351 PG 8 WC Cell Biology SC Cell Biology GA FW739 UT WOS:A1991FW73900017 PM 1712791 ER PT J AU KANO, M MOSKOWITZ, MA YOKOTA, M AF KANO, M MOSKOWITZ, MA YOKOTA, M TI PARASYMPATHETIC DENERVATION OF RAT PIAL VESSELS SIGNIFICANTLY INCREASES INFARCTION VOLUME FOLLOWING MIDDLE CEREBRAL-ARTERY OCCLUSION SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE MIDDLE CEREBRAL OCCLUSION; PARASYMPATHETIC LESIONS; ETHMOIDAL FORAMEN; CEREBRAL INFARCTION ID VASOACTIVE INTESTINAL POLYPEPTIDE; GENE-RELATED PEPTIDE; CEREBROVASCULAR NERVE-FIBERS; BLOOD-FLOW; SUBSTANCE-P; CHOLINERGIC NERVES; TRIGEMINAL ORIGIN; CAT; STIMULATION; IMMUNOREACTIVITY AB Studies were undertaken in Long Evans rats to examine the hypothesis that chronic unilateral sectioning of vasodilating nerve fibers (parasympathetic and/or sensory) innervating the circle of Willis increases infarction volume following unilateral branch occlusion of the middle cerebral artery (MCA) combined with temporary (45 min) bilateral common carotid occlusion. Infarct size was measured 24 h after surgical occlusion from seven coronal slices. Infarction volume (mean +/- SD) in sham animals (group A) and surgically naive animals (group B) measured 153 +/- 43 and 131 +/- 38 mm3, respectively. After lesions of both sensory (nasociliary nerve) and parasympathetic efferents at the ethmoidal foramen (group C, combined lesion) or selective lesions of parasympathetic efferents (group D), infarction volume increased [214 +/- 47 mm3 (p < 0.01) and 209 +/- 46 mm3 (p < 0.05), respectively]. No increases were detected after cutting the nasociliary nerve alone (group E) or occluding the external ethmoidal artery (group F) [145 +/- 39 mm3 (p < 0.05) and 124 +/- 63 mm3 (p > 0.05), respectively]. The infarct was predominantly located within cortical gray matter and became enlarged on its superior and inferior aspects after parasympathectomy. Large infarcts were noted whether animals breathed spontaneously (all of the above) or were artificially respired or whether animals were anesthetized with xylazine and ketamine or chloral hydrate. Taken together, these studies suggest a previously unrecognized protective role for autonomic parasympathetic fibers in the pathophysiology of focal cerebral ischemia that is not shared by sensory fibers. The importance of autonomic vasodilating fibers to blood flow in ischemic brain merits further study. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS 10828, NS 21558] NR 44 TC 69 Z9 70 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD JUL PY 1991 VL 11 IS 4 BP 628 EP 637 PG 10 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA FT182 UT WOS:A1991FT18200013 PM 2050751 ER PT J AU CAVINESS, VS AF CAVINESS, VS TI THE FUTURE OF CHILD NEUROLOGY SO JOURNAL OF CHILD NEUROLOGY LA English DT Discussion C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. RP CAVINESS, VS (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,PEDIAT NEUROL SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD JUL PY 1991 VL 6 IS 3 BP 273 EP 276 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA FU981 UT WOS:A1991FU98100012 PM 1875031 ER PT J AU SANTEN, RJ DEMERS, LM LYNCH, J HARVEY, H LIPTON, A MULAGHA, M HANAGAN, J GARBER, JE HENDERSON, IC NAVARI, RM MILLER, AA AF SANTEN, RJ DEMERS, LM LYNCH, J HARVEY, H LIPTON, A MULAGHA, M HANAGAN, J GARBER, JE HENDERSON, IC NAVARI, RM MILLER, AA TI SPECIFICITY OF LOW-DOSE FADROZOLE HYDROCHLORIDE (CGS-16949A) AS AN AROMATASE INHIBITOR SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID ADVANCED BREAST-CANCER; POSTMENOPAUSAL WOMEN; AMINOGLUTETHIMIDE; BIOSYNTHESIS; ALDOSTERONE; DEFICIENCY AB CGS 16949A (fadrozole hydrochloride), a potent cytochrome P450-mediated steroidogenesis inhibitor, blocks aromatase at low doses, but other biosynthetic steps at higher concentrations. Recent studies demonstrated inhibition of C-11-hydroxylase, corticosterone methyloxidase-II, and deoxycorticosterone to corticosterone conversion with this agent at somewhat higher concentrations than those required for blockade of aromatase. Based upon phase I studies, we postulated that relatively selective inhibition of aromatase might be possible if sufficiently low doses of CGS 16949A were used. A phase II study in 54 postmenopausal women with metastatic breast cancer examined the effects of low dose CGS 16949A on estrogen, mineralocorticoid, and glucocorticoid secretion. Two dose schedules and two dose levels were chosen based upon our prior dose escalation protocol study. Plasma estrone, estradiol, and estrone sulfate as well as urinary estrone and estradiol fell equally with 1.8-4 mg CGS 16949A given either on a twice daily or three times daily dose schedule. Isotopic kinetic studies demonstrated an 84% decrease in the rate of conversion of androstenedione to estrone to 0.40 +/- 0.07% (patients receiving 1.8-4 mg CGS 16949A daily). With these three regimens, basal levels of aldosterone and cortisol did not change significantly over a 12-week period of observation. Clinical examination, plasma electrolytes, and urinary sodium/potassium ratios suggested no biological evidence of mineralocorticoid deficiency. ACTH-stimulated cortisol concentrations, however, were blunted at each dose level compared pretreatment values. Nonetheless, peak responses exceeded 550 nmol/L, or a basal to peak difference of 190 nmol/L or greater, in 97% of instances. This probably reflected inhibition of C-11-hydroxylase, since basal and ACTH-stimulated levels of 11-deoxycortisol were increased in response to CGS 16949A. Androstenedione and 17-alpha-hydroxyprogesterone also exhibited an upward trend in response to drug treatment. ACTH-stimulated aldosterone levels were blunted to a greater extent than those of cortisol, probably as a reflection of corticosterone methyloxidase type II blockade. Overall, the results suggest that CGS 16949A, at doses of 1.8-2 mg daily, blocks aromatase effectively and does not produce clinically important inhibition of cortisol or aldosterone biosynthesis. Thus, this agent can probably be used safely without glucocorticoid or mineralocorticoid supplementation. C1 PENN STATE UNIV, MILTON S HERSHEY MED CTR, DEPT MED, DIV RADIAT ONCOL, HERSHEY, PA 17033 USA. PENN STATE UNIV, MILTON S HERSHEY MED CTR, CTR BIOSTAT, HERSHEY, PA 17033 USA. CIBA GEIGY CORP, SUMMIT, NJ 07901 USA. HARVARD UNIV, SCH MED, DANA FARBER INST, BOSTON, MA 02115 USA. UNIV TENNESSEE, CTR HLTH SCI, MEMPHIS, TN 38163 USA. SIMON WILLIAMSON CLIN, BIRMINGHAM, AL 35211 USA. RP SANTEN, RJ (reprint author), PENN STATE UNIV, MILTON S HERSHEY MED CTR, DEPT MED, DIV ENDOCRINOL, HERSHEY, PA 17033 USA. NR 19 TC 40 Z9 40 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 JUL PY 1991 VL 73 IS 1 BP 99 EP 106 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FR758 UT WOS:A1991FR75800016 PM 1646219 ER PT J AU STEELE, G BLEDAY, R MAYER, RJ LINDBLAD, A PETRELLI, N WEAVER, D AF STEELE, G BLEDAY, R MAYER, RJ LINDBLAD, A PETRELLI, N WEAVER, D TI A PROSPECTIVE EVALUATION OF HEPATIC RESECTION FOR COLORECTAL-CARCINOMA METASTASES TO THE LIVER - GASTROINTESTINAL-TUMOR-STUDY-GROUP PROTOCOL-6584 SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COLONIC RESECTION; CANCER; SURVIVAL; RECURRENCE; PATTERNS C1 EMMES CORP,POTOMAC,MD. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. WAYNE STATE UNIV,DETROIT,MI 48202. NR 22 TC 274 Z9 277 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 JUL PY 1991 VL 9 IS 7 BP 1105 EP 1112 PG 8 WC Oncology SC Oncology GA FU478 UT WOS:A1991FU47800003 PM 2045852 ER PT J AU HAYES, DF MESATEJADA, R PAPSIDERO, LD CROGHAN, GA KORZUN, AH NORTON, L WOOD, W STRAUCHEN, JA GRIMES, M WEISS, RB REE, HJ THOR, AD KOERNER, FC RICE, MA BARCOS, M KUFE, DW AF HAYES, DF MESATEJADA, R PAPSIDERO, LD CROGHAN, GA KORZUN, AH NORTON, L WOOD, W STRAUCHEN, JA GRIMES, M WEISS, RB REE, HJ THOR, AD KOERNER, FC RICE, MA BARCOS, M KUFE, DW TI PREDICTION OF PROGNOSIS IN PRIMARY BREAST-CANCER BY DETECTION OF A HIGH-MOLECULAR-WEIGHT MUCIN-LIKE ANTIGEN USING MONOCLONAL-ANTIBODIES DF3, F36/22, AND CU18 - A CANCER AND LEUKEMIA GROUP-B STUDY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ESTROGEN-RECEPTOR STATUS; HUMAN-MILK; DIFFERENTIATION ANTIGENS; SURFACE-ANTIGENS; CARCINOMA CELLS; EXPRESSION; NCRC-11; SURVIVAL; GLYCOPROTEINS; PROTEIN C1 HARVARD UNIV,SCH MED,CLIN PHARMACOL LAB,BOSTON,MA 02115. METPATH INC,NEW YORK,NY. COLUMBIA UNIV COLL PHYS & SURG,DEPT PATHOL,NEW YORK,NY 10032. CELLULAR PROD INC,BUFFALO,NY. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT BIOCHEM,BUFFALO,NY 14263. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT DIAGNOST IMMUNOL RES,BUFFALO,NY 14263. RP HAYES, DF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34346, CA32984, CA01041] NR 49 TC 52 Z9 52 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUL PY 1991 VL 9 IS 7 BP 1113 EP 1123 PG 11 WC Oncology SC Oncology GA FU478 UT WOS:A1991FU47800004 PM 2045853 ER PT J AU WEEKS, JC YEAP, BY CANELLOS, GP SHIPP, MA AF WEEKS, JC YEAP, BY CANELLOS, GP SHIPP, MA TI VALUE OF FOLLOW-UP PROCEDURES IN PATIENTS WITH LARGE-CELL LYMPHOMA WHO ACHIEVE A COMPLETE REMISSION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID NON-HODGKINS LYMPHOMA; BONE-MARROW TRANSPLANTATION; BREAST-CANCER PATIENTS; COMBINATION CHEMOTHERAPY; M-BACOD; COST-EFFECTIVENESS; SALVAGE THERAPY; DISEASE; PROGNOSIS; CARCINOMA C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV CLIN ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV BIOSTAT, BOSTON, MA 02115 USA. NR 41 TC 97 Z9 99 U1 0 U2 1 PU AMER SOC CLINICAL ONCOLOGY PI ALEXANDRIA PA 2318 MILL ROAD, STE 800, ALEXANDRIA, VA 22314 USA SN 0732-183X EI 1527-7755 J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUL PY 1991 VL 9 IS 7 BP 1196 EP 1203 PG 8 WC Oncology SC Oncology GA FU478 UT WOS:A1991FU47800014 PM 1710656 ER PT J AU GOLDFELD, AE STROMINGER, JL DOYLE, C AF GOLDFELD, AE STROMINGER, JL DOYLE, C TI HUMAN TUMOR-NECROSIS-FACTOR-ALPHA GENE-REGULATION IN PHORBOL ESTER STIMULATED T-CELL AND B-CELL LINES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NF-KAPPA-B; IMMUNODEFICIENCY VIRUS ENHANCER; NUCLEAR FACTOR; LYMPHOCYTES-T; FACTOR CACHECTIN; INTERFERON-BETA; CHAIN GENE; EXPRESSION; INDUCTION; ACTIVATION AB The minimal region of the human tumor necrosis factor-alpha (TNF-alpha) gene promoter necessary for its transcriptional induction by phorbol esters (PMA) in human T and B lymphocyte cell lines has been localized between - 52 and + 89 nucleotides (nt) relative to the gene's transcriptional start site. Comparison of these sequences to those required to mediate virus or lipopolysaccharide (LPS) induction of the gene reveal significant differences, and thus, the sequence requirements for PMA induction are distinct from those that mediate induction by virus or LPS. Although three sites in the TNF-alpha promoter (kappa-1, kappa-2, and kappa-3) specifically bind the transcription factor NF-kappa-B in lymphoid nuclear extracts, TNF-alpha mRNA induction by PMA does not correlate with NF-kappa-B binding activities displayed by different T and B cell lines. Moreover, kappa-1-kappa-2 can each be deleted from the TNF-alpha promoter with little effect on the genes inducibility by PMA. Therefore, TNF-alpha mRNA induction by PMA, like its induction by virus and LPS, is not primarily mediated by NF-kappa-B, but rather is mediated through other sequences and protein factors. Surprisingly, multimers of kappa-1-kappa-3 can confer PMA inducibility on a heterologous promoter in a B (Raji), but not a T (HUT78) cell line. However they are not functional on a truncated TNF-alpha promoter, indicating that promoter context and cell type specificity influence the PMA inducible function of these NF-kappa-B binding sites. RP GOLDFELD, AE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-21163] NR 37 TC 145 Z9 146 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUL 1 PY 1991 VL 174 IS 1 BP 73 EP 81 DI 10.1084/jem.174.1.73 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FU897 UT WOS:A1991FU89700010 PM 2056282 ER PT J AU DIAMOND, DJ SZALAY, P SYMER, D HAO, P SHIN, HS DINTZIS, RZ DINTZIS, HM REINHERZ, EL SILICIANO, RF AF DIAMOND, DJ SZALAY, P SYMER, D HAO, P SHIN, HS DINTZIS, RZ DINTZIS, HM REINHERZ, EL SILICIANO, RF TI MAJOR HISTOCOMPATIBILITY COMPLEX INDEPENDENT T-CELL RECEPTOR-ANTIGEN INTERACTION - FUNCTIONAL-ANALYSIS USING FLUORESCEIN DERIVATIVES SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID CONSTANT REGION GENES; EPSTEIN-BARR VIRUS; LYMPHOCYTES-T; NOMINAL ANTIGEN; CYTOCHROME-C; BINDING-SITE; ALPHA-CHAIN; ACTIVATION; MHC; SPECIFICITY AB We have isolated T cell receptor (TCR) cDNAs from fluorescein (FL)-specific human T cell clones (alpha-FL-beta-FL), and transferred them to TCR-beta- Jurkat cells in order to study direct FL-binding to the TCR. Using either FL-conjugated polymers (FL-polymer) or FL-substituted Sepharose beads, we are able to demonstrate the direct binding of antigen to the T cell surface, and the functional activation of the T cell transfectants. We present evidence against the involvement of major histocompatibility complex (MHC) molecules or antigen presentation in the interaction of FL with the alpha-FL-beta-FL transfectants. Additionally, we have examined the effect of ring substitutions on the FL molecule as well as specific alterations of substituents attached to the 5' position, and we have found that all of them interfere with the functional recognition of the alpha-FL-beta-FL TCR. These experiments demonstrate that TCRs like antibodies have intrinsic affinities for antigen, even without the involvement of MHC molecules. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOPHYS & BIOPHYS CHEM,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT CELL BIOL & ANAT,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,DEPT MED,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP DIAMOND, DJ (reprint author), CITY HOPE NATL MED CTR,BECKMAN RES INT,DIV IMMUNOL,1450 E DUARTE RD,DUARTE,CA 91010, USA. RI Symer, David/E-4173-2011; OI Diamond, Don/0000-0003-3579-7083 FU NCI NIH HHS [CA-33572]; NIAID NIH HHS [AI-19807] NR 51 TC 24 Z9 25 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 JUL 1 PY 1991 VL 174 IS 1 BP 229 EP 241 DI 10.1084/jem.174.1.229 PG 13 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FU897 UT WOS:A1991FU89700027 PM 2056277 ER PT J AU DEFOUGEROLLES, AR STACKER, SA SCHWARTING, R SPRINGER, TA AF DEFOUGEROLLES, AR STACKER, SA SCHWARTING, R SPRINGER, TA TI CHARACTERIZATION OF ICAM-2 AND EVIDENCE FOR A 3RD COUNTER-RECEPTOR FOR LFA-1 SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; FUNCTION-ASSOCIATED ANTIGEN-1; HUMAN-ENDOTHELIAL-CELLS; LEUKOCYTE INTEGRINS; IMMUNE-SYSTEM; LIGAND; EXPRESSION; DISTINCT; IMMUNOGLOBULIN; LYMPHOCYTES AB In an endeavor to further characterize human intercellular adhesion molecule-2 (ICAM-2), two murine monoclonal antibodies (mAb) were generated to ICAM-2 transfected COS cells, and designated CBR-IC2/1 and CBR-IC2/2. Immunoprecipitated, reduced ICAM-2 migrated as a broad band of M(r) 60,000 in sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Treatment with N-glycanase revealed a peptide backbone of M(r) 31,000, consistent with the size predicted from the cDNA. ICAM-2 had a broad distribution on hematopoietic cell lines and little expression on other cell lines, the sole exception being cultured endothelial cells which possess high levels of ICAM-2. Resting lymphocytes and monocytes expressed ICAM-2, while neutrophils did not. Staining of tissue sections with anti-ICAM-2 mAb confirmed their strong reactivity to vascular endothelium, but demonstrated a lack of ICAM-2 expression on other tissues. Small clusters of ICAM-2 positive cells were, however, seen in germinal centers. In contrast to ICAM-1 there was little or no induction of ICAM-2 expression on lymphocytes or cultured endothelium upon stimulation with inflammatory mediators. One of the two mAb, CBR-IC2/2, was found to totally inhibit binding of ICAM-2+ COS cells to purified lymphocyte function-associated antigen-1 (LFA-1). Using this mAb, LFA-1-dependent binding to both stimulated and unstimulated endothelium was found to be totally accounted for by ICAM-1 and ICAM-2. Homotypic aggregation of an Epstein-Barr virus-transformed B cell line, JY, was found to be solely ICAM-1 and ICAM-2-dependent, while in the case of the T cell lymphoma cell line, SKW3, anti- ICAM-2 mAb in conjunction with anti-ICAM-1 mAb could not inhibit the LFA-1-dependent aggregation. This suggests an additional LFA-1 ligand exists. Using a cell binding assay to purified LFA-1 in conjunction with anti-ICAM-1 and anti-ICAM-2 mAb, we have demonstrated that this putative third ligand for LFA-1 exists on SKW3 and other cell lines. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,COMM IMMUNOL,BOSTON,MA 02115. THOMAS JEFFERSON UNIV,DEPT PATHOL,PHILADELPHIA,PA 19107. FU NCI NIH HHS [CA-31798] NR 52 TC 462 Z9 463 U1 0 U2 5 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 JUL 1 PY 1991 VL 174 IS 1 BP 253 EP 267 DI 10.1084/jem.174.1.253 PG 15 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FU897 UT WOS:A1991FU89700029 PM 1676048 ER PT J AU SILVA, JA LEONG, GB WEINSTOCK, R FERRARI, MM AF SILVA, JA LEONG, GB WEINSTOCK, R FERRARI, MM TI MISIDENTIFIED POLITICAL FIGURES - AN UNDERAPPRECIATED DANGER SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; MISIDENTIFICATION SYNDROMES; POLITICAL FIGURES; VIOLENCE ID CAPGRAS SYNDROME; PSYCHIATRIC-PATIENTS; DELUSIONS; VIOLENCE; SERVICE AB A series of twelve patients is presented in which each patient suffered from one or more misidentification syndromes and also misidentified one or more political figures. The fact that misidentification syndromes have been associated with physical violence and that the majority of the patients studied had a history of physical violence suggests that these individuals could pose a significant danger of physical harm to others, including political figures. Persons who threaten political figures should be evaluated for misidentification syndromes. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,STUDENT PSYCHOL SERV,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV SO CALIF,SCH MED,LOS ANGELES,CA 90033. NR 38 TC 10 Z9 10 U1 1 U2 1 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JUL PY 1991 VL 36 IS 4 BP 1170 EP 1178 PG 9 WC Medicine, Legal SC Legal Medicine GA FY039 UT WOS:A1991FY03900027 PM 1919476 ER PT J AU RIGOTTI, NA SINGER, DE MULLEY, AG THIBAULT, GE AF RIGOTTI, NA SINGER, DE MULLEY, AG THIBAULT, GE TI SMOKING CESSATION FOLLOWING ADMISSION TO A CORONARY-CARE UNIT SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE SMOKING CESSATION; CORONARY CARE UNIT DISCHARGE; CARDIOVASCULAR DISEASE; CONGESTIVE HEART DISEASE; MYOCARDIAL INFARCTION AB Objective: To determine the impact of an episode of serious cardiovascular disease on smoking behavior and to identify factors associated with smoking cessation in this setting. Design: Prospective observational study in which smokers admitted to a coronary care unit (CCU) were followed for one year after hospital discharge to determine subsequent smoking behavior. Setting: Coronary care unit of a teaching hospital. Patients: Preadmission smoking status was assessed in all 828 patients admitted to the CCU during one year. The 310 smokers surviving to hospital discharge were followed and their smoking behaviors assessed by self-report at six and 12 months. Intervention: None. Measurements and main results: Six months after discharge, 32% of survivors were not smoking; the rate of sustained cessation at one year was 25%. Smokers with a new diagnosis of coronary heart disease (CHD) made during hospitalization had the highest cessation rate (53% vs. 31%, p = 0.01). On multivariate analysis, smoking cessation was more likely if patients were discharged with a diagnosis of CHD, had no prior history of CHD, were lighter smokers (< 1 pack/day), and had congestive heart failure during hospitalization. Among smokers admitted because of suspected myocardial infarction (MI), cessation was more likely if the diagnosis was CHD than it it was noncoronary (37% vs. 19%, p < 0.05), but a diagnosis of MI led to no more smoking cessation than did coronary insufficiency. Conclusion: Hospitalization in a CCU is a stimulus to long-term smoking cessation, especially for lighter smokers and those with a new diagnosis of CHD. Admission to a CCU may represent a time when smoking habits are particularly susceptible to intervention. Smoking cessation in this setting should improve patient outcomes because cessation reduces cardiovascular mortality, even when quitting occurs after the onset of CHD. RP RIGOTTI, NA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN INTERNAL MED UNIT,MED SERV,BULFINCH 1,BOSTON,MA 02114, USA. NR 0 TC 50 Z9 50 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD JUL-AUG PY 1991 VL 6 IS 4 BP 305 EP 311 DI 10.1007/BF02597426 PG 7 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA FX368 UT WOS:A1991FX36800006 PM 1890500 ER PT J AU WITT, JD JUPITER, B AF WITT, JD JUPITER, B TI KAPOSI-SARCOMA IN THE HAND SEEN AS AN ARTERIOVENOUS MALFORMATION SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB A case of Kaposi's sarcoma, which was initially thought to represent an arteriovenous malformation, is described. Angiographic findings were misleading, and careful histopathological analysis of such lesions is advocated so that correct treatment may be carried out. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,5 WHITTIER PL,SUITE 102,BOSTON,MA 02114. NR 0 TC 5 Z9 5 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JUL PY 1991 VL 16A IS 4 BP 607 EP 609 DI 10.1016/0363-5023(91)90182-B PG 3 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FW765 UT WOS:A1991FW76500007 PM 1880357 ER PT J AU GELBERMAN, RH STEINBERG, D AMIEL, D AKESON, W AF GELBERMAN, RH STEINBERG, D AMIEL, D AKESON, W TI FIBROBLAST CHEMOTAXIS AFTER TENDON REPAIR SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB Healing canine flexor tendons were treated with early controlled passive mobilization. The repair site and proximal and distal tendon stumps were stained for fibronectin and examined by light microscopy at three, seven, eleven, and seventeen days. Fibronectin increased dramatically in the epitenon adjacent to the repair site seven days after repair, a time when epitenon cellular activity was at its peak. By seventeen days, fibronectin staining had decreased substantially, both at the repair site and in the tendon stumps. A delayed increase in fibronectin activity was noted in the endotenon adjacent to the repair site. Fibronectin production appears to be an important component of the early tendon repair process. Fibroblast chemotaxis and adherence to the substratum in the days after injury and repair appears to be related directly to fibronectin secretion. This study is the first to provide documentation of fibronectin localization in a clinically relevant tendon repair model. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC 527,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR33097] NR 0 TC 54 Z9 59 U1 0 U2 2 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JUL PY 1991 VL 16A IS 4 BP 686 EP 693 DI 10.1016/0363-5023(91)90195-H PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FW765 UT WOS:A1991FW76500020 PM 1880367 ER PT J AU GELBERMAN, RH AF GELBERMAN, RH TI DIGITAL SHEATH EXCISION - REPLY SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Letter RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,WACC 427,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD JUL PY 1991 VL 16A IS 4 BP 765 EP 766 DI 10.1016/0363-5023(91)90213-U PG 2 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FW765 UT WOS:A1991FW76500038 ER PT J AU CAFARO, A OLIVA, A POLIDORI, V BOYLE, LA HERMAN, S KURNICK, JT PANDOLFI, F AF CAFARO, A OLIVA, A POLIDORI, V BOYLE, LA HERMAN, S KURNICK, JT PANDOLFI, F TI FIBROBLAST-CONDITIONED MEDIUM MEDIATES SURVIVAL OF INFLAMMATORY CELLS - DIFFERENT FACTORS ARE INVOLVED IN PRESERVING NEUTROPHIL AND LYMPHOCYTE VIABILITY SO JOURNAL OF IMMUNOLOGICAL RESEARCH LA English DT Article DE APOPTOSIS; FIBROBLASTS; LYMPHOCYTES; NEUTROPHILS; VIABILITY PRESERVATION ID COLONY-STIMULATING FACTOR; EXPRESSION AB We have investigated the ability of conditioned medium from fibroblasts (fibroblasts conditioned medium or FCM) to prolong survival and function of human blood neutrophils in vivo. As previously shown, fibroblasts or FCM from different species are capable of maintaining prolonged survival of human lymphocytes. Peripheral blood neutrophils have a very short survival in vivo. Several fibroblast lines from different sources were tested for their ability to preserve neutrophils in culture. While all the tested FCM had shown the ability to support lymphocyte viability, some could also enhance neutrophil viability for up to 96 hours, with retention of function as assessed by the NBT test. Our data also suggest that FCM from different species can work on human neutrophils and that, while fibroblasts produce factor(s) involved in both lymphocyte and neutrophil survival, there are different factors involved since some FCM that are active on lymphocytes, are not able to prolong neutrophil viability. The neutrophil preserving activity contained in the FCM is not due to IL-1, IL-2, IL-3, IL-5, IL-6, IL-11, leukemia inhibitory factor (LIF), G-CSF, M-CSF or GM-CSF. We propose that stromal cells produce different anti-apoptosis factors responsible for maintaining viability of different inflammatory cells such as neutrophils and lymphocytes. C1 UNIV ROME LA SAPIENZA,DEPT ALLERGY & CLIN IMMUNOL,I-00185 ROME,ITALY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. GENET INST,CAMBRIDGE,MA. RI Cafaro, Aurelio/K-5314-2016 NR 14 TC 4 Z9 4 U1 0 U2 0 PU PENSIERO SCIENTIFICO EDITOR PI ROME PA VIA BRADANO 3/C, 00199 ROME, ITALY SN 1120-3765 J9 J IMMUNOL RES PD JUL-SEP PY 1991 VL 3 IS 3 BP 117 EP 122 PG 6 WC Immunology SC Immunology GA GH110 UT WOS:A1991GH11000004 ER PT J AU HAHN, WC ROSENSTEIN, Y BURAKOFF, SJ BIERER, BE AF HAHN, WC ROSENSTEIN, Y BURAKOFF, SJ BIERER, BE TI INTERACTION OF CD2 WITH ITS LIGAND LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-3 INDUCES ADENOSINE 3',5'-CYCLIC-MONOPHOSPHATE PRODUCTION IN LYMPHOCYTES-T SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL ERYTHROCYTE RECEPTOR; CYTOPLASMIC FREE CALCIUM; CYCLIC-AMP; MONOCLONAL-ANTIBODY; MOLECULAR-CLONING; ALTERNATIVE PATHWAY; ADENYLATE-CYCLASE; SURFACE ANTIGENS; PROTEIN KINASE; C-FOS AB CD2(T11, the T cell E receptor), a nonpolymorphic 47- to 55-kDa glycoprotein, is a T cell-specific surface protein that plays an important role in T lymphocyte adhesion, signal transduction, and differentiation. A natural ligand of CD2 is lymphocyte function associated Ag-3 (LFA-3 (CD58)), a widely expressed glycoprotein of 50 to 70 kDa. The physiologic interaction of CD2 with LFA-3 functions to increase intercellular adhesion and plays a role in T cell activation. This interaction, however, in the absence of other stimuli, has not previously been shown to induce intracellular signals such as Ca2+ mobilization or IL-2 production. To investigate whether cAMP may play a role in ligand-triggered CD2-mediated signal transduction, we have studied the ability of purified LFA-3 and anti-CD2 mAb to induce changes in intracellular cAMP content in murine Ag-specific T cell hybridomas that stably express wild-type and mutated human CD2 molecules. By using a RIA sensitive to the femtomolar range and specific for cAMP, we demonstrate that purified LFA-3, like anti-CD2 mAb, is capable of inducing marked, transient increases in the intracellular concentrations of cAMP. Presentation of purified LFA-3 alone to CD2-expressing hybridoma cells, however, did not stimulate phosphatidylinositol turnover nor IL-2 production. The cytoplasmic domain of CD2 is necessary for these ligand-induced cAMP changes, demonstrating that LFA-3 binding to CD2 transduces a signal to the cell. Experiments using the phosphodiesterase inhibitor 3-isobutyl-1-methyl-xanthine showed that CD2-mediated regulation of cAMP levels occurs primarily by the stimulation of cAMP production rather than by the inhibition of cAMP degradation. These results demonstrate that the interaction of LFA-3 with CD2, in the absence of other stimuli, is capable of initiating intracellular biochemical changes and suggest that CD2/LFA-3 interactions may regulate T cell function at least in part through the generation of intracellular cAMP. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP HAHN, WC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1610B,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34129]; NIAID NIH HHS [AI28554] NR 60 TC 45 Z9 45 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 JUL 1 PY 1991 VL 147 IS 1 BP 14 EP 21 PG 8 WC Immunology SC Immunology GA FT763 UT WOS:A1991FT76300003 PM 1711070 ER PT J AU PINTO, VB ROCK, KL AF PINTO, VB ROCK, KL TI CHARACTERIZATION OF THE PROLIFERATIVE RESPONSE OF A CD4-8- THYMIC T-LYMPHOMA CELL-LINE TO STIMULATION BY THYMIC CELLULAR-ELEMENTS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LONG TERMINAL REPEAT; MURINE LEUKEMIA-VIRUS; MONOCLONAL-ANTIBODIES; LYMPHOCYTES-T; FUNCTIONAL-PROPERTIES; IMMATURE THYMOCYTES; ACTIVATING PROTEIN; SARCOMA-VIRUS; IDENTIFICATION; ANTIGENS AB E710.2 is a cloned T cell line that was isolated from an AKR/J thymic tumor. This clone expresses Thy-1, heat-stable Ag, and the CD3/TCR complex but does not express CD4 or CD8. When the E710.2 cell line is injected into syngeneic mice, it grows as a malignant tumor in lymphoid organs and the thymus. In contrast, this cell line does not grow in vitro under standard culture conditions. This latter property allowed us to analyze the in vitro responsiveness of this CD4-CD8- cell line to stimulation by pharmacologic agents and cellular elements from the spleen and thymus. E710.2 cells proliferate when stimulated with phorbol esters or when cocultured with thymocytes or splenocytes. We could not detect soluble stimulatory factors in cultures of E710.2 and/or lymphoid cells, suggesting that cell contact might be required for this response. The stimulatory activity in thymus and spleen appears to be broadly expressed, because all cell subsets that were examined from these tissues stimulate this cell line. The stimulation of E710.2 cells is not MHC-restricted and is not inhibited by anti-MHC mAb. Furthermore, the responsiveness of these cells is not decreased when the TCR/CD3 complex is modulated from the cell surface. Similarly, TCR/ CD3-deficient E710.2 variant clones retain their responsiveness to thymic and splenic cell stimulation. These findings suggest that there is a TCR-independent pathway of activation in E710.2 that is stimulated by a broadly expressed, non-MHC-encoded molecule(s). C1 HARVARD UNIV,MED CTR,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT LYMPHOCYTE BIOL,BOSTON,MA 02115. FU NIGMS NIH HHS [R01-GM38515] NR 51 TC 4 Z9 4 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 JUL 1 PY 1991 VL 147 IS 1 BP 42 EP 49 PG 8 WC Immunology SC Immunology GA FT763 UT WOS:A1991FT76300007 PM 1828825 ER PT J AU AKSENTIJEVICH, I SACHS, DH SYKES, M AF AKSENTIJEVICH, I SACHS, DH SYKES, M TI NATURAL ANTIBODIES AGAINST BONE-MARROW CELLS OF A CONCORDANT XENOGENEIC SPECIES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NONLETHAL PREPARATIVE REGIMEN; MONOCLONAL-ANTIBODIES; MOUSE; XENOGRAFTS; TRANSPLANTATION; ANTIGENS; MICE; MACROPHAGE; RECEPTORS; INVIVO AB Hyperacute rejection does not occur when vascularized organs are transplanted between rat and mouse, and this species combination is considered to be concordant. Since hyperacute rejection is believed to reflect the presence of pre-existing antibodies (usually of the IgM class), and lymphocytotoxic antibodies against rat cells have not been detected in normal mouse sera, it has previously been concluded that mouse anti-rat natural antibody (NAb) does not exist. However, studies have not been reported in which rat bone marrow cells (BMC) were used as targets for evaluation of normal mouse sera. Because previous work from our and other laboratories has shown that bone marrow chimerism in the rat into mouse species combination can be achieved only by transplanting large numbers of rat BMC, we have evaluated normal mouse sera for the presence of NAb against rat BMC that might explain these in vivo results. Fisher 344 rat BMC and spleen cells were incubated with serum from nonimmunized mice, then stained with fluoresceinated rat anti-mouse subclass-specific secondary reagents and analyzed using flow cytometry. NAb of the IgM and IgG3 classes were found that bound strongly to rat BMC but showed weak or absent binding to spleen cells. A low level of IgG2b binding was observed to both BMC and spleen cells. Cytotoxic activity was detected against rat BMC but not against spleen cells. The environment in which the animals were maintained played a significant role in determining the level of cytotoxic NAb in normal mouse sera. Our results are consistent with the possibility that bone marrow-specific NAb play a role in resisting engraftment of BMC across this species barrier. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT RES BIOL CTR,MGH-E,BLDG 149,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. NR 33 TC 36 Z9 36 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUL 1 PY 1991 VL 147 IS 1 BP 79 EP 85 PG 7 WC Immunology SC Immunology GA FT763 UT WOS:A1991FT76300012 PM 2051029 ER PT J AU KANOF, ME STROBER, W KWAN, WC OCONNELL, NA JAMES, SP AF KANOF, ME STROBER, W KWAN, WC OCONNELL, NA JAMES, SP TI CD4+ LEU-8+ T-CELL SUPERNATANT ACTIVITY THAT INHIBITS IG PRODUCTION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NODE HOMING RECEPTOR; IMMUNOGLOBULIN PRODUCTION; SUPPRESSOR CELLS; LYMPHOCYTES-T; GROWTH-FACTOR; SOLUBLE SUPPRESSOR; INTERFERON-GAMMA; HUMAN EQUIVALENT; B-CELLS; SUBSETS AB The subpopulation of CD4+ T cells that expresses the Leu-8 peripheral lymph node homing receptor suppresses PWM-stimulated Ig synthesis. To determine the mechanism of this suppression, the immunoregulatory activity of culture supernatants obtained from peripheral blood CD4+ Leu-8+ T cells cultured with anti-CD3 mAb and PMA (Leu-8+ supernatant) was determined. Leu-8+ supernatant suppressed PWM-stimulated Ig synthesis in cultures containing non-T cells and CD4+ Leu-8- T cells. In contrast, the supernatant from CD4+ Leu-8- T cells did not suppress Ig synthesis. The inhibitory activity of CD4+ Leu-8+ T cell supernatants could not be accounted for by a deficiency or excess of IL-2, IL-4, IFN-gamma, IL-6, or PGE2. In studies examining the effect of CD4+ Leu-8+ supernatant on T cells, the supernatant did not alter either mitogen-induced proliferation or the helper function of CD4+ Leu-8-T cells. In studies examining the effect of CD4+ Leu-8+ supernatant on B cells, the supernatant inhibited Staphylococcus aureus Cowan I strain-induced B cell Ig secretion but not B cell proliferation. The suppressor activity of Leu-8+ supernatant was eliminated by protease treatment and was eluted by HPLC in two main peaks, with molecular sizes of 44 and 12 kDa. In summary, these studies indicate that supernatants from activated CD4+ Leu-8+ T cells directly suppress B cell Ig production. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. NIAID,CLIN INVEST LAB,MUCOSAL IMMUN SECT,BETHESDA,MD 20892. FU NIAID NIH HHS [AI-07439]; NIDDK NIH HHS [DK-40918] NR 48 TC 11 Z9 11 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 JUL 1 PY 1991 VL 147 IS 1 BP 155 EP 161 PG 7 WC Immunology SC Immunology GA FT763 UT WOS:A1991FT76300023 PM 1711071 ER PT J AU KAUFMANN, Y TSENG, E SPRINGER, TA AF KAUFMANN, Y TSENG, E SPRINGER, TA TI CLONING OF THE MURINE LYMPHOCYTE FUNCTION-ASSOCIATED MOLECULE-1 ALPHA-SUBUNIT AND ITS EXPRESSION IN COS CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; LEUKOCYTE ADHESION GLYCOPROTEIN; COMPLEMENT RECEPTOR TYPE-3; AMINO-ACID SEQUENCE; BETA-SUBUNIT; P150,95 GLYCOPROTEINS; VONWILLEBRAND-FACTOR; MONOCLONAL-ANTIBODY; INTEGRIN FAMILY; LFA-1 AB The lymphocyte function-associated molecule 1 (LFA-1, CD11a/CD18) is an integrin that mediates adhesion of immune cells by interaction with two members of the Ig superfamily, ICAM-1 and ICAM-2. LFA-1 consists of an alpha-subunit (M(r) = 180,000) and a beta-subunit (M(r) = 95,000). We report here the isolation and expression of the murine alpha-subunit cDNA (GenBank accession no. M60778). The deduced sequence comprises a 1061 amino acid extracellular domain, a 29 amino acid transmembrane region, and a 50 amino acid cytoplasmic domain. It has a 72 % amino acid identity with its human counterpart and 34% identity with the murine Mac-I alpha-subunit. The murine LFA-1 alpha-subunit could be expressed on the cell surface of a fibroblastoid cell line, COS, by cotransfection with either the human or murine beta-subunit cDNA. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU PHS HHS [31798] NR 38 TC 32 Z9 33 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 JUL 1 PY 1991 VL 147 IS 1 BP 369 EP 374 PG 6 WC Immunology SC Immunology GA FT763 UT WOS:A1991FT76300054 PM 2051027 ER PT J AU TAYLOR, CR ANDERSON, RR GANGE, RW MICHAUD, NA FLOTTE, TJ AF TAYLOR, CR ANDERSON, RR GANGE, RW MICHAUD, NA FLOTTE, TJ TI LIGHT AND ELECTRON-MICROSCOPIC ANALYSIS OF TATTOOS TREATED BY Q-SWITCHED RUBY-LASER SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article ID GUINEA-PIG SKIN AB Short-pulse laser exposures can be used to alter pigmented structures in tissue by selective photothermolysis. Potential mechanisms of human tattoo pigment lightening with Q-switched ruby laser were explored by light and electron microscopy. Significant variation existed between and within tattoos. Electron microscopy of untreated tattoos revealed membrane-bound pigment granules, predominantly within fibroblasts and macrophages, and occasionally in mast cells. These granules contained pigment particles ranging from 2- in diameter. Immediately after exposure, dose-related injury was observed in cells containing pigment. Some pigment particles were smaller and lamellated. At fluences greater-than-or-equal-to 3 J/cm2, dermal vacuoles and homogenization of collagen bundles immediately adjacent to extracellular pigment were occasionally observed. A brisk neutrophilic infiltrate was apparent by 24 h. Eleven days later, the pigment was again intracellular. Half of the biopsies at 150 d revealed a mild persistent lymphocytic infiltrate. There was no fibrosis except for one case of clinical scarring. These findings confirm that short-pulse radiation can be used to selectively disrupt cells containing tattoo pigments. The physical alteration of pigment granules, redistribution, and elimination appear to account for clinical lightening of the tattoos. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. FU NIAMS NIH HHS [1R3AR38992] NR 15 TC 105 Z9 106 U1 0 U2 9 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD JUL PY 1991 VL 97 IS 1 BP 131 EP 136 DI 10.1111/1523-1747.ep12478570 PG 6 WC Dermatology SC Dermatology GA FU290 UT WOS:A1991FU29000022 PM 2056183 ER PT J AU LAMURAGLIA, G AF LAMURAGLIA, G TI CHRONIC PROSTHETIC VASCULAR GRAFT INFECTION VISUALIZATION WITH GA-67 SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP LAMURAGLIA, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VASC SURG SERV,BOSTON,MA 02114, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUL PY 1991 VL 32 IS 7 BP 1427 EP 1428 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FV990 UT WOS:A1991FV99000029 PM 2066800 ER PT J AU GOODSON, JM CUGINI, MA KENT, RL ARMITAGE, GC COBB, CM FINE, D FRITZ, ME GREEN, E IMOBERDORF, MJ KILLOY, WJ MENDIETA, C NIEDERMAN, R OFFENBACHER, S TAGGART, EJ TONETTI, M AF GOODSON, JM CUGINI, MA KENT, RL ARMITAGE, GC COBB, CM FINE, D FRITZ, ME GREEN, E IMOBERDORF, MJ KILLOY, WJ MENDIETA, C NIEDERMAN, R OFFENBACHER, S TAGGART, EJ TONETTI, M TI MULTICENTER EVALUATION OF TETRACYCLINE FIBER THERAPY .1. EXPERIMENTAL-DESIGN, METHODS, AND BASE-LINE DATA SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article DE PERIODONTAL DISEASES; TETRACYCLINE; DRUG IMPLANTS; CLINICAL TRIALS ID CLINICAL MEASUREMENTS; PERIODONTAL RESEARCH; ATTACHMENT LEVEL; IDENTIFICATION; PROBES AB The study design and baseline characteristics of a multicenter trial to test the effectiveness and safety of locally delivered tetracycline for treatment of adult periodontitis are described. Local delivery was provided by 0.5 mm diameter ethylene vinyl acetate copolymer fibers loaded 25% with tetracycline hydrochloride which were placed into periodontal pockets and maintained by an adhesive for 10 (+/- 2) days. A total of 113 subjects (56 male and 57 female; mean age 49.3 yr) at five centers participated in the study. Subjects were selected who had 4 nonadjacent teeth with 6-10 mm pockets that bled on probing. The selected sites in each subject were randomly assigned to 4 test groups: tetracycline fiber, control fiber, scaling with root planing, or untreated. A balanced experimental design was thereby established in which each subject contributed equally by providing 4 clinically comparable sites for evaluation. To provide a more specific model for testing periodontitis therapy, gingivitis was treated prior to the initiation of the study by prophylaxis with supragingival calculus removal and home care instruction. Clinical response variables measured were pocket depth reduction, attachment level gain and bleeding on controlled-force probing measured at baseline, 30 d, and 60 d. Levels of 6 bacterial species selected as probable periodontal pathogens were measured by DNA probe analysis of plaque samples. The design of this study provided several unique analytical opportunities. Controls included a comparison with conventional treatment, analysis of vehicle effects, and effects at untreated sites. Comparison of the test group with controls permitted evaluation of the principal variables that could effect interpretation of results. The balanced design created by equal representation of each subject in each test provided means to compensate for individual differences between subjects. The combination of these factors resulted in an experimental design which addresses many of the concerns that have been expressed relating to the conduct of clinical trials of periodontal treatments. C1 UNIV CALIF SAN FRANCISCO,SCH DENT,SAN FRANCISCO,CA 94143. UNIV MISSOURI,SCH DENT,KANSAS CITY,MO 64110. COLUMBIA UNIV,SCH DENT & ORAL SURG,NEW YORK,NY 10027. EMORY UNIV,SCH DENT,ATLANTA,GA 30322. RP GOODSON, JM (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. NR 18 TC 45 Z9 46 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1991 VL 26 IS 4 BP 361 EP 370 DI 10.1111/j.1600-0765.1991.tb02075.x PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FY180 UT WOS:A1991FY18000009 PM 1831504 ER PT J AU GOODSON, JM CUGINI, MA KENT, RL ARMITAGE, GC COBB, CM FINE, D FRITZ, ME GREEN, E IMOBERDORF, MJ KILLOY, WJ MENDIETA, C NIEDERMAN, R OFFENBACHER, S TAGGART, EJ TONETTI, M AF GOODSON, JM CUGINI, MA KENT, RL ARMITAGE, GC COBB, CM FINE, D FRITZ, ME GREEN, E IMOBERDORF, MJ KILLOY, WJ MENDIETA, C NIEDERMAN, R OFFENBACHER, S TAGGART, EJ TONETTI, M TI MULTICENTER EVALUATION OF TETRACYCLINE FIBER THERAPY .2. CLINICAL-RESPONSE SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article DE PERIODONTAL DISEASES; TETRACYCLINE; DELIVERY SYSTEMS; CLINICAL TRIALS ID LOCAL-DRUG DELIVERY; PERIODONTAL THERAPY; DISEASE; POCKETS; RELEASE AB The safety and efficacy of periodontal disease treatment by intrapocket placement of tetracycline (TC) fibers was investigated in a 60-day multicenter study conducted by selecting 4 sites in each subject with 6-10 mm pockets that bled on probing. Sites were randomly assigned to 1 of 4 test groups: TC fiber therapy, scaling, control fiber (fibers without drug), or untreated. TC fibers and control fibers were placed to fill the pocket and were maintained with a cyanoacrylate adhesive for 10(+/- 2) d. Scaling was performed for a minimum of 5 min under local anesthesia. Following initial tooth cleaning procedures, pocket depth, attachment level and bleeding on controlled-force probing were measured at baseline and at 30 d, and 60 d following therapy. Analysis of data from 107 subjects who had complete clinical data sets indicated that TC fiber therapy significantly decreased pocket depth, increased attachment level, and decreased bleeding on controlled-force probing to a greater extent than observed in all other test groups including scaling. These effects were greater than, and in addition to, effects that occurred due to prophylaxis and improved home care. No serious adverse side-effects attributed to TC fiber therapy were observed. No TC fiber-treated sites abscessed and superinfection was not noted. A transient redness at fiber removal was seen at 21% of the sites. Although fibers were placed without anesthesia, mild pain on initial placement was infrequent (19%) and abated rapidly. The results indicate that TC fiber placement provides a safe and effective means for treatment of periodontal infections. C1 UNIV CALIF SAN FRANCISCO,SCH DENT,SAN FRANCISCO,CA 94143. UNIV MISSOURI,SCH DENT,KANSAS CITY,MO 64110. COLUMBIA UNIV,SCH DENT & ORAL SURG,NEW YORK,NY 10027. EMORY UNIV,SCH DENT,ATLANTA,GA 30322. RP GOODSON, JM (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. NR 28 TC 135 Z9 138 U1 0 U2 5 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1991 VL 26 IS 4 BP 371 EP 379 DI 10.1111/j.1600-0765.1991.tb02076.x PG 9 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FY180 UT WOS:A1991FY18000010 PM 1831505 ER PT J AU LICHTENSTEIN, MJ PINCUS, T AF LICHTENSTEIN, MJ PINCUS, T TI RHEUMATOID-ARTHRITIS IDENTIFIED IN POPULATION BASED CROSS-SECTIONAL STUDIES - LOW PREVALENCE OF RHEUMATOID-FACTOR SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE RHEUMATOID ARTHRITIS; RHEUMATOID FACTOR; EPIDEMIOLOGY ID SIGNIFICANT RADIOGRAPHIC DAMAGE; 1ST 2 YEARS; WORK DISABILITY; FOLLOW-UP; DISEASE; MORTALITY; QUESTIONNAIRE; PROGNOSIS; CRITERIA; TIME AB All 5 cross sectional population based studies which included evaluation of all subjects for both rheumatoid factor (RF) and rheumatoid arthritis (RA) were reviewed. RF was found in only 19-33% of individuals who met the 1958 ARA criteria for RA. Many individuals identified in these studies met criteria for only "probable" or "possible" RA according to the 1958 criteria, and might not meet the 1987 criteria. However, RF was found in only 26-60% of subjects who met criteria for "definite" RA in the studies that included this information. Population based studies of RA often have been interpreted as applicable to clinical RA patients, which may explain in part different views of RA as both a mild and a progressive disease. C1 VANDERBILT UNIV,MED CTR,SCH MED,DEPT MED,DIV RHEUMATOL & IMMUNOL,T-3219 MED CTR N,NASHVILLE,TN 37232. AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM-21393] NR 45 TC 44 Z9 44 U1 0 U2 0 PU J RHEUMATOL PUBL CO PI TORONTO PA 920 YONGE ST, SUITE 115, TORONTO ON M4W 3C7, CANADA SN 0315-162X J9 J RHEUMATOL JI J. Rheumatol. PD JUL PY 1991 VL 18 IS 7 BP 989 EP 993 PG 5 WC Rheumatology SC Rheumatology GA FY159 UT WOS:A1991FY15900010 PM 1920334 ER PT J AU FOX, G HERZOG, DB AF FOX, G HERZOG, DB TI RESOLVED - THE PASS RATE FOR THE CHILD AND ADOLESCENT-PSYCHIATRY BOARD EXAMINATION SHOULD BE HIGHER THAN IT IS AT PRESENT SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Discussion ID CERTIFICATION EXAMINATION C1 MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FOX, G (reprint author), UNIV ILLINOIS,INST JUVENILE RES,CHICAGO,IL 60680, USA. NR 10 TC 3 Z9 3 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 1991 VL 30 IS 4 BP 685 EP 691 DI 10.1097/00004583-199107000-00024 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA FX321 UT WOS:A1991FX32100024 PM 1890106 ER PT J AU BARNHILL, RL DICKERSIN, GR NICKELEIT, V BHAN, AK MUHLBAUER, JE PHILLIPS, ME MIHM, MC AF BARNHILL, RL DICKERSIN, GR NICKELEIT, V BHAN, AK MUHLBAUER, JE PHILLIPS, ME MIHM, MC TI STUDIES ON THE CELLULAR-ORIGIN OF NEUROTHEKEOMA - CLINICAL, LIGHT MICROSCOPIC, IMMUNOHISTOCHEMICAL, AND ULTRASTRUCTURAL OBSERVATIONS SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID NERVE-SHEATH MYXOMA; EPITHELIAL MEMBRANE ANTIGEN; ELECTRON-MICROSCOPY; PERINEURIAL CELLS; S-100 PROTEIN; S100 PROTEIN; TUMORS; BENIGN; EXPRESSION; MARKER AB The clinical, histopathologic, and immunohistochemical features of 11 cases of neurothekeoma are reported. One case was examined by electron microscopy. The mean age of the patients was 27.1 years; the study comprised eight female and three male patients. Most lesions were nondescript papules and located on the upper part of the body, seven cases of neurothekeoma on the head. Eight cases were classified as cellular neurothekeoma on the basis of a striking fascicular pattern and three cases as myxomatous neurothekeoma because of prominent myxoid stromal change. All cellular neurothekeomas failed to express S-100 protein, whereas the three myxomatous types were strongly positive for this marker. Other than vimentin, there was no significant immunoreactivity with other immunohistochemical markers. Ultrastructural study of one case of cellular neurothekeoma was inconclusive for cell type although a perineurial origin could not be excluded. On the basis of these results, we conclude that cellular neurothekeoma differs from myxomatous neurothekeoma not only by clinical and histologic findings but also by immunoreactivity with S-100 protein. These findings also suggest the existence of two distinct subtypes of neurothekeoma and possible origin of the two variants of neurothekeoma from different cell types or at least variation in phenotypic expression of a common cell type. On the other hand, it cannot be excluded that these two variants are different stages in the natural history of neurothekeoma. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MUHLBAUER DERMATOPATHOL LAB,PITTSFORD,NY. SUNY STONY BROOK,DEPT DERMATOL,STONY BROOK,NY 11794. SUNY STONY BROOK,DEPT PATHOL,STONY BROOK,NY 11794. RP BARNHILL, RL (reprint author), MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114, USA. NR 27 TC 79 Z9 81 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD JUL PY 1991 VL 25 IS 1 BP 80 EP 88 DI 10.1016/0190-9622(91)70177-4 PN 1 PG 9 WC Dermatology SC Dermatology GA FV333 UT WOS:A1991FV33300011 PM 1880258 ER PT J AU PRESTI, CF WALLING, AD MONTEMAYOR, I CAMPBELL, JM CRAWFORD, MH AF PRESTI, CF WALLING, AD MONTEMAYOR, I CAMPBELL, JM CRAWFORD, MH TI INFLUENCE OF EXERCISE-INDUCED MYOCARDIAL-ISCHEMIA ON THE PATTERN OF LEFT-VENTRICULAR DIASTOLIC FILLING - A DOPPLER ECHOCARDIOGRAPHIC STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; PACING-INDUCED ISCHEMIA; RADIONUCLIDE ANGIOGRAPHY; FLOW VELOCITY; HYPERTROPHIC CARDIOMYOPATHY; ANGIOPLASTY; RELAXATION; REST; PERFORMANCE; DYSFUNCTION AB Previous studies using Doppler echocardiography to evaluate left ventricular diastolic filling have shown that myocardial ischemia induced by coronary balloon angioplasty or atrial pacing results in a decrease in the left ventricular inflow peak early (E) to peak atrial (A) velocity ratio. To investigate the effects of exercise-induced ischemia on Doppler-derived filling variables, 20 patients with coronary artery disease and exercise-induced electrocardiographic changes and regional wall motion abnormalities determined by two-dimensional echocardiography were evaluated and compared with 20 patients without evidence of exercise-induced ischemia. Doppler echocardiography was performed at rest and immediately after exercise before the resolution of exercise-induced wall motion abnormalities. Peak E and A velocities increased from rest to postexercise in both the ischemic and nonischemic groups, although the ischemic group demonstrated a greater increase in peak E velocity (from 68 +/- 15 cm/s at rest to 88 +/- 22 cm/s after exercise) than the nonischemic group (70 +/- 13 to 77 +/- 18 cm/s) (p < 0.05 for the difference in response between groups). Accompanying these changes was a slight increase in the peak E/A velocity ratio in the ischemic group (1.04 +/- 0.28 at rest to 1.13 +/- 0.42 after exercise) versus a decrease in the nonischemic group (1.07 +/- 0.30 to 0.90 +/- 0.28) (p < 0.05 intergroup difference). Within the ischemic group, the change from rest to postexercise in peak E/A velocity ratio was related to changes in left ventricular wall motion score (r = 0.61, p = 0.004) and inversely to changes in left ventricular ejection fraction (r = -0.61, p = 0.004) but not to changes in heart rate (r = -0.30, p = NS). This study demonstrates that during exercise-induced ischemia, early diastolic filling is not blunted but is instead maintained. This observation correlates with changes in left ventricular systolic function, suggesting that exercise-induced ischemia may lead to greater increases in left atrial pressure, which augments peak E velocity and results in pseudonormalization of the diastolic Doppler velocity profile. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CARDIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 37 TC 40 Z9 40 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUL PY 1991 VL 18 IS 1 BP 75 EP 82 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FU815 UT WOS:A1991FU81500013 PM 2050945 ER PT J AU PICARD, MH SANFILIPPO, AJ NEWELL, JB RODRIGUEZ, L GUERRERO, JL WEYMAN, AE AF PICARD, MH SANFILIPPO, AJ NEWELL, JB RODRIGUEZ, L GUERRERO, JL WEYMAN, AE TI QUANTITATIVE RELATION BETWEEN INCREASED INTRAPERICARDIAL PRESSURE AND DOPPLER FLOW VELOCITIES DURING EXPERIMENTAL CARDIAC-TAMPONADE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID EXAGGERATED RESPIRATORY VARIATION; VENTRICULAR DIASTOLIC COLLAPSE; PERICARDIAL-EFFUSION; ECHOCARDIOGRAPHIC SIGN; PULSUS PARADOXUS; COMPRESSION; DIMENSIONS; DIAGNOSIS; TIME AB To establish whether a quantitative relation exists between pericardial pressure and respiratory variation in intracardiac blood flow velocities, a spontaneously breathing closed chest canine model of pericardial tamponade was created. In seven dogs, pericardial pressure was sequentially increased in stages from a mean of -4 +/- 1 to 10 +/- 2 mm Hg while aortic and pulmonary Doppler flow velocities, pleural pressure changes (respiratory effort), blood pressure and cardiac output were measured. The variation in the Doppler-detected peak transaortic velocity (AV) during inspiration (IV) increased linearly from -5 +/- 3% at baseline (pericardial pressure -4 mm Hg) to -32 +/- 9% at a pericardial pressure of 10 mm Hg [IV(AV) = -2 (pericardial pressure) - 13.1; r = 0.78, p < 10(-6)]. The inspiratory variation in the peak transpulmonary velocity increased from 13 +/- 3% at baseline to 71 +/- 19% at a pericardial pressure of 10 mm Hg. The inspiratory variation in the pulmonary Doppler peak velocity (IV(PV)) was dependent on both pericardial pressure and degree of respiratory effort [IV(PV) = 3.8 (pericardial pressure) + 2.6 (respiratory effort) + 10.9; r = 0.88, p < 10(-8)]. Thus, quantitative relations exist between increases in intrapericardial pressure and increases in inspiratory variation of peak aortic and pulmonary flow velocities. Additionally, pulmonary artery flow velocity is influenced more than aortic velocity by intrathoracic pressure. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PICARD, MH (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,CARDIAC ULTRASOUND LAB,PHILLIPS 8,BOSTON,MA 02114, USA. RI Guerrero, Jorge/I-3666-2015; OI Guerrero, Jorge/0000-0003-4315-7318; Picard, Michael/0000-0002-9264-3243 FU NHLBI NIH HHS [HL-07535] NR 26 TC 7 Z9 7 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 JUL PY 1991 VL 18 IS 1 BP 234 EP 242 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FU815 UT WOS:A1991FU81500036 PM 2050927 ER PT J AU CUMMINGS, JL AF CUMMINGS, JL TI BEHAVIORAL COMPLICATIONS OF DRUG-TREATMENT OF PARKINSONS-DISEASE SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID BROMOCRIPTINE-INDUCED MANIA; L-DOPA; LEVODOPA THERAPY; PSYCHOSIS; HYPERSEXUALITY; HALLUCINATIONS; CLOZAPINE; SYMPTOMS; DISTURBANCES; MESULERGINE AB A variety of neuropharmacologic agents, including anticholinergic drugs, amantadine hydrochloride, levodopa, selegiline, bromocriptine, and pergolide, are now available for the treatment of Parkinson's disease. Of patients treated with dopaminergic agents, 30% develop visual hallucinations, 10% exhibit delusions, 10% have euphoria, 1% have mania, 10% to 15% experience increased anxiety, 15% have confusional periods, and a few exhibit altered sexual behaviour. Anticholinergic drugs have a greater tendency to produce confusional states than dopaminergic compounds. Elderly patients and those with underlying dementia are most likely to have untoward side effects with anti-parkinsonism treatment. Dosage reduction is the optimum management strategy, although anti-psychotic agents may be necessary in patients with delusions, and lithium may help control drug-induced mania. Dopaminergic agents share the property of stimulation of D2 dopamine receptors, and this action may play an essential role in mediating their neuropsychiatric effects. C1 UNIV CALIF LOS ANGELES,DEPT NEUROL & PSYCHIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT BEHAV SCI,LOS ANGELES,CA 90024. RP CUMMINGS, JL (reprint author), W LOS ANGLES VET AFFAIRS MED CTR,BEHAV NEUROSCI SECT,PSYCHIAT SERV,NEUROBEHAV UNIT,BLDG 256B,LOS ANGELES,CA 90073, USA. NR 89 TC 127 Z9 127 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD JUL PY 1991 VL 39 IS 7 BP 708 EP 716 PG 9 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA FU969 UT WOS:A1991FU96900012 PM 2061539 ER PT J AU NILES, JL PAN, G COLLINS, AB SHANNON, T SKATES, S FIENBERG, R ARNAOUT, MA MCCLUSKEY, RT AF NILES, JL PAN, G COLLINS, AB SHANNON, T SKATES, S FIENBERG, R ARNAOUT, MA MCCLUSKEY, RT TI ANTIGEN-SPECIFIC RADIOIMMUNOASSAYS FOR ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES IN THE DIAGNOSIS OF RAPIDLY PROGRESSIVE GLOMERULONEPHRITIS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE WEGENER GRANULOMATOSIS; MICROSCOPIC POLYARTERITIS-NODOSA; PAUCI-IMMUNE NECROTIZING AND CRESCENTIC GLOMERULONEPHRITIS; PROTEINASE-3; MYELOPEROXIDASE ID WEGENERS GRANULOMATOSIS; SYSTEMIC VASCULITIS; CRESCENTIC GLOMERULONEPHRITIS; AUTOANTIBODIES; DISEASE; ANCA; MYELOPEROXIDASE; PROTEINASE-3; MYELOBLASTIN; MECHANISMS AB Circulating anti-neutrophil cytoplasmic antibodies (ANCA) have been described in most patients with "pauci-immune" necrotizing and crescentic glomerulonephritis. A 29-kDa serine protease (p29 or proteinase 3) and myeloperoxidase are the two best characterized antigens recognized by ANCA. The study presented here was conducted to define the diagnostic value of assays for antibodies against these two antigens in rapidly progressive glomerulonephritis. Radioimmunoassays were developed for anti-29 and anti-myeloperoxidase antibodies, with purified antigens, and the results of the radioimmunoassays were compared with those obtained by immunofluorescence tests for ANCA. We performed assays on serum samples from 123 patients with the syndrome of rapidly progressive glomerulonephritis, as well as from 200 blood bank donors and from 717 additional control patients. Without knowledge of the results of ANCA tests, the renal pathologic findings in the 123 patients with rapidly progressive glomerulonephritis were analyzed, and 42 were classified as pauci-immune necrotizing and crescentic glomerulonephritis, 18 were classified as anti-glomerular basement membrane nephritis and 63 were classified as other forms of renal disease. We found radioimmunoassays to be more reliable in the diagnosis of pauci-immune necrotizing and crescentic glomerulonephritis than immunofluorescence testing. By radioimmunoassay, ANCA were found in 40 of 42 patients (95% sensitivity) with pauci-immune necrotizing and crescentic glomerulonephritis (14 with anti-p29 and 26 with anti-myeloperoxidase antibodies). The tests for antibodies to p29 and myeloperoxidase were 99.9 and 99.5% specific for pauci-immune necrotizing and crescentic glomerulonephritis, respectively. In the setting of rapidly progressive glomerulonephritis, a positive radioimmunoassay for anti-p29 or anti-myeloperoxidase antibodies (together with a negative test for anti-GBM antibodies) gives a probability of pauci-immune necrotizing and crescentic glomerulonephritis of over 99%. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA 02114. RP NILES, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,COX 5,FRUIT ST,BOSTON,MA 02114, USA. NR 41 TC 81 Z9 83 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JUL PY 1991 VL 2 IS 1 BP 27 EP 36 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA FZ094 UT WOS:A1991FZ09400004 PM 1655091 ER PT J AU SUGARBAKER, DJ HEHER, EC LEE, TH COUPER, G MENTZER, S CORSON, JM COLLINS, JJ SHEMIN, R PUGATCH, R WEISSMAN, L ANTMAN, KH AF SUGARBAKER, DJ HEHER, EC LEE, TH COUPER, G MENTZER, S CORSON, JM COLLINS, JJ SHEMIN, R PUGATCH, R WEISSMAN, L ANTMAN, KH TI EXTRAPLEURAL PNEUMONECTOMY, CHEMOTHERAPY, AND RADIOTHERAPY IN THE TREATMENT OF DIFFUSE MALIGNANT PLEURAL MESOTHELIOMA SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article; Proceedings Paper CT 70TH ANNUAL MEETING OF THE AMERICAN ASSOC FOR THORACIC SURGERY CY MAY 07-09, 1990 CL TORONTO, CANADA SP AMER ASSOC THORAC SURG ID PERITONEAL MESOTHELIOMA AB Malignant pleural mesothelioma has been considered a uniformly fatal disease associated with a median survival of 4 to 18 months. Extrapleural pneumonectomy alone has proved disappointing in the treatment of this disease, as have chemotherapy and radiotherapy. From 1980 to 1990, 31 patients with pleural mesothelioma underwent multimodality therapy that included extrapleural pneumonectomy with resection of the pericardium and diaphragm. The age of the patients was 53.4 +/- 8.6 years; 26 were male. All patients had the pathologic diagnosis reviewed before treatment. At thoracotomy six patients had residual (unresectable) gross disease, and in 23 there was histologic evidence of disease at the resection margin. The perioperative morbidity and mortality rates were 19% and 6%, respectively. The mean length of hospital stay for the 29 patients who survived the operation was 10.9 +/- 3.5 days. Postoperatively 26 patients received cyclophosphamide, doxorubicin, and cis-platinum chemotherapy with or without radiotherapy. The survival rates were 70% at 1 year and 48% at 2 years. Trends toward improved survival in the patients with complete resections approached but did not reach statistical significance. These data suggest that this multimodality protocol can be administered with acceptable morbidity and mortality. Prospective trials are justified to further clarify the role of this approach. C1 BRIGHAM & WOMENS HOSP,DEPT SURG,DIV CLIN EPIDEMIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. RP SUGARBAKER, DJ (reprint author), BRIGHAM & WOMENS HOSP,DIV OBSTET GYNECOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 15 TC 83 Z9 84 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD JUL PY 1991 VL 102 IS 1 BP 10 EP 15 PG 6 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FW773 UT WOS:A1991FW77300002 PM 2072707 ER PT J AU MATHISEN, DJ GRILLO, HC AF MATHISEN, DJ GRILLO, HC TI CARINAL RESECTION FOR BRONCHOGENIC-CARCINOMA SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article; Proceedings Paper CT 70TH ANNUAL MEETING OF THE AMERICAN ASSOC FOR THORACIC SURGERY CY MAY 07-09, 1990 CL TORONTO, CANADA SP AMER ASSOC THORAC SURG ID TRACHEAL SLEEVE PNEUMONECTOMY; LUNG; VENTILATION AB Techniques are available for carinal resection and reconstruction for bronchogenic carcinoma involving the carina. Successful outcome depends on careful patient selection, thorough preoperative evaluation, careful anesthetic management, strict attention to surgical technique, and compulsive postoperative care. Since 1973 we have performed 37 carinal resections for bronchogenic carcinoma: 21 right carinal pneumonectomies, 7 carinal resections, 7 carina plus lobe resections, and 2 carina plus pneumonectomy stump resections. Five patients had diseased N2 nodes and 13 patients had diseased N1 nodes. Complications included pulmonary (8), vocal cord paresis (3), atrial fibrillation (9), anastomotic stenosis (4), and anastomotic separation (3). There were 3 early postoperative deaths (8%). All were related to adult respiratory distress syndrome and were unresponsive to aggressive treatment. There were 4 late postoperative deaths between 2 and 4 months (10.9%). All late postoperative deaths were related to anastomotic complications (stenosis [1] and separation [3]. There are 5 absolute 5-year survivors and an actuarial 5-year survival rate of 19%. RP MATHISEN, DJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET GYNECOL,WARREN 1109,BOSTON,MA 02114, USA. NR 18 TC 72 Z9 75 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-5223 J9 J THORAC CARDIOV SUR JI J. Thorac. Cardiovasc. Surg. PD JUL PY 1991 VL 102 IS 1 BP 16 EP 23 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FW773 UT WOS:A1991FW77300003 PM 2072721 ER PT J AU OGILVY, CS AF OGILVY, CS TI AN UNUSUAL SIGN OF RECOVERY AFTER CEREBRAL INJURY IN MALE-PATIENTS SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Letter RP OGILVY, CS (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD JUL PY 1991 VL 31 IS 7 BP 1017 EP 1017 DI 10.1097/00005373-199107000-00024 PG 1 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA FX909 UT WOS:A1991FX90900023 PM 2072420 ER PT J AU HOWE, RS ISAACSON, KJ ALBERT, JL COUTIFARIS, CB AF HOWE, RS ISAACSON, KJ ALBERT, JL COUTIFARIS, CB TI EMBRYONIC HEART-RATE IN HUMAN-PREGNANCY SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Article DE CARDIAC EMBRYOLOGY; EMBRYONIC HEART RATE; FETAL DEVELOPMENT; SPONTANEOUS ABORTION; TRANSVAGINAL ULTRASOUND ID FETAL CARDIAC ACTIVITY; 1ST TRIMESTER; ULTRASOUND; SIGN AB Seventy-two women with known gestational ages underwent serial human chorionic gonadotropin (hCG) measurements and transvaginal ultrasound studies with embryonic heart rate measurements. In 53 continuing singleton pregnancies, embryonic pulse appeared between days 26 and 32, was 80 beat per minute (bpm) on day 26, and increased linearly to plateau at 160-200 bpm by day 45 (r2 = 0.72). The pulse was always seen with hCG > 21,000 mIU/mL; pulse rate was correlated to embryonic crown-rump length. Of the remaining 19 pregnancies, 8 were anembryonic, 10 showed heart activity but subsequently aborted, and 1 was terminated. Absence of embryonic pulse by 32 days after conception or a serum hCG > 21,000 mIU/mL predicts spontaneous abortion; presence of a pulse may not guarantee successful continuation of the pregnancy since incidence of spontaneous abortion after visualization of embryonic pulse may be as high as 16%. C1 HOSP UNIV PENN,DEPT OBSTET & GYNECOL,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. RP HOWE, RS (reprint author), BAYSTATE MED CTR,DEPT OBSTET & GYNECOL,WESSON WOMENS BLDG,4TH FLOOR,759 CHESTNUT ST,SPRINGFIELD,MA 01199, USA. NR 27 TC 33 Z9 35 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD JUL PY 1991 VL 10 IS 7 BP 367 EP 371 PG 5 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA FU476 UT WOS:A1991FU47600008 PM 1870180 ER PT J AU LONGNECKER, R DRUKER, B ROBERTS, TM KIEFF, E AF LONGNECKER, R DRUKER, B ROBERTS, TM KIEFF, E TI AN EPSTEIN-BARR-VIRUS PROTEIN ASSOCIATED WITH CELL-GROWTH TRANSFORMATION INTERACTS WITH A TYROSINE KINASE SO JOURNAL OF VIROLOGY LA English DT Article ID MIDDLE-T-ANTIGEN; MEDIATED SIGNAL TRANSDUCTION; MEMBRANE-PROTEIN; LATENT-INFECTION; PHOSPHATIDYLINOSITOL KINASE; RECEPTOR COMPLEX; IMMORTALIZED LYMPHOCYTES; MOLECULAR-COMPONENTS; HEMATOPOIETIC-CELLS; TUMOR-ANTIGEN AB Epstein-Barr virus (EBV) encodes two integral membrane proteins in latently infected growth-transformed cells. One of these, LMP1, can transform rodent fibroblasts and induce markers of B-lymphocyte activation. The second, LMP2, colocalizes with LMP1 in a constitutive patch in the EBV-transformed B-lymphocyte plasma membrane. The experiments reported here demonstrate that LMP2 may biochemically interact with LMP1 and that LMP2 closely associates with and is an important substrate for a B-lymphocyte tyrosine kinase in EBV-transformed B lymphocytes or in B-lymphoma cells in which LMP2 is expressed by gene transfer. LMP2 is also serine and threonine phosphorylated. LMP2 localizes to a peripheral membrane (presumably plasma membrane) patch in transfected B-lymphoma cells and colocalizes with much of the cellular tyrosine-phosphorylated proteins. LMP2 undergoes tyrosine phosphorylation in anti-LMP2 or antiphosphotyrosine immunoprecipitates from transfected B-lymphoma cells or EBV-transformed B lymphocytes. The first 167 of the 497 amino acids of LMP2 retain full ability to associate with and act as a substrate for a tyrosine kinase. A 70-kDa phosphotyrosine cell protein associates with LMP2 in transfected cells or in EBV-transformed B lymphocytes and could be a mediator of the effects of LMP2. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET & MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. FU NCI NIH HHS [CA47006] NR 65 TC 125 Z9 127 U1 0 U2 3 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 JUL PY 1991 VL 65 IS 7 BP 3681 EP 3692 PG 12 WC Virology SC Virology GA FQ940 UT WOS:A1991FQ94000035 PM 1710288 ER PT J AU BROWN, D SABOLIC, I GLUCK, S AF BROWN, D SABOLIC, I GLUCK, S TI COLCHICINE-INDUCED REDISTRIBUTION OF PROTON PUMPS IN KIDNEY EPITHELIAL-CELLS SO KIDNEY INTERNATIONAL LA English DT Article; Proceedings Paper CT SATELLITE SYMP TO THE 11TH INTERNATIONAL CONGRESS OF NEPHROLOGY : PROTON, BICARBONATE AND CHLORIDE TRANSPORT IN THE KIDNEY CY JUL 22-24, 1990 CL NARA, JAPAN ID MEDULLARY COLLECTING DUCT; BRUSH-BORDER MEMBRANES; RAT-KIDNEY; ABSORPTIVE CELLS; PLASMA-MEMBRANE; FUSION PROTEIN; BOVINE KIDNEY; MICROTUBULES; SECRETION; TRANSPORT C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. JEWISH HOSP ST LOUIS,RENAL UNIT,ST LOUIS,MO 63110. NR 49 TC 24 Z9 24 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUL PY 1991 VL 40 SU 33 BP S79 EP S83 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA FT574 UT WOS:A1991FT57400016 ER PT J AU SACHDEVA, AK ZAREN, HA SIGEL, B AF SACHDEVA, AK ZAREN, HA SIGEL, B TI SURGICAL-TREATMENT OF PEPTIC-ULCER DISEASE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID PROXIMAL GASTRIC-VAGOTOMY; BLEEDING GASTRODUODENAL ULCERS; PERFORATED DUODENAL-ULCER; UPPER GASTROINTESTINAL HEMORRHAGE; HIGHLY SELECTIVE VAGOTOMY; CONTROLLED TRIAL; SIMPLE CLOSURE; PYLORIC-STENOSIS; HEATER PROBE; MANAGEMENT C1 MED COLL PENN,SURG EDUC,PHILADELPHIA,PA 19129. VET AFFAIRS MED CTR,SURG SERV,PHILADELPHIA,PA. RP SACHDEVA, AK (reprint author), MED COLL PENN,DEPT SURG,3300 HENRY AVE,PHILADELPHIA,PA 19129, USA. NR 56 TC 16 Z9 16 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD JUL PY 1991 VL 75 IS 4 BP 999 EP 1012 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA FX347 UT WOS:A1991FX34700016 PM 2072800 ER PT J AU MITTLER, JC AF MITTLER, JC TI TESTICULAR AUTOREGULATION - POSSIBLE ROLE FOR 7-ALPHA-HYDROXYLATED ANDROGENS SO MEDICAL HYPOTHESES LA English DT Article ID FOLLICLE-STIMULATING-HORMONE; LUTEINIZING-HORMONE; MALE-RAT; SEMINIFEROUS TUBULES; GONADOTROPIN-SECRETION; INTERSTITIAL-TISSUE; IN-VITRO; HYPOPHYSECTOMIZED RATS; ANTERIOR-PITUITARY; RHESUS-MONKEY AB Pituitary FSH secretion appears to be supported by a tactor distinct from the gonadotropin-releasing hormone (Gn-RH). The ratio of FSH to LH is positively correlated with testicular steroid 5 alpha -reductase activity and negatively correlated with testicular steroid 7 alpha- hydroxylase under various experimental conditions. Literature describing interactions among the above and other factors is reviewed here. C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT MED,NEWARK,NJ 07103. RP MITTLER, JC (reprint author), US DEPT VET AFFAIRS,MED CTR,MED SERV,E ORANGE,NJ 07019, USA. NR 85 TC 1 Z9 1 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JUL PY 1991 VL 35 IS 3 BP 184 EP 191 DI 10.1016/0306-9877(91)90231-M PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FW619 UT WOS:A1991FW61900004 PM 1943861 ER PT J AU BIGGS, P CAPALUCCI, J RUSSELL, M AF BIGGS, P CAPALUCCI, J RUSSELL, M TI COMPARISON OF THE PENUMBRA BETWEEN FOCUSED AND NONDIVERGENT BLOCKS - IMPLICATIONS FOR MULTILEAF COLLIMATORS SO MEDICAL PHYSICS LA English DT Article AB The penumbra from a 10-MV x-ray beam has been measured using various field-shaping blocks located in the normal blocking tray position and compared to the penumbra of the adjustable photon jaws of the machine. The results showed that the penumbra was substantially degraded by these blocks only for field sizes greater than 15 X 15 cm2 and at the depth of maximum dose, d(max). At depths of 11 cm or greater, there was a significant difference only for the same range of field sizes in the 80% to 50% dose region. There was no significant difference at these depths for either the 95%-50% or the 90%-50% dose regions. No significant difference was observed between the use of lead and tungsten blocks and also between lead blocks with a straight edge and those with either an 0.5-mm or a 1-mm step in the face. Since the width of the 95% dose relative to the 50% dose is of greatest interest clinically, straight-edged blocks are as effective as divergent blocks in most situations. These results imply that the design and complexity of a multileaf collimator can be greatly simplified from a double focusing device to one that is single focusing in the plane orthogonal to the leaves. RP BIGGS, P (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 3 TC 13 Z9 13 U1 0 U2 1 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD JUL-AUG PY 1991 VL 18 IS 4 BP 753 EP 758 DI 10.1118/1.596669 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA GB235 UT WOS:A1991GB23500011 PM 1921882 ER PT J AU LLOVERAS, B GOOGE, PB GOLDBERG, DE BHAN, AK AF LLOVERAS, B GOOGE, PB GOLDBERG, DE BHAN, AK TI ESTROGEN-RECEPTORS IN SKIN APPENDAGE TUMORS AND EXTRAMAMMARY PAGETS-DISEASE SO MODERN PATHOLOGY LA English DT Article DE ESTROGEN RECEPTORS; SKIN APPENDAGE TUMORS; EXTRAMAMMARY PAGETS DISEASE ID SEX STEROID-RECEPTOR; PROGESTERONE RECEPTORS; PARAFFIN SECTIONS; CARCINOMA; MAMMARY; CELLS; IMMUNOPEROXIDASE; ADENOCARCINOMA; PRETREATMENT; ANTIBODIES AB Determination of estrogen receptors (ER) in breast carcinoma is valuable in the management of patients. However, little is known about the presence of these receptors in other tumors. Normal skin appendages and their neoplasms, including extramammary Paget's disease (EPD), might be expected to express ER since the breast is histogenetically related to sweat glands. In this study, 41 cases of skin appendage tumors (SAT) and 11 cases of EPD were stained using the ER-ICA monoclonal kit (Abbott, Chicago, IL) with a modified technique for paraffin-embedded sections. Controls included 10 biopsies of primary breast carcinoma and 4 cases of metastatic breast carcinoma to skin, all positive for ER. None of the samples of SAT or EPD showed staining for ER. Normal skin appendages were also negative. Normal vaginal epithelium in one case of EPD showed positive nuclear staining for ER. ER determination using immunohistochemical technique in paraffin-embedded sections may be useful in the differential diagnosis between malignant SAT and metastatic breast carcinoma in the skin. The absence of ER in normal skin appendages suggests that its apparition is a feature of specialized differentiation of breast epithelium. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,IMMUNOPATHOL UNIT,BOSTON,MA 02114. MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,NEW YORK,NY 10021. UNIV TENNESSEE,MED CTR,DEPT PATHOL,KNOXVILLE,TN 37996. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 34 TC 16 Z9 16 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JUL PY 1991 VL 4 IS 4 BP 487 EP 490 PG 4 WC Pathology SC Pathology GA FX215 UT WOS:A1991FX21500012 PM 1656434 ER PT J AU DUMITRU, D KALANTRI, A DIERSCHKE, B AF DUMITRU, D KALANTRI, A DIERSCHKE, B TI SOMATOSENSORY EVOKED-POTENTIALS OF THE MEDIAL AND LATERAL PLANTAR AND CALCANEAL NERVES SO MUSCLE & NERVE LA English DT Article DE SOMATOSENSORY EVOKED POTENTIALS; PLANTAR NERVE; TARSAL TUNNEL; ELECTRODIAGNOSIS; CALCANEAL NERVE ID TARSAL TUNNEL-SYNDROME; NERVOUS-SYSTEM; CONDUCTION; STIMULATION; NEUROPATHY; DIAGNOSIS AB The ideal electrodiagnostic procedure to assess possible plantar neuropathies continues to elude investigators. Motor studies are rarely abnormal, pure sensory studies may be difficult to obtain, needle electromyography can demonstrate membrane instability in normal feet. Mixed nerve plantar studies may be more diagnostically valuable than the other techniques but they also have shortcomings. In this report, a technique utilizing somato-sensory evoked potentials to assess the medial and lateral plantar and calcaneal nerves is demonstrated. Normative data with respect to latencies, amplitudes, and side-to-side differences are presented. Two illustrative cases are also discussed in which the more standard techniques to evaluate plantar neuropathies fail to do so, but the SEP methodology suggests compromise of the intrinsic foot nerves. C1 AUDIE L MURPHY MEM VET ADM MED CTR,REHABIL SERV,SAN ANTONIO,TX. ORTHOPAED SURG ASSOCIATES,DAVENPORT,IA. RP DUMITRU, D (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PHYS MED & REHABIL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 34 TC 11 Z9 11 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD JUL PY 1991 VL 14 IS 7 BP 665 EP 671 DI 10.1002/mus.880140710 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FT153 UT WOS:A1991FT15300009 PM 1656250 ER PT J AU SMALL, GW EBELING, SC MATSUYAMA, SS HEYMAN, A REISNER, EG RENVOIZE, EB SULKAVA, R AF SMALL, GW EBELING, SC MATSUYAMA, SS HEYMAN, A REISNER, EG RENVOIZE, EB SULKAVA, R TI VARIABLE ASSOCIATION OF HLA-A2 IN MEN WITH EARLY-ONSET ALZHEIMER-DISEASE SO NEUROBIOLOGY OF AGING LA English DT Note DE ALZHEIMER DISEASE; HLA ANTIGENS; AGE AT ONSET ID ANTIGENS AB In the present study, we attempted to replicate the finding of an increased frequency of HLA-A2 in men with early-onset (less-than-or-equal-to 60 years) Alzheimer disease (AD). HLA data obtained on 167 patients (including 19 men with early-onset AD) from three geographic regions (North Carolina. Great Britain, and Finland) failed to replicate the result. A recent prospective study from Oregon, however, confirmed the association. Studies demonstrating the association suggest its presence in sporadic rather than familial AD. These results indicate a variable HLA/AD association, with some factor such as geographic region or disease familiality contributing to this variability. C1 WAYNE STATE UNIV,DETROIT,MI 48202. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. DUKE UNIV,DURHAM,NC 27706. UNIV HELSINKI,SF-00100 HELSINKI 10,FINLAND. UNIV LEEDS,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. RP SMALL, GW (reprint author), UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. FU NIMH NIH HHS [1R29 MH46424] NR 11 TC 12 Z9 12 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0197-4580 J9 NEUROBIOL AGING JI Neurobiol. Aging PD JUL-AUG PY 1991 VL 12 IS 4 BP 375 EP 377 DI 10.1016/0197-4580(91)90026-G PG 3 WC Geriatrics & Gerontology; Neurosciences SC Geriatrics & Gerontology; Neurosciences & Neurology GA GB995 UT WOS:A1991GB99500026 PM 1961374 ER PT J AU GHIKA, J TENNIS, M HOFFMAN, E SCHOENFELD, D GROWDON, J AF GHIKA, J TENNIS, M HOFFMAN, E SCHOENFELD, D GROWDON, J TI IDAZOXAN TREATMENT IN PROGRESSIVE SUPRANUCLEAR PALSY SO NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; INDUCED MUSCULAR RIGIDITY; LOCUS COERULEUS; CEREBRAL-CORTEX; BRAIN; PROJECTIONS; INVOLVEMENT; YOHIMBINE; AGONIST AB To confirm the preliminary report that increases in norepinephrine neurotransmission improve motor performance, we administered the investigational drug idazoxan (IDA) to nine patients with progressive supranuclear palsy (PSP) according to a double-blind crossover protocol. There were seven women and two men, whose mean age was 70 years and mean duration of illness 4 years. All had an advanced parkinsonian syndrome, supranuclear ocular motor palsies, and poor responses to dopaminergic drugs. During administration of 40 mg tid of IDA, the total score and the motor subscale score of the United Parkinson's Disease Rating Scale significantly decreased. Features that improved most included mobility, balance, gait, and measures of digital dexterity. There were no significant changes in any measure during placebo administration. Corticobulbar manifestations and eye movements were not significantly improved during treatment. Side effects of IDA included transient hypertension, tachycardia, action tremor, flushing, and sweating, but none was so severe that any patient withdrew from the study. Among the few attempted treatments of PSP, IDA is the first medication shown in a double-blind study to improve aspects of motor function. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,CTR AMBULATORY CARE,SUITE 830,BOSTON,MA 02114. FU NCRR NIH HHS [5 MO1 RR01066-13] NR 53 TC 47 Z9 47 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL PY 1991 VL 41 IS 7 BP 986 EP 991 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA FX123 UT WOS:A1991FX12300005 PM 1676832 ER PT J AU FEINBERG, TE CIANCI, CD MORROW, JS PEHTA, JC REDMAN, CM HUIMA, T KOROSHETZ, WJ AF FEINBERG, TE CIANCI, CD MORROW, JS PEHTA, JC REDMAN, CM HUIMA, T KOROSHETZ, WJ TI DIAGNOSTIC-TESTS FOR CHOREOACANTHOCYTOSIS SO NEUROLOGY LA English DT Article; Proceedings Paper CT 42ND ANNUAL MEETING OF THE AMERICAN ACADEMY OF NEUROLOGY CY APR, 1990 CL MIAMI BEACH, FL SP AMER ACAD NEUROL ID CHOREA-ACANTHOCYTOSIS; ERYTHROCYTE MEMBRANE; SHAPE; DISEASE AB Two patients with striatal atrophy and a clinical syndrome consistent with choreoacanthocytosis had normal dried blood smears but their red cells demonstrated an abnormal sensitivity to various conditions known to promote discocyte-echinocyte transformation. Dilution in normal saline, in vitro aging, and contact with glass caused a great proportion of these patients' red cells to develop multiple spiny or rounded projections. Under identical conditions, such shape changes did not occur in normal patients or in those with Huntington's disease. Scanning electron microscopy showed that the age-induced increase in acanthocytic-appearing cells could be reversed with chlorpromazine. These data suggest that the red cells from these patients with striatal degeneration are deficient in their ability to preserve normal shape in the face of echinocytic stress and that this observation has diagnostic and, possibly, pathophysiologic significance. C1 BETH ISRAEL MED CTR,DEPT PSYCHIAT,NEW YORK,NY 10003. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. YALE UNIV,SCH MED,DEPT PATHOL,NEW HAVEN,CT 06510. NEW YORK BLOOD CTR,NEW YORK,NY 10021. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP FEINBERG, TE (reprint author), BETH ISRAEL MED CTR,DEPT NEUROL,CTR NEUROBEHAV,317 E 17TH ST,NEW YORK,NY 10003, USA. FU NHLBI NIH HHS [HL33841] NR 26 TC 41 Z9 42 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL PY 1991 VL 41 IS 7 BP 1000 EP 1006 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA FX123 UT WOS:A1991FX12300007 PM 1829792 ER PT J AU CHIAPPA, KH CROS, D COHEN, D AF CHIAPPA, KH CROS, D COHEN, D TI MAGNETIC STIMULATION - DETERMINATION OF COIL CURRENT FLOW DIRECTION SO NEUROLOGY LA English DT Note ID HUMAN-BRAIN; RESPONSES C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. MIT,FRANCIS BITTER NATL MAGNET LAB,CAMBRIDGE,MA 02139. FU NINDS NIH HHS [R01-NS27215] NR 10 TC 27 Z9 27 U1 0 U2 7 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL PY 1991 VL 41 IS 7 BP 1154 EP 1155 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA FX123 UT WOS:A1991FX12300042 PM 2067650 ER PT J AU LIPTON, SA SUCHER, NJ KAISER, PK DREYER, EB AF LIPTON, SA SUCHER, NJ KAISER, PK DREYER, EB TI SYNERGISTIC EFFECTS OF HIV COAT PROTEIN AND NMDA RECEPTOR-MEDIATED NEUROTOXICITY SO NEURON LA English DT Article ID AMINO-ACID NEUROTOXICITY; RETINAL GANGLION-CELLS; CEREBELLAR GRANULE CELLS; GLUTAMATE NEUROTOXICITY; ENVELOPE GLYCOPROTEIN; CENTRAL NEURONS; KINASE-C; RAT; ANTAGONISTS; AGONISTS AB Exposure of rat retinal cultures to HIV-1 coat protein gp120 for several minutes increases [Ca2+]i in approximately half of the ganglion cells; this effect is associated with delayed-onset neuronal injury, similar to that previously reported in NMDA receptor-mediated neurotoxicity. Here we show that NMDA antagonists can prevent both the rise in [Ca2+]i and subsequent neuronal damage engendered by 20 pM gp120. However, whole-cell patch-clamp recordings demonstrate that gp120 does not directly evoke an NMDA-like response or enhance glutamate/NMDA-activated currents. Moreover, complete protection from gp120-induced [Ca2+]i increases and neurotoxicity is afforded by incubation with glutamate-pyruvate transaminase, which breaks down endogenous glutamate as verified by HPLC. Since, under standard conditions in these cultures, neither glutamate nor a low picomolar concentration of gp120 is deleterious on its own, our results suggest that their neurotoxicity is synergistic. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,PROGRAM NEUROSCI,BOSTON,MA 02114. RP LIPTON, SA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [EY05477, EY09024]; NINDS NIH HHS [NS07264] NR 45 TC 351 Z9 354 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD JUL PY 1991 VL 7 IS 1 BP 111 EP 118 DI 10.1016/0896-6273(91)90079-F PG 8 WC Neurosciences SC Neurosciences & Neurology GA FY481 UT WOS:A1991FY48100011 PM 1676893 ER PT J AU ANSON, J CROWELL, RM AF ANSON, J CROWELL, RM TI CERVICOCRANIAL ARTERIAL DISSECTION SO NEUROSURGERY LA English DT Review DE ANGIOGRAPHY; ARTERIAL DISSECTION; CAROTID ARTERY; STROKE ID INTERNAL CAROTID-ARTERY; CEREBRAL-ARTERIES; ANEURYSMS; HEMORRHAGE; MANAGEMENT; RESOLUTION; OCCLUSION; STROKE AB Dissection of the cervicocranial arteries is becoming more frequently recognized as a cause of neurological disorders. Typical clinical features seen with dissection include unilateral headache, oculosympathetic palsy, amaurosis fugax, and symptoms of focal brain ischemia. The diagnosis of carotid or intracranial dissection is usually best confirmed by angiography, although magnetic resonance imaging and computed tomography have been shown to visualize intimal dissection. The prognosis in cases of spontaneous dissection is generally benign unless the initial manifestation involves infarction with substantial deficit. The best approach to treatment appears to be the administration of the anticoagulant, heparin, followed by warfarin or antiplatelet therapy. Surgical intervention is reserved for cases of progressive or recurrent ischemic complication that occurs despite the administration of adequate doses of anticoagulants. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,312 AMBULATORY CARE CTR,BOSTON,MA 02114. UNIV ILLINOIS,DEPT NEUROSURG,CHICAGO,IL 60680. NR 36 TC 138 Z9 140 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JUL PY 1991 VL 29 IS 1 BP 89 EP 96 PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FT164 UT WOS:A1991FT16400015 PM 1870693 ER PT J AU VORHEES, CV RAUCH, SL HITZEMANN, RJ AF VORHEES, CV RAUCH, SL HITZEMANN, RJ TI PRENATAL VALPROIC ACID EXPOSURE DECREASES NEURONAL MEMBRANE ORDER IN RAT OFFSPRING HIPPOCAMPUS AND CORTEX SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Note DE SYNAPTIC MEMBRANE ORDER; PRENATAL VALPROIC ACID; INUTERO VALPROIC ACID AND MEMBRANE ANISOTROPY; ANISOTROPY IN HIPPOCAMPUS; ANISOTROPY IN CORTEX; VALPROATE-INDUCED REDUCTION IN MEMBRANE ORDER; RATS ID DEVELOPMENTAL-CHANGES; PHENYTOIN EXPOSURE; MEMORY; FLUIDITY; BEHAVIOR; FETAL AB Sprague-Dawley rats were administered 0 or 200 mg/kg of valproic acid (VPA) on days 7-18 of gestation. Controls were pair-fed. On postnatal day 28, analyses of brain tissues were performed on enriched neuronal membrane fractions from cerebellum, hippocampus, and cortex for anisotropy using the membrane probe 1,6-diphenyl-1,3,5-hexatriene (DPH). No significant differences in membrane anisotropy were noted in the cerebellum, but a significant reduction in anisotropy in the hippocampus and cortex was observed. This change corresponds to a 3-5-degrees-C increase in temperature or that produced by other membrane disordering agents (ethanol, phenytoin). An association between membrane anisotropy and functional effects of prenatal VPA exposure is discussed. C1 UNIV CINCINNATI,DEPT PEDIAT,CINCINNATI,OH 45229. SUNY STONY BROOK,DEPT PSYCHIAT & BEHAV SCI,STONY BROOK,NY 11794. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. RP VORHEES, CV (reprint author), CHILDRENS HOSP RES FDN,INST DEV RES,CINCINNATI,OH 45229, USA. FU NIAAA NIH HHS [AA6032] NR 21 TC 11 Z9 11 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0892-0362 J9 NEUROTOXICOL TERATOL JI Neurotoxicol. Teratol. PD JUL-AUG PY 1991 VL 13 IS 4 BP 471 EP 474 DI 10.1016/0892-0362(91)90097-G PG 4 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA FY580 UT WOS:A1991FY58000015 PM 1921927 ER PT J AU JUWEID, M FISCHMAN, AJ RUBIN, RH BAUM, R STRAUSS, HW AF JUWEID, M FISCHMAN, AJ RUBIN, RH BAUM, R STRAUSS, HW TI COMPARISON OF TC-99M-LABELED MONOCLONAL ANTIGRANULOCYTE ANTIBODY AND IN-111 LABELED IGG FOR THE DETECTION OF FOCAL SITES OF INFECTION IN RATS SO NUCLEAR MEDICINE COMMUNICATIONS LA English DT Article AB The abilities of Tc-99m-labelled monoclonal anti-human granulocyte antibody (AGAb) and In-111-labelled nonspecific polyclonal human immunoglobulin (IgG) to localize at focal sites of inflammation were compared in rats with deep thigh infection due to E. coli. The radiolabelled antibodies were coadministered followed 4-6 and 24 h later by imaging and biodistribution studies. At 4-6 h after injection, the target to background ratio (T/B, lesion to contralateral leg) and percentage residual activity (% RA, counts in the lesion/total body counts) were nearly identical for both antibody preparations. At 24 h, T/B and % RA increased significantly (P < 0.001) for both proteins but differences between the agents were not significant. In vitro analysis of the binding of AGAb and human polyclonal IgG to rat granulocytes showed a low level of binding with both agents. These results suggest that the primary mechanism of localization, by either antibody preparation in this model, is not antigen related. In-111-labelled nonspecific human IgG and Tc-99m-AGAb are equivalent reagents for the detection of focal sites of infection in the rat. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,55 FRUIT ST,BOSTON,MA 02114. NR 0 TC 7 Z9 7 U1 0 U2 0 PU CHAPMAN HALL LTD PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8HN SN 0143-3636 J9 NUCL MED COMMUN JI Nucl. Med. Commun. PD JUL PY 1991 VL 12 IS 7 BP 637 EP 644 DI 10.1097/00006231-199107000-00008 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FX608 UT WOS:A1991FX60800008 PM 1923155 ER PT J AU BAETSCHER, M SCHMIDT, E SHIMIZU, A LEDER, P FISHMAN, MC AF BAETSCHER, M SCHMIDT, E SHIMIZU, A LEDER, P FISHMAN, MC TI SV40 T-ANTIGEN TRANSFORMS CALCITONIN CELLS OF THE THYROID BUT NOT CGRP-CONTAINING NEURONS IN TRANSGENIC MICE SO ONCOGENE LA English DT Article ID LARGE TUMOR-ANTIGEN; C-MYC; GENE; EXPRESSION; CARCINOMA; ONCOGENE; BRAIN AB Neurons are postmitotic for the adult life of animals. Tumors rarely, if ever, arise from neurons in the adult, although they do from other cells from the same lineage, such as the neuroendocrine C cells of the thyroid. We have found that 2 kb of the calcitonin gene-related peptide (CGRP)/calcitonin gene suffices to target expression to CGRP-containing neurons, such as those in the dorsal root ganglia (DRG), and to the clacitonin-secreting C cells of the thyroid. Using this promoter we have examined the effect of two potentially transforming oncogenes in these two different populations. Overexpression of c-myc for periods of up to two years does not transform either cell type, whereas SV40 Tag causes early onset medullary thyroid carcinoma, but does not transform the dorsal root ganglia neurons. This suggests that as part of the terminal differentiation process of these neurons, the cessation of mitosis is accompanied by a relative refractoriness to oncogenes that may transform other cells of the same lineage. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEV BIOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. HOWARD HUGHES MED INST,BOSTON,MA. RP FISHMAN, MC (reprint author), MASSACHUSETTS GEN HOSP,DEV BIOL LAB,MGH E,149 13TH ST,4TH FLOOR,BOSTON,MA 02129, USA. NR 31 TC 27 Z9 27 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JUL PY 1991 VL 6 IS 7 BP 1133 EP 1138 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA GV260 UT WOS:A1991GV26000006 PM 1650439 ER PT J AU BERNARDS, A AF BERNARDS, A TI PREDICTED TYK2 PROTEIN CONTAINS 2 TANDEM PROTEIN-KINASE DOMAINS SO ONCOGENE LA English DT Note ID TYROSINE KINASES; SIGNAL TRANSDUCTION; CATALYTIC DOMAINS; CLONING; GENES AB Tyk2 was recently described as an 1187 amino acid protein with a putative protein-tyrosine kinase domain near its C-terminus and no similarity to other proteins in the approximately 900 amino acids preceding the kinase domain. I report here, however, that tyk2 contains an additional protein kinase domain, and that the two tandem kinase domains are preceded by an SH2-like, putative regulatory domain. RP BERNARDS, A (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DEPT MOLEC GENET,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 13 TC 24 Z9 24 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JUL PY 1991 VL 6 IS 7 BP 1185 EP 1187 PG 3 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA GV260 UT WOS:A1991GV26000013 PM 1861866 ER PT J AU WESTFALL, CT SHORE, JW AF WESTFALL, CT SHORE, JW TI ISOLATED FRACTURES OF THE ORBITAL FLOOR - RISK OF INFECTION AND THE ROLE OF ANTIBIOTIC-PROPHYLAXIS SO OPHTHALMIC SURGERY AND LASERS LA English DT Review AB The application of antibiotic prophylaxis to fractures of the orbital floor is controversial. The incidence of infection following this injury remains undefined. We report a case of orbital cellulitis following orbital floor fracture, and attempt to define guidelines for the appropriate use of antibiotics in the setting of an isolated blowout fracture. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,EYE PLAST & ORBIT SERV,BOSTON,MA 02114. NR 13 TC 21 Z9 21 U1 1 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD JUL PY 1991 VL 22 IS 7 BP 409 EP 411 PG 3 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA FU148 UT WOS:A1991FU14800009 PM 1891188 ER PT J AU BLICKMAN, JG HERRIN, JT CLEVELAND, RH JARAMILLO, D AF BLICKMAN, JG HERRIN, JT CLEVELAND, RH JARAMILLO, D TI COEXISTING NEPHROLITHIASIS AND CHOLELITHIASIS IN PREMATURE-INFANTS SO PEDIATRIC RADIOLOGY LA English DT Article ID FUROSEMIDE THERAPY; ASSOCIATION AB Though the coexistence of nephrolithiasis and cholelithiasis in premature infants is extremely rare, we report four patients seen in a two year period. All patients weighed less than 1100 grams at birth, developed severe bronchopulmonary dysplasia, and all had Grade III or IV bilateral intraventricular hemorrhages. All four infants received prolonged furosemide therapy lasting at least 28 consecutive days. The renal stones disappeared in all four upon cessation of therapy, while in none have the gallstones disappeared after a mean follow-up period of 13 months. Ultrasound was superior in identifying and monitoring these stones. Their presence resulted in manipulating diuretic therapy which then was shown to limit renal and possibly biliary complications. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT NEPHROL SECT,BOSTON,MA 02114. RP BLICKMAN, JG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT RADIOL SECT,BOSTON,MA 02114, USA. NR 11 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD JUL PY 1991 VL 21 IS 5 BP 363 EP 364 DI 10.1007/BF02011489 PG 2 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA FW509 UT WOS:A1991FW50900013 PM 1909776 ER PT J AU KERNAN, WJ MULLENIX, PJ AF KERNAN, WJ MULLENIX, PJ TI STABILITY AND REPRODUCIBILITY OF TIME STRUCTURE IN SPONTANEOUS BEHAVIOR OF MALE-RATS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE SPONTANEOUS BEHAVIOR; TIME STRUCTURE; K-FUNCTION; MEASURE STABILITY; SPRAGUE-DAWLEY RATS ID ACTS; STATISTICS; SYSTEM; MODEL AB The computer pattern recognition system for the study of spontaneous rat behavior has allowed new analytical techniques which expand the definition of experimentally induced changes in behavior. As with any technique, the stability of the measures must be considered when evaluating overall sensitivity. This study evaluates the stability and reproducibility of three behavioral measures: a measure of the number of initiations of specific behavioral acts, a measure of the total time of each act, and a measure of behavioral time structure. Normal statistical parameters are used to evaluate the significance of changes detected using the first two measures, but the third measure utilizes K-functions, the bootstrap and ad hoc criteria to evaluate significance of observed changes. This study compares the stability of results from these three measures as applied to fourteen different groups of control Sprague-Dawley male rats. All three measures provided stable and reproducible results, but the measure of time structure, the K-function analysis, provided the greatest consistency. Behavior, particularly spontaneous behavior, has traditionally been perceived as being intrinsically variable. However, this study shows that the computer pattern recognition system and its analytical techniques provide stable and reproducible values that vary only a few percent. C1 IOWA STATE UNIV SCI & TECHNOL,VET DIAGNOST LAB,AMES,IA 50011. FORSYTH RES INST,DEPT TOXICOL,BOSTON,MA 02115. IOWA STATE UNIV SCI & TECHNOL,DEPT PHYS,AMES,IA 50011. NR 17 TC 6 Z9 6 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD JUL PY 1991 VL 39 IS 3 BP 747 EP 754 DI 10.1016/0091-3057(91)90158-X PG 8 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA GD543 UT WOS:A1991GD54300032 PM 1784603 ER PT J AU PARIS, JM LORENS, SA LEE, JM MITSUSHIO, H RITCHIE, JC NEMEROFF, CB AF PARIS, JM LORENS, SA LEE, JM MITSUSHIO, H RITCHIE, JC NEMEROFF, CB TI MUSCIMOL INJECTIONS INTO THE MEDIAN RAPHE NUCLEUS INCREASE SERUM ACTH AND CORTICOSTERONE CONCENTRATIONS VIA A NONSEROTONERGIC MECHANISM SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Note DE MEDIAN RAPHE NUCLEUS; GABA; MUSCIMOL; ACTH; CORTICOSTERONE; SEROTONIN ID CORTICOTROPIN-RELEASING-FACTOR; DORSAL RAPHE; PARAVENTRICULAR NUCLEUS; INDUCED HYPERACTIVITY; SEROTONERGIC NEURONS; INHIBITORY INFLUENCE; RAT HYPOTHALAMUS; CONSCIOUS RATS; SECRETION; AGONISTS AB Midbrain raphe serotonin (5-HT) neurons can influence the pituitary-adrenal axis. The midbrain raphe nuclei also contain a number of non-5-HT neurons, including gamma-aminobutyric acid (GABA) interneurons which can modulate 5-HT neuronal activity. We investigated the effects of intraraphe injections of the GABA(A) agonist, muscimol, on serum adrenocorticotropin hormone (ACTH) and corticosterone concentrations. Rats were infused with muscimol (0, 25, 50, and 100 ng in 0.5-mu-l saline) into the median raphe nucleus (MR). The animals were killed 30 min later, and trunk blood was collected for measurement of serum concentrations of ACTH and corticosterone by radioimmunoassay. Muscimol dose dependently increased plasma concentrations of these two pituitary-adrenal hormones. In order to determine the role of MR 5-HT neurons in these effects, separate groups of implanted animals were infused with either the serotonergic neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT) or ascorbic acid vehicle into the MR. Two weeks later, the animals were infused with muscimol (100 ng in 0.5-mu-l) and sacrificed as above. Treatment with 5,7-DHT, which markedly reduced hippocampal concentrations of 5-HT (-83%) and 5-HIAA (-73%), did not block intra-MR muscimol-induced elevations in ACTH and corticosterone. Thus, 5-HT neurons within the MR apparently do not mediate the increased activity of the pituitary-adrenal axis produced by stimulation of MR GABA(A) receptors. C1 LOYOLA UNIV,MED CTR,DEPT PHARMACOL,MAYWOOD,IL 60153. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROPATHOL,BOSTON,MA 02114. DUKE UNIV,MED CTR,DEPT PSYCHIAT,DURHAM,NC 27710. DUKE UNIV,MED CTR,DEPT PHARMACOL,DURHAM,NC 27710. FU NIMH NIH HHS [MH-42088] NR 32 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 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD JUL PY 1991 VL 39 IS 3 BP 765 EP 768 DI 10.1016/0091-3057(91)90161-T PG 4 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA GD543 UT WOS:A1991GD54300035 PM 1723800 ER PT J AU VANDERSTRAETEN, D RODRIGUESPOUSADA, RA GOODMAN, HM VANMONTAGU, M AF VANDERSTRAETEN, D RODRIGUESPOUSADA, RA GOODMAN, HM VANMONTAGU, M TI PLANT ENOLASE - GENE STRUCTURE, EXPRESSION, AND EVOLUTION SO PLANT CELL LA English DT Article ID AMINO-ACID-SEQUENCE; BACTERIOPHAGE-T7 RNA-POLYMERASE; POST-TRANSCRIPTIONAL CONTROL; PENTOSE-PHOSPHATE PATHWAY; NEURON-SPECIFIC ENOLASE; YEAST ENOLASE; MESSENGER-RNA; SACCHAROMYCES-CEREVISIAE; NUCLEOTIDE-SEQUENCE; SECONDARY-STRUCTURE AB Enolase genes were cloned from tomato and Arabidopsis. Comparison of their primary structures with other enolases revealed a remarkable degree of conservation, except for the presence of an insertion of 5 amino acids unique to plant enolases. Expression of the enolase genes was studied under various conditions. Under normal growth conditions, steady-state messenger and enzyme activity levels were significantly higher in roots than in green tissue. Large inductions of mRNA, accompanied by a moderate increase in enzyme activity, were obtained by an artificial ripening treatment in tomato fruits. However, there was little effect of anaerobiosis on the abundance of enolase messenger. In heat shock conditions, no induction of enolase mRNA was observed. We also present evidence that, at least in Arabidopsis, the hypothesis that there exists a complete set of glycolytic enzymes in the chloroplast is not valid, and we propose instead the occurrence of a substrate shuttle in Arabidopsis chloroplasts for termination of the glycolytic cycle. C1 STATE UNIV GHENT,GENET LAB,KL LEDEGANCKSTR 35,B-9000 GHENT,BELGIUM. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. OI RODRIGUES POUSADA, Renato Alberto/0000-0003-2551-4705; Van Der Straeten, Dominique/0000-0002-7755-1420 NR 91 TC 105 Z9 109 U1 1 U2 8 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 1040-4651 J9 PLANT CELL JI Plant Cell PD JUL PY 1991 VL 3 IS 7 BP 719 EP 735 DI 10.1105/tpc.3.7.719 PG 17 WC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology SC Biochemistry & Molecular Biology; Plant Sciences; Cell Biology GA FX732 UT WOS:A1991FX73200009 PM 1841726 ER PT J AU MAY, JW AF MAY, JW TI THE BROW FAT PAD - REPLY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,DIV PLAST & RECONSTRUCT SURG,LEVEL 4,SUITE 453,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUL PY 1991 VL 88 IS 1 BP 177 EP 178 PG 2 WC Surgery SC Surgery GA FT959 UT WOS:A1991FT95900044 ER PT J AU MAY, JW AF MAY, JW TI IN ORIENTALS, BE CAREFUL WHEN YOURE ON THE ROOF - REPLY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,DIV PLAST & RECONSTRUCT SURG,LEVEL 4,SUITE 453,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUL PY 1991 VL 88 IS 1 BP 178 EP 178 DI 10.1097/00006534-199107000-00055 PG 1 WC Surgery SC Surgery GA FT959 UT WOS:A1991FT95900046 ER PT J AU SMITH, FE ROSEN, KM VILLAKOMAROFF, L WEIR, GC BONNERWEIR, S AF SMITH, FE ROSEN, KM VILLAKOMAROFF, L WEIR, GC BONNERWEIR, S TI ENHANCED INSULIN-LIKE GROWTH FACTOR-I GENE-EXPRESSION IN REGENERATING RAT PANCREAS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SOMATOMEDIN-C; PANCREATIC BETA CELL; PANCREATIC DUCTULES; INSITU HYBRIDIZATION ID MESSENGER RIBONUCLEIC-ACIDS; BETA-CELL REPLICATION; SOMATOMEDIN-C; MONOLAYER-CULTURES; ENDOTHELIAL-CELLS; SKELETAL-MUSCLE; HUMAN-FETUS; B-CELLS; IGF-I; FETAL AB Insulin-like growth factor I (IGF-I) mRNA expression was studied after 90% partial pancreatectomy in the rat to determine whether IGF-I was associated with pancreatic regeneration. The level of IGF-I mRNA was maximally increased (4-fold above control value) 3 days after pancreatectomy, but thereafter gradually decreased, returning to control levels by 14 days after surgery. By in situ hybridization, IGF-I mRNA in both pancreatectomized and sham-operated rats was localized to capillary endothelial cells, indicating that this is the site of IGF-I expression in the normal rat pancreas. However, enhanced IGF-I mRNA expression was localized to focal areas of regeneration unique to pancreatectomized rats. In these areas, epithelial cells of proliferating ductules and individual connective tissue cells expressed IGF-I, suggesting that IGF-I may play an important role in the growth or differentiation of pancreatic tissue. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP SMITH, FE (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,EP JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02115, USA. FU NICHD NIH HHS [HD18655]; NIDDK NIH HHS [DK35449, DK07260] NR 40 TC 114 Z9 116 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 JUL PY 1991 VL 88 IS 14 BP 6152 EP 6156 DI 10.1073/pnas.88.14.6152 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FW761 UT WOS:A1991FW76100044 PM 1712481 ER PT J AU RAMER, SE WINKLER, DG CARRERA, A ROBERTS, TM WALSH, CT AF RAMER, SE WINKLER, DG CARRERA, A ROBERTS, TM WALSH, CT TI PURIFICATION AND INITIAL CHARACTERIZATION OF THE LYMPHOID-CELL PROTEIN-TYROSINE KINASE P56LCK FROM A BACULOVIRUS EXPRESSION SYSTEM SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ROUS-SARCOMA VIRUS; TRANSFORMING PROTEIN; HUMAN-PLATELETS; GROWTH-FACTOR; GENE-PRODUCT; PHOSPHORYLATION; ACTIVATION; PP60C-SRC; CD4; PEPTIDES AB The lymphocyte-specific protein-tyrosine kinase p56lck has been purified 90-fold to almost-equal-to 30% purity in 30% yield from a baculovirus expression system by a two-column purification procedure. At least two forms of p56lck were isolated, differing in the extent of phosphorylation and migrating as 56- and 59-kDa species on SDS/PAGE but as a single 56-kDa band after treatment with potato acid phosphatase. Autophosphorylation of purified p56lck occurred at a rate of 25 fmol/min to a maximum incorporation of almost-equal-to of phosphate per mol of p56lck with tyrosine-394 (but not tyrosine-505) and other, unidentified tyrosine residue(s) being the major sites of phosphorylation in vitro. Phosphorylation of tyrosine-containing peptides was monitored using an automated HPLC system. Although peptide substrate K(m) values were in the 1-5 mM range, the V(max) for the 13-amino acid peptide RRLIEDAEYAARG modified p60src autophosphorylation site) was 120 (min-1 (350 min-1 when adjusted for p56lck purity), suggesting that the enzyme purified from recombinant baculovirus-infected Sf9 cells has a high catalytic turnover compared with other tyrosine kinases. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM CELLULAR & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OI Carrera, Ana/0000-0002-3999-5434 FU NCI NIH HHS [CA43803]; NIGMS NIH HHS [GM20011] NR 54 TC 35 Z9 35 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 JUL PY 1991 VL 88 IS 14 BP 6254 EP 6258 DI 10.1073/pnas.88.14.6254 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FW761 UT WOS:A1991FW76100065 PM 2068105 ER PT J AU HELD, KD EPP, ER AWAD, S BIAGLOW, JE AF HELD, KD EPP, ER AWAD, S BIAGLOW, JE TI POSTIRRADIATION SENSITIZATION OF MAMMALIAN-CELLS BY THE THIOL-DEPLETING AGENT DIMETHYL FUMARATE SO RADIATION RESEARCH LA English DT Article ID NON-PROTEIN THIOLS; STRAND DNA BREAKS; HUMAN-FIBROBLASTS; X-IRRADIATION; BUTHIONINE SULFOXIMINE; GLUTATHIONE DEPLETION; CHEMICAL-COMPOUNDS; CELLULAR-RESPONSE; RADIATION; RADIOSENSITIZATION C1 UNIV PENN,DEPT RADIAT THERAPY,PHILADELPHIA,PA 19104. RP HELD, KD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 18614, CA 44982] NR 26 TC 15 Z9 15 U1 0 U2 1 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 JUL PY 1991 VL 127 IS 1 BP 75 EP 80 DI 10.2307/3578091 PG 6 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA FX438 UT WOS:A1991FX43800011 PM 2068274 ER PT J AU SPIRO, IJ MCPHERSON, S COOK, JA LING, CC DEGRAFF, W MITCHELL, JB AF SPIRO, IJ MCPHERSON, S COOK, JA LING, CC DEGRAFF, W MITCHELL, JB TI SENSITIZATION OF LOW-DOSE-RATE IRRADIATION BY NONLETHAL HYPERTHERMIA SO RADIATION RESEARCH LA English DT Note ID DEPENDENCE; REPAIR; DAMAGE; CELLS C1 NCI,RADIAT ONCOL BRANCH,BETHESDA,MD 20892. MEM SLOAN KETTERING CANC CTR,DEPT MED PHYS,NEW YORK,NY 10021. RP SPIRO, IJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 11 TC 22 Z9 22 U1 0 U2 1 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 JUL PY 1991 VL 127 IS 1 BP 111 EP 114 DI 10.2307/3578097 PG 4 WC Biology; Biophysics; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Radiology, Nuclear Medicine & Medical Imaging GA FX438 UT WOS:A1991FX43800017 PM 2068266 ER PT J AU KAMMER, B SAINI, S BRINK, JA KNOEFEL, WT FERRUCCI, JT SIMEONE, JF MUELLER, PR AF KAMMER, B SAINI, S BRINK, JA KNOEFEL, WT FERRUCCI, JT SIMEONE, JF MUELLER, PR TI OPTIMAL TECHNIQUE FOR DETECTION OF GALLSTONES AT INJECTION CHOLECYSTOGRAPHY - INVITRO ANALYSIS SO RADIOLOGY LA English DT Article DE BILE DUCT RADIOGRAPHY, CONTRAST MEDIA; BILE DUCT RADIOGRAPHY, TECHNOLOGY; GALLBLADDER, CALCULI; GALLBLADDER, RADIOGRAPHY ID BILE-DUCT STONES; GALLBLADDER STONES; LITHOTRIPSY; DISSOLUTION AB Injection cholecystography is often employed during invasive gallbladder procedures to determine the number of gallstones that are present. The authors undertook this study to define the optimal radiographic technique for performance of injection cholecystography. Condoms filled with 100 mL of contrast medium at four different iodine concentrations (30%, 15%, 7.5%, and 3.8% [wt/vol]) and containing up to five 4-mm-thick gallstones or a single 10-mm-thick gallstone were radiographed in a 20-cm-deep water bath by using four kilovolt peak settings (70, 80, 90, and 100 kVp). Images were read by three radiologists who were blinded to the radiographic technique. Decreasing iodine concentration significantly (P < .05) improved detection of 4-mm-thick gallstones at a constant kilovolt peak setting. However, increasing the kilovolt peak setting while using the same concentration of contrast medium had no statistically significant influence on gallstone detectability, although radiologists did indicate a preference for the high-kilovolt peak technique. Results of the authors' experiments showed that for detection of small gallstones at injection cholecystography, use of a low-concentration contrast medium and a high kilovolt peak setting is the recommended radiographic technique. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 12 TC 0 Z9 0 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 JUL PY 1991 VL 180 IS 1 BP 43 EP 45 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FR679 UT WOS:A1991FR67900011 PM 2052720 ER PT J AU GEANMARTON, AD VEZINA, LG MARTON, KI STIMAC, GK PEYSTER, RG TAVERAS, JM DAVIS, KR AF GEANMARTON, AD VEZINA, LG MARTON, KI STIMAC, GK PEYSTER, RG TAVERAS, JM DAVIS, KR TI ABNORMAL CORPUS-CALLOSUM - A SENSITIVE AND SPECIFIC INDICATOR OF MULTIPLE-SCLEROSIS SO RADIOLOGY LA English DT Article DE CORPUS CALLOSUM, ABNORMALITIES; CORPUS CALLOSUM, MR STUDIES; SCLEROSIS, MULTIPLE ID WHITE-MATTER; PERIVENTRICULAR LESIONS; MR; BRAIN; CORD; DIAGNOSIS; LUCENCIES; DEMENTIA; ATROPHY; AGE AB The authors investigated whether identification of corpus callosal (CC) involvement might increase the specificity of magnetic resonance (MR) imaging in differentiating multiple sclerosis (MS) from other periventricular white matter diseases (PWDs). They prospectively evaluated 42 patients with MS and 127 control patients with other PWDs. Ninety-three percent of the MS patients demonstrated confluent and/or focal lesions involving the callosal-septal interface (CSI). These lesions characteristically involved the inferior aspect of the callosum and radiated from the ventricular surface into the overlying callosum. CSI lesions were optimally demonstrated on sagittal long repetition time (TR)/short echo time (TE) images and frequently (45% of cases) went undetected on axial images. Only 2.4% of the control patients had lesions of the CC. The authors conclude that midsagittal long TR/short TE images are highly sensitive and specific for MS and that callosal involvement in MS is more common than previously reported. C1 MASSACHUSETTS GEN HOSP,DIV NEURORADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. FIRST HILL DIAGNOST IMAGING,SEATTLE,WA. HAHNEMANN UNIV,MED CTR,DEPT RADIOL,PHILADELPHIA,PA 19102. NR 59 TC 128 Z9 130 U1 2 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 JUL PY 1991 VL 180 IS 1 BP 215 EP 221 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FR679 UT WOS:A1991FR67900045 PM 2052698 ER PT J AU MANSCHRECK, TC MAHER, BA ROSENTHAL, JE BERNER, J AF MANSCHRECK, TC MAHER, BA ROSENTHAL, JE BERNER, J TI REDUCED PRIMACY AND RELATED FEATURES IN SCHIZOPHRENIA SO SCHIZOPHRENIA RESEARCH LA English DT Article DE MEMORY; REPETITION; PRIMACY; RECENCY; SPEECH; (SCHIZOPHRENIA) ID ANTICHOLINERGIC DRUGS; CONTEXTUAL CONSTRAINT; THOUGHT-DISORDER; TOKEN RATIO; MEMORY; RECALL AB Subtle memory disturbances are widely reported in schizophrenia. We investigated one such disturbance, reduced primacy in serial position recall among 20 schizophrenic patients, 20 depressed patients, and 20 normal controls. The main finding is that schizophrenic subjects show reduced primacy and middle position performance, but are able to match the recency recall of controls. We further demonstrate that primacy performance is associated with another memory anomaly frequently noted in schizophrenia, decreased context associated gain in recall. Among schizophrenic subjects, primacy performance is also related to increased repetition in speech, a feature associated with formal thought disorder in schizophrenia. These observations suggest that memory deviances and disordered speech may have a common pathogenesis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. NR 41 TC 19 Z9 20 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD JUL-AUG PY 1991 VL 5 IS 1 BP 35 EP 41 DI 10.1016/0920-9964(91)90051-R PG 7 WC Psychiatry SC Psychiatry GA FP597 UT WOS:A1991FP59700004 PM 1677264 ER PT J AU FREI, E AF FREI, E TI THE MODULATION OF ALKYLATING-AGENTS SO SEMINARS IN HEMATOLOGY LA English DT Article; Proceedings Paper CT KEYSTONE SYMP WORKSHOP : CURING LEUKEMIA CY NOV 26-28, 1990 CL MARTHAS VINEYARD, MA SP ADRIA LAB, FARMITALIA CARLO ERBA ID RESISTANT; CELLS RP FREI, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 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 0037-1963 J9 SEMIN HEMATOL JI Semin. Hematol. PD JUL PY 1991 VL 28 IS 3 SU 4 BP 22 EP 24 PG 3 WC Hematology SC Hematology GA FY818 UT WOS:A1991FY81800006 PM 1664143 ER PT J AU CAMPBELL, LH SILVERMAN, PR PATTI, PB AF CAMPBELL, LH SILVERMAN, PR PATTI, PB TI REUNIONS BETWEEN ADOPTEES AND BIRTH PARENTS - THE ADOPTEES EXPERIENCE SO SOCIAL WORK LA English DT Article ID ADULT ADOPTEES; ADOPTION C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. CATHOLIC CHAR,N SUBURBAN OFF,LYNN,MA. RP CAMPBELL, LH (reprint author), NOTRE DAME COLL MARYLAND,CONTINUING EDUC,GIBBONS HALL,4701 N CHARLES ST,BALTIMORE,MD 21210, USA. FU NIMH NIH HHS [MH17058] NR 18 TC 31 Z9 31 U1 1 U2 4 PU NATL ASSOC SOCIAL WORKERS PI WASHINGTON PA 750 FIRST ST, NE, STE 700, WASHINGTON, DC 20002-4241 SN 0037-8046 J9 SOC WORK JI Soc. Work PD JUL PY 1991 VL 36 IS 4 BP 329 EP 335 PG 7 WC Social Work SC Social Work GA FT994 UT WOS:A1991FT99400010 PM 1896888 ER PT J AU MACDONALD, ME SCOTT, HS WHALEY, WL POHL, T WASMUTH, JJ LEHRACH, H MORRIS, CP FRISCHAUF, AM HOPWOOD, JJ GUSELLA, JF AF MACDONALD, ME SCOTT, HS WHALEY, WL POHL, T WASMUTH, JJ LEHRACH, H MORRIS, CP FRISCHAUF, AM HOPWOOD, JJ GUSELLA, JF TI HUNTINGTON DISEASE-LINKED LOCUS D4S111 EXPOSED AS THE ALPHA-L-IDURONIDASE GENE SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Note ID CELL HYBRID; DNA MARKERS; SHORT ARM; LOCALIZATION; CHROMOSOME-4; RECOMBINATION; ASSIGNMENT; TELOMERE; SEGMENT; LIBRARY AB Alpha-L-Iduronidase (IDUA) has been intensively studied due to its causative role in mucopolysaccharidosis type I (Hurler, Scheie and Hurler/Scheie syndromes). The recent cloning of a human IDUA cDNA has resulted in a reevaluation of the chromosomal location of this gene. Previously assigned to chromosome 22, IDUA now has been localized to 4p16.3, the region of chromosome 4 associated with Huntington's disease (HD). The existence of a battery of cloned DNA, physical map information, and genetic polymorphism data for this region has allowed the rapid fine mapping of IDUA within the terminal cytogenetic band of 4p. IDUA was found to be coincident with D4S111, an anonymous locus displaying a highly informative multiallele DNA polymorphism. This map location, 1.1 x 10(6) bp from the telomere, makes IDUA the most distal cloned gene assigned to 4p. However, it falls within a segment of 4p16.3 that has been eliminated from the HD candidate region, excluding a role for IDUA in this disorder. C1 UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. ADELAIDE CHILDRENS HOSP INC,DEPT CHEM PATHOL,LYSOSOMAL DIS RES UNIT,ADELAIDE,SA 5006,AUSTRALIA. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. EUROPEAN MOLEC BIOL LAB,W-6900 HEIDELBERG,GERMANY. RP MACDONALD, ME (reprint author), MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114, USA. RI Scott, Hamish/B-2122-2009 OI Scott, Hamish/0000-0002-5813-631X FU NHGRI NIH HHS [HG00169]; NINDS NIH HHS [NS16367, NS22031] NR 30 TC 28 Z9 28 U1 0 U2 1 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0740-7750 J9 SOMAT CELL MOLEC GEN JI Somat.Cell Mol.Genet. PD JUL PY 1991 VL 17 IS 4 BP 421 EP 425 DI 10.1007/BF01233067 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA GE701 UT WOS:A1991GE70100010 PM 1832239 ER PT J AU SURGENOR, DM WALLACE, EL CHURCHILL, WH HAO, SHS CHAPMAN, RH POSS, R AF SURGENOR, DM WALLACE, EL CHURCHILL, WH HAO, SHS CHAPMAN, RH POSS, R TI RED-CELL TRANSFUSIONS IN TOTAL KNEE AND TOTAL HIP-REPLACEMENT SURGERY SO TRANSFUSION LA English DT Article ID BLOOD AB To explore how red cell transfusions were used to support patients who underwent primary and revision hip and knee replacements classified within diagnosis-related group (DRG) 209 (major joint and limb reattachment procedures), we studied abstracted patient discharge records from 151 United States hospitals in 1986. A total of 9684 units of whole blood and/or separated red cells was used to support 6472 patients. The transfusion use varied by surgical procedure, with patient gender as an influencing factor. Large proportions of patients underwent surgery without requiring transfusion. Among transfused patients, the majority received 1 to 3 units of red cells; however, a minority of patients required multiple transfusions, thereby utilizing a disproportionate share of the blood resource. Comparison of transfusion practice within the seven most active hospitals revealed significant differences (p less-than-or-equal-to 0.01) in the percentage of patients actually transfused, but not in the mean number of units of red cell components transfused per transfused patient. Similar findings emerged from comparison of transfusion practice when all hospitals were segregated into five hospital classes on the basis of orthopedic surgical service activity. These effects were seen for both total knee and total hip replacement procedures. It can be concluded that the lack of clearly defined criteria for transfusion contributed to the variations observed. C1 SUNY BUFFALO,SCH MANAGEMENT,BUFFALO,NY 14260. CTR MANAGEMENT SYST,WILLIAMSVILLE,NY. RP SURGENOR, DM (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-33774] NR 16 TC 66 Z9 68 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD JUL-AUG PY 1991 VL 31 IS 6 BP 531 EP 537 DI 10.1046/j.1537-2995.1991.31691306252.x PG 7 WC Hematology SC Hematology GA FY567 UT WOS:A1991FY56700013 PM 1906649 ER PT J AU NATHAN, DM FOGEL, H NORMAN, D RUSSELL, PS TOLKOFFRUBIN, N DELMONICO, FL AUCHINCLOSS, H CAMUSO, J COSIMI, AB AF NATHAN, DM FOGEL, H NORMAN, D RUSSELL, PS TOLKOFFRUBIN, N DELMONICO, FL AUCHINCLOSS, H CAMUSO, J COSIMI, AB TI LONG-TERM METABOLIC AND QUALITY-OF-LIFE RESULTS WITH PANCREATIC RENAL-TRANSPLANTATION IN INSULIN-DEPENDENT DIABETES-MELLITUS SO TRANSPLANTATION LA English DT Article ID REJECTION; KIDNEY AB Evaluation of whole-organ pancreas transplantation in the therapy of IDDM has been difficult because of generally poor graft survival and significant complications in past experience. We report a technically successful simultaneous pancreas/kidney transplant program with patient and graft survival of 85% over 3 years of follow-up (mean 21 months) in 33 subjects with IDDM. Glucose metabolism was normalized without need for exogenous insulin immediately posttransplant in all but one recipient and remained normal in 85% of recipients. The outcome in pancreas/kidney recipients was compared with that in 18 insulin-dependent diabetic recipients of kidney transplant only performed in the same period. Quality of life was assessed with one general and one diabetes-specific questionnaire. General quality of life issues improved significantly in both pancreas/kidney and kidney recipients, but diabetes specific quality of life improved only in the pancreas/kidney recipients. Pancreas/kidney recipients required twice as long a period of hospitalization for the transplant and two times as many readmissions for a variety of complications. Only a minority of hospital admissions was strictly attributable to the pancreas graft. Of the five deaths in the pancreas/kidney recipients, two were attributable to the pancreas transplant. Pancreas transplantation in IDDM can now be accomplished with a high degree of success, resulting in normalized glucose metabolism and with overall mortality similar to kidney transplantation alone. Successful pancreas transplantation improves quality of life with respect to diabetes but this benefit is accomplished at a cost of increased hospital admissions and complications related to the transplanted pancreas. The effects of pancreas transplantation on the long-term complications of insulin-dependent diabetes remain unknown. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, TRANSPLANT UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02115 USA. RP NATHAN, DM (reprint author), MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. NR 20 TC 91 Z9 92 U1 0 U2 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0041-1337 EI 1534-6080 J9 TRANSPLANTATION JI Transplantation PD JUL PY 1991 VL 52 IS 1 BP 85 EP 91 DI 10.1097/00007890-199107000-00018 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA FX180 UT WOS:A1991FX18000018 PM 1858159 ER PT J AU DICKERSIN, GR ERLANDSON, RA AF DICKERSIN, GR ERLANDSON, RA TI CONTROVERSIAL SPINDLE CELL TUMORS - AN OVERVIEW SO ULTRASTRUCTURAL PATHOLOGY LA English DT Review C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,NEW YORK,NY 10021. RP DICKERSIN, GR (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0191-3123 J9 ULTRASTRUCT PATHOL JI Ultrastruct. Pathol. PD JUL-OCT PY 1991 VL 15 IS 4-5 BP 315 EP 316 PG 2 WC Microscopy; Pathology SC Microscopy; Pathology GA GF888 UT WOS:A1991GF88800002 PM 1755096 ER PT J AU DICKERSIN, GR AF DICKERSIN, GR TI SYNOVIAL SARCOMA - A REVIEW AND UPDATE, WITH EMPHASIS ON THE ULTRASTRUCTURAL CHARACTERIZATION OF THE NONGLANDULAR COMPONENT SO ULTRASTRUCTURAL PATHOLOGY LA English DT Review DE ELECTRON MICROSCOPY; SYNOVIAL SARCOMA; ULTRASTRUCTURE ID EPITHELIAL DIFFERENTIATION; SOFT-TISSUE; FEATURES; LIGHT; TUMOR AB Classic biphasic synovial sarcoma is usually not a problem in identification, whereas the monophasic spindle cell form continues to be a challenge in the differential diagnosis of spindle cell neoplasms. Most synovial sarcomas do not arise from a joint or tendon sheath, and by electron microscopy and immunohistochemistry they differ in several ways from nonneoplastic synovium. The cell of origin of synovial sarcoma is unknown, but certain features are rather consistently observed in the biphasic tumors and are useful in identifying monophasic samples. These features are apparent by immunohistochemistry and electron microscopy, both of which indicate early epithelial differentiation in the nonglandular component of the neoplasm. With immunohistochemistry, some of these cells stain for keratin. By electron microscopy, a gradient of differentiation from unclassifiable spindle cells to fully differentiated epithelial lining cells is demonstrable. A review and illustration of the ultrastructural characteristics in this spectrum of intermediate cells constitute the main emphasis of the article. The cells tend to be oval and polygonal; to be arranged in clusters surrounded by basal lamina or flocculent matrix; to have junctions, including tight junctions, and to form villuslike filopodia, true microvilli, canaliculi, and microlumina. This range of ultrastructural features is usually diagnostic of the nonglandular phase of synovial sarcoma. C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. RP DICKERSIN, GR (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. NR 30 TC 34 Z9 34 U1 0 U2 1 PU HEMISPHERE PUBL CORP PI BRISTOL PA 1900 FROST ROAD, SUITE 101, BRISTOL, PA 19007-1598 SN 0191-3123 J9 ULTRASTRUCT PATHOL JI Ultrastruct. Pathol. PD JUL-OCT PY 1991 VL 15 IS 4-5 BP 379 EP 402 PG 24 WC Microscopy; Pathology SC Microscopy; Pathology GA GF888 UT WOS:A1991GF88800008 PM 1721748 ER PT J AU NEWMAN, LH SALTZMAN, B AF NEWMAN, LH SALTZMAN, B TI IDENTIFYING RISK-FACTORS IN DEVELOPMENT OF CLINICALLY SIGNIFICANT POST-SHOCK-WAVE LITHOTRIPSY SUBCAPSULAR HEMATOMAS SO UROLOGY LA English DT Article ID EXTRACORPOREAL; COMPLICATIONS AB A retrospective study of 1,012 shock-wave lithotripsy treatments was performed to identify and analyze the risk factors for the development of six clinically significant post-extracorporeal shock-wave lithotripsy (ESWL) subcapsular hematomas. The patients studied had clinical signs and symptoms that on evaluation were confirmed as originating from a subcapsular hematoma. Common factors identified which we believe may put patients at increased risk for the development of subcapsular hematoma included hypertension, diabetes mellitus, coronary artery disease, and obesity. C1 BRONX VET AFFAIRS MED CTR,NEW YORK,NY. RP NEWMAN, LH (reprint author), MT SINAI MED CTR,SCH MED,DEPT UROL,5 E 98TH ST,NEW YORK,NY 10029, USA. NR 12 TC 36 Z9 40 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD JUL PY 1991 VL 38 IS 1 BP 35 EP 38 DI 10.1016/0090-4295(91)80009-V PG 4 WC Urology & Nephrology SC Urology & Nephrology GA FW772 UT WOS:A1991FW77200008 PM 1866855 ER PT J AU OFFENSPERGER, WB OFFENSPERGER, S WALTER, E BLUM, HE GEROK, W AF OFFENSPERGER, WB OFFENSPERGER, S WALTER, E BLUM, HE GEROK, W TI INHIBITION OF DUCK HEPATITIS-B VIRUS-INFECTION BY LYSOSOMOTROPIC AGENTS SO VIROLOGY LA English DT Note ID RECEPTOR-BINDING SITE; REVERSE-TRANSCRIPTASE; ANTIVIRAL STRATEGIES; ENVELOPED VIRUSES; INVITRO; DNA; REPLICATION; CELLS; SERUM; LIVER C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,GASTROINTESTINAL UNIT & MOLEC HEPATOL,BOSTON,MA 02129. RP OFFENSPERGER, WB (reprint author), UNIV FREIBURG,DEPT MED,W-7800 FREIBURG,GERMANY. NR 27 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 0042-6822 J9 VIROLOGY JI Virology PD JUL PY 1991 VL 183 IS 1 BP 415 EP 418 DI 10.1016/0042-6822(91)90157-7 PG 4 WC Virology SC Virology GA FQ368 UT WOS:A1991FQ36800046 PM 2053292 ER PT J AU KOSKI, G LAWRENCE, K RIGHI, D AF KOSKI, G LAWRENCE, K RIGHI, D TI INHIBITION BY ETHANOL OF 45CA2+ UPTAKE IN PC12 PHEOCHROMOCYTOMA CELLS - INTERACTIONS BETWEEN ALCOHOL AND CARBACHOL SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Note RP KOSKI, G (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BIOCHEM PHARMACOL LAB,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 28 PY 1991 VL 625 BP 448 EP 450 DI 10.1111/j.1749-6632.1991.tb33876.x PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FZ455 UT WOS:A1991FZ45500052 PM 2058900 ER PT J AU MILLER, KW WOOD, SC FORMAN, SA BUGGE, B HILL, WAG ABADJI, V AF MILLER, KW WOOD, SC FORMAN, SA BUGGE, B HILL, WAG ABADJI, V TI THE NICOTINIC ACETYLCHOLINE-RECEPTOR IN ITS MEMBRANE ENVIRONMENT SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID POSTSYNAPTIC MEMBRANES; ION CHANNEL; TORPEDO; ANESTHETICS; INHIBITION; INCREASES; PROTEINS; PROCAINE; AGONIST; ETHANOL C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP MILLER, KW (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NIAAA NIH HHS [AA 07040]; NIGMS NIH HHS [GM 15904] NR 35 TC 14 Z9 14 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD JUN 28 PY 1991 VL 625 BP 600 EP 615 DI 10.1111/j.1749-6632.1991.tb33895.x PG 16 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FZ455 UT WOS:A1991FZ45500071 PM 1711816 ER PT J AU CHO, HJ RAMER, SE ITOH, M WINKLER, DG KITAS, E BANNWARTH, W BURN, P SAITO, H WALSH, CT AF CHO, HJ RAMER, SE ITOH, M WINKLER, DG KITAS, E BANNWARTH, W BURN, P SAITO, H WALSH, CT TI PURIFICATION AND CHARACTERIZATION OF A SOLUBLE CATALYTIC FRAGMENT OF THE HUMAN TRANSMEMBRANE LEUKOCYTE ANTIGEN RELATED (LAR) PROTEIN TYROSINE PHOSPHATASE FROM AN ESCHERICHIA-COLI EXPRESSION SYSTEM SO BIOCHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTOR; BACTERIOPHAGE-T7 RNA-POLYMERASE; SOLID-PHASE SYNTHESIS; HUMAN-PLACENTA; PEPTIDE-SYNTHESIS; COMMON ANTIGEN; KINASE; PHOSPHORYLATION; FAMILY; SUBSTRATE AB A 350 amino acid soluble fragment of the intracellular catalytic domain of the human transmembrane leukocyte antigen related (LAR) protein tyrosine phosphatase has been purified 17-fold to > 90% purity from an Escherichia coli expression vector in quantities sufficient for kinetic and structural characterization. To assess substrate specificity, phosphotyrosine peptides corresponding to autophosphorylation sites of the two major classes of tyrosine kinases have been synthesized. Thus 6-12-residue phosphotyrosine peptides of the insulin receptor and epidermal growth factor receptor kinase domains and of the autophosphorylation and C-terminal regulatory sites of p60src and p56lck have been analyzed for k(cat) and K(M) by using a nonradioactive chromogenic assay for P(i) release. The catalytic domain of LAR PTPase shows k(cat) values of 20-70 s-1 for phosphotyrosine peptides and affinities that vary 150-fold from 27-mu-M to 4.1 mM. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. F HOFFMANN LA ROCHE & CO LTD,CENT RES DEPT,CH-4002 BASEL,SWITZERLAND. FU NCI NIH HHS [CA51132]; NIGMS NIH HHS [GM20011] NR 47 TC 75 Z9 75 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 JUN 25 PY 1991 VL 30 IS 25 BP 6210 EP 6216 DI 10.1021/bi00239a019 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FT936 UT WOS:A1991FT93600019 PM 1711896 ER PT J AU WATKINS, SC SLAYTER, HS CODINGTON, JF AF WATKINS, SC SLAYTER, HS CODINGTON, JF TI INTRACELLULAR PATHWAY OF A MUCIN-TYPE MEMBRANE GLYCOPROTEIN IN MOUSE MAMMARY-TUMOR CELLS SO CARBOHYDRATE RESEARCH LA English DT Article ID TA3 TUMOR; SURFACE GLYCOPROTEINS; MONOCLONAL-ANTIBODIES; CARCINOMA-CELLS; ASCITES CELL; SIALIC-ACID; 2 SUBLINES; EPIGLYCANIN; ADENOCARCINOMA; ALLOTRANSPLANTABILITY AB Epiglycanin, a mucin-type glycoprotein, was found by immunoelectron microscopy to be located in cytoplasmic compartments, as well as at the surface of the TA3-Ha mammary carcinoma ascites cell. The glycoprotein was identified by means of gold-labeled secondary antibody bound to a primary antiepiglycanin monoclonal antibody or by lectins specific for carbohydrate structures in epiglycanin. The primary antibody recognized a glycopeptide component containing a beta-D-(1 --> 3)-D-GalNAc chain attached to a serine or threonine residue. Two routes to the cell surface from epiglycanins's first-recognized location in the trans-Golgi reticulum were suggested. Its presence in vesicles, which fuse with the cell surface, would explain the presence of epiglycanin as an integral membrane protein. Some of these observed vesicles, however, may be endocytotic in character. Epiglycanin was also found in large multivesiculate sacs which were observed on occasion to be open to the extracellular milieu. This finding, as well as the observed fusion of small vesicles from the trans-Golgi network with the sacs, strongly suggested exocytotic migration for the large sacs. Endocytotic migration may also be possible, although incubation of viable cells with gold-labeled antiepiglycanin antibody resulted in minimal uptake within the intracellular sacs, and incubation with [I-125]-epiglycanin under metabolic conditions resulted in no detectable uptake of radiolabel by the cells. C1 HARVARD UNIV,SCH MED,BOSTON BIOMED RES INST,20 STANIFORD ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-18600, CA-08418]; NIGMS NIH HHS [GM14237] NR 53 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JUN 25 PY 1991 VL 213 BP 185 EP 200 DI 10.1016/S0008-6215(00)90608-6 PG 16 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA GA193 UT WOS:A1991GA19300020 PM 1933937 ER PT J AU ALROY, J DEGASPERI, R WARREN, CD AF ALROY, J DEGASPERI, R WARREN, CD TI APPLICATION OF LECTIN HISTOCHEMISTRY AND CARBOHYDRATE ANALYSIS TO THE CHARACTERIZATION OF LYSOSOMAL STORAGE DISEASES SO CARBOHYDRATE RESEARCH LA English DT Article ID BETA-GALACTOSIDASE DEFICIENCY; GM1 GANGLIOSIDOSIS; CEROID-LIPOFUSCINOSIS; SWAINSONINE TOXICOSIS; LIQUID-CHROMATOGRAPHY; GLYCOPROTEIN STORAGE; ALPHA-MANNOSIDASE; CONCANAVALIN-A; OLIGOSACCHARIDES; SHEEP AB In lysosomal storage diseases that involve a defect in the catabolism of glycoconjugates, lectin histochemistry adds a new dimension to the characterization of stored carbohydrates as it identifies sugar residues in situ in the affected cells and, thus, determines which cell types are affected by storage. It may be combined with chemical and biochemical analysis by h.p.l.c. The present review summarizes recent results for a variety of storage diseases and presents new data for G(M1)-gangliosidosis. C1 TUFTS UNIV,SCH MED,SCH VET MED,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CARBOHYDRATE RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ALROY, J (reprint author), TUFTS UNIV,SCH MED,DEPT PATHOL,136 HARRISON AVE,BOSTON,MA 02111, USA. FU NICHD NIH HHS [HD 21087]; NINDS NIH HHS [NS 2176] NR 88 TC 23 Z9 24 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6215 J9 CARBOHYD RES JI Carbohydr. Res. PD JUN 25 PY 1991 VL 213 BP 229 EP 250 DI 10.1016/S0008-6215(00)90611-6 PG 22 WC Biochemistry & Molecular Biology; Chemistry, Applied; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA GA193 UT WOS:A1991GA19300023 PM 1933939 ER PT J AU ERDILE, LF HEYER, WD KOLODNER, R KELLY, TJ AF ERDILE, LF HEYER, WD KOLODNER, R KELLY, TJ TI CHARACTERIZATION OF A CDNA-ENCODING THE 70-KDA SINGLE-STRANDED DNA-BINDING SUBUNIT OF HUMAN REPLICATION PROTEIN-A AND THE ROLE OF THE PROTEIN IN DNA-REPLICATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIMIAN VIRUS-40 DNA; SACCHAROMYCES-CEREVISIAE; POLYMERASE-ALPHA; SV40 ORIGIN; INVITRO REPLICATION; PURIFIED PROTEINS; GENE-32 PROTEIN; PURIFICATION; SEQUENCES; CLONING AB Replication protein A (RP-A) is a three-subunit single-stranded DNA-binding protein that has been isolated from human cells. RP-A is essential for SV40 DNA replication and may also be important in genetic recombination. The sequence of a cDNA encoding the 70-kDa subunit of human RP-A is reported. The 616-amino acid predicted open reading frame of the human protein is 31% identical with the 62 1 -amino acid open reading frame of the 70-kDa subunit of RP-A from the yeast Saccharomyces cerevisiae. Both proteins share a highly conserved putative metal binding domain of the 4-cysteine type. The human cDNA directs production in Escherichia coli of a 70-kDa protein that reacts with a monoclonal antibody directed against the 70-kDa subunit of human RP-A. The recombinant 70-kDa subunit, purified from bacteria, exhibits single-stranded DNA binding activity comparable to that of the complete RP-A complex. The 70-kDa subunit is able to substitute for the complete human RP-A complex in stimulating the activity of DNA polymerase alpha-primase on a poly(dA).oligo(dT) template. However, the 70-kDa subunit alone cannot substitute for the complete RP-A complex in SV40 DNA replication in vitro, suggesting an important functional role for the other subunits. C1 UNIV BERN,INST GEN MICROBIOL,CH-3012 BERN,SWITZERLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC GENET LAB,BOSTON,MA 02115. RP ERDILE, LF (reprint author), JOHNS HOPKINS UNIV,SCH MED,DEPT MOLEC BIOL & GENET,BALTIMORE,MD 21205, USA. FU NIGMS NIH HHS [GM29383, GM42780] NR 45 TC 123 Z9 125 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 JUN 25 PY 1991 VL 266 IS 18 BP 12090 EP 12098 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FT762 UT WOS:A1991FT76200101 PM 2050703 ER PT J AU RICHARDS, EJ GOODMAN, HM AUSUBEL, FM AF RICHARDS, EJ GOODMAN, HM AUSUBEL, FM TI THE CENTROMERE REGION OF ARABIDOPSIS-THALIANA CHROMOSOME-1 CONTAINS TELOMERE-SIMILAR SEQUENCES SO NUCLEIC ACIDS RESEARCH LA English DT Article ID YEAST SCHIZOSACCHAROMYCES-POMBE; ALPHA-SATELLITE DNA; FISSION YEAST; NUCLEOTIDE-SEQUENCES; FUNCTIONAL-ANALYSIS; PLASMODIUM-BERGHEI; ORGANIZATION; EVOLUTION; GENE AB We describe the structure of an Arabidopsis thaliana genomic clone containing two classes of repetitive DNA elements derived from the centromere region of chromosome 1. One class is comprised of tandem arrays of a highly reiterated repeat containing degenerate telomere sequence motifs. Adjacent to these telomere-similar repeats we found a dispersed repetitive element reiterated approximately five times in the A. thaliana genome. The nucleotide sequence of the dispersed repeat is unusual, being extremely AT-rich and composed of numerous, overlapping repeat motifs. C1 MASSACHUSETTS GEN HOSP, DEPT MOLEC BIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA. RI Richards, Eric/E-6866-2012 NR 34 TC 104 Z9 106 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 25 PY 1991 VL 19 IS 12 BP 3351 EP 3357 DI 10.1093/nar/19.12.3351 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FU512 UT WOS:A1991FU51200027 PM 1648204 ER PT J AU UEMURA, Y KOWALL, NW MOSKOWITZ, MA AF UEMURA, Y KOWALL, NW MOSKOWITZ, MA TI FOCAL ISCHEMIA IN RATS CAUSES TIME-DEPENDENT EXPRESSION OF C-FOS PROTEIN IMMUNOREACTIVITY IN WIDESPREAD REGIONS OF IPSILATERAL CORTEX SO BRAIN RESEARCH LA English DT Article DE C-FOS; IMMEDIATE EARLY GENE; IMMUNOHISTOCHEMISTRY; NEURAL PLASTICITY; FOCAL CEREBRAL ISCHEMIA; RAT ID EPIDERMAL GROWTH-FACTOR; CEREBRAL-ISCHEMIA; GENE-EXPRESSION; BRAIN INJURY; MAMMALIAN BRAIN; NERVOUS-SYSTEM; MESSENGER-RNA; SPINAL-CORD; INDUCTION; MK-801 AB c-Fos protein expression was examined in brain by immunohistochemistry following permanent middle cerebral artery (MCA) occlusion above the rhinal fissure and ipsilateral common carotid artery (CCA) occlusion in Long-Evans rats. In sham-operated animals, c-fos protein-like immunoreactivity (CFPLI) was confined to neuronal nuclei of the hypothalamus and was not present in other regions including cerebral cortex. In the core territory of the MCA, CFPLI was not detected when examined at 15 and 30 min, 1, 4 and 8 h and 1, 2, 4 and 7 days after occlusion. Focal ischemia induced two temporal and spatial patterns of CFPLI. At 1 h, c-fos protein was expressed in the nuclei of many neurons in layers II-V of the ipsilateral cortex both immediately adjacent to and remote from the ischemic territory. Within regions outside the MCA territory (e.g. cingulate gyrus and piriform cortices), CFPLI in these neurons peaked at 2-4 h and was undetectable after 2 days. Neurons in the zone immediately surrounding the ischemic core within MCA territory also expressed CFPLI, but in contrast, continued to express c-fos up to 4 days after ischemia. Immunoreactivity surrounding the ischemic core was found in neuronal nuclei predominantly, although from 1 to 4 days, CFPLI was found in perikarya and dendrites as well. MK-801 (3 mg/kg, i.p., 30 min prior to occlusion) completely blocked the early c-fos protein induction in all regions but expression within neurons surrounding the ischemic core was present 1 day after a single injection. The initial induction of c-fos protein in cortical neurons distant from the ischemic core lesion and prolonged c-fos expression surrounding the infarct suggests that c-fos expression is linked to both early onset-short lasting stimulation and more persistent excitatory or plasticity-related phenomena associated with focal ischemic brain injury. C1 MASSACHUSETTS GEN HOSP,STROKE RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Moskowitz, Michael/D-9916-2011; Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NINDS NIH HHS [NS 10828] NR 35 TC 142 Z9 144 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 JUN 21 PY 1991 VL 552 IS 1 BP 99 EP 105 DI 10.1016/0006-8993(91)90665-I PG 7 WC Neurosciences SC Neurosciences & Neurology GA FU388 UT WOS:A1991FU38800015 PM 1913186 ER PT J AU FAUSTMAN, D COE, C AF FAUSTMAN, D COE, C TI PREVENTION OF XENOGRAFT REJECTION BY MASKING DONOR HLA CLASS-I ANTIGENS SO SCIENCE LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; ISLET ALLOGRAFT SURVIVAL; T-CELL RECEPTORS; AUTOIMMUNE ENCEPHALOMYELITIS; MONOCLONAL-ANTIBODY; RENAL-ALLOGRAFTS; ADHESION; INVIVO; MICE; PROLONGATION AB Destruction of target cells by cytotoxic T lymphocytes requires the presence of HLA (human lymphocyte antigen) class I antigens on the target cells for adhesion as well as for triggering of the antigen-specific T cell receptor. Rejection of xenogeneic human pancreatic islets and liver was circumvented by masking, before transplantation, donor antigens with F(ab')2 antibody fragments to HLA class I or tissue-specific epitopes. This strategy eliminated the need for recipient immunosuppression and allowed islet xenograft survival beyond 200 days, as demonstrated functionally by C peptide secretion as well as by histology. These in vivo observations are consistent with the importance of donor HLA class I in eliciting graft rejection and have potential applicability to the successful transplantation of other HLA class I-bearing donor tissues. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIABET UNIT,BOSTON,MA 02114. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 26 TC 104 Z9 105 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 JUN 21 PY 1991 VL 252 IS 5013 BP 1700 EP 1702 DI 10.1126/science.1710828 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FT114 UT WOS:A1991FT11400044 PM 1710828 ER PT J AU FINBERG, RW WAHL, SM ALLEN, JB SOMAN, G STROM, TB MURPHY, JR NICHOLS, JC AF FINBERG, RW WAHL, SM ALLEN, JB SOMAN, G STROM, TB MURPHY, JR NICHOLS, JC TI SELECTIVE ELIMINATION OF HIV-1-INFECTED CELLS WITH AN INTERLEUKIN-2 RECEPTOR SPECIFIC CYTOTOXIN SO SCIENCE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HIV-INFECTED CELLS; FUSION PROTEIN; DIPHTHERIA-TOXIN; ENVELOPE GLYCOPROTEIN; LYMPHOCYTES; ACTIVATION; ENTRY; MONOCYTES; CD4 AB Infection by human immunodeficiency virus type 1 (HIV-1) is associated with cellular activation and expression of the interleukin-2 (IL-2) receptor. A genetically engineered fusion toxin, DAB486 IL-2, that contains the enzymatic site and translocation domain of diphtheria toxin and the receptor binding domain of IL-2 specifically kills cells that express high-affinity IL-2 receptors. This toxin selectively eliminated the HIV-1-infected cells from mixed cultures of infected and uninfected cells and inhibited production of viral proteins and infectious virus. Thus, cellular activation antigens present a target for early antiviral intervention. C1 SERAGEN,HOPKINTON,MA 01748. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NIDR,IMMUNOL LAB,BETHESDA,MD 20892. BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,THORNDIKE LAB,BOSTON,MA 02215. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. BOSTON UNIV MED,BOSTON UNIV HOSP,BOSTON,MA 02118. RP FINBERG, RW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 NR 28 TC 47 Z9 47 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 JUN 21 PY 1991 VL 252 IS 5013 BP 1703 EP 1705 DI 10.1126/science.1904628 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FT114 UT WOS:A1991FT11400045 PM 1904628 ER PT J AU NEMUNAITIS, J RABINOWE, SN SINGER, JW BIERMAN, PJ VOSE, JM FREEDMAN, AS ONETTO, N GILLIS, S OETTE, D GOLD, M BUCKNER, CD HANSEN, JA RITZ, J APPELBAUM, FR ARMITAGE, JO NADLER, LM AF NEMUNAITIS, J RABINOWE, SN SINGER, JW BIERMAN, PJ VOSE, JM FREEDMAN, AS ONETTO, N GILLIS, S OETTE, D GOLD, M BUCKNER, CD HANSEN, JA RITZ, J APPELBAUM, FR ARMITAGE, JO NADLER, LM TI RECOMBINANT GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR AFTER AUTOLOGOUS BONE-MARROW TRANSPLANTATION FOR LYMPHOID CANCER SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID NON-HODGKINS-LYMPHOMA; GM-CSF; ADVANCED MALIGNANCY; HEMATOPOIESIS; CHEMOTHERAPY; PRIMATES; CELLS; MICE; IL-3 AB Background. The period of neutropenia after autologous bone marrow transplantation results in substantial morbidity and mortality. The results of previous phase I-II clinical trials suggest that recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) may accelerate neutrophil recovery and thereby reduce complications in patients after autologous bone marrow transplantation. Methods. We conducted a randomized, double-blind, placebo-controlled trial at three institutions. The study design and treatment schedules were identical, and the results were pooled for analysis. One hundred twenty-eight patients were enrolled. Sixty-five patients received rhGM-CSF in a two-hour intravenous infusion daily for 21 days, starting within four hours of the marrow infusion, and 63 patients received placebo. Results. No toxic effects specifically ascribed to rhGM-CSF were observed. The patients given rhGM-CSF had a recovery of the neutrophil count to 500 x 10(6) per liter 7 days earlier than the patients who received placebo (19 vs. 26 days, P < 0.001), had fewer infections, required 3 fewer days of antibiotic administration (24 vs. 27 days, P = 0.009), and required 6 fewer days of initial hospitalization (median, 27 vs. 33 days; P = 0.01). There was no difference in the survival rate at day 100. Conclusions. In patients undergoing autologous bone marrow transplantation for lymphoid neoplasia, rhGM-CSF significantly lessens morbidity. Further studies will be required to establish its optimal dosage and schedule of administration. C1 IMMUNEX CORP,SEATTLE,WA. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. UNIV WASHINGTON,SEATTLE,WA 98195. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. HOECHST ROUSSEL PHARMACEUT PTY LTD,SOMERVILLE,NJ 08876. RP NEMUNAITIS, J (reprint author), VET AFFAIRS MED CTR,111-ONC,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. OI Singer, Jack/0000-0003-4001-4549 FU NCI NIH HHS [CA 34183, CA 47748, CA 18029] NR 30 TC 443 Z9 444 U1 1 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 JUN 20 PY 1991 VL 324 IS 25 BP 1773 EP 1778 DI 10.1056/NEJM199106203242504 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FR681 UT WOS:A1991FR68100004 PM 1903847 ER PT J AU TANAKA, J TEICHER, BA HERMAN, TS HOLDEN, SA DEZUBE, B FREI, E AF TANAKA, J TEICHER, BA HERMAN, TS HOLDEN, SA DEZUBE, B FREI, E TI ETOPOSIDE WITH LONIDAMINE OR PENTOXIFYLLINE AS MODULATORS OF ALKYLATING AGENT ACTIVITY INVIVO SO INTERNATIONAL JOURNAL OF CANCER LA English DT Article ID ASCITES TUMOR-CELLS; MURINE TUMOR; DNA TOPOISOMERASES; ARTERIAL-DISEASE; HOECHST 33342; TRANSPORT; REPAIR; RADIATION; MELPHALAN; THERAPY AB In an effort to improve the additive anti-tumor efficacy of commonly used alkylating agents, the topoisomerase-II inhibitor etoposide was used in combination with either the mitochondrial poison and energy-depleting agent Ionidamine or the hemorheologic agent and tumor-blood-flow-increasing agent pentoxifylline. In the FSaIIC murine fibrosarcoma system, these modulators were evaluated for modulation of whole-tumor cell killing vs. bone-marrow CFU-GM toxicity with the alkylating drugs CDDP, CTX, L-PAM or BCNU. Etoposide alone was essentially additive with the alkylating drugs for both tumor-cell and bone-marrow killing, except for BCNU, where a substantial increase in tumor-cell killing occurred (0.5 to 2.0 Logs over the dose range of BCNU tested) without a significant increase in bone-marrow toxicity. Etoposide plus Ionidamine was significantly more active than etoposide alone only with CTX and BCNU in tumor-cell vs. bone-marrow killing. Etoposide plus pentoxifylline was also most active with these two alkylating agents, where increases in tumor-cell killing of 0.5 to 1.0 log were observed. Hoechst-33342-defined tumor-cell sub-population studies revealed that etoposide significantly improved the killing of dim (putative hypoxic) cells by CDDP, but neither Ionidamine nor pentoxifylline significantly improved killing of bright or dim cells together. With CTX, etoposide plus Ionidamine or pentoxifylline substantially improved killing of dim cells over etoposide alone (each by about 0.8 logs). These data indicate that a therapeutic advantage may be achievable by combining etoposide with Ionidamine or pentoxifylline for use with alkylating drugs. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. FU NCI NIH HHS [1PO1-CA38493] NR 40 TC 14 Z9 14 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0020-7136 J9 INT J CANCER JI Int. J. Cancer PD JUN 19 PY 1991 VL 48 IS 4 BP 631 EP 637 DI 10.1002/ijc.2910480424 PG 7 WC Oncology SC Oncology GA FT311 UT WOS:A1991FT31100023 PM 2045206 ER PT J AU THRALL, JH AF THRALL, JH TI NUCLEAR-MEDICINE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PULMONARY-EMBOLISM; METAIODOBENZYLGUANIDINE; INFECTION RP THRALL, JH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 13 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD JUN 19 PY 1991 VL 265 IS 23 BP 3137 EP 3139 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FQ770 UT WOS:A1991FQ77000027 PM 2041129 ER PT J AU MAYER, RJ AF MAYER, RJ TI TRAINING IN MEDICAL ONCOLOGY - REGAINING THE LUSTER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material RP MAYER, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 6 Z9 6 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 19 PY 1991 VL 83 IS 12 BP 806 EP 807 DI 10.1093/jnci/83.12.806 PG 2 WC Oncology SC Oncology GA FQ595 UT WOS:A1991FQ59500001 PM 2061939 ER PT J AU MEISSEN, GJ MASTROMAURO, CA KIELY, DK MCNAMARA, DS MYERS, RH AF MEISSEN, GJ MASTROMAURO, CA KIELY, DK MCNAMARA, DS MYERS, RH TI UNDERSTANDING THE DECISION TO TAKE THE PREDICTIVE TEST FOR HUNTINGTON DISEASE SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE RESTRICTION FRAGMENT LENGTH POLYMORPHISM; HD; GENETIC COUNSELING ID DNA MARKER; CHOREA; ATTITUDES; RISK; GENETICS AB The predictive test for Huntington disease (HD) has allowed those at risk to determine gene status prior to symptoms. The purpose of this research was to understand the motivation and the anticipated reactions of those requesting the test. Forty persons at 50% risk for HD and 31 companions participated in a structured personal interview as part of the predictive test protocol. Reasons for taking the test centered on the reduction of anxiety and uncertainty associated with being at risk and enhanced planning and decision making. Participants also believed that taking the test would produce more positive than negative outcomes. With a favorable result, most anticipated a reduction of anxiety, a more normal future, and relief knowing their children would be at a very low risk. Most also cited benefits as more likely than consequences with an unfavorable result. Making the most of life, easier planning, and reduced uncertainty were rated as more likely than any of the adverse impacts, including short-term depression and becoming frightened. Almost all participants (95%) said they would rather learn that they have the HD gene than remain at 50% risk. The uncertainty, anxiety, and chronic stress associated with being at risk appears to underlie the motivation of many seeking the predictive test for HD. C1 BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SOCIAL SERV,BOSTON,MA 02114. RP MEISSEN, GJ (reprint author), WICHITA STATE UNIV,DEPT PSYCHOL,COMMUNITY PSYCHOL PROGRAM,WICHITA,KS 67208, USA. FU NINDS NIH HHS [NS16367] NR 29 TC 51 Z9 51 U1 3 U2 4 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD JUN 15 PY 1991 VL 39 IS 4 BP 404 EP 410 DI 10.1002/ajmg.1320390408 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA FM879 UT WOS:A1991FM87900007 PM 1678928 ER PT J AU BOOTH, RG BALDESSARINI, RJ CAMPBELL, A AF BOOTH, RG BALDESSARINI, RJ CAMPBELL, A TI INHIBITION OF DOPAMINE SYNTHESIS IN RAT STRIATAL MINCES - EVIDENCE OF DOPAMINE AUTORECEPTOR SUPERSENSITIVITY TO S(+)-N-NORMAL-PROPYLNORAPOMORPHINE BUT NOT R(-)-N-NORMAL-PROPYLNORAPOMORPHINE AFTER PRETREATMENT WITH FLUPHENAZINE SO BIOCHEMICAL PHARMACOLOGY LA English DT Note ID SUPER-SENSITIVITY; RECEPTORS; APOMORPHINE; DRUGS; ACID C1 HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHIAT RES LABS,BELMONT,MA. UNIV N CAROLINA,SCH PHARM,DIV MED CHEM & NAT PROD,CHAPEL HILL,NC 27599. RP BOOTH, RG (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115, USA. FU NIMH NIH HHS [MH-34006, MH-14275, MH-47370] NR 17 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD JUN 15 PY 1991 VL 41 IS 12 BP 2040 EP 2043 DI 10.1016/0006-2952(91)90148-X PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FN572 UT WOS:A1991FN57200034 PM 1674873 ER PT J AU LIND, SE AF LIND, SE TI THE BLEEDING-TIME DOES NOT PREDICT SURGICAL BLEEDING SO BLOOD LA English DT Review ID ASPIRIN-INDUCED PROLONGATION; PARTIAL THROMBOPLASTIN TIME; PERCUTANEOUS LIVER-BIOPSY; PERIOPERATIVE BLOOD-LOSS; OPEN-HEART SURGERY; CARDIOPULMONARY BYPASS; RENAL BIOPSY; POSTOPERATIVE HEMORRHAGE; EPIDURAL-ANESTHESIA; SCREENING-TEST C1 MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 58 TC 235 Z9 237 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 15 PY 1991 VL 77 IS 12 BP 2547 EP 2552 PG 6 WC Hematology SC Hematology GA FR682 UT WOS:A1991FR68200001 PM 2043759 ER PT J AU BARNHILL, RL ROUSH, GC AF BARNHILL, RL ROUSH, GC TI CORRELATION OF CLINICAL AND HISTOPATHOLOGIC FEATURES IN CLINICALLY ATYPICAL MELANOCYTIC NEVI SO CANCER LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; DYSPLASTIC NEVUS; DIAGNOSIS; LESIONS; PRECURSORS; MICROSCOPY AB To define better the evolving entity of dysplastic melanocytic nevus (DMN), studies correlating clinical with histologic features of DMN are essential. However, based on a literature search, no previous quantitative analysis was found of the relationship between gross morphologic features and histologic features of DMN. The authors correlated individual clinical features with histopathologic features and histologic diagnosis of the clinically most atypical nevus in 153 melanoma patients. This nevus was identified, evaluated clinically, and removed for histologic evaluation from each patient. Gross morphologic features assessed for nevi included: size (in mm), the presence of a macular component, irregular border, ill-defined border, haphazard coloration, distortion of skin cleavage lines on tangential lighting, asymmetry, and number of colors present (12 features in all). Nineteen histologic features were assessed in each nevus by a single dermatopathologist. These included architectural, nuclear, and cytoplasmic parameters ascribed to dysplastic nevi. Each of these histologic features was correlated with the 12 individual clinical features. Seventeen percent of the nevi fulfilled the criteria for the histologic diagnosis of DMN. Among individual nevus parameters, size (in mm), irregular border, ill-defined border, macular component, and pink color were associated significantly with histologic DMN. Nevus size (in mm) and irregular borders correlated with the greatest number of individual histologic parameters. A comparison of clinicopathologic correlations for two different examiners revealed that certain clinical features are probably more important than others for the recognition of dysplastic nevi and that individual examiners have different thresholds for the perception of some gross morphologic features. These observations are relevant to the development of clinical criteria for dysplastic nevi. C1 CANC PREVENT RES INST,NEW YORK,NY. MASSACHUSETTS GEN HOSP,DERMATOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BARNHILL, RL (reprint author), MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,FRUIT ST,BOSTON,MA 02114, USA. NR 20 TC 22 Z9 22 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUN 15 PY 1991 VL 67 IS 12 BP 3157 EP 3164 DI 10.1002/1097-0142(19910615)67:12<3157::AID-CNCR2820671237>3.0.CO;2-6 PG 8 WC Oncology SC Oncology GA FR254 UT WOS:A1991FR25400036 PM 2044059 ER PT J AU PANDOLFI, F BOYLE, LA TRENTIN, L KURNICK, JT ISSELBACHER, KJ GATTONICELLI, S AF PANDOLFI, F BOYLE, LA TRENTIN, L KURNICK, JT ISSELBACHER, KJ GATTONICELLI, S TI EXPRESSION OF HLA-A2 ANTIGEN IN HUMAN-MELANOMA CELL-LINES AND ITS ROLE IN T-CELL RECOGNITION SO CANCER RESEARCH LA English DT Article ID CLASS-I ANTIGENS; TUMOR-INFILTRATING LYMPHOCYTES; HUMAN SOLID TUMORS; HISTOCOMPATIBILITY ANTIGEN; METASTATIC MELANOMA; BINDING-SITE; C-MYC; GROWTH; INTERLEUKIN-2; SUPPRESSION AB Previous studies have suggested that, in human melanoma, expression of HLA-A2 antigen is important for tumor cell recognition by autologous T-lymphocytes. Because of the recent demonstration that expression of HLA Class I antigens may be selectively lost in several human tumors, including melanoma, we derived pairs of tumor infiltrating lymphocytes (TIL) and melanoma cell lines from 4 human lymphocytic antigen (HLA)-A2+ patients with metastatic melanoma. We observed that, although all 4 TIL cultures expressed HLA-A2 antigen, only 2 melanoma cell lines did so. Melanoma cells derived from the other 2 patients showed neither surface expression of the HLA-A2 antigen nor presence of the corresponding mRNA. We also observed some correlation between loss of HLA-A2 expression and level of c-myc transcription. TIL derived from patients whose melanoma cell lines had normal expression of HLA-A2 had a CD8 phenotype and were capable of lysing autologous melanoma cells. Melanoma cell killing was CD3 and major histocompatibility complex Class I restricted in both cases, but HLA-A2 restricted in only one case. On the other hand, TIL derived from the 2 patients whose melanoma cell lines had lost expression of HLA-A2 had a predominant CD4 phenotype and virtually no cytotoxic activity. Preincubation of the HLA-A2 negative melanoma cell lines with alpha- or gamma-interferon did not induce the re-expression of the HLA-A2 antigen. In an attempt to restore HLA-A2 antigen expression in one of the melanoma cell lines that were HLA-A2 negative, we transfected these cells with the HLA-A2 gene subcloned in the pSV2-neo vector. Four transfected clones, with high levels of HLA-A2 antigen expression, were expanded and characterized. Proliferative and cytotoxic activities of TIL against the autologous transfected clones as well as the untransfected parental melanoma cell line were measured and compared. CD4+ TIL showed no difference in the proliferative response to autologous parental and HLA-A2 transfected clones. However, we observed selective recognition of the HLA-A2 expressing clones by autologous cultured peripheral blood lymphocytes (which contained CD8 cells) as well as allogeneic CD8+ TIL with a HLA-A2 restricted pattern of recognition. In contrast, virtually no cytotoxic activity was detected against either parental or HLA-A2 transfected clones. Overall, our data suggest that selective down-regulation of HLA-A2 antigen expression in melanoma cells may represent one of the mechanisms by which tumor cells escape immunological recognition. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP PANDOLFI, F (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,149 13TH ST,BOSTON,MA 02129, USA. RI TRENTIN, LIVIO/J-7676-2016 OI TRENTIN, LIVIO/0000-0003-1222-6149 FU NCI NIH HHS [CA 44324]; NIAMS NIH HHS [AR 39993]; NIDDK NIH HHS [DK 36350] NR 34 TC 62 Z9 62 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1991 VL 51 IS 12 BP 3164 EP 3170 PG 7 WC Oncology SC Oncology GA FQ967 UT WOS:A1991FQ96700014 PM 1904004 ER PT J AU OKUNIEFF, P DOLS, S LEE, J SINGER, S VAUPEL, P NEURINGER, LJ BESHAH, K AF OKUNIEFF, P DOLS, S LEE, J SINGER, S VAUPEL, P NEURINGER, LJ BESHAH, K TI ANGIOGENESIS DETERMINES BLOOD-FLOW, METABOLISM, GROWTH-RATE, AND ATPASE KINETICS OF TUMORS GROWING IN AN IRRADIATED BED - P-31 AND H-2 NUCLEAR-MAGNETIC-RESONANCE STUDIES SO CANCER RESEARCH LA English DT Article ID RADIATION-INDUCED INJURY; MURINE SARCOMAS; FAST-NEUTRONS; X-RAYS; SPECTROSCOPY; RADIOCURABILITY; PREIRRADIATION; HYDRALAZINE; CARCINOMAS; FRACTION AB Experimental tumors growing in irradiated tissue have been used to study the biological differences characteristic of locally recurrent tumors. Since the hypoxic cell fraction of tumors growing in irradiated tissue is increased and growth rate is slowed, these tumors are assumed to be metabolically deprived with hypoperfusion. In this study, we directly measured the effect of tumor bed irradiation on blood flow, growth rate, rate of nucleoside triphosphate (NTP) turnover, and metabolic state using P-31 and H-2 nuclear magnetic resonance, and an intradermal assay for angiogenesis. (NTP turnover refers to ATP-synthetase mediated NTP turnover that is visible to P-31 nuclear magnetic resonance using the technique of saturation transfer.) A decrease in the number of small blood vessels perfusing tumors in a preirradiated bed was found. Most of the decrease was due to a loss of vessels with diameters less than 0.04 mm. When tumors growing in preirradiated tissue reached almost-equal-to 100 mm3 in volume, a high frequency of gross and microscopic necrosis and hemorrhage was already observed in most tumors. Consistent with these observations, the phosphocreatine/inorganic phosphate and nucleoside triphosphate/inorganic phosphate ratios were significantly lower in the tumors growing in a preirradiated bed compared with tumors in a nonirradiated bed. The blood flow rate was similar to control for tumors less than 100 mm3 (45.8 versus 40.5 ml/100 g/min, P = not significant), but was significantly lower than control for tumors greater than 100 mm3 (40.4 versus 12.2 ml/100 g/min, P < 0.01). The NTP turnover rates correlated (P < 0.005, r = 0.66) with the volume doubling rate (1/tumor volume doubling time), but for tumors almost-equal-to 100 mm3 in size neither the volume doubling rate nor the NTP turnover rate of tumors growing in an irradiated bed was statistically lower than control [NTP turnover: 14 +/- 3%/s versus 9 +/- 2%/s; volume doubling rate: 0.47 +/- 0.07/day versus 0.33 +/- 0.04/day, (mean +/- SE)]. A large intertumor variability of all metabolic parameters was observed. RP OKUNIEFF, P (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, DEPT RADIAT ONCOL, EDWIN L STEELE LAB, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA13311, CA48096]; NCRR NIH HHS [RR00995] NR 35 TC 39 Z9 39 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 15 PY 1991 VL 51 IS 12 BP 3289 EP 3295 PG 7 WC Oncology SC Oncology GA FQ967 UT WOS:A1991FQ96700033 PM 1710169 ER PT J AU WEBER, GF MAERTENS, P MENG, X PIPPENGER, CE AF WEBER, GF MAERTENS, P MENG, X PIPPENGER, CE TI GLUTATHIONE-PEROXIDASE DEFICIENCY AND CHILDHOOD SEIZURES SO LANCET LA English DT Note AB 4 children with intractable seizures, repeated infections, and intolerance to anticonvulsants had evidence of glutathione peroxidase deficiency. 2 had low intracellular enzyme activity but normal blood selenium and high plasma glutathione peroxidase concentrations. The other 2 had low intracellular glutathione peroxidase activity with low circulating glutathione peroxidase and selenium concentrations. The clinical state of the children improved after discontinuation of anticonvulsant medication and selenium substitution. C1 UNIV SO ALABAMA,MED CTR,DEPT NEUROL,MOBILE,AL 36617. CLEVELAND CLIN FDN,DEPT BIOCHEM,CLEVELAND,OH 44195. RP WEBER, GF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 78 Z9 80 U1 3 U2 3 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD JUN 15 PY 1991 VL 337 IS 8755 BP 1443 EP 1444 DI 10.1016/0140-6736(91)93130-2 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FR060 UT WOS:A1991FR06000007 PM 1675321 ER PT J AU SUCHER, NJ LEI, SZ LIPTON, SA AF SUCHER, NJ LEI, SZ LIPTON, SA TI CALCIUM-CHANNEL ANTAGONISTS ATTENUATE NMDA RECEPTOR-MEDIATED NEUROTOXICITY OF RETINAL GANGLION-CELLS IN CULTURE SO BRAIN RESEARCH LA English DT Note DE EXCITATORY AMINO ACID; N-METHYL-D-ASPARTATE; CALCIUM CHANNEL ANTAGONIST; NEUROTOXICITY; RAT CENTRAL NEURON; CELL CULTURE ID AMINO-ACID RECEPTORS; SPINAL-CORD NEURONS; GLUTAMATE NEUROTOXICITY; STRIATAL NEURONS; RAT; TOXICITY; INVITRO; EXCITOTOXICITY; MODULATION; DEPENDENCE AB Dihydropyridine calcium channel antagonists block a prolonged or 'L-type' component of voltage-dependent Ca2+ current in patch-clamp recordings of postnatal rat retinal ganglion cells. In the present study on these neurons, calcium channel antagonists were found at 500-1000 nM concentrations to attenuate the early rise in [Ca2+]i and the subsequent toxic effects of exogenous glutamate, N-methyl-D-aspartate (NMDA), or an endogenous glutamate-related compound present in the retinal cultures. Previous data have shown that the neurotoxicity engendered by these agents can also be prevented by selective NMDA antagonists. The present observations raise the possibility, at least in this preparation, that activation of both voltage-dependent calcium channels and NMDA receptor-operated channels contribute to the injurious effects triggered by molecules binding to the NMDA receptor. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,ENDERS BLDG,SUITE 361,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [EY05477]; NICHD NIH HHS [HD06276] NR 36 TC 92 Z9 95 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 JUN 14 PY 1991 VL 551 IS 1-2 BP 297 EP 302 DI 10.1016/0006-8993(91)90944-Q PG 6 WC Neurosciences SC Neurosciences & Neurology GA FV304 UT WOS:A1991FV30400040 PM 1680525 ER PT J AU DIAMOND, MS STAUNTON, DE MARLIN, SD SPRINGER, TA AF DIAMOND, MS STAUNTON, DE MARLIN, SD SPRINGER, TA TI BINDING OF THE INTEGRIN MAC-1 (CD11B/CD18) TO THE 3RD IMMUNOGLOBULIN-LIKE DOMAIN OF ICAM-1 (CD54) AND ITS REGULATION BY GLYCOSYLATION SO CELL LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; MONOCLONAL-ANTIBODY; ANTIGEN-1 LFA-1; HUMAN CD4; TRANSENDOTHELIAL MIGRATION; NEUTROPHIL ADHERENCE; GLYCOPROTEIN FAMILY; COMPLEMENT RECEPTOR; ELECTRON-MICROSCOPY; ENDOTHELIAL-CELLS AB Both the integrins LFA-1 and Mac-1 bind to ICAM-1, an immunoglobulin superfamily member. Previously, we localized the binding sites of LFA-1 and the major group of human rhinoviruses to the first NH2-terminal immunoglobulin-like domain of ICAM-1. Here, we show that the binding site on ICAM-1 for Mac-1 is unexpectedly distinct from that for LFA-1 and maps to the third NH2-terminal immunoglobulin-like domain. These findings provide a function for the tandem duplication of immunoglobulin-like domains in ICAM-1 and have implications for other immunoglobulin superfamily members. Mutations at two sites in the third domain that destroy consensus sequences for N-linked glycosylation enhance binding to purified Mac-1. Agents that interfere with carbohydrate processing provide evidence that the size of the N-linked oligosaccharide side chains on ICAM-1 affects binding to Mac-1 but not to LFA- 1. Thus, we suggest that the extent of glycosylation on ICAM-1 may regulate adhesion to LFA-1 or Mac-1 in vivo. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. BOEHRINGER INGELHEIM PHARMACEUT,RIDGEFIELD,CT 06877. RP DIAMOND, MS (reprint author), HARVARD UNIV,SCH MED,COMM CELL & DEV BIOL,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA31799]; NIGMS NIH HHS [T32 GM007753, T32GM07753-11] NR 73 TC 687 Z9 706 U1 1 U2 12 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUN 14 PY 1991 VL 65 IS 6 BP 961 EP 971 DI 10.1016/0092-8674(91)90548-D PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FR047 UT WOS:A1991FR04700007 PM 1675157 ER PT J AU CHITTENDEN, T LIVINGSTON, DM KAELIN, WG AF CHITTENDEN, T LIVINGSTON, DM KAELIN, WG TI THE T/E1A-BINDING DOMAIN OF THE RETINOBLASTOMA PRODUCT CAN INTERACT SELECTIVELY WITH A SEQUENCE-SPECIFIC DNA-BINDING PROTEIN SO CELL LA English DT Article ID E2F TRANSCRIPTION FACTOR; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGENS; SUSCEPTIBILITY GENE; REGULATORY PROTEINS; TRANS-ACTIVATION; CELL-CYCLE; RB GENE; SV40; PROMOTER AB A DNA-binding site selection and enrichment procedure revealed a sequence-specific DNA-binding activity selectively associated with glutathione S-transferase-retinoblastoma protein chimeras (GST-RB) that had been incubated with a human cell extract. Appropriate mutant forms of GST-RB, incubated in equivalent extracts, did not associate with this specific DNA-binding activity, and a peptide replica of the HPV E7 RB-binding segment selectively inhibited the association of GST-RB with the sequence-specific DNA-binding protein(s). Sequence analysis of oligonucleotides with high affinity for GST-RB complexes, as well as the results of competition binding studies, strongly suggest that RB can associate specifically with the transcription factor E2F or with a protein having closely related DNA-binding properties. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP CHITTENDEN, T (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 41 TC 389 Z9 393 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD JUN 14 PY 1991 VL 65 IS 6 BP 1073 EP 1082 DI 10.1016/0092-8674(91)90559-H PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FR047 UT WOS:A1991FR04700018 PM 1828394 ER PT J AU LIANG, TJ HASEGAWA, K RIMON, N WANDS, JR BENPORATH, E AF LIANG, TJ HASEGAWA, K RIMON, N WANDS, JR BENPORATH, E TI A HEPATITIS-B VIRUS MUTANT ASSOCIATED WITH AN EPIDEMIC OF FULMINANT-HEPATITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID E-ANTIGEN; PRECORE REGION; CORE ANTIGEN; NON-A; GENOME; LIVER; HBE; DNA; IDENTIFICATION; REPLICATION AB Background. A nosocomial outbreak of fulminant hepatitis B occurred in five patients in Haifa, Israel. Previous investigations identified the suspected source as a carrier of hepatitis B surface antigen who was positive for antibodies to hepatitis B e antigen and had chronic liver disease. We examined the strain of hepatitis B virus (HBV) that caused this epidemic, in order to identify specific mutations in the precore or core region. Methods. The presence of HBV was identified by polymerase-chain-reaction amplification of viral DNA in serum from the source patient, the five patients with fulminant hepatitis B, and five controls with acute, self-limited hepatitis B. The amplified viral HBV DNA samples were then cloned and sequenced. Results. Sequence analysis of viral DNA established that the same HBV mutant with two mutations in the precore region was present in the source patient and the five patients with fulminant hepatic failure. This HBV mutant had significant sequence divergence from other known HBV subtypes in the X, precore, and core regions. Cloned HBV DNA derived from a hospitalized patient who had subclinical hepatitis B at the same time as the outbreak and from four other control subjects with acute, self-limited hepatitis B all contained the wild-type sequence in the precore region. Conclusions. In the outbreak we studied, a mutant hepatitis B viral strain was transmitted from a common source to five patients who subsequently died of fulminant hepatitis B infection. Naturally occurring viral mutations in the HBV genome may predispose the infected host to more severe liver injury. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. TECHNION ISRAEL INST TECHNOL,RAMBAM MED CTR,FAC MED,VIROL LAB,HAIFA,ISRAEL. RP LIANG, TJ (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,7TH FL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666, AA-08169] NR 38 TC 407 Z9 419 U1 0 U2 2 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 13 PY 1991 VL 324 IS 24 BP 1705 EP 1709 DI 10.1056/NEJM199106133242405 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FQ155 UT WOS:A1991FQ15500005 PM 2034247 ER PT J AU HUSAIN, SS AF HUSAIN, SS TI SINGLE-CHAIN UROKINASE-TYPE PLASMINOGEN-ACTIVATOR DOES NOT POSSESS MEASURABLE INTRINSIC AMIDOLYTIC OR PLASMINOGEN-ACTIVATOR ACTIVITIES SO BIOCHEMISTRY LA English DT Article ID SITE-SPECIFIC MUTAGENESIS; PRO-UROKINASE; AFFINITY-CHROMATOGRAPHY; SARCOMA-CELLS; 2-CHAIN FORMS; HUMAN-PLASMA; HUMAN-URINE; CLOT LYSIS; FACTOR-VII; PURIFICATION AB The question whether single-chain urokinase-type plasminogen activator (Sc-uPA) possesses an enzymatic activity has been a subject of intense investigation for a number of years but still remains unresolved. Recent studies from several laboratories suggest that Sc-uPA or its plasmin-resistant mutants obtained by site-directed mutagenesis possess significant, albeit low, amidolytic and plasminogen activator activities, ranging from 0.1% to 1% of that observed for two-chain urokinase (Tc-uPA). In an effort to characterize these putative intrinsic activities, Sc-uPA was repeatedly treated with dansyl-Glu-Gly-Arg chloromethyl ketone (dansyl-EGRck) or diisopropyl fluorophosphate (DFP) (0.1-0.25 mM added thrice over a period of 24 h at 0-degrees-C). This treatment exhaustively inactivated the Tc-uPA contaminant but did not affect Sc-uPA, as evidenced by the lack of significant incorporation of radiolabeled inhibitor in Sc-uPA and full activation of the inhibitor-treated Sc-uPA by plasmin. Assayed in the presence of excess DFP or dansyl-EGRck to ensure trapping of any Tc-uPA generated in the assay mixture, Sc-uPA (84-mu-g/mL, 10500 latent units/mL) did not elicit any detectable cleavage of the chromogenic substrate S-2444 (detection limit 0.1 unit of Tc-uPA/mL). However, if the Tc-uPA inhibitors were removed prior to assay, a trace amount of amidolytic activity invariably reappeared in the Sc-uPA preparation. Incorporation experiments with [H-3]DFP suggested that the appearance of this amidolytic activity was due to formation of Tc-uPA. Plasminogen activator assay of DFP- and dansyl-EGRck-treated Sc-uPA (0.45 - 2.25-mu-M), performed in the presence of these inhibitors and Trasylol (10-mu-M) to ensure entrapment of any Tc-uPA or plasmin generated in the reaction mixture, showed no significant cleavage of I-125-labeled plasminogen (detection limit 0.1 nM). However, if dansyl-EGRck and DFP were removed from the inhibitor-treated Sc-uPA and the assay was performed in the presence of Trasylol alone, there was significant cleavage of I-125-plasminogen due to contamination by Tc-uPA. Fibrin, a positive effector of plasminogen activation by Tc-uPA or Sc-uPA preparations in the absence of DFP and dansyl-EGRck, did not promote cleavage of plasminogen or S-2444 by Sc-uPA in the presence of the Tc-uPA inhibitors. The present findings indicate that, under conditions stringently excluding Tc-uPA contamination, neither recombinant human Sc-uPA expressed in Chinese hamster ovary cells nor Sc-uPA secreted by fetal kidney cells or a transformed line of kidney cells shows measurable amidolytic activity above the detection limit of 0.001 % or plasminogen activator activity above the detection limit of 0.01% of Tc-uPA activity. These studies suggest that the intrinsic activities ascribed to Sc-uPA or its plasmin-resistant mutants arise from small amounts of Tc-uPA, possibly generated from Sc-uPA by the action of traces of contaminating proteases that are not susceptible to inactivation by usual inhibitors of trypsin-like serine proteases. 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 39 TC 30 Z9 30 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 JUN 11 PY 1991 VL 30 IS 23 BP 5797 EP 5805 DI 10.1021/bi00237a024 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FQ553 UT WOS:A1991FQ55300024 PM 1828371 ER PT J AU SCHMAHMANN, JD PANDYA, DN AF SCHMAHMANN, JD PANDYA, DN TI PROJECTIONS TO THE BASIS PONTIS FROM THE SUPERIOR TEMPORAL SULCUS AND SUPERIOR TEMPORAL REGION IN THE RHESUS-MONKEY SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE TEMPOROPONTINE; PONS; CEREBELLUM; CONNECTIONS; BEHAVIOR ID INFERIOR PARIETAL LOBULE; FRONTAL EYE FIELD; CORTICOPONTINE PROJECTION; MACAQUE MONKEY; VISUAL AREAS; SUBCORTICAL PROJECTIONS; HORSERADISH-PEROXIDASE; CORTICAL CONNECTIONS; MACACA-FASCICULARIS; NEURONAL-ACTIVITY AB The present investigation was designed to determine the origins in the temporal lobe, and terminations in the pons, of the temporopontine pathway. Injections of tritiated amino acids were placed in multimodal regions in the upper bank of the superior temporal sulcus (STS), and in unimodal visual, somatosensory, and auditory areas in different sectors of the lower bank of the STS, the superior temporal gyrus (STG), and the supratemporal plane (STP). The distribution of terminal label in the nuclei of the basis pontis was studied using the autoradiographic technique. Following injections of isotope into the multimodal areas (TPO and PGa) in the upper bank of the STS, intense aggregations of label were observed in the extreme dorsolateral, dorsolateral, and lateral nuclei of the pons, and modest amounts of label were seen in the peripeduncular nucleus. The caudalmost area TPO projected in addition to the ventral and intrapeduncular pontine nuclei. The second auditory area, AII, and the adjacent auditory association areas of the STG and STP contributed modest projections to the dorsolateral, lateral, and peripedunuclar nuclei, but generally spared the extreme dorsolateral nucleus. The lower bank of the STS, which subserves central vision, the somatosensory associated region at the fundus of the rostral STS, and the primary auditory area did not project to the pons. The higher order, multimodal STS contribution to the corticopontocerebellar circuit may provide a partial anatomical substrate for the hypothesis that the cerebellum contributes to the modulation of nonmotor functions. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. EDITH NOURSE ROGERS MEM VET ADM HOSP,BEDFORD,MA 01730. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT ANAT,BOSTON,MA 02118. HARVARD UNIV,BETH ISRAEL HOSP,NEUROL UNIT,BOSTON,MA 02215. RP SCHMAHMANN, JD (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. FU PHS HHS [16841] NR 125 TC 116 Z9 116 U1 2 U2 3 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 JUN 8 PY 1991 VL 308 IS 2 BP 224 EP 248 DI 10.1002/cne.903080209 PG 25 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA FP840 UT WOS:A1991FP84000008 PM 1716269 ER PT J AU RUSKIN, JN AF RUSKIN, JN TI CATHETER ABLATION FOR SUPRAVENTRICULAR TACHYCARDIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID ACCESSORY ATRIOVENTRICULAR PATHWAY; CLOSED-CHEST ABLATION RP RUSKIN, JN (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 13 TC 19 Z9 19 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 6 PY 1991 VL 324 IS 23 BP 1660 EP 1662 DI 10.1056/NEJM199106063242309 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA FP307 UT WOS:A1991FP30700009 PM 2030722 ER PT J AU KYRIAKIS, JM BRAUTIGAN, DL INGEBRITSEN, TS AVRUCH, J AF KYRIAKIS, JM BRAUTIGAN, DL INGEBRITSEN, TS AVRUCH, J TI PP54 MICROTUBULE-ASSOCIATED PROTEIN-2 KINASE REQUIRES BOTH TYROSINE AND SERINE THREONINE PHOSPHORYLATION FOR ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID GROWTH-FACTOR; S6 KINASE; INSULIN; ACTIVATION; INVIVO; FORMS AB pp54 microtubule-associated protein-2 (MAP-2) kinase, a recently discovered protein serine/threonine kinase (Kyriakis, J., and Avruch, J. (1990) J. Biol. Chem. 265, 17355-17363), is shown to contain immunoreactive phosphotyrosine residues. Treatment with recombinant rat brain protein tyrosine phosphatase-1 deactivates pp54 MAP-2 kinase, concomitant with the removal of phosphotyrosine residues. Protein (serine/threonine) phosphatase-1 also deactivates pp54 MAP-2 kinase in a specific fashion. pp54 MAP-2-kinase joins pp42 MAP-2 kinase and cdc2/maturation-promoting factor as one of only three serine/threonine protein kinases known to be regulated by phosphorylation at both tyrosine and, independently, at serine/threonine residues. In view of these shared regulatory properties, a role for pp54 MAP-2 kinase in the control of cell division is likely. C1 MASSACHUSETTS GEN HOSP,DIABET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. BROWN UNIV,DIV BIOL & MED,PROVIDENCE,RI 02912. IOWA STATE UNIV SCI & TECHNOL,DEPT ZOOL & GENET,AMES,IA 50011. FU NHLBI NIH HHS [HL07680]; NIDDK NIH HHS [DK41513, DK41762] NR 23 TC 95 Z9 96 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1991 VL 266 IS 16 BP 10043 EP 10046 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP086 UT WOS:A1991FP08600007 PM 1645334 ER PT J AU PULIDO, R ELICES, MJ CAMPANERO, MR OSBORN, L SCHIFFER, S GARCIAPARDO, A LOBB, R HEMLER, ME SANCHEZMADRID, F AF PULIDO, R ELICES, MJ CAMPANERO, MR OSBORN, L SCHIFFER, S GARCIAPARDO, A LOBB, R HEMLER, ME SANCHEZMADRID, F TI FUNCTIONAL EVIDENCE FOR 3 DISTINCT AND INDEPENDENTLY INHIBITABLE ADHESION ACTIVITIES MEDIATED BY THE HUMAN INTEGRIN VLA-4 - CORRELATION WITH DISTINCT ALPHA-4 EPITOPES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BINDING-SITE; FIBRONECTIN RECEPTOR; VITRONECTIN RECEPTOR; MONOCLONAL-ANTIBODY; PLASMA FIBRONECTIN; CELL DISTRIBUTION; T-CELLS; IDENTIFICATION; SUBUNIT; LFA-1 AB The human integrin VLA (very late activation antigens)-4 (CD49d/CD29), the leukocyte receptor for both the CS-1 region of plasma fibronectin (Fn) and the vascular cell surface adhesion molecule-1 (VCAM-1), also mediates homotypic aggregation upon triggering with specic anti-VLA-4 monoclonal antibody (mAb). Epitope mapping of this integrin of the human B-cell line Ramos, performed with a wide panel of anti-VLA-4 mAb by both cross-competitive cell binding and protease sensitivity assays, revealed the existence of three topographically distinct epitopes on the alpha-4 chain, referred to as epitopes A-C. By testing this panel of anti-VLA-4 mAb for inhibition of cecell binding to both a 38-kDa Fn fragment containing CS-1 and to VCAM-1, as well as for induction and inhibition of VLA-4 mediated homotypic cell adhesion, we have found overlapping but different functiional properties associated with each epitope. Anti-alpha-4 mAb recognizing epitope B inhibited cell attachment to both Fn and VCAM-1, whereas mAb against epitope A did not block VCAM-1 binding and only partially inhibited binding to Fn. In contrast, mAb directed to epitope C did not affect cell adhesion to either of the two VLA-4 ligands. All mAb directed to site A, as well as a subgroup of mAb recognizing epitope B (called B2), were able to induce cell aggregation, but this effect was not exerted by mAb specific to site C and by a subgroup against epitope B (called B1). Moreover, although anti-epitope C and anti-epitope B1 mAb did not trigger aggregation, those mAb blocked aggregation induced by anti-epitope A or B2 mAb. In addition, anti-epitope A mAb blocked B2-induced aggregation, and conversely, anti-epitope B2 mAb blocked A-induced aggregation. Further evidence for multiple VLA-4 functions is that anti-Fn and anti-VCAM-1 antibodies inhibited binding to Fn or to VCAM-1, respectively, but did not affect VLA-4-mediated aggregation. In summary, we have demonstrated that there are at least three different VLA-4-mediated adhesion functions, we have defined three distinct VLA-4 epitopes, and we have correlated these epitopes with the different functions of VLA-4. C1 CTR INVEST BIOL,E-28006 MADRID,SPAIN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,BOSTON,MA 02115. BIOGEN INC,CAMBRIDGE,MA 02142. RP PULIDO, R (reprint author), UNIV AUTONOMA MADRID,HOSP PRINCESA,SECC INMUNOL,DIEGO DE LEON 62,E-28006 MADRID,SPAIN. RI Campanero, Miguel/A-4052-2013; Garcia Pardo, Angeles/G-5987-2015; Sanchez-Madrid, Francisco/M-7889-2016 OI Campanero, Miguel/0000-0003-1410-8621; Garcia Pardo, Angeles/0000-0001-5577-2954; Sanchez-Madrid, Francisco/0000-0001-5303-0762 FU NIGMS NIH HHS [GM 38903] NR 35 TC 248 Z9 249 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 JUN 5 PY 1991 VL 266 IS 16 BP 10241 EP 10245 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP086 UT WOS:A1991FP08600039 PM 1709929 ER PT J AU LANIER, SM DOWNING, S DUZIC, E HOMCY, CJ AF LANIER, SM DOWNING, S DUZIC, E HOMCY, CJ TI ISOLATION OF RAT GENOMIC CLONES ENCODING SUBTYPES OF THE ALPHA-2-ADRENERGIC RECEPTOR - IDENTIFICATION OF A UNIQUE RECEPTOR SUBTYPE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MUSCARINIC ACETYLCHOLINE-RECEPTOR; ALPHA-2 ADRENOCEPTOR HETEROGENEITY; BETA-ADRENERGIC-RECEPTOR; H-3 RAUWOLSCINE; ALPHA-2B-ADRENOCEPTOR SUBTYPES; COMPLEMENTARY-DNA; MOLECULAR-CLONING; CELL LINE; EXPRESSION; BINDING AB Alpha-2-Adrenergic receptors (alpha-2-AR) exist as subtypes that are expressed in a tissue-specific manner and differ in 1) their ligand recognition properties, 2) their extent of receptor protein glycosylation, and possibly 3) their mechanism of signal transduction. Genomic or cDNA clones encoding three receptor subtypes have been characterized; however, both functional and radioligand binding studies in rodents suggest the existence of a fourth receptor subtype. To isolate the rat genes encoding receptor subtypes we screened a rat genomic library with an oligonucleotide probe encompassing the third membrane span of the human C-4 alpha-2-AR. Two intronless rat genes were isolated that encode distinct receptor subtypes (RG10, RG20). RG10 and RG20 encode proteins of 458 and 450 amino acids, respectively, that are 56% homologous and possess the structural features expected of this class of membrane-bound receptors. RG10 identifies a mRNA species of approximately 2500 nucleotides that is found primarily in brain, whereas RG20 identifies a larger mRNA species (approximately 4000 nucleotides) that is found in several tissues including brain, kidney, and salivary gland. RG10 is 88% homologous to the human C-4-alpha-2-AR and exhibits similar binding properties ([H-3]rauwolscine K(D) = 0.7 +/- 0.3 nM) as determined following transient expression of the receptor in COS-1 cells. RG20 exhibits ligand binding properties distinct from the three receptor subtypes identified by molecular cloning. Saturation binding studies indicate an affinity constant of 15 +/- 1.2 nM for the alpha-2-AR antagonist [H-3]rauwolscine, a value 6-20 times higher than that observed for the three cloned receptor subtypes. In competition binding studies the potency order of competing ligands for RG20 is phentolamine > idazoxan > yohimbine > rauwolscine > prazosin. Of the three previously cloned alpha-2-AR, RG20 is most closely related to the human C-10-alpha-2-AR (89% homology) and is also capable of mediating adenylylcyclase inhibition as determined following its stable expression in NIH-3T3 fibroblasts. However, in contrast to RG20, [H-3]rauwolscine exhibits a K(D) of 2 nM for the C-10 receptor, and the potency order for competing ligands is rauwolscine greater-than-or-equal-to yohimbine > idazoxan > phentolamine > prazosin. RG20 and C-10 are also distinguished by their affinity for SKF-10478 (RG20 K(i) = 531 nM, C-10 K(i) = 101 nm), a compound that may functionally distinguish pre- and postsynaptic alpha-2-AR. These data suggest that RG20 represents a fourth alpha-2-AR subtype distinct from the known alpha-2-A-C receptor subtypes. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CELLULAR & MOLEC RES LAB,CARDIAC UNIT,JACKSON 13,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-19259]; NINDS NIH HHS [NS-24821] NR 70 TC 248 Z9 250 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1991 VL 266 IS 16 BP 10470 EP 10478 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP086 UT WOS:A1991FP08600072 PM 1645350 ER PT J AU TSAI, AYM ITOH, M STREULI, M THAI, T SAITO, H AF TSAI, AYM ITOH, M STREULI, M THAI, T SAITO, H TI ISOLATION AND CHARACTERIZATION OF TEMPERATURE-SENSITIVE AND THERMOSTABLE MUTANTS OF THE HUMAN RECEPTOR-LIKE PROTEIN TYROSINE PHOSPHATASE LAR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BACTERIOPHAGE-T7 RNA-POLYMERASE; LEUKOCYTE COMMON ANTIGEN; AMINO-ACID REPLACEMENTS; HIGH-LEVEL EXPRESSION; ESCHERICHIA-COLI; LAMBDA-REPRESSOR; CLONED GENES; MUTATIONS; CLONING; MEMBER AB Human LAR is a transmembrane receptor-like protein whose cytoplasmic region contains two tandemly duplicated domains homologous to protein tyrosine phosphatases (PTPases). Whereas the membrane-proximal domain I has enzymatic activity, the membrane-distal domain II has no apparent catalytic activity but seems to have a regulatory function. In order to study structure-function relationships of the LAR PTPase, LAR domain I was expressed in Escherichia coli, and mutants that have reduced catalytic activity or reduced thermostability were isolated and characterized. We isolated 18 unique hydroxylamine-induced missense mutations in the LAR domain I segment, of which three were temperature-sensitive. Five additional temperature-sensitive mutations were isolated using N-methyl-N'-nitro-N-nitrosoguanidine. All eight temperature-sensitive mutations are confined within a short segment of the LAR domain I sequence between amino acid positions 1329 and 1407. To examine whether this region is particularly prone to temperature-sensitive mutations, tyrosine at aminoacid position 1379 was changed to a phenylalanine by oligonucleotide-directed mutagenesis. This mutant, Y1379-F, was indeed temperature-sensitive. We also isolated a revertant of a temperature-sensitive mutant. The revertant contained a second-site mutation (C1446-Y) that suppresses several temperature-sensitive mutations and also enhances the folding of LAR protein produced in E. coli. C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL, 44 BINNEY ST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH DENT MED, DEPT PERIODONTOL, CAMBRIDGE, MA 02138 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA51132]; NIAID NIH HHS [AI-26598] NR 34 TC 59 Z9 60 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1991 VL 266 IS 16 BP 10534 EP 10543 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP086 UT WOS:A1991FP08600081 PM 1645351 ER PT J AU MYERS, MG BACKER, JM SIDDLE, K WHITE, MF AF MYERS, MG BACKER, JM SIDDLE, K WHITE, MF TI THE INSULIN-RECEPTOR FUNCTIONS NORMALLY IN CHINESE-HAMSTER OVARY CELLS AFTER TRUNCATION OF THE C-TERMINUS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE-ACTIVITY; MONOCLONAL-ANTIBODIES; BETA-SUBUNIT; PROTEIN-KINASE; PHOSPHORYLATION; AUTOPHOSPHORYLATION; REPLACEMENT; BINDING; SITES; ENDOCYTOSIS AB We studied the structure and function of the human insulin receptor (IR) and a mutant which lacked the last 43 amino acids of the beta-subunit (IR-DELTA-ct). This deletion removed tyrosine (Tyr1322, Tyr1316) and threonine (Thr1336) phosphorylation sites. In Chinese hamster ovary (CHO) cells, insulin binding to the mutant receptor was normal, and [S-35]methionine labeling indicated that both the IR and IR-DELTA-ct were processed normally; however, the beta-subunit of IR-DELTA-ct was 5 kDa smaller than that of the IR. The time course of insulin-stimulated autophosphorylation of the partially purified IR-DELTA-ct was normal, but the maximum autophosphorylation was reduced 20-30%. Tryptic phosphopeptide mapping confirmed the absence of the C-terminal phosphorylation sites and indicated that phosphorylation of the regulatory region (Tyr1146, Tyr1150, Tyr1151) occurred normally; kinase activity of the IR and IR-DELTA-ct was activated normally by insulin-stimulated autophosphorylation. In the intact CHO cells, insulin-stimulated serine and threonine phosphorylation of the IR-DELTA-ct was reduced 20%, suggesting that most Ser/Thr phosphorylation sites are located outside of the C terminus. During insulin stimulation, the wild-type and mutant insulin receptor activated the phosphatidylinositol 3-kinase. Moreover, insulin itself or human-specific anti-insulin receptor antibodies stimulated glycogen and DNA synthesis equally in both CHO/IR and CHO/IR-DELTA-ct cells. These data suggest that the C terminus plays a minimal role in IR function and signal transmission in CHO cells. C1 HARVARD UNIV,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK38712, DK36836, DK08126] NR 31 TC 83 Z9 83 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 JUN 5 PY 1991 VL 266 IS 16 BP 10616 EP 10623 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP086 UT WOS:A1991FP08600092 PM 1645354 ER PT J AU ODA, A DRUKER, B SMITH, M SALZMAN, EW AF ODA, A DRUKER, B SMITH, M SALZMAN, EW TI ASSOCIATION OF THE TYROSINE KINASE PP60SRC WITH THE CORE CYTOSKELETON AND SLOW TYROSINE PHOSPHORYLATION ARE REGULATED BY AGGREGATION AGGLUTINATION SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR MOLEC BIOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 730 EP 730 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96600242 ER PT J AU LU, HR GOLD, HK WU, ZM DECOCK, F PAUWELS, P COLLEN, D AF LU, HR GOLD, HK WU, ZM DECOCK, F PAUWELS, P COLLEN, D TI ACCELERATION AND PERSISTENCE OF RT-PA INDUCED ARTERIAL EVERSION GRAFT RECANALIZATION WITH A SINGLE BOLUS INJECTION OF F(AB)2 FRAGMENTS OF THE ANTIPLATELET GPIIB SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 TAKEDA CHEM IND LTD,CTR THROMBOSIS & VASC RES,OSAKA 532,JAPAN. TAKEDA CHEM IND LTD,EXPTL CARDIOL LAB,OSAKA 532,JAPAN. TAKEDA CHEM IND LTD,DEPT HISTOPATHOL,OSAKA 532,JAPAN. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 788 EP 788 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96600399 ER PT J AU ODA, A DALEY, JF SMITH, M KANG, J SALZMAN, EW AF ODA, A DALEY, JF SMITH, M KANG, J SALZMAN, EW TI NON-EQUIVALENCE OF GPIIBIIIA COMPLEXES WITH NI2+-INHIBITABLE MN2+-PERMEABLE CALCIUM CHANNELS OF BLOOD-PLATELETS SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 BETH ISRAEL HOSP,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 835 EP 835 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96600525 ER PT J AU CAREW, JA QUINN, SM LYNCH, DC AF CAREW, JA QUINN, SM LYNCH, DC TI THE O-LINKED CARBOHYDRATES OF VONWILLEBRAND-FACTOR MODULATE ITS BINDING TO GLYCOPROTEIN-1B SO THROMBOSIS AND HAEMOSTASIS 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 F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 841 EP 841 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96600540 ER PT J AU TAKADA, Y MURPHY, E PIL, P CHEN, C GINSBERG, MH HEMLER, ME AF TAKADA, Y MURPHY, E PIL, P CHEN, C GINSBERG, MH HEMLER, ME TI MOLECULAR-CLONING AND EXPRESSION OF THE CDNA FOR ALPHA-3 CHAIN OF HUMAN ENDOTHELIAL-CELL VLA-3 (ALPHA-3-BETA-1), AN INTEGRIN RECEPTOR FOR FIBRONECTIN, LAMININ AND COLLAGEN SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 Scripps Res Inst, RES INST, COMMITTEE VASC BIOL, LA JOLLA, CA 92037 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR VIROL, BOSTON, MA 02115 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 876 EP 876 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96600631 ER PT J AU ARKIN, CF GANDA, OP AF ARKIN, CF GANDA, OP TI HYPERFIBRINOGENEMIA IN DIABETES-MELLITUS - ITS RELATIONSHIP TO VASCULAR COMPLICATIONS AND OTHER CLINICAL FINDINGS IN 116 PATIENTS SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 NEW ENGLAND DEACONESS HOSP,DEPT PATHOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 987 EP 987 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96601044 ER PT J AU ODA, A DALEY, JF SMITH, M KANG, J SALZMAN, EW AF ODA, A DALEY, JF SMITH, M KANG, J SALZMAN, EW TI CAPACITATIVE CALCIUM ENTRY IN THE ACTIVATION OF PHOSPHOLIPASE-C AND GRANULE SECRETION IN HUMAN BLOOD-PLATELETS SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INST TUMOR IMMUNOL,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT SURG,BOSTON,MA 02215. NR 0 TC 1 Z9 1 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 1012 EP 1012 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96601135 ER PT J AU JAHROUDI, N HAQUE, Z LYNCH, DC AF JAHROUDI, N HAQUE, Z LYNCH, DC TI TRANSCRIPTIONAL REGULATION OF VONWILLEBRAND-FACTOR GENE-EXPRESSION SO THROMBOSIS AND HAEMOSTASIS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 5 PY 1991 VL 65 IS 6 BP 1129 EP 1129 PG 1 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA FZ966 UT WOS:A1991FZ96601561 ER PT J AU HUA, QX WEISS, MA AF HUA, QX WEISS, MA TI COMPARATIVE 2D-NMR STUDIES OF HUMAN INSULIN AND DES-PENTAPEPTIDE INSULIN - SEQUENTIAL RESONANCE ASSIGNMENT AND IMPLICATIONS FOR PROTEIN DYNAMICS AND RECEPTOR RECOGNITION SO BIOCHEMISTRY LA English DT Article ID CHAIN DES-(B30) INSULIN; TWO-DIMENSIONAL H-1-NMR; TYROSINE KINASE DOMAIN; SHORTENED INSULIN; INVITRO POTENCY; B26-30 INSULIN; PHOTO-CIDNP; SIDE-CHAIN; RESOLUTION; HEXAMER AB The solution structure and dynamics of human insulin are investigated by 2D H-1 NMR spectroscopy in reference to a previously analyzed analogue, des-pentapeptide(B26-B30) insulin (DPI; Hua, Q. X., & Weiss, M. A. (1990) Biochemistry 29, 10545-10555). This spectroscopic comparison is of interest since (i) the structure of the C-terminal region of the B-chain has not been determined in the monomeric state and (ii) the role of this region in binding to the insulin receptor has been the subject of long-standing speculation. The present NMR studies are conducted in the presence of an organic cosolvent (20% acetic acid), under which conditions both proteins are monomeric and stably folded. Complete sequential assignment of human insulin is obtained and leads to the following conclusions. (1) The secondary structure of the insulin monomer (three alpha-helices and B-chain beta-turn) is similar to that observed in the 2-Zn crystal state. (2) The folding of DPI is essentially the same as the corresponding portion of intact insulin, in accord with the similarities between their respective crystal structures. However, differences between insulin and DPI are observed in the extent of conformational broadening of amide resonances, indicating that the presence or absence of residues B26-B30 influences the overall dynamics of the protein on the millisecond time scale. (3) Residues B24-B28 adopt an extended configuration in the monomer and pack against the hydrophobic core as in crystallographic dimers; residues B29 and B30 are largely disordered. This configuration differs from that described in a more organic milieu (35% acetonitrile; Kline, A. D., & Justice, R. M., Jr. (1990) Biochemistry 29, 2906-2913), suggesting that the conformation of insulin in the latter study may have been influenced by solvent composition. (4) The insulin fold is shown to provide a model for collective motions in a protein with implications for the mechanism of protein-protein recognition. To our knowledge, this paper describes the first detailed analysis of a protein NMR spectrum under conditions of extensive conformational broadening. Such an analysis is made possible in the present case by comparative study of an analogue (DPI) with more tractable spectroscopic properties. 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 S10 RR04862-01] NR 51 TC 115 Z9 118 U1 0 U2 7 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 4 PY 1991 VL 30 IS 22 BP 5505 EP 5515 DI 10.1021/bi00236a025 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP306 UT WOS:A1991FP30600025 PM 2036420 ER PT J AU MAHLER, ME CUMMINGS, JL AF MAHLER, ME CUMMINGS, JL TI BEHAVIORAL NEUROLOGY OF MULTIINFARCT DEMENTIA SO ALZHEIMER DISEASE & ASSOCIATED DISORDERS LA English DT Article ID CEREBRAL BLOOD-FLOW; ALZHEIMERS-DISEASE; VASCULAR DEMENTIA; PERSONALITY ALTERATIONS; MULTIINFARCT DEMENTIA; BINSWANGER TYPE; MOOD DISORDERS; LANGUAGE; STROKE; PERFORMANCE AB Multi-infarct dementia (MID) is a heterogeneous entity in which a variety of cerebrovascular disorders leads to intellectual impairment. A variety of patterns of behavioral changes may be observed in MID, depression, psychosis, and personality change are common. The neurobehavioral syndromes of MID are determined by the specific arteries involved and the location and extent of tissue infarction. C1 W LOS ANGELES VET AFFAIRS MED CTR, NEUROBEHAV UNIT B111, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA 90024 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT PSYCHIAT & BIOBEH SCI, LOS ANGELES, CA 90024 USA. NR 52 TC 29 Z9 29 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0893-0341 J9 ALZ DIS ASSOC DIS JI Alzheimer Dis. Assoc. Dis. PD SUM PY 1991 VL 5 IS 2 BP 122 EP 130 DI 10.1097/00002093-199100520-00009 PG 9 WC Clinical Neurology; Pathology SC Neurosciences & Neurology; Pathology GA GU430 UT WOS:A1991GU43000009 PM 2059404 ER PT J AU HAINES, JL AF HAINES, JL TI THE GENETICS OF ALZHEIMER-DISEASE - A TEASING PROBLEM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID BETA-PROTEIN GENE; 1ST-DEGREE RELATIVES; CLINICAL-FEATURES; COLOR-BLINDNESS; LINKAGE; DEMENTIA; RISK; HETEROGENEITY; DISORDER; PEDIGREE C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP HAINES, JL (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BLDG 149,6TH FLOOR,13TH ST,BOSTON,MA 02114, USA. RI Haines, Jonathan/C-3374-2012 NR 44 TC 18 Z9 18 U1 1 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JUN PY 1991 VL 48 IS 6 BP 1021 EP 1025 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA FP092 UT WOS:A1991FP09200001 PM 2035522 ER PT J AU IONASESCU, VV TROFATTER, J HAINES, JL SUMMERS, AM IONASESCU, R SEARBY, C AF IONASESCU, VV TROFATTER, J HAINES, JL SUMMERS, AM IONASESCU, R SEARBY, C TI HETEROGENEITY IN X-LINKED RECESSIVE CHARCOT-MARIE-TOOTH NEUROPATHY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DNA PROBES; LINKAGE; LOCALIZATION; DISEASE; CARRIERS AB Three families presenting with X-linked recessive Charcot-Marie-Tooth neuropathies (CMT) were studied both clinically and genetically. The disease phenotype in family 1 was typical of CMT type 1, except for an infantile onset; two of five affected individuals were mentally retarded, and obligate-carrier females were unaffected. Families 2 and 3 showed distal atrophy with weakness, juvenile onset, and normal intelligence. Motor-nerve conduction velocities were significantly slowed, and electromyography data were consistent with denervation in affected CMT males in all three families. Thirty X-linked RFLPs were tested for linkage studies against the CMT disease loci. Family 1 showed tight linkage (recombination fraction [theta] = 0) to Xp22.2 markers DXS16, DXS143, and DXS43, with peak lod scores of 1.75, 1.78, and 2.04, respectively. A maximum lod score of 3.48 at DXS16 (theta = 0) was obtained by multipoint linkage analysis of the map DXS143-DXS16-DXS43. In families 2 and 3 there was suggestion of tight linkage (theta = 0) to Xq26 markers DXS86, DXS144, and DXS105, with peak lod scores of 2.29, 1.33, and 2.32, respectively. The combined maximum multipoint lod score of 1.81 at DXS144 (theta = 0) for these two families occurred in the map DXS10-DXS144-DXS51-DXS105-DXS15-DXS52. A joint homogeneity analysis including both regions (Xp22.2 and Xq26-28) provided evidence against homogeneity (chi-2 = 9.12, P < .005). No linkage to Xp11.12-q22 markers was observed, as was reported for X-linked dominant CMT and the Cowchock CMT variant. Also, the chromosomes 1 and 17 CMT loci were excluded by pairwise linkage analysis in all three families. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. N YORK GEN HOSP,DEPT GENET,N YORK M2K 1E1,ONTARIO,CANADA. RP IONASESCU, VV (reprint author), UNIV IOWA HOSP & CLIN,DEPT PEDIAT,PEDIAT GENET MUSCLE LAB,IOWA CITY,IA 52242, USA. RI Haines, Jonathan/C-3374-2012 NR 22 TC 64 Z9 64 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD JUN PY 1991 VL 48 IS 6 BP 1075 EP 1083 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA FP092 UT WOS:A1991FP09200008 PM 1674639 ER PT J AU WARPINSKI, JR BUSH, RK AF WARPINSKI, JR BUSH, RK TI LATEX HYPERSENSITIVITY SO AMERICAN JOURNAL OF MEDICINE LA English DT Letter C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP WARPINSKI, JR (reprint author), INTERMT ALLERGY & ASTHMA CLIN,SALT LAKE CITY,UT, USA. NR 4 TC 2 Z9 2 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD JUN PY 1991 VL 90 IS 6 BP 769 EP 769 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FR832 UT WOS:A1991FR83200024 PM 2042700 ER PT J AU TODD, R DONOFF, BR CHIANG, T CHOU, MY ELOVIC, A GALLAGHER, GT WONG, DTW AF TODD, R DONOFF, BR CHIANG, T CHOU, MY ELOVIC, A GALLAGHER, GT WONG, DTW TI THE EOSINOPHIL AS A CELLULAR SOURCE OF TRANSFORMING GROWTH FACTOR-ALPHA IN HEALING CUTANEOUS WOUNDS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID MESSENGER-RNA; TGF-ALPHA; INDUCTION; CELLS; MACROPHAGES AB Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha) are known to promote the healing of epithelial wounds. Eosinophils are present in healing wounds and have recently been shown to be capable of producing TGF-alpha. This investigation was done to determine if eosinophils infiltrated into healing wounds are capable of expressing this cytokine. Using the rabbit cutaneous open wound model, the study found that the eosinophil is one of the predominant cell types in the healing wound, beginning from the seventh day and thereafter. Most surprisingly, the majority of the eosinophils present in the healing wound were found to contain TGF-alpha mRNA and protein by in situ hybridization and immunohistochemistry. Thus it is proposed that the delivery of TGF-alpha by eosinophils to epithelial wound healing sites represents a normal body mechanism whereby this multifunctional cytokine can accelerate the wound healing process. C1 HARVARD UNIV,SCH DENT MED,DEPT ORAL MED & ORAL PATHOL,188 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,DEPT PROSTHET DENT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NIDCR NIH HHS [K16 DE 00275, DE-08680] NR 21 TC 99 Z9 101 U1 0 U2 1 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1991 VL 138 IS 6 BP 1307 EP 1313 PG 7 WC Pathology SC Pathology GA FR746 UT WOS:A1991FR74600003 PM 2053590 ER PT J AU ROLLINS, BJ POBER, JS AF ROLLINS, BJ POBER, JS TI INTERLEUKIN-4 INDUCES THE SYNTHESIS AND SECRETION OF MCP-1-JE BY HUMAN ENDOTHELIAL-CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Note ID TUMOR-NECROSIS-FACTOR; SMOOTH-MUSCLE CELLS; GENE-EXPRESSION; GROWTH-FACTOR; STIMULATORY FACTOR; HUMAN-MONOCYTES; IFN-GAMMA; B-CELLS; IA-ANTIGENS; IL-4 AB The authors have demonstrated that human interleukin-4 (IL-4) induces increased expression of the mRNA encoding the monocyte-specific chemoattractant and activator, MCP-1/JE, in human endothelial cells (EC). In addition, treatment of ECs with IL-4 resulted in the synthesis and secretion of MCP-1/JE protein. While IL-4 did not significantly influence the induced expression of MCP-1/JE mRNA by interleukin-1 (IL-1) or tumor necrosis factor, concomitant treatment with IL-4 and IL-1 caused more secretion of MCP-1/JE protein than either cytokine alone. These results suggest that EC-produced MCP-1/JE may mediate some of IL-4's effects on monocyte physiology in vivo, including IL-4's anti-tumor properties. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROLLINS, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA53091]; NHLBI NIH HHS [HL36003] NR 36 TC 148 Z9 149 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1991 VL 138 IS 6 BP 1315 EP 1319 PG 5 WC Pathology SC Pathology GA FR746 UT WOS:A1991FR74600004 PM 2053591 ER PT J AU CHIANG, YY TAKEBAYASHI, S OBERLEY, TD AF CHIANG, YY TAKEBAYASHI, S OBERLEY, TD TI INVITRO ANALYSIS OF EXTRACELLULAR-MATRIX PRODUCTION BY PORCINE GLOMERULAR MESANGIAL AND VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID LAMININ; FIBRONECTIN; CULTURE; GROWTH; MODULATION; COMPONENTS; NEURONS AB Proliferation potential and extracellular matrix production were compared in cultured porcine glomerular mesangial cells and arterial and venous smooth muscle cells. Mesangial and arterial smooth muscle cells proliferated more rapidly than venous smooth muscle cells. In immunofluorescence studies, mesangial and arterial smooth muscle cells stained strongly for collagen types I, III, and V; venous smooth muscle showed weaker staining for collagens III and V. Total collagen synthesis in cultured mesangial and arterial smooth muscle cells was lower than in venous smooth muscle cells. Electrophoretic analysis showed type I collagen predominated in all cell types, although levels were highest in mesangial and arterial smooth muscle cells. Collagen V (alpha-3) occurred only in venous smooth muscle cells. Mesangial and arterial smooth muscle cells showed cell-bound fibronectin and laminin, which also were secreted into the medium. Venous smooth muscle cells secreted fibronectin, but all laminin was cell bound. The findings suggest a strong similarity between mesangial and arterial smooth muscle cells. C1 UNIV WISCONSIN,DEPT PATHOL,MADISON,WI 53706. FUKUOKA UNIV,DEPT PATHOL 2,FUKUOKA 81401,JAPAN. RP CHIANG, YY (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 39 TC 12 Z9 12 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1991 VL 138 IS 6 BP 1349 EP 1358 PG 10 WC Pathology SC Pathology GA FR746 UT WOS:A1991FR74600007 PM 2053592 ER PT J AU PALMER, WE CHEW, FS AF PALMER, WE CHEW, FS TI RENAL ONCOCYTOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 4 TC 1 Z9 1 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUN PY 1991 VL 156 IS 6 BP 1144 EP 1144 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM539 UT WOS:A1991FM53900002 PM 2028856 ER PT J AU MCLOUD, TC FLOWER, CDR AF MCLOUD, TC FLOWER, CDR TI IMAGING THE PLEURA - SONOGRAPHY, CT, AND MR IMAGING SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Review ID PERCUTANEOUS CATHETER DRAINAGE; COMPUTED-TOMOGRAPHY; ROUNDED ATELECTASIS; THORACIC EMPYEMA; CHEST-WALL; MESOTHELIOMA; DIAGNOSIS; EFFUSION; ULTRASOUND; DISEASE AB A variety of imaging techniques can be used to evaluate the pleura and the pleural space. Standard radiographs are the most common. In this article, however, we review the use of three other imaging techniques: sonography, CT, and MR imaging. Sonography allows easy identification of pleural fluid and loculation and differentiation from pleural masses; CT is best for characterizing location and composition of pleural masses; MR is somewhat limited, but is best for imaging superior sulcus carcinoma. C1 ADDENBROOKES HOSP,DEPT DIAGNOST RADIOL,CAMBRIDGE CB2 2QQ,ENGLAND. RP MCLOUD, TC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114, USA. NR 66 TC 112 Z9 117 U1 1 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUN PY 1991 VL 156 IS 6 BP 1145 EP 1153 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM539 UT WOS:A1991FM53900003 PM 2028857 ER PT J AU LEE, MJ SAINI, S BRINK, JA HAHN, PF SIMEONE, JF MORRISON, MC RATTNER, D MUELLER, PR AF LEE, MJ SAINI, S BRINK, JA HAHN, PF SIMEONE, JF MORRISON, MC RATTNER, D MUELLER, PR TI TREATMENT OF CRITICALLY ILL PATIENTS WITH SEPSIS OF UNKNOWN CAUSE - VALUE OF PERCUTANEOUS CHOLECYSTOSTOMY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID ACUTE CHOLECYSTITIS; GALLBLADDER; SCINTIGRAPHY; ASPIRATION; DIAGNOSIS AB Because of the difficulty in diagnosing acute cholecystitis in critically ill patients with severe intercurrent illness by clinical and imaging methods or percutaneous aspiration of the gallbladder, a trial of percutaneous cholecystostomy was performed in 24 patients in the intensive-care unit with persistent, unexplained sepsis after a complete clinical, laboratory, and radiologic search showed no alternative source of infection. Persistent high fevers, despite antibiotic therapy, were present in all patients, with elevated WBC count in 18 patients, vague abdominal tenderness in 11, and septic shock requiring vasopressors in 15. Sonographically, all patients had distended, spherical gallbladders, six had gallstones, eight had wall thickening, three had pericholecystic fluid, and four had Murphy's sign. All patients were seen by a senior abdominal surgeon, who agreed to a trial of percutaneous cholecystostomy. Fourteen patients (58%) responded to percutaneous cholecystostomy, as evidenced by a decrease in WBC count, defervescence, and the ability to be weaned off vasopressors. Bile cultures were positive in four patients. Ten patients (42%) did not respond to percutaneous cholecystostomy; five eventually died of unrelated causes. A respiratory source of infection was eventually found in three of these 10 patients, with no proved source of infection in the remainder. No complications related to catheter insertion occurred in this group of patients. Bile leaks occurred in two patients when the percutaneous cholecystostomy catheter was removed, but without serious consequence. Our experience suggests that a lower threshold for performing percutaneous cholecystostomy in this difficult clinical subset of patients is worthwhile. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. NR 16 TC 50 Z9 51 U1 0 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUN PY 1991 VL 156 IS 6 BP 1163 EP 1166 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM539 UT WOS:A1991FM53900006 PM 2028859 ER PT J AU THRALL, JH WITTENBERG, J AF THRALL, JH WITTENBERG, J TI RADIOLOGY SUMMIT 1990 - SPECIALIZATION IN RADIOLOGY - TRENDS, IMPLICATIONS, AND RECOMMENDATIONS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material RP THRALL, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 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 JUN PY 1991 VL 156 IS 6 BP 1273 EP 1276 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM539 UT WOS:A1991FM53900034 PM 2028877 ER PT J AU ZUKERBERG, LR HARRIS, NL YOUNG, RH AF ZUKERBERG, LR HARRIS, NL YOUNG, RH TI CARCINOMAS OF THE URINARY-BLADDER SIMULATING MALIGNANT-LYMPHOMA - A REPORT OF 5 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE URINARY BLADDER; TRANSITIONAL CELL CARCINOMA; LYMPHOEPITHELIAL-LIKE CARCINOMA ID LYMPHOEPITHELIOMA-LIKE CARCINOMA; LYMPHOCYTES-T; STROMA; TRACT; LUNG AB We report five carcinomas of the urinary bladder, four of them transitional cell carcinomas and one undifferentiated carcinoma, with unusual features that have received little or no comment in the literature and may be the cause of diagnostic difficulty because of their possible confusion with malignant lymphoma. Four patients were male and one female. They ranged from 61 to 76 years of age. Three tumors from these patients had a prominent (2 cases) or massive (1 case) lymphoid infiltrate that partially obscured the invasive carcinoma in two cases and largely obscured it in the third case, which closely resembled a lymphoepithelioma. The diagnosis of malignant lymphoma was only excluded with confidence in the last case after thorough immunohistochemical study. The lymphoid infiltrate was composed of numerous T-cells (UCHL-1 and Leu 22 positive) and polytypic plasma cells with admixed eosinophils; occasional germinal centers were present in one case. The tumors were deeply invasive in two patients, one of whom is alive with no evidence of disease 4 years after treatment with chemotherapy and radiation therapy; the other two cases are too recent for meaningful follow-up. Two other transitional cell carcinomas had diffuse patterns that simulated lymphoma or plasmacytoma. Recognition of these patterns of vesical carcinoma is important in order to avoid the misdiagnosis of the very rare malignant lymphoma of the urinary bladder. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LAB,WARREN 2,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 24 TC 88 Z9 97 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 JUN PY 1991 VL 15 IS 6 BP 569 EP 576 DI 10.1097/00000478-199106000-00005 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA FM530 UT WOS:A1991FM53000005 PM 2031529 ER PT J AU KILLICK, KA AF KILLICK, KA TI ANALYSIS OF GLUTATHIONE-S-TRANSFERASE FROM HUMAN LIVER BY ISOELECTRIC-FOCUSING IN A UREA MINIGEL SYSTEM SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID DRUG-RESISTANCE; BINDING; FORMS 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 15 TC 7 Z9 7 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 JUN PY 1991 VL 195 IS 2 BP 255 EP 261 DI 10.1016/0003-2697(91)90325-N PG 7 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FP885 UT WOS:A1991FP88500010 PM 1750675 ER PT J AU KASSEL, DB MUSSELMAN, BD SMITH, JA AF KASSEL, DB MUSSELMAN, BD SMITH, JA TI PRIMARY STRUCTURE DETERMINATION OF PEPTIDES AND ENZYMATICALLY DIGESTED PROTEINS USING CAPILLARY LIQUID-CHROMATOGRAPHY MASS-SPECTROMETRY AND RAPID LINKED-SCAN TECHNIQUES SO ANALYTICAL CHEMISTRY LA English DT Article ID FAST-ATOM-BOMBARDMENT; ELECTROSPRAY IONIZATION; COLLISIONAL ACTIVATION; PERFORMANCE; MICROBORE AB Primary protein sequences were determined for both peptides and enzymatically digested proteins by rapid linked-scan (B/E) liquid chromatography/mass spectrometry/mass spectrometry (LC/MS/MS) at the low-picomole level (10-50 pmol). During the course of a single LC/MS/MS analysis, we demonstrated that it is possible to generate interpretable collison-induced dissociation spectra of the eluting proteolytic peptides. Molecular weights of tryptic peptides were established by using 1/10 of the protein digest by operating in the capillary LC/frit-FABMS mode. Peptides exhibiting the strongest MH+ ions were then selected for subsequent LC/MS/MS analysis (typically 1/5 of the remaining protein digest). Elution times for each chromatographic peak were generally > 30 s. It was therefore possible to obtain a minimum of six B/E fast linked-scan spectra during the course of elution of each peptide component. Typically, B/E linked scans of the greatest ion abundance (obtained at the chromatographic peak maximum) were averaged to enhance the signal/noise ratio at these low-picomole levels. Unit resolution was observed for product ions below m/z 1000. Rapid linked scanning by LC/frit-FABMS/MS provided mass assignments for product ions within 0.2-0.3 amu of theoretical values. Side-chain fragment ions (w(n) and d(n)) were also observed, which allowed for the differentiation of isobaric amino acids (e.g., leucine and isoleucine). Examples of the application of this fast linked-scan technique to LC/MS/MS are presented for complex mixtures of unknown peptides and the tryptic digestion of phosphorylated beta-casein. C1 JEOL USA INC,PEABODY,MA 01960. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU PHS HHS [G-2321] NR 31 TC 26 Z9 26 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0003-2700 J9 ANAL CHEM JI Anal. Chem. PD JUN 1 PY 1991 VL 63 IS 11 BP 1091 EP 1097 DI 10.1021/ac00011a008 PG 7 WC Chemistry, Analytical SC Chemistry GA FN812 UT WOS:A1991FN81200010 PM 1883067 ER PT J AU COTE, CJ ROLF, N LIU, LMP GOUDSOUZIAN, NG RYAN, JF ZASLAVSKY, A GORE, R TODRES, ID VASSALLO, S POLANER, D ALIFIMOFF, JK AF COTE, CJ ROLF, N LIU, LMP GOUDSOUZIAN, NG RYAN, JF ZASLAVSKY, A GORE, R TODRES, ID VASSALLO, S POLANER, D ALIFIMOFF, JK TI A SINGLE-BLIND STUDY OF COMBINED PULSE OXIMETRY AND CAPNOGRAPHY IN CHILDREN SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, PEDIATRIC; ANESTHESIA COMPLICATIONS, DESATURATION; HYPERCARBIA; ANESTHESIA TECHNIQUES, TRACHEAL INTUBATION; MONITORING, PULSE OXIMETRY; CAPNOGRAPHY ID CARBON-DIOXIDE; ESOPHAGEAL INTUBATION; ENDOTRACHEAL-TUBE AB This single-blind study examined four levels of monitoring in 402 pediatric cases. Patients were randomly assigned to one of four groups: 1) oximeter and capnograph; 2) only oximeter; 3) only capnograph; or 4) neither oximeter nor capnograph data available to the anesthesia team. An anesthesiologist, not involved in patient care, observed all cases and continuously recorded hemoglobin oxygen saturation (Sp(o2)), ECG, expired CO2, and the oximeter plethysmographic output. Mean age, weight, ASA physical status, airway management (mask or endotracheal tube), and anesthetic technique were similar in each group. Two-hundred sixty problems were documented in 153 patients. Fifty-nine events in 43 patients resulted in "major" desaturation (Sp(o2) less-than-or-equal-to 85% for greater-than-or-equal-to 30 s). Fifteen "major" canpnograph events (esophageal intubation, disconnection, accidental extubation, or obstructed end tracheal tube) were observed in 11 patients; 8 of these also developed varying degrees of desaturation. One-hundred thirty "minor" desaturation events (Sp(o2) less-than-or-equal-to 95% for greater-than-or-equal-to 60 s) and 79 "minor" capnograph events (hypercarbia or hypocarbia) were observed. A number of problems fulfilled criteria in multiple categories. Infants less-than-or-equal-to 6 months of age had the highest incidence of major desaturation events (18 of 65 [27%]) compared to toddlers 7-24 months of age or children > 24 months of age (P < 0.001). Blinding the oximeter data increased the number of patients (12 vs. 31) experiencing major desaturation events (P = 0.003); blinding the capnograph data altered neither the frequency of desaturation events nor the incidence of major capnograph events. Blinding the capnograph data increased the number of patients with minor capnograph events (22 vs. 47; P = 0.0026). More patients experienced multiple problems when neither capnograph nor oximeter data were available compared to when both were available (23 vs. 11; P = 0.04). We conclude: 1) The pulse oximeter is far superior to either the capnograph or clinical judgment in providing the earliest warning of desaturation events. 2) Capnography can provide an early warning to potentially life-threatening problems, but such problems often result in desaturation. 3) Capnography reduces the incidence of hypercarbia and hypocarbia. 4) Infants less-than-or-equal-to 6 months of age are at greatest risk for major desaturation and major capnograph events. 5) The number of problems observed can be significantly reduced when both monitors are used. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP COTE, CJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. OI Polaner, David/0000-0001-8716-6289 NR 12 TC 99 Z9 99 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 JUN PY 1991 VL 74 IS 6 BP 980 EP 987 PG 8 WC Anesthesiology SC Anesthesiology GA FR380 UT WOS:A1991FR38000003 PM 1904206 ER PT J AU HURFORD, WE LYNCH, KE STRAUSS, HW LOWENSTEIN, E ZAPOL, WM AF HURFORD, WE LYNCH, KE STRAUSS, HW LOWENSTEIN, E ZAPOL, WM TI MYOCARDIAL PERFUSION AS ASSESSED BY TL-201 SCINTIGRAPHY DURING THE DISCONTINUATION OF MECHANICAL VENTILATION IN VENTILATOR-DEPENDENT PATIENTS SO ANESTHESIOLOGY LA English DT Article DE HEART, BLOOD FLOW; LUNGS, RESPIRATORY FAILURE; VENTILATION, MECHANICAL, VENTILATOR DEPENDENCE ID CORONARY-ARTERY DISEASE; INTRA-THORACIC PRESSURE; ASSISTED VENTILATION; TL-201 SCINTIGRAPHY; LEFT-VENTRICLE; ELECTROCARDIOGRAPHY; DILATION; ISCHEMIA; CHARGES; SCANS AB Patients who cannot be separated from mechanical ventilation (MV) after an episode of acute respiratory failure often have co-existing coronary artery disease. The authors hypothesized that increased left ventricular (LV) wall stress during periods of spontaneous ventilation (SV) could alter myocardial perfusion in these patients. Using thallium-201 (201TI) myocardial scintigraphy, the authors studied the occurrence of myocardial perfusion abnormalities during periods of SV in 15 MV-dependent patients (nine women, six men; aged 71 +/- 7 yr, mean +/- SD). Fourteen of these patients were studied once with 201TI myocardial scintigraphy during intermittent mechanical ventilation (IMV) and again on another day, after at least 10 min of SV through a T-piece. One patient was studied during SV only. Thirteen of 14 of the patients (93%) studied during MV had abnormal patterns of initial myocardial 201TI uptake, but only 1 patient demonstrated redistribution of 201TI on delayed images. The remainder of the abnormalities observed during MV were fixed defects. SV produced significant alterations of myocardial 201TI distribution or transient LV dilation, or both, in 7 of the 15 patients (47%). Four patients demonstrated new regional decreases of LV myocardial thallium concentration with redistribution of the isotope on delayed images. The patient studied only during SV also had myocardial 201TI defects with redistribution. Five patients (3 also having areas of 201TI redistribution) had transient LV dilation during SV. The change from MV to SV was accompanied by increased spontaneous minute ventilation (3.5 +/- 2.6 to 8.4 +/- 3.7 1/min) and mean arterial blood pressure (90 +/- 2 to 98 +/- 3 mmHg), and decreased pH(a) (7.41 +/- 0.02 to 7.37 +/- 0.03) (P < 0.05 by paired t test for each comparison); the Pa(O2), Pa(CO2), heart rate, 12-lead ECG, tidal volume, vital capacity, and maximum inspiratory pressure were unchanged. The frequent occurrence of new regions of altered myocardial 201TI uptake and LV dilation during SV suggests that myocardial perfusion often is altered and myocardial ischemia may be present during SV in MV-dependent patients. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. RP HURFORD, WE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 FU NHLBI NIH HHS [HL23591] NR 30 TC 44 Z9 45 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 JUN PY 1991 VL 74 IS 6 BP 1007 EP 1016 DI 10.1097/00000542-199106000-00007 PG 10 WC Anesthesiology SC Anesthesiology GA FR380 UT WOS:A1991FR38000007 PM 2042755 ER PT J AU RAINES, DE HOGUE, CW WICKENS, C WELCH, J RISK, SC AF RAINES, DE HOGUE, CW WICKENS, C WELCH, J RISK, SC TI ARTIFACTUAL HYPERTENSION DUE TO TRANSDUCER CABLE MALFUNCTION SO ANESTHESIOLOGY LA English DT Article DE MONITORING, ARTERIAL BLOOD PRESSURE; COMPLICATIONS, INVASIVE MONITORING; HYPERTENSION ID HYPOTENSION C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIOL,CARDIAC ANESTHESIA GRP,BOSTON,MA 02114. NR 7 TC 1 Z9 1 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD JUN PY 1991 VL 74 IS 6 BP 1149 EP 1151 DI 10.1097/00000542-199106000-00027 PG 3 WC Anesthesiology SC Anesthesiology GA FR380 UT WOS:A1991FR38000027 PM 2042769 ER PT J AU BROD, SA ALSABBAGH, A SOBEL, RA HAFLER, DA WEINER, HL AF BROD, SA ALSABBAGH, A SOBEL, RA HAFLER, DA WEINER, HL TI SUPPRESSION OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS BY ORAL-ADMINISTRATION OF MYELIN ANTIGENS .4. SUPPRESSION OF CHRONIC RELAPSING DISEASE IN THE LEWIS RAT AND STRAIN-13 GUINEA-PIG SO ANNALS OF NEUROLOGY LA English DT Article ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; COLLAGEN-INDUCED ARTHRITIS; BASIC-PROTEIN; MULTIPLE-SCLEROSIS; II COLLAGEN; ANTI-L3T4 ANTIBODIES; IMMUNE-RESPONSES; INHIBITION; TOLERANCE; MODEL AB Oral administration of proteins is a long-recognized method of inducing antigen-specific peripheral immune tolerance. We previously showed that oral administration of myelin basic protein suppresses monophasic experimental autoimmune encephalomyelitis in the Lewis rat when it is given in association with immunization and prior to disease onset. As a potential therapy for human autoimmune disease, it is crucial to determine whether oral tolerance can ameliorate an ongoing immune response. We therefore asked whether oral administration of myelin antigens, after sensitization and disease expression has occurred, could affect immunological, clinical, or pathological features of experimental autoimmune encephalomyelitis. Chronic relapsing experimental autoimmune encephalomyelitis was induced in the Lewis rat and strain 13 guinea pig by immunization with whole guinea pig cord homogenate, complete Freund's adjuvant, and Mycobacterium tuberculosis. Following recovery from the first attack, animals were orally given bovine myelin, guinea pig myelin, or guinea pig myelin basic protein three times per week for up to 3 months. Animals receiving myelin products orally had decreased severity and frequency of clinical relapses, decreased delayed-type hypersensitivity responses to myelin antigens, diminished inflammation in the central nervous system (CNS), and decreased areas of CNS demyelination. In the rat, guinea pig myelin basic protein was as effective as guinea pig myelin in ameliorating the disease and also resulted in decreased serum anti-myelin basic protein antibody levels. No exacerbation of disease or worsening of pathological findings occurred in the animals given myelin products. These results demonstrate that oral administration of myelin antigens can suppress chronic relapsing experimental autoimmune encephalomyelitis and have direct relevance to therapy of human demyelinating disorders such as multiple sclerosis. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BROD, SA (reprint author), BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,DEPT MED,DIV NEUROL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NINDS NIH HHS [NS RO1-26773] NR 27 TC 70 Z9 72 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD JUN PY 1991 VL 29 IS 6 BP 615 EP 622 DI 10.1002/ana.410290608 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FQ342 UT WOS:A1991FQ34200007 PM 1716432 ER PT J AU WILKINS, EW GRILLO, HC SCANNELL, JG MONCURE, AC MATHISEN, DJ AF WILKINS, EW GRILLO, HC SCANNELL, JG MONCURE, AC MATHISEN, DJ TI ROLE OF STAGING IN PROGNOSIS AND MANAGEMENT OF THYMOMA SO ANNALS OF THORACIC SURGERY LA English DT Article ID MEDULLARY DIFFERENTIATION; THYMIC CARCINOMA; EPITHELIAL-CELLS; TUMORS AB Eighty-five patients operated on for thymoma from 1972 to 1989 were evaluated, 32 with myasthenia gravis and 53 without. Masaoka staging revealed stage I disease in 45 (53%), stage II in 23 (27%), stage III in 14 (16%), and stage IVa in 3 (4%). There was no operative mortality. Actuarial survival at 10 years was 63.7% for all patients: 78.3% for those in stage I, 74.7% for those in stage II, and 20.8% for those in stage III. There was no recurrence in patients in stage I. Mediastinal recurrence developed in 4 patients in stage II considered to have noninvasive disease by the surgeon. It is recommended that all patients be followed up for a minimum of 10 years and that all patients in stages II and III receive postoperative radiotherapy. The presence of myasthenia gravis is no longer considered as an adverse factor in survival. C1 MASSACHUSETTS GEN HOSP,SURG SERV,THORAC SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 16 TC 104 Z9 107 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD JUN PY 1991 VL 51 IS 6 BP 888 EP 892 PG 5 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FQ352 UT WOS:A1991FQ35200005 PM 2039316 ER PT J AU ALLEN, MS MATHISEN, DJ GRILLO, HC WAIN, JC MONCURE, AC HILGENBERG, AD AF ALLEN, MS MATHISEN, DJ GRILLO, HC WAIN, JC MONCURE, AC HILGENBERG, AD TI BRONCHOGENIC-CARCINOMA WITH CHEST-WALL INVASION SO ANNALS OF THORACIC SURGERY LA English DT Article ID EN BLOC RESECTION; FACTORS AFFECTING SURVIVAL; LUNG AB Bronchogenic carcinoma with chest wall involvement continues to present a major clinical challenge. We have treated 52 patients since 1973, excluding those with superior sulcus tumors. There were 37 male and 15 female patients with an average age of 62.9 years. Chest pain was an initial symptom in 37%. All patients had negative mediastinoscopy results. Squamous cell carcinoma was present in 53% and adenocarcinoma in 35%. The median number of ribs resected was two (range, one to six), and only 2 patients required chest wall reconstruction. Pathologic staging was T3 N0 M0 in 83% and T3 N1 M0 in 17%. Operative mortality was 3.8%. Absolute 5-year survival was 26.3%. Patients who had N1 disease had a 5-year survival of only 11%. Radiation therapy was employed in 46% for positive nodes or close margins. Bronchogenic carcinoma with chest wall invasion remains potentially curable if N2 nodes are not involved. The role of radiation therapy has not been clearly defined. Morbidity and mortality should be minimal. C1 MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,WARREN 1109,BOSTON,MA 02114. NR 19 TC 55 Z9 55 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD JUN PY 1991 VL 51 IS 6 BP 948 EP 951 PG 4 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FQ352 UT WOS:A1991FQ35200015 PM 2039324 ER PT J AU JENIKE, MA BAER, L BALLANTINE, T MARTUZA, RL TYNES, S GIRIUNAS, I BUTTOLPH, ML CASSEM, NH AF JENIKE, MA BAER, L BALLANTINE, T MARTUZA, RL TYNES, S GIRIUNAS, I BUTTOLPH, ML CASSEM, NH TI CINGULOTOMY FOR REFRACTORY OBSESSIVE-COMPULSIVE DISORDER - A LONG-TERM FOLLOW-UP OF 33 PATIENTS SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID GLUCOSE METABOLIC RATES; ABNORMALITIES; RELIABILITY; SCALE AB To evaluate the feasibility of cingulotomy as a treatment for patients with intractable obsessive-compulsive disorder, we evaluated the records of all 35 patients with this diagnosis who had undergone one or more such procedures at Massachusetts General Hospital, Boston, during the last 25 years. Retrospectively, all but two of these patients met DSM-III-R criteria for obsessive-compulsive disorder. Six patients were deceased; four by suicide. Questionnaires were sent to the remaining 27 patients with obsessive-compulsive disorder; 17 patients returned the questionnaire and another agreed to an interview without completing the forms. Sixteen of these 18 patients participated in a telephone interview, and patient reports were corroborated by an informant in 10 cases. Despite the presence of some side effects, such as easily controlled seizures (9%) and transient mania (6%), the results of this investigation support the use of cingulotomy as a potentially effective treatment for patients with severe and disabling obsessive-compulsive disorder. With the use of very conservative criteria, we estimated that at least 25% to 30% of the patients benefited substantially from this procedure. Similar results were found in a preliminary prospective study of four patients who recently underwent cingulotomy after state-of-the-art preoperative treatments had failed. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. RP JENIKE, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BULFINCH 3,FRUIT ST,BOSTON,MA 02114, USA. NR 29 TC 148 Z9 154 U1 1 U2 1 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 JUN PY 1991 VL 48 IS 6 BP 548 EP 555 PG 8 WC Psychiatry SC Psychiatry GA FQ353 UT WOS:A1991FQ35300006 PM 2039338 ER PT J AU MANSON, JE COLDITZ, GA STAMPFER, MJ WILLETT, WC KROLEWSKI, AS ROSNER, B ARKY, RA SPEIZER, FE HENNEKENS, CH AF MANSON, JE COLDITZ, GA STAMPFER, MJ WILLETT, WC KROLEWSKI, AS ROSNER, B ARKY, RA SPEIZER, FE HENNEKENS, CH TI A PROSPECTIVE-STUDY OF MATURITY-ONSET DIABETES-MELLITUS AND RISK OF CORONARY HEART-DISEASE AND STROKE IN WOMEN SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID MYOCARDIAL-INFARCTION; MORTALITY; FRAMINGHAM; POPULATION; INSULIN; LIPIDS; ATHEROSCLEROSIS; COMMUNITY; GLUCOSE; COHORT AB We examined the relationship of maturity-onset clinical diabetes mellitus with the subsequent incidence of coronary heart disease, stroke, total cardiovascular mortality, and all-cause mortality in a cohort of 116 177 US women who were 30 to 55 years of age and free of known coronary heart disease, stroke, and cancer in 1976. During 8 years of follow-up (889 255 person-years), we identified 338 nonfatal myocardial infarctions, 111 coronary deaths, 259 strokes, 238 cardiovascular deaths, and 1349 deaths from all causes. Diabetes was associated with a markedly increased risk of nonfatal myocardial infarction and fatal coronary heart disease (age-adjusted relative risk [RR] = 6.7; 95% confidence interval [Cl], 5.3 to 8.4), ischemic stroke (RR = 5.4; 95% Cl, 3.3 to 9.0), total cardiovascular mortality (RR = 6.3; 95% Cl, 4.6 to 8.6), and all-cause mortality (RR = 3.0; 95% Cl, 2.5 to 3.7). A major independent effect of diabetes persisted in multivariate analyses after simultaneous control for other known coronary risk factors (for these end points, RR [95% Cl] = 3.1 [2.3 to 4.2], 3.0 [1.6 to 5.7], 3.0 [1.9 to 4.8], and 1.9 [1.4 to 2.4], respectively). The absolute excess coronary risk due to diabetes was greater in the presence of other risk factors, including cigarette smoking, hypertension, and obesity. These prospective data indicate that maturity-onset clinical diabetes is a strong determinant of coronary heart disease, ischemic stroke, and cardiovascular mortality among middle-aged women. The adverse effect of diabetes is amplified in the presence of other cardiovascular risk factors, many of which are modifiable. C1 HARVARD UNIV,SCH MED,DEPT MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PREVENT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA. MT AUBURN HOSP,CAMBRIDGE,MA 02138. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA 40356]; NHLBI NIH HHS [HL 34594]; NIDDK NIH HHS [DK 36798] NR 53 TC 484 Z9 493 U1 0 U2 4 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD JUN PY 1991 VL 151 IS 6 BP 1141 EP 1147 DI 10.1001/archinte.151.6.1141 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA FQ681 UT WOS:A1991FQ68100013 PM 2043016 ER PT J AU KORNMEHL, EW STEINERT, RF PULIAFITO, CA AF KORNMEHL, EW STEINERT, RF PULIAFITO, CA TI A COMPARATIVE-STUDY OF MASKING FLUIDS FOR EXCIMER LASER PHOTOTHERAPEUTIC KERATECTOMY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID PHOTOREFRACTIVE KERATECTOMY; CORNEA; SURGERY AB Several fluids of different viscosity were used to mask deeper tissues while exposing protruding irregularities during therapeutic keratectomy of an irregular anterior corneal surface with the 193-nm argon fluoride excimer laser. A model of an irregular anterior corneal surface was developed in deepithelialized calf eyes using grade 8-0 sandpaper. Therapeutic keratectomy was then performed on 28 eyes at a fluence of 180 mJ/cm2, a repetition rate of 10 Hz, and 500 pulses per eye. Solutions of 0.3% hydroxypropylmethylcellulose 2910 and a 0.1% dextran 70 solution, 1% carboxymethylcellulose sodium solution, or 0.9% saline solution were applied to the corneal surface of 21 eyes. Seven control eyes underwent ablation without the addition of fluid. Scanning electron microscopy demonstrated that corneas treated with dextran 70 had the least surface irregularity, and those treated with carboxymethylcellulose or saline solution had intermediate surface irregularity. Corneas that were ablated without additional fluid had the greatest surface irregularity. The application of a moderately viscous solution during therapeutic excimer laser keratectomy enhances the smoothing effect of surface ablation. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,MORSE LASER CTR,LASER RES LAB,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 15 TC 61 Z9 61 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 JUN PY 1991 VL 109 IS 6 BP 860 EP 863 PG 4 WC Ophthalmology SC Ophthalmology GA FQ676 UT WOS:A1991FQ67600034 PM 2043076 ER PT J AU RONDINELLI, RD MURPHY, JR WILSON, DH MILLER, CC AF RONDINELLI, RD MURPHY, JR WILSON, DH MILLER, CC TI PREDICTORS OF FUNCTIONAL OUTCOME AND RESOURCE UTILIZATION IN INPATIENT REHABILITATION SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE FUNCTIONAL; REHABILITATION; RESOURCE AB Consecutive patients (n = 1,289) discharged from two inpatient rehabilitation facilities were prospectively examined to determine the extent to which rehabilitative outcomes, functionally based progress, and associated resource utilization (in terms of rehabilitation length of stay) can be concomitantly predicted using the Tufts/New England Medical Center functional assessment tool and bivariate and multivariate statistical comparisons. A high percentage (> 50%) of statistically significant associations between the predictor variables and seven outcome measures were seen. The R2s corresponding to these associations were generally small and resistant to enhancement by commonly accepted statistical manipulations. Consequently, they are, in general, of limited predictive value for determining functional prognosis or resource utilization among rehabilitation inpatients. Although functionally based predictors appear to be the best predictors of functional progress, their effectiveness as predictors of other domains (eg, discharge outcome and rehabilitation length of stay) is variable. The implication is that a prospective payment system using such an array of predictors and directed primarily at cost containment is likely to overlook potentially important gains in functional progress and patient outcome. Furthermore, the functionally based predictors, taken individually, varied in effectiveness as predictors among facilities, and, taken collectively, they varied in effectiveness as predictors for different diagnostic groupings within a facility. The inconsistency of predictions according to the various domains appears to further limit their application to a prospective payment model. C1 DENVER VET AFFAIRS MED CTR,INFORMAT RESOURCES MANAGEMENT SERV,DENVER,CO. UNIV COLORADO,SCH MED,DEPT PREVENT MED,DENVER,CO 80202. RP RONDINELLI, RD (reprint author), ROSE MED CTR,DEPT PM&R,4567 E 9TH AVE,DENVER,CO 80220, USA. NR 11 TC 23 Z9 23 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD JUN PY 1991 VL 72 IS 7 BP 447 EP 453 PG 7 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA FP702 UT WOS:A1991FP70200001 PM 1905529 ER PT J AU BURKE, JF AF BURKE, JF TI WHO IS RESPONSIBLE FOR PROGRESS SO ARCHIVES OF SURGERY LA English DT Editorial Material CT 71ST ANNUAL MEETING OF THE NEW ENGLAND SURGICAL SOC CY SEP 15, 1990 CL NEWPORT, RI SP NEW ENGLAND SURG SOC C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP BURKE, JF (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 5 Z9 5 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD JUN PY 1991 VL 126 IS 6 BP 677 EP 680 PG 4 WC Surgery SC Surgery GA FQ354 UT WOS:A1991FQ35400001 PM 2039353 ER PT J AU STEELE, G BUSSE, P HUBERMAN, MS LECLAIR, JM FALCHUK, ZM MAYER, RJ BOTHE, A RAVIKUMAR, TS STONE, M JESSUP, JM AF STEELE, G BUSSE, P HUBERMAN, MS LECLAIR, JM FALCHUK, ZM MAYER, RJ BOTHE, A RAVIKUMAR, TS STONE, M JESSUP, JM TI A PILOT-STUDY OF SPHINCTER-SPARING MANAGEMENT OF ADENOCARCINOMA OF THE RECTUM SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 71ST ANNUAL MEETING OF THE NEW ENGLAND SURGICAL SOC CY SEP 15, 1990 CL NEWPORT, RI SP NEW ENGLAND SURG SOC ID LOCAL EXCISION; RADIATION-THERAPY; CANCER; ELECTROCOAGULATION; CARCINOMA AB After analysis of 26 prospectively accrued patients with distal rectal adenocarcinomas who underwent sphincter preservation treatment, we have concluded that tumors that invade only the submucosa can safely be treated with surgery alone and that tumors that invade the muscularis or further can be safely treated with surgery combined with chemoradiotherapy. None of the patients had either local or distant recurrence, with a median follow-up of 21 months. All patients have been fully continent. The results, although preliminary, imply that resection of distal rectal adenocarcinoma with sphincter preservation, and adjuvant therapy when appropriate, have achieved local and distant control equal to the conventional Miles' abdominoperineal resection, but without the need for a permanent colostomy. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT RADIAT THERAPY,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT SURG,NEW HAVEN,CT 06510. RP STEELE, G (reprint author), HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DEPT SURG,110 FRANCIS ST,SUITE 3-A,BOSTON,MA 02215, USA. FU NCI NIH HHS [P01 CA 44704] NR 24 TC 40 Z9 40 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD JUN PY 1991 VL 126 IS 6 BP 696 EP 702 PG 7 WC Surgery SC Surgery GA FQ354 UT WOS:A1991FQ35400005 PM 2039356 ER PT J AU MARKOWITZ, JS COSIMI, LA CAREY, RW KANG, S PADYK, C SOBER, AJ COSIMI, AB AF MARKOWITZ, JS COSIMI, LA CAREY, RW KANG, S PADYK, C SOBER, AJ COSIMI, AB TI PROGNOSIS AFTER INITIAL RECURRENCE OF CUTANEOUS MELANOMA SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 71ST ANNUAL MEETING OF THE NEW ENGLAND SURGICAL SOC CY SEP 15, 1990 CL NEWPORT, RI SP NEW ENGLAND SURG SOC ID I MALIGNANT-MELANOMA; METASTASES AB We reviewed 231 patients who developed recurrent disease 1 to 218 months after surgical therapy for clinical stage I cutaneous melanoma. Metastatic lesions amenable to surgery, including visceral recurrences, were resected. Adjuvant systemic chemotherapy/immunotherapy or regional hyperthermic perfusion was added in patients with unresected disease. Local irradiation was employed for nonresectable brain or other isolated symptomatic metastases. The overall 5-year survival rate after initial recurrence was 36%. In patients with soft tissue or nodal recurrence, the 5-year survival rates were 49% and 38%, respectively; six (11%) of 53 patients whose initial recurrence was in a visceral organ achieved prolonged remission. Primary lesion anatomic site, thickness, pathologic type, and interval from initial therapy to recurrence were unrelated to survival. Significant prognostic factors included the site of initial metastasis, stage of primary disease, and the successful complete eradication of gross disease by surgical excision or intensive chemotherapy. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,GEN SURG SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DERMATOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 16 TC 58 Z9 59 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD JUN PY 1991 VL 126 IS 6 BP 703 EP 708 PG 6 WC Surgery SC Surgery GA FQ354 UT WOS:A1991FQ35400006 PM 2039357 ER PT J AU HARE, JW AF HARE, JW TI COMPLICATED DIABETES COMPLICATING PREGNANCY SO BAILLIERES CLINICAL OBSTETRICS AND GYNAECOLOGY LA English DT Article ID RENAL-TRANSPLANTATION; SPONTANEOUS-ABORTION; MELLITUS; NEPHROPATHY; DISEASE; RETINOPATHY; WOMEN; HYPOGLYCEMIA; RAT C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA 02215. RP HARE, JW (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 41 TC 5 Z9 5 U1 0 U2 0 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0950-3552 J9 BAILLIERE CLIN OB GY JI Baillieres Clin. Obstet. Gynaecol. PD JUN PY 1991 VL 5 IS 2 BP 349 EP 367 DI 10.1016/S0950-3552(05)80102-6 PG 19 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA FZ802 UT WOS:A1991FZ80200007 PM 1954718 ER PT J AU MOORE, DF TSIATIS, A AF MOORE, DF TSIATIS, A TI ROBUST ESTIMATION OF THE VARIANCE IN MOMENT METHODS FOR EXTRA-BINOMIAL AND EXTRA-POISSON VARIATION SO BIOMETRICS LA English DT Article DE CLUSTER RANDOMIZATION; ERROR RATIO; EXTRA-BINOMIAL VARIATION; EXTRA-POISSON VARIATION; GENERALIZED ESTIMATING EQUATION; MOMENT METHOD; ROBUST VARIANCE ESTIMATE; TERATOLOGY ID QUASI-LIKELIHOOD FUNCTIONS; GENERALIZED LINEAR-MODELS; REGRESSION AB When faced with data in the form of overdispersed counts or proportions, moment methods allow consistent parameter estimation when only the form of the mean and variance is specified. If the variance form is misspecified, these methods still yield consistent parameter estimates, though with lower efficiency, and the variances of the estimates will be inconsistent. A variance correction is available that yields consistent variance estimates in these circumstances. The asymptotic and small-sample efficiencies of this correction are calculated, and its performance under variance misspecification is studied. A group-randomized breast self-examination prevention study that is now underway serves as a focal point for the study of these properties. The use of the variance correction in modelling is illustrated on a teratology data set. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP MOORE, DF (reprint author), TEMPLE UNIV,DEPT STAT,SPEAKMAN HALL,PHILADELPHIA,PA 19122, USA. FU NCI NIH HHS [CA-23415, CA-09337] NR 24 TC 63 Z9 64 U1 0 U2 4 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1991 VL 47 IS 2 BP 383 EP 401 DI 10.2307/2532133 PG 19 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA FV774 UT WOS:A1991FV77400003 PM 1912253 ER PT J AU KALISH, LA AF KALISH, LA TI REDUCING MEAN SQUARED ERROR IN THE ANALYSIS OF STRATIFIED EPIDEMIOLOGIC STUDIES - RESPONSE SO BIOMETRICS LA English DT Letter RP KALISH, LA (reprint author), HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT BIOSTAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 1 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1991 VL 47 IS 2 BP 776 EP 776 PG 1 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA FV774 UT WOS:A1991FV77400036 ER PT J AU ZELEN, M AF ZELEN, M TI COMPLIANCE, BIAS, AND POWER IN CLINICAL-TRIALS - REPLY SO BIOMETRICS LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ZELEN, M (reprint author), HARVARD UNIV,SCH PUBL HLTH,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 2 TC 9 Z9 9 U1 0 U2 0 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD JUN PY 1991 VL 47 IS 2 BP 778 EP 779 PG 2 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA FV774 UT WOS:A1991FV77400038 ER PT J AU CANTIELLO, HF PATENAUDE, C ZANER, K AF CANTIELLO, HF PATENAUDE, C ZANER, K TI OSMOTICALLY INDUCED ELECTRICAL SIGNALS FROM ACTIN-FILAMENTS SO BIOPHYSICAL JOURNAL LA English DT Article ID POISSON-BOLTZMANN EQUATION; GLYCEROL-EXTRACTED MUSCLE; DIVALENT-CATIONS; GELS; CONTRACTION; CHARGE; FIELDS AB Actin filaments, F-actin, a major component of the cortical cytoskeleton, play an important role in a variety of cell functions. In this report we have assessed the role of osmotic stress on the electrochemical properties of F-actin. The spontaneous Donnan potential of a polymerized actin solution (5 mg/ml) was -3.93 +/- 1.84 mV, which was linearly reduced by osmotic stress on the order of 1-20 mOsm (0.28 +/- 0.06 mV/mM). Calculated surface charge density was reduced and eventually reversed by increasing the osmotic stress as expected for a phase transition behavior. The electro-osmotic behavior of F-actin disappeared at pH 5.5 and was dependent on its filamentous nature. Furthermore, osmotically stressed F-actin displayed a nonlinear electric response upon application of electric fields on the order of 500-2,000 V/cm. These data indicate that F-actin in solution may display nonideal electro-osmotic properties consistent with ionic "cable" behavior which may be of biological significance in the processing and conduction of electrical signals within the cellular compartment. C1 BOSTON UNIV,SCH MED,DEPT MED & BIOCHEM,HEMATOL ONCOL SERV,BLDG S3E,80 E CONCORD ST,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIGMS NIH HHS [GM 37590] NR 25 TC 34 Z9 34 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD JUN PY 1991 VL 59 IS 6 BP 1284 EP 1289 PG 6 WC Biophysics SC Biophysics GA FP158 UT WOS:A1991FP15800013 PM 1873465 ER PT J AU PARRY, RL CHIN, TW DONAHOE, PK AF PARRY, RL CHIN, TW DONAHOE, PK TI COMPUTER-AIDED CELL COLONY COUNTING SO BIOTECHNIQUES LA English DT Article ID NUDE-MICE; GROWTH AB Counting cell colonies is a tedious task when performed with the light microscope. Moreover, unless strict double-blind protocols are adhered to, biased counts are difficult to avoid. Presented here is a computer software application that performs accurate, reproducible cell colony counts with a minimum of user generated bias. The application is based upon the Apple(R) IICX computer system with Image software and AppleScan(R). Colonies are grown on 24-well plates and prepared in such a way as to permit good quality scanning. The scans are then transferred to Image and the individual colonies in each well are counted. Good correlation with counts done by light microscopy is achieved. C1 USN HOSP,BETHESDA,MD 20814. RP PARRY, RL (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,WARREN 11,BOSTON,MA 02114, USA. NR 4 TC 14 Z9 14 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD JUN PY 1991 VL 10 IS 6 BP 772 EP 774 PG 3 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FQ809 UT WOS:A1991FQ80900017 PM 1878212 ER PT J AU ROY, DC GRIFFIN, JD BELVIN, M BLATTLER, WA LAMBERT, JM RITZ, J AF ROY, DC GRIFFIN, JD BELVIN, M BLATTLER, WA LAMBERT, JM RITZ, J TI ANTI-MY9-BLOCKED-RICIN - AN IMMUNOTOXIN FOR SELECTIVE TARGETING OF ACUTE MYELOID-LEUKEMIA CELLS SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA; ACUTE MYELOBLASTIC-LEUKEMIA; MONOCLONAL-ANTIBODY; CLONOGENIC CELLS; RICIN; PROGENITORS; LYMPHOMA; CHAIN C1 IMMUNOGEN INC,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA34183] NR 35 TC 57 Z9 57 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 1 PY 1991 VL 77 IS 11 BP 2404 EP 2412 PG 9 WC Hematology SC Hematology GA FP517 UT WOS:A1991FP51700014 PM 2039821 ER PT J AU FREEDMAN, AS RITZ, J NEUBERG, D ANDERSON, KC RABINOWE, SN MAUCH, P TAKVORIAN, T SOIFFER, R BLAKE, K YEAP, B CORAL, F NADLER, LM AF FREEDMAN, AS RITZ, J NEUBERG, D ANDERSON, KC RABINOWE, SN MAUCH, P TAKVORIAN, T SOIFFER, R BLAKE, K YEAP, B CORAL, F NADLER, LM TI AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN 69 PATIENTS WITH A HISTORY OF LOW-GRADE B-CELL NON-HODGKINS-LYMPHOMA SO BLOOD LA English DT Article ID HIGH-DOSE THERAPY; CHRONIC MYELOGENOUS LEUKEMIA; DISEASE-FREE SURVIVAL; COMBINATION CHEMOTHERAPY; MALIGNANT-LYMPHOMA; POOR-PROGNOSIS; HISTOLOGIC CONVERSION; BODY IRRADIATION; SALVAGE THERAPY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FREEDMAN, AS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA-06516, CA01105, CA34183] NR 37 TC 182 Z9 182 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 JUN 1 PY 1991 VL 77 IS 11 BP 2524 EP 2529 PG 6 WC Hematology SC Hematology GA FP517 UT WOS:A1991FP51700030 PM 2039834 ER PT J AU TROP, M SCHIFFRIN, EJ CARTER, EA AF TROP, M SCHIFFRIN, EJ CARTER, EA TI EFFECT OF PLATELET-ACTIVATING-FACTOR ON RETICULOENDOTHELIAL SYSTEM FUNCTION SO BURNS LA English DT Article AB The effect of platelet activating factor (PAF) injections on the uptake of Tc-99m-SC (Tc-99m-SC (Tc-99m-sulphur colloid) was determined in vivo. PAF (2-mu-g) injected intravenously into unanaesthetized, unrestrained rats was associated with the development of lesions in the small intestine and alteration of Tc-99m-SC uptake in vivo. Tc-99m-SC uptake into the lung was increased while spleen uptake was decreased. Pretreatment of the animals with a PAF antagonist, SRI-64-441, prevented the intestinal lesions and alterations of Tc-99m-SC uptake. Macrophages, isolated from lung lavage of the PAF-treated rats, demonstrated a decreased generation of hydrogen peroxide in vitro. The present results suggest that, in addition to its other effects on the immune system, PAF can also alter the in vivo phagocytic activity of the reticuloendothelial system in the rat. C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. FU NIDDK NIH HHS [DK 34854] NR 0 TC 1 Z9 1 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0305-4179 J9 BURNS JI Burns PD JUN PY 1991 VL 17 IS 3 BP 193 EP 197 DI 10.1016/0305-4179(91)90102-M PG 5 WC Critical Care Medicine; Dermatology; Surgery SC General & Internal Medicine; Dermatology; Surgery GA FR436 UT WOS:A1991FR43600004 PM 1892549 ER PT J AU MCCORMICK, ML OBERLEY, TD ELWELL, JH OBERLEY, LW SUN, Y LI, JJ AF MCCORMICK, ML OBERLEY, TD ELWELL, JH OBERLEY, LW SUN, Y LI, JJ TI SUPEROXIDE-DISMUTASE AND CATALASE LEVELS DURING ESTROGEN-INDUCED RENAL TUMORIGENESIS, IN RENAL TUMORS AND THEIR AUTONOMOUS VARIANTS IN THE SYRIAN-HAMSTER SO CARCINOGENESIS LA English DT Article ID OXYGEN RADICALS; KIDNEY; TRANSFORMATION; PROMOTION; ENZYMES; INVITRO; CELLS AB Antioxidant enzyme levels were determined in kidneys during estrogen-induced cortical renal tumorigenesis in male Syrian hamsters. The activity of these enzymes in renal tumors were compared to those in the kidney cortex of untreated male castrated hamsters of different ages and in age-matched animals treated with diethylstilbestrol (DES) for varying periods. A transient increase in kidney Mn superoxide dismutase (MnSOD) and total SOD activity was seen after 1.5 and 3.1 months of DES treatment compared to untreated controls. However, after 4.4 months of DES exposure the activities of these antioxidant enzymes fell below untreated levels. The level of MnSOD and CuZnSOD was 3- to 10-fold lower compared to castrated male renal cortical values in DES-induced primary, serially transplanted and in autonomous renal tumour variants. Catalase activity declined steadily at 1.5 to 4.4 months of DES treatment. Low levels of catalase activity were found in all tumors examined. In general, Western blot analysis of immunoreactive proteins confirmed these findings, indicating that the low enzyme activities were due to low levels of enzyme proteins. Immunohistochemistry of the earliest tumor foci exhibited negligible antioxidant enzyme activity. The levels of these antioxidant enzymes were similar in all tumors surveyed, both primary and autonomous variants and in newborn kidneys, and they were about 10-fold lower than in normal kidney cortex or isolated proximal tubules. C1 UNIV MINNESOTA,SCH MED,DEPT PHARMACOL,MINNEAPOLIS,MN 55417. WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,MADISON,WI 53705. UNIV IOWA,RADIAT RES LAB,IOWA CITY,IA 52242. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53705. VET ADM MED CTR,HORMONAL CARCINOGENESIS LAB,MINNEAPOLIS,MN 55417. FU NCI NIH HHS [CA 22009, CA 41267] NR 29 TC 38 Z9 38 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0143-3334 J9 CARCINOGENESIS JI Carcinogenesis PD JUN PY 1991 VL 12 IS 6 BP 977 EP 983 DI 10.1093/carcin/12.6.977 PG 7 WC Oncology SC Oncology GA FQ426 UT WOS:A1991FQ42600006 PM 2044204 ER PT J AU BERNSTEIN, SH KHARBANDA, SM SHERMAN, ML SUKHATME, VP KUFE, DW AF BERNSTEIN, SH KHARBANDA, SM SHERMAN, ML SUKHATME, VP KUFE, DW TI POSTTRANSCRIPTIONAL REGULATION OF THE ZINC FINGER-ENCODING EGR-1 GENE BY GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR IN HUMAN U-937 MONOCYTIC LEUKEMIA-CELLS - INVOLVEMENT OF A PERTUSSIS TOXIN-SENSITIVE G-PROTEIN SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID C-FOS; 3T3 CELLS; CULTURED-CELLS; GROWTH-FACTORS; BINDING; EXPRESSION; TRANSCRIPTION; SERUM; ONCOGENE; JUN AB The EGR-1 gene is an immediate early response gene encoding a zinc finger DNA-binding protein. The present studies have examined the regulation of EGR-1 gene expression in human U-937 monocytic leukemia cells treated with granulocyte-macrophage colony-stimulating factor (GM-CSF). The results demonstrate that GM-CSF rapidly and transiently increases EGR-1 gene expression in U-937 cells. Similar findings were obtained in GM-CSF-treated human monocytes. We also show that the regulation of EGR-1 expression by GM-CSF is a pertussis toxin-sensitive event. The results of nuclear run-on assays further demonstrate that the EGR-1 gene is constitutively transcribed in untreated U-937 cells and that GM-CSF has little effect on this rate of transcription. Inhibition of protein synthesis with cycloheximide also had no detectable effect on EGR-1 gene transcription but was associated with superinduction of EGR-1 mRNA levels in GM-CSF-treated cells. Moreover, the half-life of GM-CSF-induced EGR-1 transcripts was prolonged from 33 to 70 min following inhibition of protein synthesis. Taken together, the results indicate that GM-CSF activates signaling pathways which regulate EGR-1 gene expression through a pertussis toxin-sensitive G protein and that these events increase EGR-1 mRNA levels by a posttranscriptional mechanism. This GM-CSF-dependent regulation of EGR-1 expression may provide a mechanism for transducing signals to the nucleus that are involved in the control of gene transcription. C1 UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. RP BERNSTEIN, SH (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA42802, CA01092] NR 41 TC 25 Z9 25 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 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD JUN PY 1991 VL 2 IS 6 BP 273 EP 278 PG 6 WC Cell Biology SC Cell Biology GA FQ211 UT WOS:A1991FQ21100002 PM 2064996 ER PT J AU DIMITRIADOU, V BUZZI, MG THEOHARIDES, TC MOSKOWITZ, MA AF DIMITRIADOU, V BUZZI, MG THEOHARIDES, TC MOSKOWITZ, MA TI ANTIINFLAMMATORY EFFECTS OF DIHYDROERGOTAMINE AND SUMATRIPTAN IN BLOOD-VESSELS AND MAST-CELLS OF DURA-MATER SO CEPHALALGIA LA English DT Article C1 TUFTS UNIV,DEPT PHARMACOL,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 1 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0333-1024 J9 CEPHALALGIA JI Cephalalgia PD JUN PY 1991 VL 11 SU 11 BP 9 EP 10 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FU338 UT WOS:A1991FU33800005 ER PT J AU RUNGE, MS HABER, E AF RUNGE, MS HABER, E TI IMPORTANCE OF EXPERIMENTAL-MODELS IN STUDY OF THROMBOSIS AND THROMBOLYSIS - INTRODUCTION SO CIRCULATION LA English DT Editorial Material C1 BRISTOL MYERS SQUIBB PHARMACEUT,RES INST,PRINCETON,NJ. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP RUNGE, MS (reprint author), EMORY UNIV,DIV CARDIOL,ATLANTA,GA 30322, USA. NR 0 TC 3 Z9 3 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1991 VL 83 IS 6 SU S BP 1 EP 2 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FQ624 UT WOS:A1991FQ62400001 ER PT J AU GOLD, HK YASUDA, T JANG, IK GUERRERO, JL FALLON, JT LEINBACH, RC COLLEN, D AF GOLD, HK YASUDA, T JANG, IK GUERRERO, JL FALLON, JT LEINBACH, RC COLLEN, D TI ANIMAL-MODELS FOR ARTERIAL THROMBOLYSIS AND PREVENTION OF REOCCLUSION - ERYTHROCYTE-RICH VERSUS PLATELET-RICH THROMBUS SO CIRCULATION LA English DT Article DE THROMBOLYSIS; OCCLUSIONS ID ACUTE MYOCARDIAL-INFARCTION; TISSUE PLASMINOGEN-ACTIVATOR; CANINE CORONARY-ARTERIES; HIGH-GRADE STENOSIS; INTRACORONARY STREPTOKINASE; REPERFUSION; TRIAL; THERAPY; ANGIOPLASTY; INHIBITOR AB Experimental animal models for erythrocyte-rich (ER) and platelet-rich (PR) arterial thrombosis were developed in dogs and rabbits and used for the evaluation of the effect of antithrombin and antiplatelet agents on thrombolysis with recombinant tissue-type plasminogen activators (rt-PA). The canine models consist of a whole blood clot produced in the left anterior descending coronary artery (ER thrombus) or a 1-cm everted (inside-out) segment graft in the circumflex coronary artery that predisposes to occlusion with PR material (PR thrombus). The rabbit models consist of a femoral arterial whole blood clot (ER thrombus) or a femoral arterial eversion graft (PR thrombus). The whole blood clot models are sensitive to recanalization with rt-PA but are consistently associated with reocclusion, notwithstanding the concomitant use of heparin and/or aspirin. Clot lysis is accelerated and reocclusion is prevented by the administration of F(ab')2 fragments of a monoclonal antibody 7E3 directed against the platelet glycoprotein IIb/IIIa receptor; of Argatroban, a synthetic thrombin inhibitor; or of kistrin, a glycoprotein IIb/IIIa-blocking polypeptide from the Malayan pit viper venom. The PR thrombus models are very resistant to recanalization with rt-PA, but this resistance can be overcome by the concomitant use of the platelet glycoprotein IIb/IIIa-blocking antibody. Thus, selective platelet glycoprotein IIb/IIIa inhibitors are more effective than aspirin, heparin, or both in accelerating arterial thrombolysis with rt-PA; in preventing reocclusion after clot lysis; and in overcoming the resistance of PR thrombus to dispersion with rt-PA. These experimental animal models may be useful in the development of improved thrombolytic strategies using plasminogen activators in conjunction with specifically targeted antiplatelet and anticoagulant agents. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,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. RP GOLD, HK (reprint author), MASSACHUSETTS GEN HOSP,DIV CARDIAC,WACC 4,ROOM 480,15 PARKMAN ST,BOSTON,MA 02114, USA. RI Guerrero, Jorge/I-3666-2015 OI Guerrero, Jorge/0000-0003-4315-7318 NR 53 TC 63 Z9 63 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1991 VL 83 IS 6 SU S BP 26 EP 40 PG 15 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FQ624 UT WOS:A1991FQ62400004 ER PT J AU HABER, E COLLEN, D HARKER, L GOLD, HK FOLTS, J LIGHT, RT ANTONACCIO, MJ BADIMON, JJ SCHUMACHER, W FLEMING, JS NICHOLS, T ONDETTI, MA AF HABER, E COLLEN, D HARKER, L GOLD, HK FOLTS, J LIGHT, RT ANTONACCIO, MJ BADIMON, JJ SCHUMACHER, W FLEMING, JS NICHOLS, T ONDETTI, MA TI ANIMAL-MODELS FOR THE STUDY OF THROMBOLYSIS INVIVO - ROUND-TABLE DISCUSSION SO CIRCULATION LA English DT Discussion DE DISCUSSION; THROMBOSIS ID BLEEDING-TIME; DISEASE C1 BRISTOL MYERS SQUIBB PHARMACEUT,RES INST,PRINCETON,NJ. EMORY UNIV,SCH MED,HEMATOL & ONCOL DEPT A,ATLANTA,GA 30322. MASSACHUSETTS GEN HOSP,DIV CARDIAC,BOSTON,MA 02114. CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,B-3000 LOUVAIN,BELGIUM. UNIV WISCONSIN,CARDIOL SECT,MADISON,WI 53792. UNIV N CAROLINA,SCH MED,DEPT MED,CHAPEL HILL,NC 27514. RP HABER, E (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 8 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 JUN PY 1991 VL 83 IS 6 SU S BP 73 EP 79 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FQ624 UT WOS:A1991FQ62400008 ER PT J AU FROSTELL, C FRATACCI, MD WAIN, JC JONES, R ZAPOL, WM AF FROSTELL, C FRATACCI, MD WAIN, JC JONES, R ZAPOL, WM TI INHALED NITRIC-OXIDE - A SELECTIVE PULMONARY VASODILATOR REVERSING HYPOXIC PULMONARY VASOCONSTRICTION SO CIRCULATION LA English DT Article DE ENDOTHELIUM-DERIVED RELAXING FACTOR; PULMONARY HYPERTENSION; THROMBOXANE ANALOG; HYPOXIA ID RELAXING FACTOR; NITROGEN-DIOXIDE; NITROPRUSSIDE; LUNGS; RELAXATION; HEMOGLOBIN; ARTERY; INVITRO; BLOOD; VEIN AB Background. We examined the effects of inhalation of 5-80 ppm nitric oxide (NO) gas on the normal and acutely constricted pulmonary circulation in awake lambs. Methods and Results. Spontaneous breathing of nitric oxide (an endothelium-derived relaxing factor) at 40 ppm or more reversed acute pulmonary vasoconstriction within 3 minutes either because of infusion of the stable thromboxane endoperoxide analogue U46619 or because of pulmonary hypertension due to breathing a hypoxic gas mixture. Systemic vasodilation did not occur. Pulmonary vasodilation by NO inhalation was produced during infusion of U46619 for periods of 1 hour without observing evidence of short-term tolerance. Pulmonary hypertension resumed within 3-6 minutes of ceasing NO inhalation. In the normal lamb, the pulmonary vascular resistance, systemic vascular resistance, cardiac output, left atrial and central venous pressures were unaltered by NO inhalation. Conclusion. Breathing 80 ppm NO for 3 hours did not increase either methemoglobin or extravascular lung water levels or modify lung histology compared with those in control lambs. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT PATHOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-42397] NR 49 TC 814 Z9 823 U1 2 U2 10 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1991 VL 83 IS 6 BP 2038 EP 2047 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FP800 UT WOS:A1991FP80000022 PM 2040056 ER PT J AU CHEN, C RODRIGUEZ, L GUERRERO, JL MARSHALL, S LEVINE, RA WEYMAN, AE THOMAS, JD AF CHEN, C RODRIGUEZ, L GUERRERO, JL MARSHALL, S LEVINE, RA WEYMAN, AE THOMAS, JD TI NONINVASIVE ESTIMATION OF THE INSTANTANEOUS 1ST DERIVATIVE OF LEFT-VENTRICULAR PRESSURE USING CONTINUOUS-WAVE DOPPLER ECHOCARDIOGRAPHY SO CIRCULATION LA English DT Article DE ECHOCARDIOGRAPHY, DOPPLER; LEFT VENTRICULAR FUNCTION; LEFT VENTRICULAR DP/DT ID ACUTE MITRAL REGURGITATION; SYSTOLIC PRESSURE; MYOCARDIAL-INFARCTION; AORTIC-STENOSIS; DUAL CATHETER; FLOW; CONTRACTILITY; VALIDATION; VOLUME; RELAXATION AB Background. The complete continuous-wave Doppler mitral regurgitant velocity curve should allow reconstruction of the ventriculoatrial (VA) pressure gradient from mitral valve closure to opening, including left ventricular (LV) isovolumic contraction, ejection, and isovolumic relaxation. Assuming that the left atrial pressure fluctuation is relatively minor in comparison with the corresponding LV pressure changes during systole, the first derivative of the Doppler-derived VA pressure gradient curve (Doppler dP/dt) might be used to estimate the LV dP/dt curve, previously measurable only at catheterization (catheter dP/dt). Methods and Results. This hypothesis was examined in an in vivo mitral regurgitant model during 30 hemodynamic stages in eight dogs. Contractility and relaxation were altered by inotropic stimulation and hypothermia. The Doppler mitral regurgitant velocity spectrum was recorded along with simultaneously acquired micromanometer LV and left atrial pressures. The regurgitant velocity profiles were digitized and converted to VA pressure gradient curves using the simplified Bernoulli equation. The instantaneous dP/dt of the VA pressure gradient curve was then derived. The instantaneous Doppler-derived VA pressure gradients, instantaneous Doppler dP/dt, dP/dt(max), and -dP/dt(max) were compared with corresponding catheter measurements. This method of estimating dP/dt(max) from the instantaneous dP/dt curve was also compared with a previously proposed Doppler method of estimating dP/dt(max) using the Doppler-derived mean rate of LV pressure rise over the time period between velocities of 1 and 3 m/sec on the ascending slope of the Doppler velocity spectrum. Both instantaneous Doppler-derived VA pressure gradients (r = 0.95, p < 0.0001) and Doppler dP/dt (r = 0.92, p < 0.0001) correlated well with corresponding measurements by catheter during systolic contraction and isovolumic relaxation (pooled data). The Doppler dP/dt(max) (1,266 +/- 701 mm Hg/sec) also correlated well (r = 0.94) with the catheter dP/dt(max) (1,200 +/- 573 mm Hg/sec). There was no difference between the two methods for measurement of dP/dt(max) (p = NS). Although Doppler - dP/dt(max) was slightly lower than the catheter measurement (961 +/- 511 versus 1,057 +/- 540 mm Hg/sec, p < 0.01), the correlation between measurements by Doppler and catheter was excellent (r = 0.93, p < 0.0001). The alternative method of mean isovolumic pressure rise (896 +/- 465 mm Hg/sec) underestimated the catheter dP/dt(max) (1,200 +/- 573 mm Hg/sec) significantly (on average, 25%; p < 0.001). Conclusions. The present study demonstrated an accurate and reliable noninvasive Doppler method for estimating instantaneous LV dP/dt, dP/dt(max), and -dP/dt(max). C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-38176] NR 31 TC 86 Z9 93 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1991 VL 83 IS 6 BP 2101 EP 2110 PG 10 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FP800 UT WOS:A1991FP80000029 PM 2040059 ER PT J AU KHURANA, JS ROSENBERG, AE KATTAPURAM, SV FERNANDEZ, OS EHARA, S AF KHURANA, JS ROSENBERG, AE KATTAPURAM, SV FERNANDEZ, OS EHARA, S TI MALIGNANCY SUPERVENING ON AN INTRAMEDULLARY NAIL SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article ID REPLACEMENT; SARCOMA AB A primary, malignant, fibrous histiocytoma of bone occurring in association with a Hansen Street intramedullary nail occurred in a 39-year-old man. The physical and chemical characteristics of materials, in relation to the generation of secondary neoplasia are reviewed, but the problem of coincidence is difficult to exclude. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. CHILDRENS HOSP,NATL MED CTR,DEPT ORTHOPED,WASHINGTON,DC 20010. SAN JUAN HLTH CTR,SAN JUAN,PR. NR 14 TC 11 Z9 11 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 JUN PY 1991 IS 267 BP 251 EP 254 PG 4 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FQ673 UT WOS:A1991FQ67300040 PM 1646091 ER PT J AU ANDERSON, BJ AF ANDERSON, BJ TI CHRONIC ILLNESS DURING CHILDHOOD AND ADOLESCENCE - PSYCHOLOGICAL-ASPECTS - GARRISON,WT, MCQUISTON,S SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ANDERSON, BJ (reprint author), JOSLIN DIABET FDN INC,BOSTON,MA 02215, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD JUN PY 1991 VL 36 IS 6 BP 511 EP 512 PG 2 WC Psychology, Multidisciplinary SC Psychology GA FP585 UT WOS:A1991FP58500034 ER PT J AU VANKERCKHOVE, C RUSSELL, GJ PARKER, CM BRENNER, MB AF VANKERCKHOVE, C RUSSELL, GJ PARKER, CM BRENNER, MB TI ANTIGEN RECEPTORS AND ADHESION MOLECULES ON T LYMPHOCYTES IN THE GUT SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article AB The gut-associated lymphoid tissue represents an important site of initial contact with foreign antigens from the intestinal lumen. It is a complex immune system comprising of Peyer's patches, mesenteric lymph nodes, mucosal lymphocytes present in the lamina propria, and intraepithelial lymphocytes located on the luminal surface of the basement membrane and adjacent to the basolateral side of enterocytes. The function and immunoregulation of the gut-associated lyphoid tissue and its role in the pathogenesis of intestinal diseases are only partly understood. We summarize selected advances in understanding the cell-surface molecules involved in homing and adhesion of T cells in the gut-associated lymphoid tissue and the nature of the T-cell antigen receptor repertoire expressed by intraepithelial lymphocytes. RP VANKERCKHOVE, C (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD JUN PY 1991 VL 7 IS 3 BP 432 EP 436 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FQ273 UT WOS:A1991FQ27300013 ER PT J AU SANDERSON, IR WALKER, WA AF SANDERSON, IR WALKER, WA TI NUTRITION AND IMMUNITY SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article AB It is appealing to believe that improved nutrition enhances the capability of the immune system to ward off pathogens. Manipulating the diet is often a simple task, whereas adjusting the immune system at a cellular level involves the interplay of very complex elements. It is heartening, therefore, that evidence has accumulated to substantiate this link and that evidence has continued to increase over the past year. RP SANDERSON, IR (reprint author), MASSACHUSETTS GEN HOSP,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD JUN PY 1991 VL 7 IS 3 BP 463 EP 470 DI 10.1097/00001574-199106000-00019 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FQ273 UT WOS:A1991FQ27300017 ER PT J AU MCCULLOCH, DK KOERKER, DJ KAHN, SE BONNERWEIR, S PALMER, JP AF MCCULLOCH, DK KOERKER, DJ KAHN, SE BONNERWEIR, S PALMER, JP TI CORRELATIONS OF INVIVO BETA-CELL FUNCTION-TESTS WITH BETA-CELL MASS AND PANCREATIC INSULIN CONTENT IN STREPTOZOCIN-ADMINISTERED BABOONS SO DIABETES LA English DT Article ID HLA-IDENTICAL SIBLINGS; I DIABETES-MELLITUS; B-CELLS; 1ST-DEGREE RELATIVES; DEPENDENT DIABETICS; GLUCOSE; SENSITIVITY; SECRETION; ISLET; DYSFUNCTION AB In vivo beta-cell function tests are used increasingly in humans during the preclinical phase of insulin-dependent diabetes mellitus (IDDM), but the severity of the beta-cell loss responsible for the abnormalities seen in these tests is unknown. We have measured several physiological beta-cell function tests-fasting plasma glucose, glucose disappearance constant, fasting insulin, acute insulin responses to arginine (AIR(arginine)) and glucose (AIR(glucose)), and glucose potentiation of AIR(arginine) (DELTA-AIR(arginine)/DELTA-G) and two direct objective measurements (pancreatic insulin content [PIC] and quantitative beta-cell mass)-in adolescent male baboons (Papio anubis/cyanocephalus). We have correlated in vivo measurements obtained within 3 days after the animals were killed with in vitro estimates of PIC and beta-cell mass in 15 animals, (2 nondiabetic requiring insulin treatment and 13 after varying doses of streptozocin to induce degrees of beta-cell damage ranging from normoglycemia to severe hyperglycemia). There was a strong linear correlation between beta-cell mass and PIC (r = 0.79, P < 0.001). Physiological measures of beta-cell function were significantly correlated with both PIC and beta-cell mass. The correlations between physiological measures and beta-cell mass were linear and intercepted the beta-cell mass axis at 0.15-0.2 g, suggesting that in vivo measures of beta-cell function approach 0 when there is still approximately 40-50% of the beta-cell mass detectable histologically. With PIC, the linear correlations intercepted the axes close to 0. These findings provide considerable validity to the measurements of beta-cell function used in preclinical IDDM in humans. Our data suggest that such physiological measurements give an accurate valid reflection of changes in beta-cell mass and pancreatic insulin content. C1 UNIV WASHINGTON,DIABET ENDOCRINOL RES CTR,DEPT BIOPHYS,SEATTLE,WA 98108. DEPT VET AFFAIRS,SEATTLE,WA. JOSLIN DIABET CTR,BOSTON,MA. UNIV WASHINGTON,DIABET ENDOCRINOL RES CTR,DEPT MED,SEATTLE,WA 98108. UNIV WASHINGTON,DIABET ENDOCRINOL RES,DEPT PHYSIOL,SEATTLE,WA 98108. RP MCCULLOCH, DK (reprint author), UNIV WASHINGTON,VET AFFAIRS MED CTR,MED SERV 111,ZB-20,1660 S COLUMBIAN WAY,SEATTLE,WA 98108, USA. FU NCRR NIH HHS [RR-00166]; NIDDK NIH HHS [DK-02456, DK-17047] NR 54 TC 108 Z9 109 U1 1 U2 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD JUN PY 1991 VL 40 IS 6 BP 673 EP 679 DI 10.2337/diabetes.40.6.673 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FN617 UT WOS:A1991FN61700004 PM 2040383 ER PT J AU ZIEGLER, R ALPER, CA AWDEH, ZL CASTANO, L BRINK, SJ SOELDNER, JS JACKSON, RA EISENBARTH, GS AF ZIEGLER, R ALPER, CA AWDEH, ZL CASTANO, L BRINK, SJ SOELDNER, JS JACKSON, RA EISENBARTH, GS TI SPECIFIC ASSOCIATION OF HLA-DR4 WITH INCREASED PREVALENCE AND LEVEL OF INSULIN AUTOANTIBODIES IN 1ST-DEGREE RELATIVES OF PATIENTS WITH TYPE-I DIABETES SO DIABETES LA English DT Article ID ISLET-CELL ANTIBODIES; MAJOR HISTOCOMPATIBILITY COMPLEX; HLA-DR; GENETIC-POLYMORPHISM; IMMUNE-RESPONSE; PROTEIN-A; MELLITUS; ASSAY; CHILDREN; ALLOANTIGENS AB First-degree relatives of patients with insulin-dependent (type I) diabetes (n = 264 from 106 families) were evaluated with HLA typing and determination of competitive insulin autoantibodies (CIAAs) and islet cell autoantibodies (ICAs). The levels of CIAAs in 30 relatives exceeded our upper limit of normal (greater-than-or-equal-to 39 nU/ml), and 30 had high-titer ICAs (greater-than-or-equal-to 40 Juvenile Diabetes Foundation units [JDF U]). Eleven of the HLA-typed relatives developed diabetes during follow-up. Twenty-three percent (28 of 123) of the relatives with at least one HLA-DR4 allele were CIAA + (CIAA greater-than-or-equal-to 39 nU/ml) versus 4% (6 of 141) among DR4- relatives (P < 0.0001). Twenty-one of 22 of the highest CIAA values were all in the DR4+ group (DR4+ vs. DR4-, P = 0.003, Wilcoxon's rank-sum test). HLA-DR3 did not correlate with the level of CIAAs, and neither DR3 nor DR4 correlated with titer of ICAs measured in JDF U. We conclude that, in first-degree relatives of patients with type I diabetes, there is a striking association with HLA-DR4 in both the prevalence of relatives exceeding the normal CIAA range and in the level of CIAAs. These data suggest that a gene on HLA-DR4 haplotypes contributes to the level of anti-insulin autoimmunity, and we hypothesize that DR4-associated diabetes susceptibility, distinct from DR3-associated susceptibility, may be secondary to this influence. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215. NEW ENGLAND DIABET & ENDOCRINOL CTR,CTR BLOOD RES,CHESTNUT HILL,MA. UNIV CALIF DAVIS,SACRAMENTO MED CTR,SACRAMENTO,CA 95817. RI Castano, Luis/C-3084-2009 FU NIDDK NIH HHS [DK-26844, DK-33790, DK-36836] NR 41 TC 56 Z9 56 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 JUN PY 1991 VL 40 IS 6 BP 709 EP 714 DI 10.2337/diabetes.40.6.709 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FN617 UT WOS:A1991FN61700009 PM 2040387 ER PT J AU LAFFEL, L AF LAFFEL, L TI INCREASED BLOOD-PRESSURE AND ERYTHROCYTE SODIUM LITHIUM COUNTERTRANSPORT ACTIVITY ARE NOT INHERITED IN DIABETIC NEPHROPATHY SO DIABETOLOGIA LA English DT Letter ID HYPERTENSION RP LAFFEL, L (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,EPIDEMIOL & GENET UNIT,1 JOSLIN PL,BOSTON,MA 02115, USA. NR 7 TC 4 Z9 4 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD JUN PY 1991 VL 34 IS 6 BP 452 EP 453 DI 10.1007/BF00403187 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FR268 UT WOS:A1991FR26800015 PM 1884904 ER PT J AU COULSTON, DR AF COULSTON, DR TI HEPATITIS-B VACCINE SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Editorial Material ID HEALTH-CARE WORKERS; VIRUS RP COULSTON, DR (reprint author), DEACONESS MED CTR,INTERNAL MED RESIDENCY PROGRAM,800 W 5TH AVE,RM 629,SPOKANE,WA 99210, USA. NR 7 TC 1 Z9 1 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD JUN PY 1991 VL 25 IS 6 BP 671 EP 672 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FR210 UT WOS:A1991FR21000023 PM 1831580 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI HOMOLOGOUS DESENSITIZATION OF THE INSULINOTROPIC GLUCAGONLIKE PEPTIDE-I(7-37) RECEPTOR ON INSULINOMA (HIT-T15) CELLS SO ENDOCRINOLOGY LA English DT Article ID GASTRIC-INHIBITORY POLYPEPTIDE; STIMULATED ADENYLATE-CYCLASE; PERFUSED RAT PANCREAS; PEPTIDE-I; GENE-EXPRESSION; GIP RECEPTORS; BETA-CELLS; SECRETION; LINE; SOMATOSTATIN AB Glucagon-like peptide-I(7-37) [GLP-I(7-37)] is an intestinal peptide with potent insulinotropic activities on pancreatic beta-cells in vivo and in vitro. In earlier studies elevated concentrations GLP-I(7-37) inhibited insulin release and cAMP generation in beta-cells. We now show that the GLP-I(7-37) receptor in the glucose-responsive B-cell line HIT-T15 undergoes rapid and reversible homologous desensitization in response to supraphysiological concentrations of GLP-I(7-37). GLP-I(7-37) stimulated insulin release and cAMP generation in a glucose-dependent biphasic manner with a maximum stimulation at 10 nmol/liter. The first-phase insulin secretory response was reduced by 41% at doses of GLP-I(7-37) of 100 nmol/liter and higher. Preperifusion of B-cells with 100 nmol/liter GLP-I(7-37) for 5 or 10 min reduced a subsequent insulin secretory response to 10 nmol/liter GLP-I(7-37) after hormone washout and recovery periods of 10 min (52% and 55% reduction) or 30 min (33% reduction or full recovery). Preperifusion of HIT-T15 cells with 100 nmol/liter glucagon (10 min) or 100 nmol/liter gastric inhibitory peptide (GIP) (10 min) had no effect on the insulin secretory response to 10 nmol/liter GLP-I(7-37). Prior exposure of cells to 100 nmol/liter GLP-(7-37) (10 min) did not alter the GIP-induced (10 nmol/liter) insulin release, but 100 nmol/liter GIP (10 min) reduced the insulin secretion during stimulation with 10 nmol/liter GIP by 56%. These data indicate that: 1) the GLP-I(7-37) receptor is subject to rapid and reversible homologous desensitization and, 2) the GLP-I(7-37) receptor on beta-cells is distinct from that of GIP. The recent finding of elevated GLP-I(7-36) amide levels in subjects with noninsulin-dependent diabetes suggests the possibility that a homologous desensitization of the GLP-I(7-37) receptor might contribute to the impaired insulin secretion in this disorder. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02114. RP FEHMANN, HC (reprint author), MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK-30834] NR 41 TC 65 Z9 65 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD JUN PY 1991 VL 128 IS 6 BP 2880 EP 2888 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FN112 UT WOS:A1991FN11200028 PM 1645253 ER PT J AU SAGER, R AF SAGER, R TI SENESCENCE AS A MODE OF TUMOR SUPPRESSION SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article ID HUMAN PAPILLOMAVIRUS TYPE-16; MAMMARY EPITHELIAL-CELLS; HUMAN-FIBROBLASTS; KERATINOCYTES; GROWTH; DNA; TRANSFORMATION AB Two independent lines of experimental evidence are presented in support of the hypothesis that senescence is a normal mechanism of tumor suppression, a homeostatic device designed through evolution to limit cell proliferation irreversibly and thereby to protect the organism against cancer. One set of experiments uses normal human foreskin fibroblasts, transfected at early passage with SV40 DNA and subsequently infected with the K-ras virus. If the cells are immortal prior to infection, they become tumorigenic and make large tumors in nude mice, whereas if they are not immortal, though expressing SV40 T-antigen, they make tiny tumors that senesce in the test mouse after as many doublings as similar cells make in culture. This result demonstrates that immortalization is essential for progressive tumor growth in vivo. The second set of experiments demonstrate that normal human mammary epithelial cells can be immortalized by transfection with viral DNA from human papilloma virus 16 or 18, although these viruses have not been associated with breast cancer. The effective immortalization and other premalignant changes induced by human papilloma virus transfection are accompanied by chromosome changes that may contribute to the partially transformed phenotypes. None of the cloned or pooled transfectants have been tumorigenic in the nude mouse assay. Here, too, immortalization is experimentally separable from tumor-forming ability. RP SAGER, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 39814] NR 15 TC 124 Z9 124 U1 1 U2 2 PU NATL INST ENVIRON HEALTH SCI PI RES TRIANGLE PK PA PO BOX 12233, RES TRIANGLE PK, NC 27709 SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD JUN PY 1991 VL 93 BP 59 EP 62 DI 10.2307/3431170 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA GC052 UT WOS:A1991GC05200011 PM 1663451 ER PT J AU ERICKSONLAMY, K ROHEN, JW GRANT, WM AF ERICKSONLAMY, K ROHEN, JW GRANT, WM TI OUTFLOW FACILITY STUDIES IN THE PERFUSED HUMAN OCULAR ANTERIOR SEGMENT SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE OUTFLOW FACILITY; HUMAN EYE; ORGAN CULTURE; TRABECULAR MESHWORK; PERFUSION ID MESHWORK ORGAN-CULTURE; ENUCLEATED HUMAN EYE C1 UNIV ERLANGEN NURNBERG,DEPT ANAT,W-8520 ERLANGEN,GERMANY. RP ERICKSONLAMY, K (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY07321] NR 23 TC 45 Z9 46 U1 1 U2 6 PU ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD JUN PY 1991 VL 52 IS 6 BP 723 EP 731 DI 10.1016/0014-4835(91)90024-9 PG 9 WC Ophthalmology SC Ophthalmology GA FR434 UT WOS:A1991FR43400009 PM 1855546 ER PT J AU TSAI, SF STRAUSS, E ORKIN, SH AF TSAI, SF STRAUSS, E ORKIN, SH TI FUNCTIONAL-ANALYSIS AND INVIVO FOOTPRINTING IMPLICATE THE ERYTHROID TRANSCRIPTION FACTOR GATA-1 AS A POSITIVE REGULATOR OF ITS OWN PROMOTER SO GENES & DEVELOPMENT LA English DT Article DE GATA-1; ERYTHROID TRANSCRIPTION FACTOR; INVIVO FOOTPRINTING; PROMOTER ACTIVITY ID DOMINANT CONTROL REGION; PORPHOBILINOGEN DEAMINASE GENE; DNA-BINDING FACTOR; GLOBIN GENE; MAMMALIAN-CELLS; PLASMID DNA; EXPRESSION; ENHANCER; ONCOGENE; PROTEIN AB Transcription of erythroid-expressed genes and normal erythroid development in vivo are dependent on a regulatory protein (GATA-1) that recognizes a consensus GATA motif. GATA-1 expression is itself restricted to erythroid progenitors and to two related hematopoietic lineages, megakaryocytes and mast cells. During cellular maturation the levels of GATA-1 RNA and protein increase progressively. In an effort to delineate mechanisms by which this pivotal transcription factor is itself regulated we have characterized the mouse GATA-1 gene and cis-elements within its promoter. We find that the isolated promoter retains cell specificity exhibited by the intact gene. Full promoter activity requires the presence of proximal CACCC box sequences and an upstream, double GATA motif that binds a single GATA-1 molecule in an asymmetric fashion. Using in vivo footprinting of mouse erythroleukemic cells we detect protein binding in vivo to both cis-elements. On the basis of these findings we propose that a positive feedback loop mediated through GATA-1 serves two complementary functions: maintenance of the differentiated state by locking the promoter into an "on" state, and programming the progressive increase in protein content throughout cellular maturation. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02138. HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MICROBIOL IMMUNOL,BOSTON,MA 02115. RI Tsai, Shih-Feng/E-3997-2010 NR 55 TC 293 Z9 295 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 JUN PY 1991 VL 5 IS 6 BP 919 EP 931 DI 10.1101/gad.5.6.919 PG 13 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA FQ554 UT WOS:A1991FQ55400003 PM 2044960 ER PT J AU ZHANG, K SMOUSE, D PERRIMON, N AF ZHANG, K SMOUSE, D PERRIMON, N TI THE CROOKED NECK GENE OF DROSOPHILA CONTAINS A MOTIF FOUND IN A FAMILY OF YEAST-CELL CYCLE GENES SO GENES & DEVELOPMENT LA English DT Article DE CROOKED NECK; TPR MOTIF; NEUROGENESIS; CELL CYCLE; DROSOPHILA ID SACCHAROMYCES-CEREVISIAE; NERVOUS-SYSTEM; X-CHROMOSOME; PROTEIN; MELANOGASTER; SEQUENCE; NUCLEAR; MUTANTS; MUTATIONS; EMBRYOS AB The crooked neck (crn) gene of Drosophila encodes a protein of 702 amino acids and contains 16 tandemly arranged copies of a 34-amino-acid repeat that is similar to the tetratrico peptide repeat (TPR). Multiple copies of the TPR motif have also been found in a family of yeast genes, including several members that are necessary for cell division. TPR-containing proteins encoded by the yeast genes CDC16, CDC23, and nuc2+ are required for progression through the G2/M transition of the cell cycle. Loss of zygotic expression of crn causes defects in the proliferation of brain neuroblasts and results in the absence of identified neuronal lineages in the central and peripheral nervous systems. The sequence similarity and mutant phenotypes are consistent with a cell cycle requirement for the crn gene product. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RI Perrimon, Norbert/F-9766-2011 FU NICHD NIH HHS [HD23684]; NIGMS NIH HHS [GM10300] NR 59 TC 46 Z9 48 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 JUN PY 1991 VL 5 IS 6 BP 1080 EP 1091 DI 10.1101/gad.5.6.1080 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA FQ554 UT WOS:A1991FQ55400016 PM 2044955 ER PT J AU ROLLINS, BJ MORTON, CC LEDBETTER, DH EDDY, RL SHOWS, TB AF ROLLINS, BJ MORTON, CC LEDBETTER, DH EDDY, RL SHOWS, TB TI ASSIGNMENT OF THE HUMAN SMALL INDUCIBLE CYTOKINE A2 GENE, SCYA2 (ENCODING JE OR MCP-1), TO 17Q11.2-12 - EVOLUTIONARY RELATEDNESS OF CYTOKINES CLUSTERED AT THE SAME LOCUS SO GENOMICS LA English DT Note ID CHEMOATTRACTANT PROTEIN-1 MCP-1; GROWTH-FACTOR; CLONING; TRANSLOCATION; LOCALIZATION; SEQUENCE; CELLS; CDNA; EXPRESSION C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BAYLOR UNIV,INST MOLEC GENET,HOUSTON,TX 77030. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14263. RP ROLLINS, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA53091]; NHGRI NIH HHS [HG0333]; NIGMS NIH HHS [GM20454] NR 29 TC 33 Z9 35 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 JUN PY 1991 VL 10 IS 2 BP 489 EP 492 DI 10.1016/0888-7543(91)90338-F PG 4 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FL240 UT WOS:A1991FL24000027 PM 2071154 ER PT J AU MILLARD, WJ ROMANO, TM LAYDEN, MP RUSSELL, WE MARTIN, RJ AF MILLARD, WJ ROMANO, TM LAYDEN, MP RUSSELL, WE MARTIN, RJ TI GROWTH-HORMONE SECRETION IN THE OBESE MALE-RAT - MODULATION BY THE GONADAL AND THYROID AXES SO GROWTH DEVELOPMENT AND AGING LA English DT Article DE GROWTH HORMONE; OBESITY; TESTOSTERONE; EPISODIC SECRETION; GROWTH HORMONE-RELEASING FACTOR; THYROID HORMONE; TSH ID GH-RELEASING HORMONE; HEMOLYTIC PLAQUE-ASSAY; ZUCKER RATS; (GH)-RELEASING FACTOR; ULTRADIAN RHYTHM; SOMATOSTATIN; INVITRO; PYRIDOSTIGMINE; RESPONSIVENESS; STEROIDS AB The present study was designed to determine if either the testes or thyroid plays a role in the blunted GH secretion observed in the obese male rat. Analysis of individual GH secretory profiles in adult lean and obese Zucker rats revealed a severe attenuation of both mean GH levels and individual GH pulse amplitudes in obese rats as well as a significant lowering of circulating testosterone levels. Normalization of the testosterone levels by the use of sc Silastic capsules elevated but did not normalize GH pulse amplitudes in obese animals. Further, the GH response to either rat GH-releasing factor (5-mu/kg) or morphine (1 mg/kg) were reduced in obese male rats. In contrast, the thyroid axis showed minimal change in obese animals. A slight reduction in free T3 levels in serum was observed while free and total T4 and total T3 were normal in obese rats. Further, mean circulating TSH levels and the TSH response to 500 ng/kg TRH were not altered in fat rats. Thus, the reduced GH secretion observed in the obese rat is not paramount to an alteration in either gonadal or thyroid function. This alteration of the GH secretory axis may not be attributable to one factor but more likely caused by a number of concomitant deficits which may act in concert to manifest impaired GH secretion. C1 MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. UNIV GEORGIA,COLL HOME ECON,DEPT FOODS & NUTR,ATHENS,GA 30602. RP MILLARD, WJ (reprint author), UNIV FLORIDA,COLL PHARM,DEPT PHARMACODYNAM,GAINESVILLE,FL 32610, USA. RI Russell, William/A-7307-2009 FU NICHD NIH HHS [HD-22199, HD-22226] NR 55 TC 11 Z9 11 U1 0 U2 0 PU GROWTH PUBL CO INC PI BAR HARBOR PA PO BOX 42, BAR HARBOR, ME 04609-0042 SN 0017-4793 J9 GROWTH DEVELOP AGING JI Growth Dev. Aging PD SUM PY 1991 VL 55 IS 2 BP 91 EP 103 PG 13 WC Developmental Biology; Geriatrics & Gerontology SC Developmental Biology; Geriatrics & Gerontology GA GB542 UT WOS:A1991GB54200003 PM 1682282 ER PT J AU CAREY, TS WEIS, K HOMER, C AF CAREY, TS WEIS, K HOMER, C TI PREPAID VERSUS TRADITIONAL MEDICAID PLANS - LACK OF EFFECT ON PREGNANCY OUTCOMES AND PRENATAL-CARE SO HEALTH SERVICES RESEARCH LA English DT Article ID BIRTH-WEIGHT; HEALTH; TRIAL; HMO C1 UNIV N CAROLINA,DEPT SOCIAL MED,CHAPEL HILL,NC 27599. UNIV N CAROLINA,DEPT HLTH POLICY & ADM,CHAPEL HILL,NC 27599. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. RP CAREY, TS (reprint author), UNIV N CAROLINA,DEPT MED,CB 7110,5025 B OLD CLIN BLDG,CHAPEL HILL,NC 27599, USA. NR 24 TC 42 Z9 42 U1 0 U2 0 PU HEALTH ADMINISTRATION PRESS PI MELROSE PARK PA C/O FOUNDATION AMER COLL HEALTHCARE EXECUTIVES 1951 CORNELL AVE, MELROSE PARK, IL 60160 SN 0017-9124 J9 HEALTH SERV RES JI Health Serv. Res. PD JUN PY 1991 VL 26 IS 2 BP 165 EP 181 PG 17 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA FR010 UT WOS:A1991FR01000002 PM 2061055 ER PT J AU LIANG, TJ BARUCH, Y BENPORATH, E ENAT, R BASSAN, L BROWN, NV RIMON, N BLUM, HE WANDS, JR AF LIANG, TJ BARUCH, Y BENPORATH, E ENAT, R BASSAN, L BROWN, NV RIMON, N BLUM, HE WANDS, JR TI HEPATITIS-B VIRUS-INFECTION IN PATIENTS WITH IDIOPATHIC LIVER-DISEASE SO HEPATOLOGY LA English DT Article ID POLYMERASE CHAIN-REACTION; NON-A; C VIRUS; HEPATOCELLULAR-CARCINOMA; SURFACE-ANTIGEN; DNA; SERUM; ANTIBODIES; GENOME; ASSAY AB We studied 67 HBsAg-negative Israeli patients (36 negative for all HBV serological markers as group 1 and 31 positive for antibodies to HBs and HBc as group 2) with chronic liver disease and cirrhosis of unknown origin using a rapid, sensitive and specific assay for the detection of low levels of hepatitis B virus in serum. This technique uses a high-affinity monoclonal antibody to HBs against an a domain epitope of HBsAg to capture the virion, followed by hepatitis B virus DNA amplification with the polymerase chain reaction. In addition, 55 subjects without liver disease served as controls: Group 3 (n = 32) was negative for all hepatitis B virus markers; group 4 (n = 23) was positive for antibodies to HBs and HBc. We found 11 individuals in group 1 (31%) and 10 in group 2 (29%) harboring low levels of hepatitis B virus DNA in serum. In contrast, no one in group 3 or group 4 was positive by this technique (p < 0.0001). Using polymerase chain reaction primers spanning other regions of the hepatitis B virus genome and a method of restriction-fragment analysis of polymerase chain reaction-amplified sequences, we detected significant DNA sequence heterogeneity, suggesting infection with distinct hepatitis B virus strains. DNA extracted from paraffin-embedded liver biopsy specimens of 42 patients from groups 1 and 2 was shown to contain hepatitis B virus DNA by polymerase chain reaction in 11 of 12 patients with circulating virion DNA. More important, 18 additional patients whose sera were negative by HBs-antibody capture/polymerase chain reaction amplification had hepatitis B virus DNA sequences in their livers. Hepatitis C virus antibodies were found in 71% of group 1, in 65% of group 2, in 3% of group 3 and in 4% of group 4 (p < 0.0001). Coexistence of hepatitis B virus infection and hepatitis C virus antibodies were common (> 30%). We conclude that infection with hepatitis B virus undetectable by conventional assays and with hepatitis C virus may represent important unrecognized causes of idiopathic chronic liver disease in Israel, accounting for the possible origin in more than 90% of patients. C1 TECHNION ISRAEL INST TECHNOL,RAMBAM MED CTR,FAC MED,DEPT PATHOL,IL-31096 HAIFA,ISRAEL. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. TECHNION ISRAEL INST TECHNOL,RAMBAM MED CTR,FAC MED,VIROL LAB,IL-31096 HAIFA,ISRAEL. TECHNION ISRAEL INST TECHNOL,RAMBAM MED CTR,FAC MED,DEPT MED B,IL-31096 HAIFA,ISRAEL. RP LIANG, TJ (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,149 13TH ST,7TH FLOOR,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-08169, AA-02666] NR 37 TC 113 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 0270-9139 J9 HEPATOLOGY JI Hepatology PD JUN PY 1991 VL 13 IS 6 BP 1044 EP 1051 DI 10.1016/0270-9139(91)92470-S PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FT650 UT WOS:A1991FT65000006 PM 2050320 ER PT J AU FLOTTE, TJ AF FLOTTE, TJ TI MALIGNANT-MELANOMA INSITU - ANOTHER PERSPECTIVE - REPLY SO HUMAN PATHOLOGY LA English DT Letter RP FLOTTE, TJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD JUN PY 1991 VL 22 IS 6 BP 627 EP 627 DI 10.1016/0046-8177(91)90250-S PG 1 WC Pathology SC Pathology GA GJ608 UT WOS:A1991GJ60800026 ER PT J AU GOODFRIEND, TL BALL, DL WEINBERGER, MH MOORE, TJ WEDER, AB EGAN, BM AF GOODFRIEND, TL BALL, DL WEINBERGER, MH MOORE, TJ WEDER, AB EGAN, BM TI SALT LOADS RAISE PLASMA FATTY-ACIDS AND LOWER INSULIN SO HYPERTENSION LA English DT Article; Proceedings Paper CT 44TH ANNUAL FALL CONF AND SCIENTIFIC SESSION OF THE COUNCIL FOR HIGH BLOOD PRESSURE RESEARCH CY SEP 12-15, 1990 CL BALTIMORE, MD SP COUNCIL HIGH BLOOD PRESSURE RES DE BLOOD PRESSURE; SODIUM-DEPENDENT HYPERTENSION; INSULIN; NOREPINEPHRINE ID LIQUID-CHROMATOGRAPHIC ANALYSIS; BLOOD-PRESSURE; IDENTIFICATION; EPINEPHRINE; ALDOSTERONE; INHIBITORS; POTASSIUM; DIETS; TRIAL; RAT AB Some fatty acids are potent inhibitors of angiotensin binding and aldosterone production in adrenal glomerulosa cells and thereby may be involved in regulating salt and water balance. To study the possible regulation of fatty acids by salt, we measured the levels of unesterified fatty acids in plasma from patients subjected to extremes of dietary salt intake and saline infusion. Insulin and catecholamines, two known regulators of plasma fatty acids, also were measured. Infusion of 2 1 saline over 4 hours caused the levels of most unesterified fatty acids to rise. Total unesterified fatty acids rose 60-100%. A high salt diet caused a smaller rise in total unesterified fatty acids (approximately 33%). In both instances, oleic and palmitoleic acids showed the greatest proportionate increases, whereas stearic acid was relatively unaffected. When salt loads were administered by either intravenous or dietary routes, plasma insulin levels fell by approximately 50%. Plasma norepinephrine increased after saline infusion but not during a high salt diet. Postsaline levels of fatty acids correlated inversely with postsaline levels of aldosterone, supporting a possible role for fatty acids as physiological regulators of the adrenal glomerulosa. A rise in plasma fatty acids and fall in insulin in response to salt loads could act in concert to increase sodium excretion, constituting a physiological mechanism contributing to salt and water balance. C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. INDIANA UNIV,SCH MED,INDIANAPOLIS,IN 46202. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MICHIGAN,SCH MED,ANN ARBOR,MI 48104. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. FU NHLBI NIH HHS [HL-18575, HL-37717, HL-36568] NR 28 TC 24 Z9 24 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JUN PY 1991 VL 17 IS 6 SU S BP 958 EP 964 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FR814 UT WOS:A1991FR81400020 PM 2045176 ER PT J AU SKLAR, RM HUDSON, A BROWN, RH AF SKLAR, RM HUDSON, A BROWN, RH TI GLUCOCORTICOIDS INCREASE MYOBLAST PROLIFERATION RATES BY INHIBITING DEATH OF CYCLING CELLS SO IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY LA English DT Letter ID SERUM-FREE MEDIUM; SKELETAL-MUSCLE; GROWTH RP SKLAR, RM (reprint author), MASSACHUSETTS GEN HOSP,CECIL B DAY NEUROMUSCULAR RES LABS,149 13TH ST,NAVY YARD,BOSTON,MA 02129, USA. NR 11 TC 7 Z9 7 U1 0 U2 0 PU SOC IN VITRO BIOLOGY PI COLUMBIA PA 8815 CENTRE PARK DRIVE SUITE 210, COLUMBIA, MD 21045 SN 0073-5655 J9 IN VITRO CELL DEV B PD JUN PY 1991 VL 27 IS 6 BP 433 EP 434 PG 2 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA GB181 UT WOS:A1991GB18100001 ER PT J AU MICHEL, JL MADOFF, LC KLING, DE KASPER, DL AUSUBEL, FM AF MICHEL, JL MADOFF, LC KLING, DE KASPER, DL AUSUBEL, FM TI CLONED ALPHA AND BETA C-PROTEIN ANTIGENS OF GROUP-B STREPTOCOCCI ELICIT PROTECTIVE IMMUNITY SO INFECTION AND IMMUNITY LA English DT Article ID GROUP-A STREPTOCOCCI; IBC PROTEINS; IMMUNOGLOBULIN-A; ESCHERICHIA-COLI; EXPRESSION; IDENTIFICATION; ANTIBODIES; BINDING; STRAINS; IMMUNIZATION AB Streptococcus agalactiae (group B streptococci [GBS]) is the leading cause of neonatal sepsis and meningitis in the United States. The surface-associated C proteins of GBS play a role in immunity, but their number, size, structure, function, and virulence properties have not been well characterized. A recombinant library of DNA fragments from GBS strain A909 (type Ia/C) was prepared in the plasmid pUX12, a specially constructed Escherichia coli expression vector. The library was screened with a rabbit antiserum shown to be protective for passive immunity to GBS infection in a mouse lethality model. Clones were divided into two distinct groups on the basis of DNA-DNA cross-hybridization, restriction enzyme analysis, and the expression of antigenic proteins in E. coli. A characteristic clone from each group was chosen for further study. Clone pJMS23 expresses gene products that biochemically and immunologically correspond to the trypsin-resistant, C-protein alpha antigen. Clone pJMS1 expresses a gene product that binds to immunoglobulin A and is similar to the trypsin-sensitive, C-protein beta antigen. Antisera raised in rabbits against E. coli containing each of the plasmid clones were able to elicit protective immunity in mice challenged by GBS strains carrying the C proteins but not by non-C-protein-bearing strains. Southern blot analysis shows no DNA homology between the clones, and there is no immunological cross-reactivity between the antigens they express. Therefore, pJMS23 and pJMS1 encode two different C proteins that define unique protective epitopes. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,DIV INFECT DIS,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP MICHEL, JL (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,CHANNING LAB,180 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI23339, AI28500, AI00981] NR 40 TC 73 Z9 75 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUN PY 1991 VL 59 IS 6 BP 2023 EP 2028 PG 6 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA FN775 UT WOS:A1991FN77500025 PM 1674738 ER PT J AU HAUSER, ST HOULIHAN, J POWERS, SI JACOBSON, AM NOAM, GG WEISSPERRY, B FOLLANSBEE, D BOOK, BK AF HAUSER, ST HOULIHAN, J POWERS, SI JACOBSON, AM NOAM, GG WEISSPERRY, B FOLLANSBEE, D BOOK, BK TI ADOLESCENT EGO DEVELOPMENT WITHIN THE FAMILY - FAMILY STYLES AND FAMILY SEQUENCES SO INTERNATIONAL JOURNAL OF BEHAVIORAL DEVELOPMENT LA English DT Article; Proceedings Paper CT PRE-CONF WORKSHOP ON FAMILY CONTEXTS OF ADOLESCENT DEVELOPMENT CY MAR 20, 1986 CL MADISON, WI SP SOC RES ADOLESCENCE ID RELIABILITY C1 HARVARD UNIV,SCH MED,JUDGE BAKER GUIDANCE CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS MENT HLTH CTR,DEPT PSYCHIAT,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA. BOSTON UNIV,CTR ACAD COMP,BOSTON,MA 02215. UNIV MASSACHUSETTS,DEPT PSYCHOL,AMHERST,MA 01003. MCLEAN HOSP,BELMONT,MA 02178. NORTHWESTERN UNIV,EVANSTON,IL 60201. NR 44 TC 18 Z9 18 U1 1 U2 2 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0165-0254 J9 INT J BEHAV DEV JI Int. J. Behav. Dev. PD JUN PY 1991 VL 14 IS 2 BP 165 EP 193 PG 29 WC Psychology, Developmental SC Psychology GA FP643 UT WOS:A1991FP64300003 ER PT J AU CORN, BW TAYLOR, BW KNOX, SJ MARTZ, KL FLYNN, DF AF CORN, BW TAYLOR, BW KNOX, SJ MARTZ, KL FLYNN, DF TI RESULTS OF THE 1989 ASSOCIATION OF RESIDENTS IN RADIATION ONCOLOGY SURVEY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article; Proceedings Paper CT 31ST ANNUAL MEETING OF THE AMERICAN SOC OF THERAPEUTIC RADIOLOGY AND ONCOLOGY CY OCT 01-06, 1989 CL SAN FRANCISCO, CA SP AMER SOC THERAPEUT RADIOL & ONCOL DE ASSOCIATION OF RESIDENTS IN RADIATION ONCOLOGY (ARRO); RESIDENT SURVEY ID MEDICINE; CAREER AB To assess a variety of issues concerning physician-trainees in radiation oncology, a survey was conducted by the Association of Residents in Radiation Oncology (ARRO). Ultimately, 70% of residents responded to the survey. The survey identified perceived strengths as well as shortcomings in training programs. We conclude that residents are generally satisfied with their training. Future surveys are planned to expand this important database. C1 FOX CHASE CANC INST,PHILADELPHIA,PA 19111. WILLIAM A SHANDS TEACHING HOSP & CLIN,DIV RADIAT THERAPY,GAINESVILLE,FL. STANFORD UNIV HOSP,DEPT RADIAT ONCOL,STANFORD,CA 94305. AMER COLL RADIOL,STAT UNIT,PHILADELPHIA,PA. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. NR 12 TC 12 Z9 12 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD JUN PY 1991 VL 20 IS 6 BP 1363 EP 1367 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FQ581 UT WOS:A1991FQ58100027 PM 2045310 ER PT J AU RO, JY BUCKNER, CK BRENDEL, JK FISHLEDER, RI GRAZIANO, FM AF RO, JY BUCKNER, CK BRENDEL, JK FISHLEDER, RI GRAZIANO, FM TI INFLUENCE OF INDOMETHACIN AND L-CYSTEINE ON HISTAMINE AND PEPTIDOLEUKOTRIENE RELEASE FROM SUPERFUSED TRACHEAS TAKEN FROM GUINEA-PIGS PASSIVELY SENSITIZED WITH IGG1 AND IGE ANTIBODIES SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID ARACHIDONIC-ACID METABOLISM; SLOW-REACTING SUBSTANCE; IMMUNOLOGICAL RELEASE; INDUCED CONTRACTION; MEDIATOR RELEASE; MAST-CELLS; HUMAN LUNG; ANAPHYLAXIS; INVITRO; ANTIGEN AB We have previously reported differences in mediator release during equivalent levels of antigen (Ag)-induced smooth muscle contraction of guinea pig pulmonary tissues after passive sensitization with IgG1 versus IgE antibodies (Abs). In the present study, we have examined the influence of indomethacin (5 x 10(-6) mol/L) and L-cysteine (3 or 10 mmol/L) on mediator release from superfused trachea taken from guinea pigs passively sensitized with IgG1 or IgE Ab 1 day before in vitro studies. Tissues were challenged with Ag (oxazolone-human serum albumin conjugate), and contractions and superfusate histamine and peptidoleukotrienes were monitored at discrete time intervals thereafter. Superfusate mediator contents were determined by spectrophotofluorimetry (histamine) and RAST (peptidoleukotrienes). The profiles of peptidoleukotrienes were examined with high-pressure liquid chromatography. At equivalent levels of contraction, significantly less histamine and peptidoleukotrienes were found in superfusate samples after sensitization with IgE Abs. None of the drug pretreatments significantly altered Ag-induced histamine release after IgG1 or IgE sensitization. Indomethacin resulted in an increase in total measurable peptidoleukotrienes found only after IgG1 receptor activation, but it did prolong tracheal contractions with both Abs. L-cysteine, 10 mmol/L, resulted in an increase in total measurable superfusate peptidoleukotriene content under all experimental conditions. The percentage increase in peptidoleukotriene content from that found without drug pretreatment was larger in the case of IgE compared to IgG1 sensitization. During early time periods, after Ag challenge, measurable peptidoleukotriene levels in superfusate samples were similar for both Abs in the presence of L-cysteine, 10 mmol/L. These data suggest that there is a differential pattern of peptidoleukotriene metabolism after activation of IgG1 versus IgE receptors in guinea pig trachea. C1 UNIV WISCONSIN,SCH PHARM,MADISON,WI 53706. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NHLBI NIH HHS [HL 33237, HL 28585]; NIAID NIH HHS [AI 00652] NR 37 TC 15 Z9 15 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD JUN PY 1991 VL 87 IS 6 BP 1150 EP 1160 DI 10.1016/0091-6749(91)92161-S PG 11 WC Allergy; Immunology SC Allergy; Immunology GA FR066 UT WOS:A1991FR06600015 PM 1710633 ER PT J AU FANTIN, B EBERT, S LEGGETT, J VOGELMAN, B CRAIG, WA AF FANTIN, B EBERT, S LEGGETT, J VOGELMAN, B CRAIG, WA TI FACTORS AFFECTING DURATION OF INVIVO POSTANTIBIOTIC EFFECT FOR AMINOGLYCOSIDES AGAINST GRAM-NEGATIVE BACILLI SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID DOSING INTERVALS; THIGH-INFECTION; MICE C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,ROOM D-3224,2500 OVERLOOK TERRACE,MADISON,WI 53705. UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. NR 11 TC 41 Z9 41 U1 1 U2 1 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD JUN PY 1991 VL 27 IS 6 BP 829 EP 836 DI 10.1093/jac/27.6.829 PG 8 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FT015 UT WOS:A1991FT01500016 PM 1938689 ER PT J AU SCHEIBE, RJ GINTY, DD WAGNER, JA AF SCHEIBE, RJ GINTY, DD WAGNER, JA TI RETINOIC ACID STIMULATES THE DIFFERENTIATION OF PC12 CELLS THAT ARE DEFICIENT IN CAMP-DEPENDENT PROTEIN-KINASE SO JOURNAL OF CELL BIOLOGY LA English DT Article ID NERVE GROWTH-FACTOR; BINDING-PROTEIN; CYCLIC-AMP; NEURITE OUTGROWTH; MORPHOLOGICAL-DIFFERENTIATION; PHEOCHROMOCYTOMA CELLS; GENE-EXPRESSION; MESSENGER-RNA; C-FOS; ACETYLCHOLINESTERASE ACTIVITY AB Retinoic acid (RA) induced neuronal differentiation in A126-1B2 cells and 123.7 cells, two mutant lines of PC12 that are deficient in cAMP-dependent protein kinase, but not in the parental PC12 cell line. A single exposure to RA was sufficient to cause neurite formation and inhibit cell division for a period of > 3 wk, suggesting that RA may cause a long-term, stable change in the state of these cells. In A126-1B2 cells, RA also induced the expression of other markers of differentiation including acetylcholinesterase and the mRNAs for neurofilament (NF-M) and GAP-43 as effectively as nerve growth factor (NGF). Neither NGF nor RA stimulated an increase in the expression of smg-25A in A126-1B2 cells, suggesting that the cAMP-dependent protein kinases may be required for an increase in the expression of this marker. RA also caused a rapid increase in the expression of the early response gene, c-fos, but did not effect the expression of egr-1. RA equivalently inhibited the division of A126-1B2 cells, 123.7 cells and parental PC12 cells, so RA induced differentiation is not an indirect response to growth arrest. In contrast, the levels of retinoic acid receptors (RAR-alpha and RAR-beta), and retinoic acid binding protein (CRABP) mRNA were strikingly higher in both A126-1B2 cells and 123.7 cells than in the parental PC12 cells. The deficiencies in cAMP-dependent protein kinase may increase the expression of CRABP and the RARs; and, thus, cAMP may indirectly regulate the ability of RA to control neurite formation and neural differentiation. Thus, RA appears to regulate division and differentiation of PC12 cells by a biochemical mechanism that is quite distinct from those used by peptide growth factors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. RP SCHEIBE, RJ (reprint author), HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA40929]; NINDS NIH HHS [NS08764] NR 66 TC 56 Z9 56 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD JUN PY 1991 VL 113 IS 5 BP 1173 EP 1182 DI 10.1083/jcb.113.5.1173 PG 10 WC Cell Biology SC Cell Biology GA FN341 UT WOS:A1991FN34100017 PM 1645738 ER PT J AU TOJO, K LEE, ARC AF TOJO, K LEE, ARC TI PENETRATION AND BIOCONVERSION OF DRUGS IN THE SKIN SO JOURNAL OF CHEMICAL ENGINEERING OF JAPAN LA English DT Article DE SKIN METABOLISM; PERCUTANEOUS ABSORPTION; PROVITAMIN; VITAMIN-C; VITAMIN-E; PRODRUG ID ESTRADIOL ESTERS; DELIVERY; PERMEATION; KINETICS; PRODRUGS AB The dynamic phenomena of skin diffusion/bioconversion of a provitamin have been described by assuming a bilayer skin consisting of the stratum corneum as a main diffusion barrier and the viable skin as a major site of bioconversion. The mathematical model adequately describes the time courses of the in vitro appearance profiles of the provitamin and its metabolites, vitamins C and E, in the hairless mouse skin. The present model can be used not only to investigate transdermal delivery of prodrugs but also to elucidate mechanisms of skin detoxification of xenobiotics entering the skin. C1 MASSACHUSETTS GEN HOSP,WANG AMBULATORY CARE CTR,DEPT SURG,BOSTON,MA 02114. RP TOJO, K (reprint author), KYUSHU INST TECHNOL,COLL COMP SCI & SYST ENGN,DEPT BIOCHEM SCI & ENGN,IIZUKA CAMPUS,FUKUOKA 820,JAPAN. NR 15 TC 2 Z9 2 U1 0 U2 3 PU SOC CHEMICAL ENG JAPAN PI BUNKYO KU TOKYO PA KYORITSU BUILDING 4-16-19 KOHINATA, BUNKYO KU TOKYO 112, JAPAN SN 0021-9592 J9 J CHEM ENG JPN JI J. Chem. Eng. Jpn. PD JUN PY 1991 VL 24 IS 3 BP 297 EP 300 DI 10.1252/jcej.24.297 PG 4 WC Engineering, Chemical SC Engineering GA FU147 UT WOS:A1991FU14700004 ER PT J AU PRINCE, RL MACLAUGHLIN, DT GAZ, RD NEER, RM AF PRINCE, RL MACLAUGHLIN, DT GAZ, RD NEER, RM TI LACK OF EVIDENCE FOR ESTROGEN-RECEPTORS IN HUMAN AND BOVINE PARATHYROID TISSUE SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID POST-MENOPAUSAL WOMEN; POSTMENOPAUSAL WOMEN; PRIMARY HYPERPARATHYROIDISM; CALCIUM; BINDING; REPLACEMENT; SECRETION; BONE AB It has been hypothesized that estrogen may have a direct effect to reduce the set-point for PTH secretion which may be implicated in its hypocalcemic action. If this is so, estrogen receptors should be demonstrable within parathyroid tissue. Seven human parathyroid adenomas and five samples of normal bovine parathyroid tissue were examined using classical hormone-binding techniques. In no case was there evidence of displaceable estrogen binding of high affinity and low capacity. To exclude the presence of receptors within a small subset of the cells, five of the human adenomas were further studied by immunohistochemistry using a monoclonal antibody to the human estrogen receptor. In no case was there evidence of estrogen receptors. We conclude that the hypocalcemic action of estrogen replacement is unlikely to be mediated via a classical estrogen receptor within the parathyroid, although normal parathyroid tissue was not studied. C1 UNIV WESTERN AUSTRALIA, SIR CHARLES GALRDNER HOSP, DEPT MED, NEDLANDS, WA 6009, AUSTRALIA. MASSACHUSETTS GEN HOSP, DEPT ENDOCRINE SURG, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT GYNECOL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT ENDOCRINOL, BOSTON, MA 02114 USA. NR 16 TC 22 Z9 22 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1991 VL 72 IS 6 BP 1226 EP 1228 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FM319 UT WOS:A1991FM31900010 PM 2026745 ER PT J AU ALEXANDER, JM JAMESON, JL BIKKAL, HA SCHWALL, RH KLIBANSKI, A AF ALEXANDER, JM JAMESON, JL BIKKAL, HA SCHWALL, RH KLIBANSKI, A TI THE EFFECTS OF ACTIVIN ON FOLLICLE-STIMULATING-HORMONE SECRETION AND BIOSYNTHESIS IN HUMAN GLYCOPROTEIN HORMONE-PRODUCING PITUITARY-ADENOMAS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID RIBONUCLEIC-ACID LEVELS; BETA-SUBUNIT; ALPHA-SUBUNIT; CELL-CULTURES; INHIBIN; FSH; TUMORS; RAT AB The effects of activin on pituitary FSH biosynthesis have been previously characterized using primary rat pituitary cultures; however, little is known of the effects of activin on FSH biosynthesis and secretion in human pituitary tissue. Production of intact glycoprotein hormones and free subunits is increasingly recognized in pituitary tumors; however, the regulation of gonadotropins in such tumors has not been addressed. We have investigated the effects of human recombinant activin on glycoprotein hormone biosynthesis and secretion in primary cultures of 12 human glycoprotein hormone-producting pituitary adenomas and compared this with the effects of activin in normal rat anterior pituitary cells. In 33% of the human pituitary tumors studied, significant (P < 0.05) increases in FSH-beta secretion occurred in response to incubation with 20 ng/mL activin for 24 h (19-287% stimulation), without changes in the production of intact FSH. A Northern analysis performed on cells derived from one tumor indicated that FSH-beta mRNA levels increased 350% after activin treatments; however, FSH secretion did not parallel the mRNA changes. None of the human glycoprotein hormone-producing tumors significantly increased FSH secretion in response to activin. To validate the biological activity of recombinant human activin-A and to confirm time and dose conditions for the human tumor cultures, we also examined its ability to stimulate FSH production in rat pituitary cultures. Activin (20 ng/mL) added to the culture medium significantly increased FSH secretion and steady state levels of FSH-beta mRNA after 24 h. These data indicate that some glycoprotein hormone-producing pituitary tumors treated with purified activin have discordant responses of intact gonadotropins and free subunit responses. In contrast to responses in normal rat gonadotrophs, FSH-beta biosynthetic pathways may be uncoupled from intact FSH secretion in a subset of glycoprotein hormone-producing pituitary adenomas. C1 MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, BOSTON, MA 02114 USA. GENENTECH INC, DEPT DEV BIOL, SAN FRANCISCO, CA 94080 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-23519]; NIDDK NIH HHS [DK-07028, DK-40947] NR 32 TC 23 Z9 23 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1991 VL 72 IS 6 BP 1261 EP 1267 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FM319 UT WOS:A1991FM31900016 PM 1902844 ER PT J AU RICHTER, JM WANG, TC FAWAZ, K BYNUM, TE FALLON, D SHAPLEIGH, C AF RICHTER, JM WANG, TC FAWAZ, K BYNUM, TE FALLON, D SHAPLEIGH, C TI PRACTICE PATTERNS AND COSTS OF HOSPITALIZATION FOR UPPER GASTROINTESTINAL HEMORRHAGE SO JOURNAL OF CLINICAL GASTROENTEROLOGY LA English DT Article DE HOSPITAL COSTS; UPPER GASTROINTESTINAL HEMORRHAGE; PRACTICE PATTERNS ID CONTROLLED TRIAL; EARLY ENDOSCOPY; ELECTROCOAGULATION; RADIOLOGY; THERAPY; ULCER AB We conducted an observational study at three hospitals in Boston to examine the patterns of practice and the costs involved in the medical management of noncirrhotic, upper gastrointestinal bleeding. A total of 111 patients were identified and studied: 42 from hospital 1, 38 from hospital 2, and 31 from hospital 3. There were no significant differences in the management of the patients, except for the more frequent use of upper gastrointestinal radiography at hospital 3 and the more frequent use of cimetidine at hospital 2. Only a small percentage (3-7%) of patients required surgery, and overall mortality (0-8%) was low. The average cost of hospitalization, determined by using the New England Medical Center cost model, was calculated for direct costs ($3,180). The majority of costs incurred were for hospital bed or intensive care unit stay (63%) and transfusion of blood products (14%), with costs for physicians' services (9%), endoscopy (2%), and upper gastrointestinal radiography (1%) accounting for only a small percentage. This study demonstrates remarkable similarity in practice patterns and resource utilization at three different hospitals and provides data on the actual costs involved in hospitalization for noncirrhotic, uper gastrointestinal hemorrhage. C1 NEW ENGLAND MED CTR HOSP,MED SERV,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV GASTROENTEROL,MED SERV,BOSTON,MA 02115. RP RICHTER, JM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,GASTROINTESTINAL UNIT,JACKSON 7,BOSTON,MA 02114, USA. NR 23 TC 22 Z9 22 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-0790 J9 J CLIN GASTROENTEROL JI J. Clin. Gastroenterol. PD JUN PY 1991 VL 13 IS 3 BP 268 EP 273 DI 10.1097/00004836-199106000-00005 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FM900 UT WOS:A1991FM90000004 PM 2066543 ER PT J AU HEAGY, W CRUMPACKER, C LOPEZ, PA FINBERG, RW AF HEAGY, W CRUMPACKER, C LOPEZ, PA FINBERG, RW TI INHIBITION OF IMMUNE FUNCTIONS BY ANTIVIRAL DRUGS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE LYMPHOCYTES; VIRUS REPLICATION; HIV; IMMUNOSUPPRESSION; HERPES VIRUS ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS-RELATED COMPLEX; HEMATOPOIETIC PROGENITOR CELLS; PHASE-I TRIAL; 2',3'-DIDEOXYINOSINE DDI; LYMPHOCYTE-PROLIFERATION; HTLV-III/LAV; RNA-CONTENT; INVITRO; 3'-AZIDO-3'-DEOXYTHYMIDINE AB Immune functions were evaluated in vitro for PBMC isolated from healthy donors and cultured with the antiviral agents, 3'-azido-3'-deoxythymidine (AZT), ribavirin, ganciclovir, 2'3'-dideoxyinosine (ddI), or acyclovir. To identify methods for assessing the effects of antiviral drugs on immune cells, the PBMC response to mitogens, Con A, or phytohemagglutinin was evaluated from measurements of [H-3]thymidine and [C-14]leucine incorporation, cell growth, cellular RNA, DNA, and protein levels, and the PBMC proliferative cycle (i.e., progression from G0 --> G1 --> S --> G2 + M). At clinically relevant concentrations, AZT, ribavirin, or ganciclovir diminished PBMC responsiveness to mitogen. The numbers of proliferating cells in G1, S, and G2 + M phases of the cell cycle, DNA content, and [H-3]thymidine uptake were decreased in cultures treated with AZT, ribavirin, or ganciclovir. AZT or ribavirin but not ganciclovir reduced RNA and protein in the cultures and inhibited cell growth. Whereas AZT, ribavirin, or ganciclovir were antiproliferative, ddI or acyclovir had little, if any, effect on PBMC mitogenesis. The inhibitory effects of antivirals on immune cells may contribute to the immune deterioration observed in patients following prolonged use of the drugs. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HARVARD THORNDIKE RES LAB,DIV INFECT DIS,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,FLOW CYTOMETRY LAB,BOSTON,MA 02115. RP HEAGY, W (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 NCI NIH HHS [CA-34979]; NIAID NIH HHS [AI-27659, AI-29173] NR 41 TC 113 Z9 115 U1 1 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1991 VL 87 IS 6 BP 1916 EP 1924 DI 10.1172/JCI115217 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FP851 UT WOS:A1991FP85100007 PM 1904068 ER PT J AU WAKABAYASHI, G GELFAND, JA JUNG, WK CONNOLLY, RJ BURKE, JF DINARELLO, CA AF WAKABAYASHI, G GELFAND, JA JUNG, WK CONNOLLY, RJ BURKE, JF DINARELLO, CA TI STAPHYLOCOCCUS-EPIDERMIDIS INDUCES COMPLEMENT ACTIVATION, TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-1, A SHOCK-LIKE STATE AND TISSUE-INJURY IN RABBITS WITHOUT ENDOTOXEMIA - COMPARISON TO ESCHERICHIA-COLI SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE C5A; CYTOKINE; DISSEMINATED INTRAVASCULAR COAGULATION; LIPOTEICHOIC ACID; NEUTROPHIL AGGREGATION ID MONONUCLEAR-CELLS INVITRO; SEPTIC SHOCK; FACTOR PAF; ENDOGENOUS PYROGEN; LETHAL BACTEREMIA; CACHECTIN; ANTIBODIES; MORTALITY; INDUCTION; C5A AB Tumor necrosis factor (TNF) and IL-1 are thought to mediate many of the pathophysiologic changes of endotoxemia and Gram-negative bacteremia. In these studies, heat-killed Staphylococcus epidermidis were infused into rabbits to determine whether an endotoxin (LPS)-free microorganism also elicits cytokinemia and the physiologic abnormalities seen in Gram-negative bacteremia. S. epidermidis induced complement activation, circulating TNF and IL-1, and hypotension to the same degree as did one-twentieth the number of heat-killed Escherichia coli. Circulating IL-1-beta levels had a greater correlation coefficient (r = 0.81, P < 0.001) with the degree of hypotension than TNF levels (r = 0.48, P < 0.02). Leukopenia, thrombocytopenia, diffuse pulmonary capillary aggregation of neutrophils, and hepatic necrosis with neutrophil infiltration were observed to the same extent after either S. epidermidis or E. coli infusion. However, S. epidermidis infusion did not induce significant (< 60 pg/ml) endotoxemia, whereas E. coli infusion resulted in high (11,000 pg/ml) serum endotoxin levels. S. epidermidis, E. coli, LPS, or S. epidermidis-derived lipoteichoic acid (LTA) induced TNF and IL-1 from blood mononuclear cells in vitro. E. coli organisms and LPS were at least 100-fold more potent than S. epidermidis or LTA. Thus, a shock-like state with similar levels of complement activation as well as circulating levels of IL-1 and TNF were observed following either S. epidermidis or E. coli. These data provide further evidence that host factors such as IL-1 and TNF are common mediators of the septic shock syndrome regardless of the organism. 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. TUFTS UNIV,DEPT SURG,BOSTON,MA 02111. FU NIAID NIH HHS [AI-15614]; NIGMS NIH HHS [GM-21700] NR 52 TC 225 Z9 227 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1991 VL 87 IS 6 BP 1925 EP 1935 DI 10.1172/JCI115218 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FP851 UT WOS:A1991FP85100008 PM 2040686 ER PT J AU KRISHNA, V CHATTERJEE, K NAGAYA, T MADISON, LD DATTA, S RENTOUMIS, A JAMESON, JL AF KRISHNA, V CHATTERJEE, K NAGAYA, T MADISON, LD DATTA, S RENTOUMIS, A JAMESON, JL TI THYROID-HORMONE RESISTANCE SYNDROME - INHIBITION OF NORMAL RECEPTOR FUNCTION BY MUTANT THYROID-HORMONE RECEPTORS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE TRANSCRIPTIONAL REGULATION; ERBA; THYROID-STIMULATING HORMONE; THYROID HORMONE RESISTANCE; THYROID HORMONE ID EUKARYOTIC TRANSCRIPTIONAL ACTIVATORS; C-ERBA; RESPONSE ELEMENT; GENERALIZED RESISTANCE; NEGATIVE REGULATION; GENE-TRANSCRIPTION; BINDING; PROTEIN; BETA; TISSUES AB Thyroid hormone (T3) resistance is inherited in most cases in an autosomal dominant manner. The disorder is characterized by elevated free thyroid hormone levels and partial resistance to thyroid hormone at the cellular level. Distinct single amino acid substitutions in the ligand binding domain of the beta form of the thyroid hormone receptor have been described in two kindreds with this disorder. We used transient expression assays to characterize the functional properties of these receptor mutants, one containing a Gly to Arg change at amino acid 340 (G340R) and the other a Pro to His change at amino acid 448 (P448H). A nine amino acid carboxy terminal deletion (DELTA-448-456), analogous to an alteration that occurs in v-erbA, was also studied for comparison with the mutations that occur in the T3 resistance syndrome. None of the receptor mutants were able to mediate thyroid hormone dependent activation (TreTKCAT) or repression (TSH-alpha-CAT) of reporter genes when compared with the wild type receptor. In addition, the mutants inhibited the activity of normal alpha and beta receptor isoforms when examined in coex-pression assays. This activity, referred to as dominant negative inhibition, was manifest with respect to both the positively and negatively regulated reporter genes. Although mutant receptor binding to DNA was unaffected, ligand binding studies showed that the G340R and DELTA-448-456 mutants failed to bind T3, whereas the P448H mutant bound hormone with reduced affinity (approximately 10% of normal) compared to the wild type receptor. Consistent with this finding, the P448H mutant receptor was partially active at higher T3 concentrations. Furthermore, the dominant negative inhibition elicited by the P448H receptor mutant at higher T3 concentrations was reversed in the presence of high doses of T3. These findings indicate that mutant beta receptors in patients with thyroid hormone resistance have reduced affinity for T3 and are functionally deficient, but impair the activity of normal receptors, thereby providing a mechanism for the dominant mode of inheritance in this disorder. C1 MASSACHUSETTS GEN HOSP,THYROID UNIT,JACKSON 1021,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. OI Jameson, James/0000-0001-9538-4059 NR 42 TC 92 Z9 93 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1991 VL 87 IS 6 BP 1977 EP 1984 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FP851 UT WOS:A1991FP85100015 ER PT J AU SUEMORI, S CIACCI, C PODOLSKY, DK AF SUEMORI, S CIACCI, C PODOLSKY, DK TI REGULATION OF TRANSFORMING GROWTH-FACTOR EXPRESSION IN RAT INTESTINAL EPITHELIAL-CELL LINES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE AUTOCRINE; PARACRINE; EPIDERMAL GROWTH FACTOR; EXTRACELLULAR MATRIX ID COLON CANCER LINES; FACTOR-BETA; FACTOR-ALPHA; FACTOR RECEPTOR; DIFFERENTIATION; MODULATION; MEMBRANE; INVITRO; LAMININ AB Autocrine and paracrine modulation of transforming growth factor expression was assessed in rat intestinal epithelial cell lines designated IEC-6 and IEC-17. Addition of the transforming growth factor-alpha (TGF-alpha) homologue epidermal growth factor (EGF) to media of subconfluent IEC-6 cells led to autocrine stimulation of TGF-alpha expression as well as increased expression of the transforming growth factor-beta-1 (TGF-beta-1). Increased expression of TGF-alpha was maximal between 3 and 6 h after addition of EGF and subsequently declined coincident with increasing level of expression of TGF-beta-1, which achieved maximal levels 6 h after addition of EGF and was sustained for more than 12 h. Addition of TGF-beta-1 also led to autocrine induction of its own expression coincident with suppression of TGF-alpha expresion. Addition of TGF-beta-1 was associated with increased expression of beta-actin when standardized to a constitutive transcript (GAPDH). Similar responses to addition of EGF and TGF-beta-1, were observed in another intestinal epithelial cell line, designated IEC-17. Modulation of expression of TGFs was attenuated when cells were grown on the complex extracellular matrix produced by the Engelbreth-Holm-Swarm tumor (Matrigel), reflecting the baseline induction of TGF-beta-1 expression when compared to IEC-6 and IEC-17 cells maintained on plastic. These observations suggest that expression of TGFs is controlled by autocrine mechanisms in intestinal epithelial cell lines and proliferation stimulated by TGF-alpha may be initially self-reinforcing but ultimately downregulated by induction of TGF-beta-1. C1 MASSACHUSETTS GEN HOSP, DEPT MED, GASTROINTESTINAL UNIT, BOSTON, MA 02114 USA. RI ciacci, carolina/A-2594-2012 OI ciacci, carolina/0000-0002-7426-1145 FU NIDDK NIH HHS [DK41557] NR 33 TC 111 Z9 111 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD JUN PY 1991 VL 87 IS 6 BP 2216 EP 2221 DI 10.1172/JCI115256 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FP851 UT WOS:A1991FP85100046 PM 2040702 ER PT J AU WEISSMANN, D SPARGO, J WENNERSTEN, C FERRARO, MJ AF WEISSMANN, D SPARGO, J WENNERSTEN, C FERRARO, MJ TI DETECTION OF ENTEROCOCCAL HIGH-LEVEL AMINOGLYCOSIDE RESISTANCE WITH MICROSCAN FREEZE-DRIED PANELS CONTAINING NEWLY MODIFIED MEDIUM AND VITEK GRAM-POSITIVE SUSCEPTIBILITY CARDS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID STREPTOCOCCUS-FAECALIS; ENDOCARDITIS; GENTAMICIN; BACTEREMIA AB Both conventional and modified MicroScan Type 5 panels and Vitek Gram-Positive Susceptibility cards were compared with agar dilution screen plates for their abilities to detect high-level resistance to gentamicin and streptomycin in 235 enterococcal isolates, including 167 Enterococcus faecalis and 63 E. faecium isolates. The modified Type 5 panels contained dextrose-phosphate broth instead of Mueller-Hinton broth in their high-level-resistance screen wells. The sensitivities for detection of gentamicin and streptomycin high-level resistance were 100 and 100% (E. faecalis) and 100 and 94% (E. faecium) for the modified MicroScan panels, 100 and 89% (E. faecalis) and 100 and 98% (E. faecium) for the conventional MicroScan panels, and 81 and 86% (E. faecalis) and 85 and 94% (E. faecium) for the Vitek cards. All specificities were 100% except for the Vitek cards with streptomycin, where it was 96%. Isolates that showed resistance on the streptomycin agar screen plates were rescreened on plates containing 32,000-mu-g/ml to detect ribosomally mediated resistance. For all three systems, every failure to detect streptomycin high-level resistance occurred in isolates with enzymatic, not ribosomal, resistance. The modified MicroScan Type 5 panels are a suitable method for detecting enterococcal high-level resistance to gentamicin and streptomycin. The Vitek cards are too insensitive for this purpose. C1 MASSACHUSETTS GEN HOSP,FRANCIS BLAKE BACTERIOL LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,INFECT DIS LAB,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 30 TC 17 Z9 17 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JUN PY 1991 VL 29 IS 6 BP 1232 EP 1235 PG 4 WC Microbiology SC Microbiology GA FM520 UT WOS:A1991FM52000026 PM 1907609 ER PT J AU GOFF, DC MIDHA, KK BROTMAN, AW MCCORMICK, S WAITES, M AMICO, ET AF GOFF, DC MIDHA, KK BROTMAN, AW MCCORMICK, S WAITES, M AMICO, ET TI AN OPEN TRIAL OF BUSPIRONE ADDED TO NEUROLEPTICS IN SCHIZOPHRENIC-PATIENTS SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Note ID ANTI-ANXIETY DRUG; INDUCED AKATHISIA; AGGRESSIVE-BEHAVIOR; PHARMACOLOGY; HALOPERIDOL; ANXIOLYTICS; METABOLISM; GEPIRONE; MONKEYS AB Twenty chronic schizophrenic patients completed at least 2 weeks of a 6-week trial of buspirone (mean dose 23.8 mg/day) added to a stable dose of neuroleptic. At week 6, mean scores were significantly improved (p < 0.01) on the Brief Psychiatric Rating Scale, the Simpson Angus Scale for Extrapyramidal Symptoms and the Global Assessment Scale. Overall measures of akathisia and tardive dyskinesia were not significantly changed at week 6. In the 7 patients taking oral haloperidol, mean plasma concentrations of haloperidol were significantly increased (p < 0.05) by 26% 6 weeks after adding buspirone. C1 ERICH LINDEMANN MENTAL HLTH CTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. UNIV SASKATCHEWAN,COLL PHARM & MED,SASKATOON S7N 0W0,SASKATCHEWAN,CANADA. FU NIMH NIH HHS [MH-31154, MH-36224, MH-19052] NR 36 TC 80 Z9 80 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 JUN PY 1991 VL 11 IS 3 BP 193 EP 197 PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA FN817 UT WOS:A1991FN81700008 PM 2066458 ER PT J AU BARNHILL, RL AF BARNHILL, RL TI CURRENT STATUS OF THE DYSPLASTIC MELANOCYTIC NEVUS SO JOURNAL OF CUTANEOUS PATHOLOGY LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; PRECURSOR LESIONS; TUMOR PROGRESSION; BENIGN NEVI; POLYGENIC INHERITANCE; MONOCLONAL-ANTIBODIES; NONFAMILIAL MELANOMA; FAMILIAL MELANOMA; NEVOCELLULAR NEVI; RISK-FACTORS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BARNHILL, RL (reprint author), MASSACHUSETTS GEN HOSP,DIV DERMATOPATHOL,BOSTON,MA 02114, USA. NR 90 TC 33 Z9 34 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6987 J9 J CUTAN PATHOL JI J. Cutan. Pathol. PD JUN PY 1991 VL 18 IS 3 BP 147 EP 159 DI 10.1111/j.1600-0560.1991.tb00147.x PG 13 WC Dermatology; Pathology SC Dermatology; Pathology GA FW538 UT WOS:A1991FW53800002 PM 1918502 ER PT J AU TAVARES, M DEPAOLA, P SOPARKAR, P JOSHIPURA, K AF TAVARES, M DEPAOLA, P SOPARKAR, P JOSHIPURA, K TI THE PREVALENCE OF ROOT CARIES IN A DIABETIC POPULATION SO JOURNAL OF DENTAL RESEARCH LA English DT Article ID DENTAL DISEASE; MELLITUS; CHILDREN; CARBOHYDRATE AB The objective of this study was to assess the level of root caries in a population of diabetic adults. Diabetics are of special interest because they are alleged to be periodontally compromised and have atypical patterns of refined carbohydrate ingestion. Diabetic subjects were patients of the Joslin Diabetic Center in Boston and had significantly elevated blood glucose and glycosylated hemoglobin levels over at least a ten-year period. Eligible subjects had to be between the ages of 45 and 65 and have a minimum of ten teeth and three sites with recession. Data were collected on coronal caries, oral hygiene, gingivitis, pocket depth, recession, and root caries and were compared with data from control subjects from a larger nondiabetic study group. There were 88 diabetics and 185 controls with mean ages of 55.7 and 56.3 years, respectively. The groups were found to be similar with respect to the numbers of buccal surface sites with gingival recession and the numbers of carious root lesions. There was a distinct difference, however, with respect to restored root surfaces: 1.76 mean filled surfaces were observed in the controls, as compared with 0.49 in the diabetics. A Katz Root Caries Index (for which lesions are calculated as a percentage of the numbers of exposed root surfaces) was determined to be 15.2 for the controls and 7.1 for the diabetics. A reasonable inference is that these differences are the result of a restricted ingestion of refined carbohydrates by the diabetic group. This was confirmed by a dietary survey of subsamples from the diabetic and non-diabetic groups. RP TAVARES, M (reprint author), FORSYTH DENT CTR,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-07009-04] NR 32 TC 15 Z9 16 U1 0 U2 1 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD JUN PY 1991 VL 70 IS 6 BP 979 EP 983 DI 10.1177/00220345910700061401 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FR234 UT WOS:A1991FR23400009 PM 2045579 ER PT J AU HERZOG, DB KELLER, MB LAVORI, PW BRADBURN, IS AF HERZOG, DB KELLER, MB LAVORI, PW BRADBURN, IS TI BULIMIA-NERVOSA IN ADOLESCENCE SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE BULIMIA NERVOSA; OUTCOME; ADOLESCENCE ID EATING DISORDERS; ANOREXIA-NERVOSA; MEDICAL COMPLICATIONS; DOUBLE-BLIND; PLACEBO; PSYCHOTHERAPY AB Investigations of bulimia nervosa have focused primarily on adult samples, although bulimia nervosa commonly has its onset in adolescence. Pediatricians are often questioned about its etiology, course, and treatment. In an attempt to provide pediatricians with answers, we integrate findings from recent epidemiological and treatment studies with a clinical report of 18 women who developed bulimia nervosa during their teens and sought treatment at our eating disorders clinic. C1 MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,BOSTON,MA 02114. BROWN UNIV,RES,PROVIDENCE,RI 02912. UNIV CALIF BERKELEY,BERKELEY,CA 94720. NR 41 TC 3 Z9 3 U1 3 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD JUN PY 1991 VL 12 IS 3 BP 191 EP 195 PG 5 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA FQ272 UT WOS:A1991FQ27200008 PM 1869624 ER PT J AU PETEET, JR ABRAMS, HE ROSS, DM STEARNS, NM AF PETEET, JR ABRAMS, HE ROSS, DM STEARNS, NM TI PRESENTING A DIAGNOSIS OF CANCER - PATIENTS VIEWS SO JOURNAL OF FAMILY PRACTICE LA English DT Article DE PHYSICIAN-PATIENT RELATIONSHIP; DIAGNOSIS; PROGNOSIS; NEOPLASMS ID INFORMATION; ATTITUDES; PHYSICIAN; CARE AB Background. Although in general, patients in the United States are now told if they have been diagnosed as having cancer, little information is available either about the way in which this is done or about patients' satisfaction with how they are told. Methods. Thirty-two patients were interviewed who had been given a diagnosis of cancer; one half were being treated at a comprehensive cancer center and one half at a community hospital. The study instrument, presented in a semistructured interview conducted by psychosocial clinicians, included specific questions about the setting and the manner in which the patients were told, their reactions to the diagnosis, and their suggestions of how physicians should inform others who have to be informed of a similar diagnosis. Results. All patients were told of their diagnosis by a physician; 84% of the time the diagnosis was given in person. Patients said that being told with hope, information, and caring, and with respect for their privacy and wishes to have a supportive person present were particularly helpful. Almost 40% of patients reported at the time of the interview that their hopes were directed toward remission and optimal quality of life rather than toward a cure. Four of the six patients whose conditions had initially been misdiagnosed described subsequent mistrust of information received from physicians. Conclusions. These findings confirm the importance of a physician providing hope for and fostering trust in patients to whom they are presenting the diagnosis of cancer. The results indicate that physicians' help in providing treatment information contributes more to hope than does cheerfulness or optimism, and that patients who have been given a misdiagnosis require special consideration in order to reestablish trust. C1 SALEM HOSP,SALEM,MA. RP PETEET, JR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 27 TC 46 Z9 46 U1 2 U2 4 PU APPLETON & LANGE PI E NORWALK PA 25 VAN ZANT ST, E NORWALK, CT 06855 SN 0094-3509 J9 J FAM PRACTICE JI J. Fam. Pract. PD JUN PY 1991 VL 32 IS 6 BP 577 EP 581 PG 5 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA FR074 UT WOS:A1991FR07400009 PM 2040882 ER PT J AU DUBIN, D PRATT, RE HUI, KY DZAU, VJ AF DUBIN, D PRATT, RE HUI, KY DZAU, VJ TI CHARACTERIZATION OF PRORENIN ACTIVATION USING A SYNTHETIC PEPTIDE SUBSTRATE SO JOURNAL OF HYPERTENSION LA English DT Note DE PRORENIN ACTIVATION; PRORENIN BIOSYNTHESIS; PRORENIN PROCESSING ID PLASMA INACTIVE RENIN; IDENTIFICATION; BIOSYNTHESIS; KALLIKREIN; PEPSIN; GENE AB Human renin is synthesized as an inactive zymogen (prorenin) which is processed to the active form. We synthesized an 11-amino acid peptide which spans the human prorenin processing site in order to develop a simple assay to study human prorenin activation. Six enzymes which are capable of activating recombinant prorenin in vitro were studied. Four of these enzymes digested the synthetic peptide in a specific fashion, as analyzed by reverse-phase high-performance liquid chromatography. Amino acid analysis of the purified digestion products revealed that trypsin cleaves between Arg-Leu, the authentic processing site, while kallikrein, plasmin and elastase all cleaved at alternate sites. On the other hand, pepsin and cathepsin D did not cleave this substrate, suggesting that the activation of prorenin by these proteases might occur at a site distinct from the authentic processing site. Our data suggest that this synthetic peptide may be used as a simple and specific assay for prorenin activation. C1 STANFORD UNIV,MED CTR,SCH MED,DIV CARDIOVASC MED,FALK CARDIOVASC RES CTR,300 PASTEUR DR,STANFORD,CA 94305. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL35252, HL35610, HL42663] NR 14 TC 4 Z9 4 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0263-6352 J9 J HYPERTENS JI J. Hypertens. PD JUN PY 1991 VL 9 IS 6 BP 483 EP 486 DI 10.1097/00004872-199106000-00001 PG 4 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FQ810 UT WOS:A1991FQ81000001 PM 1653285 ER PT J AU MATSUYAMA, T YAMADA, A DEUSCH, K SLEASMAN, J DALEY, JF TORIMOTO, Y ABE, T AF MATSUYAMA, T YAMADA, A DEUSCH, K SLEASMAN, J DALEY, JF TORIMOTO, Y ABE, T TI CYTOCHALASINS ENHANCE THE PROLIFERATION OF CD4 CELLS THROUGH THE CD3-TI ANTIGEN RECEPTOR COMPLEX OR THE CD2 MOLECULE THROUGH AN EFFECT ON EARLY EVENTS OF ACTIVATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CONCANAVALIN-A; HUMAN LYMPHOCYTES; PLASMA-MEMBRANE; HELPER-INDUCER; T-CELLS; IMMUNOGLOBULIN; PHAGOCYTOSIS; STIMULATION; INHIBITION; LEUKOCYTES AB Cytochalasins are known to inhibit or enhance the proliferation of T cells induced by mitogens in a concentration-dependent fashion. To clarify the mechanism by which cytochalasins enhance T cell proliferation, we examined which activation pathways and events in signal transduction were affected by cytochalasins. We also examined subsets of CD4 cells for a preferential response to cytochalasins. Cytochalasins enhanced the proliferation of CD4 cells induced by optimal doses of anti-CD3 antibody or suboptimal doses of anti-CD2 antibodies. Cytochalasins, at low concentrations enhanced the rise in intracellular Ca2+ and production of IP3 in CD4 cells activated by anti-CD2 or CD3 antibodies. Cytochalasins also enhanced the modulation of CD3 induced by anti-CD3 antibody. These results suggest that cytochalasins enhance the proliferation of CD4 cells by affecting early events in signal transduction after activation through the CD3-Ti Ag-receptor complex or CD2 molecule. At the doses used, cytochalasins appear to interact with cytochalasin-binding sites in the cell membrane. Cytochalasins predominantly enhanced CD3-mediated proliferation in the CD29-subset of CD4 cells. C1 KURUME UNIV,KURUME,FUKUOKA 830,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP MATSUYAMA, T (reprint author), SAITAMA MED SCH,SAITAMA MED CTR,DEPT INTERNAL MED 2,1981 KAMODA,KAWAGOE CITY 3501,JAPAN. NR 32 TC 15 Z9 15 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 JUN 1 PY 1991 VL 146 IS 11 BP 3736 EP 3741 PG 6 WC Immunology SC Immunology GA FN054 UT WOS:A1991FN05400008 PM 1709660 ER PT J AU TOLTZIS, P MARX, CM KLEINMAN, N LEVINE, EM SCHMIDT, EV AF TOLTZIS, P MARX, CM KLEINMAN, N LEVINE, EM SCHMIDT, EV TI ZIDOVUDINE-ASSOCIATED EMBRYONIC TOXICITY IN MICE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; ANTIRETROVIRAL ACTIVITY; REVERSE-TRANSCRIPTASE; AZIDOTHYMIDINE AZT; RETROVIRAL DISEASE; DNA-POLYMERASES; XENOPUS-LAEVIS; DOUBLE-BLIND; 3'-AZIDO-3'-DEOXYTHYMIDINE AB A novel toxicity associated with zidovudine (AZT), the standard antiviral therapy for infection with human immunodeficiency virus, is described. When AZT was administered to mice to evaluate its safety during gestation, the animals failed to complete pregnancy successfully. Mice receiving AZT during gestation yielded fewer fetuses (P = .003) and greater numbers of resorptions (P = .003) per pregnant mouse compared with untreated animals. Drug effects on adult mice were assessed to determine if toxicity could account for the pregnancy failures. However, adult animals receiving AZT demonstrated no adverse effects with regard to growth, food consumption, activity, or ovarian histology. A direct toxic effect of AZT on the mouse embryo was tested by cultivating single-cell fertilized oocytes in vitro in the presence of increasing concentrations of drug. Exposure to AZT was highly correlated with failure to develop to the blastocyst stage (P < .001). These data indicate that AZT has a direct toxic effect on the developing mouse embryo. Further analysis of the nature of this toxicity may be important in designing less toxic antiretroviral agents and in planning future uses of AZT. C1 CASE WESTERN RESERVE UNIV,SCH MED,DEPT PEDIAT,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SCH MED,CTR ANIM RESOURCE,CLEVELAND,OH 44106. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. NR 26 TC 49 Z9 52 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1991 VL 163 IS 6 BP 1212 EP 1218 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA FP534 UT WOS:A1991FP53400006 PM 2037787 ER PT J AU WARREN, HS GLENNON, M DEDECKKER, FA TELLO, D AF WARREN, HS GLENNON, M DEDECKKER, FA TELLO, D TI ROLE OF NORMAL SERUM IN THE BINDING OF LIPOPOLYSACCHARIDE TO IGG FRACTIONS FROM RABBIT ANTISERA TO ESCHERICHIA-COLI J5 AND OTHER GRAM-NEGATIVE BACTERIA SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HIGH-DENSITY LIPOPROTEINS; SALMONELLA-TYPHIMURIUM LIPOPOLYSACCHARIDES; MONOCLONAL-ANTIBODIES; CROSS-REACTIVITY; O-ANTIGENS; R MUTANTS; LIPID-A; ENDOTOXIN; IMMUNIZATION; NEUTRALIZATION AB Because lipopolysaccharide (LPS) bound to lipoprotein is less active than unbound LPS in multiple assay systems, the binding of radiolabeled LPS to lipoproteins in sera prepared from normal rabbits and rabbits made hyperimmune to Escherichia coli J5 were compared. LPS-lipoprotein binding in hyperimmune sera to E. coli J5 was not greater than that in normal serum as assessed by ultracentrifugation, but more LPS was precipitated from hyperimmune antisera than normal sera under conditions designed to precipitate LPS-lipoprotein complexes with calcium and dextran. Radiolabeled LPS was precipitated by delipidated antisera and fractions of IgG purified by anion exchange chromatography, but the precipitation was dependent on the presence of normal serum in the reaction mixture. These data suggest that a fluid-phase RIA done in the presence of normal serum may facilitate the detection of IgG in antisera raised to E. coli J5 that binds to heterologous smooth LPS. C1 INST PASTEUR,EXPTL IMMUNOL LAB,F-75724 PARIS 15,FRANCE. SHRINERS BURN INST,INFECT DIS UNIT,CINCINNATI,OH 45219. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WARREN, HS (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,149 13TH ST,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI-28943] NR 51 TC 10 Z9 10 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1991 VL 163 IS 6 BP 1256 EP 1266 PG 11 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA FP534 UT WOS:A1991FP53400013 PM 1709961 ER PT J AU SUNDKVIST, G LIND, P BERGSTROM, B LILJA, B RABINOWE, SL AF SUNDKVIST, G LIND, P BERGSTROM, B LILJA, B RABINOWE, SL TI AUTONOMIC NERVE ANTIBODIES AND AUTONOMIC NERVE FUNCTION IN TYPE-1 AND TYPE-2 DIABETIC-PATIENTS SO JOURNAL OF INTERNAL MEDICINE LA English DT Article DE ANTIBODIES; AUTOIMMUNITY; AUTONOMIC NEUROPATHY; SYMPATHETIC NERVE ANTIBODIES; SYMPATHETIC NEUROPATHY; VAGAL NERVE ANTIBODIES; VAGAL NEUROPATHY ID ANTI-ADRENAL MEDULLARY; ISLET CELL ANTIBODIES; HEART-RATE; PLASMA-CATECHOLAMINES; DEVELOPING IDDM; HIGH-RISK; NEUROPATHY; MELLITUS; DURATION; COMPLICATIONS AB Complement-fixing adrenal medulla (CF-ADM), sympathetic ganglion (CF-SG), and vagal (CF-V) nerve antibodies were determined in diabetic patients. Among 74 patients with Type 1 diabetes, CF-ADM was detected in 7 (10 %) cases, CF-SG in 14 (19 %) cases, and CF-V in 8 (11 %) cases. Among 38 patients with Type 2 diabetes, CF-ADM was detected in 5 (13 %) cases, CF-SG in 4 (11 %) cases, and CF-V in 6 (16 %) cases. There were associations between autonomic nerve antibodies and autonomic nerve function. CF-ADM and/or CF-SG were significantly (P < 0.002) less prevalent in Type 1 diabetic patients with autonomic neuropathy than in those without [5/44 (11 %) vs. 14/30 (47 %)] and, in agreement with this, the brake index, a sign of parasympathetic and sympathetic autonomic nerve function, was significantly (P < 0.005) higher (more normal) in these patients (-0.56 +/- 0.13 vs. - 1.04 +/- 0.12). In Type 2 diabetic patients, the E/I ratio, an index of parasympathetic nerve function, was significantly (P < 0.03) lower (more abnormal) in those with CF-V than in those without (- 1.81 +/- 0.17 vs. - 1.20 +/- 0.11). In conclusion, the frequency of sympathetic nerve antibodies was decreased in Type 1 diabetic patients with autonomic neuropathy, while in Type 2 diabetic patients parasympathetic nerve antibodies were related to severe parasympathetic neuropathy. C1 UNIV LUND,MALMO GEN HOSP,DEPT CLIN PHYSIOL,S-21401 MALMO,SWEDEN. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,IMMUNOL SECT,BOSTON,MA 02115. RP SUNDKVIST, G (reprint author), UNIV LUND,MALMO GEN HOSP,DEPT MED,S-21401 MALMO,SWEDEN. NR 27 TC 34 Z9 34 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-6820 J9 J INTERN MED JI J. Intern. Med. PD JUN PY 1991 VL 229 IS 6 BP 505 EP 510 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FQ458 UT WOS:A1991FQ45800007 PM 2045757 ER PT J AU HERZOG, DB NEWMAN, KL WARSHAW, M AF HERZOG, DB NEWMAN, KL WARSHAW, M TI BODY-IMAGE DISSATISFACTION IN HOMOSEXUAL AND HETEROSEXUAL MALES SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID EATING DISORDERS; BULIMIA; NERVOSA; WEIGHT; MEN AB A nonclinical sample of 43 homosexual and 32 heterosexual men completed two self-report inventories regarding weight, body satisfaction, eating attitudes, and behaviors. Subjects were also asked to select their current and ideal figures, the weight they felt would be most attractive to a potential partner, and the weight to which they would be most attracted in a potential partner from figures representing very thin to very heavy physiques. Heterosexual men were significantly heavier than homosexual men and desired a significantly heavier ideal weight. Although the current and ideal physiques selected by the homosexual and heterosexual men were almost identical, homosexual men were more likely to desire an underweight ideal. A heightened pursuit of thinness may place homosexual men at an increased risk for developing eating disorders. RP HERZOG, DB (reprint author), MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 16 TC 45 Z9 45 U1 1 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD JUN PY 1991 VL 179 IS 6 BP 356 EP 359 DI 10.1097/00005053-199106000-00009 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA FR292 UT WOS:A1991FR29200009 PM 2051150 ER PT J AU HOCHBERG, FH LOEFFLER, JS PRADOS, M AF HOCHBERG, FH LOEFFLER, JS PRADOS, M TI THE THERAPY OF PRIMARY BRAIN LYMPHOMA SO JOURNAL OF NEURO-ONCOLOGY LA English DT Review DE PRIMARY BRAIN LYMPHOMA; RADIATION THERAPY; CHEMOTHERAPY; AIDS ID CENTRAL-NERVOUS-SYSTEM; EPSTEIN-BARR VIRUS; HIGH-DOSE METHOTREXATE; NON-HODGKINS LYMPHOMA; RETICULUM-CELL SARCOMA; PRIMARY CEREBRAL LYMPHOMA; I-131 MONOCLONAL-ANTIBODIES; IMMUNE-DEFICIENCY SYNDROME; RADIATION-THERAPY; MALIGNANT-LYMPHOMA AB Recommendations regarding the current therapy of primary brain lymphoma (NHL-CNS) take into account the occurrence of this tumor in immunocompetent and immunosuppressed hosts. Immunohistochemical evaluation of biopsy material or spinal fluid provides the diagnosis in 90% of patients. For the immunocompetent, pre-irradiation intra-venous or intra-arterial chemotherapy with Methotrexate alone or in combination with other agents is provided to treat tumor within multiple brain sites. Subarachnoid deposits are treated with Methotrexate by intrathecal administration. Radiation is provided after chemotherapy and for the treatment of vitreal/retinal deposits or symptomatic lesions within the spinal axis. The therapy of recurrent NHL-CNS makes use of intravenous Methotrexate or high dose Cytosine Arabinoside. Immunosuppressed patients respond to reduction of immunosuppressive medication. The therapy of NHL-CNS in the AIDS patient makes use of corticosteroids followed by cranial irradiation. A discussion of emerging trends in the therapy of NHL-CNS in the AIDS and non-AIDS population is provided. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. JOINT CTR RADIAT THERAPY,BOSTON,MA. UNIV CALIF SAN FRANCISCO,NEUROONCOL SERV,SAN FRANCISCO,CA 94143. NR 65 TC 56 Z9 56 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JUN PY 1991 VL 10 IS 3 BP 191 EP 201 PG 11 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA FT051 UT WOS:A1991FT05100001 PM 1895164 ER PT J AU KRETSCHMAR, CS LINGGOOD, RM AF KRETSCHMAR, CS LINGGOOD, RM TI CHEMOTHERAPEUTIC TREATMENT OF EXTENSIVE OPTIC PATHWAY TUMORS IN INFANTS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE OPTIC GLIOMA; CHEMOTHERAPY; BRAIN NEOPLASM; CHILDREN ID PRIMARY BRAIN-TUMORS; LONG-TERM; RADIATION-THERAPY; NATURAL-HISTORY; SAN-FRANCISCO; NERVE GLIOMA; PHASE-II; CHILDREN; MANAGEMENT; CHILDHOOD AB Two infants, ages 14 and 4 months, with extensive optic pathway tumors were treated with intensive chemotherapy called MADDOC: nitrogen mustard, doxorubicin, cis-platinum, dacarbazine, vincristine, and cyclophosphamide. The first child had hydrocephalus with an enhancing mass at the hypothalamus which followed the optic radiation to include the lateral geniculate body and medial temporal lobe. A v-p shunt was placed, and biopsy revealed a Grade II astrocytoma. One month later, the child developed malignant ascites. Intensive induction chemotherapy was then begun with cis-platinum 100 mg/m2 and cyclophosphamide 3 g/m2 for two initial cycles. The ascites resolved within one week, and chemotherapy was continued for 10 courses of the 6-drug MADDOC regimen. CT scans showed a gradual shrinkage of the tumor mass by approximately 70%. The enhancing areas continued to decrease in size through 20 months after completing MADDOC. The child has not received radiation and is well 4 years 7 months post diagnosis. The second infant had massive enlargement of the right optic nerve with an enhancing chiasmatic mass extending into the suprasellar space, hypothalamus, and brain stem. This infant was not biopsied; she also received induction MADDOC chemotherapy for 12 cycles. CT scans showed a definite decrease in the chiasmatic mass by the fifth cycle, with continued reduction by approximately 40% after 10 months. Twenty-three months from diagnosis there was asymptomatic evidence of tumor growth. The child is being treated with carboplatinum and remains ophthalmologically and radiographically stable 43 months from dignosis. C1 HARVARD UNIV,SCH MED,MASSACHUSETS GEN HOSP,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02115. NR 41 TC 11 Z9 11 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JUN PY 1991 VL 10 IS 3 BP 263 EP 270 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA FT051 UT WOS:A1991FT05100009 PM 1895167 ER PT J AU KATZELNICK, DJ DAVAR, G SCANLON, JP AF KATZELNICK, DJ DAVAR, G SCANLON, JP TI REVERSIBILITY OF PSYCHIATRIC-SYMPTOMS IN A CHRONIC SOLVENT ABUSER - A CASE-REPORT SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID ORGANIC-SOLVENTS; TOLUENE ABUSE; ENCEPHALOPATHY; SECONDARY; SEQUELAE AB The acute mental status changes associated with inhaled solvent use have been well described. 1 The potential long-term neuropsychiatric sequelae of inhaled solvent use are not as well characterized. We present here the case of a 20-year-old male with a 7-year history of inhaled solvent (toluene) use whose neurological and psychiatric status were followed closely over a 1-month period on an inpatient psychiatric unit. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. NR 13 TC 1 Z9 1 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 1991 VL 3 IS 3 BP 319 EP 321 PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA GC876 UT WOS:A1991GC87600010 PM 1821248 ER PT J AU BEAL, MF FERRANTE, RJ SWARTZ, KJ KOWALL, NW AF BEAL, MF FERRANTE, RJ SWARTZ, KJ KOWALL, NW TI CHRONIC QUINOLINIC ACID LESIONS IN RATS CLOSELY RESEMBLE HUNTINGTONS-DISEASE SO JOURNAL OF NEUROSCIENCE LA English DT Article ID PERFORMANCE LIQUID-CHROMATOGRAPHY; KAINIC ACID; NEUROPEPTIDE-Y; STRIATAL NEURONS; BASAL GANGLIA; CEREBROSPINAL-FLUID; NADPH-DIAPHORASE; KYNURENIC ACID; ANIMAL-MODEL; QUANTITATIVE AUTORADIOGRAPHY AB We previously found a relative sparing of somatostatin and neuropeptide Y neurons 1 week after producing striatal lesions with NMDA receptor agonists. These results are similar to postmortem findings in Huntington's disease (HD), though in this illness there are two- to threefold increases in striatal somatostatin and neuropeptide Y concentrations, which may be due to striatal atrophy. In the present study, we examined the effects of striatal excitotoxin lesions at 6 months and 1 yr, because these lesions exhibit striatal shrinkage and atrophy similar to that occurring in HD striatum. At 6 months and 1 yr, lesions with the NMDA receptor agonist quinolinic acid (QA) resulted in significant increases (up to twofold) in concentrations of somatostatin and neuropeptide Y immunoreactivity, while concentrations of GABA, substance P immunoreactivity, and ChAT activity were significantly reduced. In contrast, somatostatin and neuropeptide Y concentrations did not increase 6 months after kainic acid (KA) or alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) lesions. At both 6 months and 1 yr, QA lesions showed striking sparing of NADPH-diaphorase neurons as compared with both AMPA and KA lesions, neither of which showed preferential sparing of these neurons. Long-term QA lesions also resulted in significant increases in concentrations of both 5-HT and 5-hydroxyindoleacetic acid (HIAA), similar to findings in HD. Chronic QA lesions therefore closely resemble the neurochemical features of HD, because they result in increases in somatostatin and neuropeptide Y and in 5-HT and HIAA. These findings strengthen the possibility that an NMDA receptor-mediated excitotoxic process could play a role in the pathogenesis of HD. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,EXPTL NEUROPATHOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,CS KUBIK LAB NEUROPATHOL,BOSTON,MA 02114. RP BEAL, MF (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU PHS HHS [16367] NR 79 TC 378 Z9 385 U1 0 U2 4 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JUN PY 1991 VL 11 IS 6 BP 1649 EP 1659 PG 11 WC Neurosciences SC Neurosciences & Neurology GA FR284 UT WOS:A1991FR28400016 PM 1710657 ER PT J AU RORDORF, G UEMURA, Y BONVENTRE, JV AF RORDORF, G UEMURA, Y BONVENTRE, JV TI CHARACTERIZATION OF PHOSPHOLIPASE-A2 (PLA2) ACTIVITY IN GERBIL BRAIN - ENHANCED ACTIVITIES OF CYTOSOLIC, MITOCHONDRIAL, AND MICROSOMAL FORMS AFTER ISCHEMIA AND REPERFUSION SO JOURNAL OF NEUROSCIENCE LA English DT Article ID FREE FATTY-ACIDS; TRANSIENT CEREBRAL-ISCHEMIA; GLOMERULAR MESANGIAL CELLS; RAT-LIVER MITOCHONDRIA; ARACHIDONIC-ACID; LIPOXYGENASE METABOLITES; CALCIUM-CONCENTRATION; MEMBRANE DYSFUNCTION; POTASSIUM CHANNELS; C ACTIVITY AB Brain phospholipase A2 (PLA2) activity has not been well characterized. Given the importance of this enzymatic activity for a variety of cellular functions in the brain, we characterized the subcellular distribution of PLA2 activity in gerbil brain and evaluated how PLA2 activity was altered by ischemia and reperfusion. Cytosolic, mitochondrial, and microsomal fractions were prepared by differential centrifugation of forebrain homogenates. PLA2 activities of each fraction were assayed by measuring release of arachidonic acid (AA) from exogenous C-14-AA-phosphatidylcholine (PC), -phosphatidylethanolamine (PE), and -phosphatidylinositol (Pl). Two forms of PLA2 were present in the cytosolic fraction: a high-molecular-weight form, active against PC and PE, and a smaller form with an M(r) of approximately 14 kDa, active against PE. In the mitochondrial and microsomal fractions, a single form (M(r) almost-equal-to 14 kDa) was dominant, active against both PC and PE. The role of PLA2 activation in ischemic brain injury remains controversial. PLA2 enzymatic activity was characterized in gerbil brain after 10 min of common carotid occlusion, followed by 10 min of reperfusion. Ischemic/reperfused brains had significantly higher PLA2 specific activities in each subcellular fraction. Ischemia and reperfusion did not change the gel-filtration elution patterns of PLA2 activity of the various forms of the enzyme. Cytosolic, mitochondrial, and microsomal activities were optimal at a pH of approximately 8.5. Cytosolic PLA2 activity was enhanced when Ca2+ concentration ([Ca2+]) was increased over the physiological range (10(-7) to 10(-6) M). Mitochondrial and microsomal PLA2 activities were also [Ca2+] dependent. In conclusion, gerbil brain has various forms of Ca2+-dependent PLA2 activities. Ischemia and reperfusion result in stable activation of both soluble and membrane-associated forms. This stable activation of PLA2 may play a major role in cellular injury associated with ischemia and reperfusion in the brain. C1 MASSACHUSETTS GEN HOSP, MED SERV, RENAL UNIT, JACKSON 8, FRUIT ST, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROSURG SERV, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT NEUROSURG, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK 38452, DK 39249, DK 39773] NR 66 TC 126 Z9 128 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 USA SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JUN PY 1991 VL 11 IS 6 BP 1829 EP 1836 PG 8 WC Neurosciences SC Neurosciences & Neurology GA FR284 UT WOS:A1991FR28400032 PM 2045888 ER PT J AU OLDENDORF, WH AF OLDENDORF, WH TI SATURATION OF AMINO-ACID-UPTAKE BY HUMAN BRAIN-TUMOR DEMONSTRATED BY SPECT SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material RP OLDENDORF, WH (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,B-151C,LOS ANGELES,CA 90024, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUN PY 1991 VL 32 IS 6 BP 1229 EP 1230 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FP827 UT WOS:A1991FP82700016 PM 2045938 ER PT J AU KANKE, M MATSUEDA, GR STRAUSS, HW YASUDA, T LIAU, CS KHAW, BA AF KANKE, M MATSUEDA, GR STRAUSS, HW YASUDA, T LIAU, CS KHAW, BA TI LOCALIZATION AND VISUALIZATION OF PULMONARY EMBOLI WITH RADIOLABELED FIBRIN-SPECIFIC MONOCLONAL-ANTIBODY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID VENOUS THROMBI; INFARCTION; TC-99M AB Indium-111-labeled monoclonal antibody 64C5 specific for the beta-chain of fibrin monomer was used to image canine (n = 6) experimental pulmonary emboli (at least one barium-thrombin and one copper-coil induced clot per dog). Uptake of in-111-64C5 and I-125-control-DIG26-11 were compared in 10 clots (7 barium-thrombin and 3 copper-coil) identified in the lungs. There was no difference in the blood clearance of In-111-64C5 and I-125-DIG26-11. Uptake of In-111-64C5 (0.183 +/- 0.105, mean %ID/g) was greater than I-125-DIG26-11 (0.024 +/- 0.025) in pulmonary clots (p < 0.001). Mean thrombus to blood ratios at 24 hr were 6.78:1 for 64C5 and 0.57:1 for DIG26-11. The clots visualized in vivo were larger (0.315 +/- 0.381 g) than clots not visualized (0.089 +/- 0.098). Negative images were recorded in three dogs with pulmonary emboli, injected with In-111-labeled control monoclonal antibody 3H3. These data suggest that In-111-labeled antifibrin can detect large pulmonary emboli in vivo. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP KANKE, M (reprint author), MASSACHUSETTS GEN HOSP,DIV NUCL MED,TILTON 2,FRUIT ST,BOSTON,MA 02114, USA. NR 22 TC 16 Z9 16 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD JUN PY 1991 VL 32 IS 6 BP 1254 EP 1260 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FP827 UT WOS:A1991FP82700023 PM 2045943 ER PT J AU RUGGIERO, SL DONOFF, RB AF RUGGIERO, SL DONOFF, RB TI BONE REGENERATION AFTER MANDIBULAR RESECTION - REPORT OF 2 CASES SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Article ID HEMIMANDIBULECTOMY RP RUGGIERO, SL (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORAL & MAXILLOFACIAL SURG,ORAL & MAXILLOFACIAL SURG SERV,BOSTON,MA 02114, USA. NR 18 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-2391 J9 J ORAL MAXIL SURG JI J. Oral Maxillofac. Surg. PD JUN PY 1991 VL 49 IS 6 BP 647 EP 652 DI 10.1016/0278-2391(91)90349-Q PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FN444 UT WOS:A1991FN44400016 PM 2037923 ER PT J AU GOLDSTEIN, B HERRIN, JT TODRES, ID AF GOLDSTEIN, B HERRIN, JT TODRES, ID TI INCREASED INTRAABDOMINAL PRESSURE AND ANURIA IN THE NEWBORN SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE ASCITES; NEONATAL C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT NEPHROL,CHILDRENS SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEONATAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PEDIAT INTENS CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 3 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 0022-3468 J9 J PEDIATR SURG JI J. Pediatr. Surg. PD JUN PY 1991 VL 26 IS 6 BP 749 EP 750 DI 10.1016/0022-3468(91)90027-Q PG 2 WC Pediatrics; Surgery SC Pediatrics; Surgery GA FP688 UT WOS:A1991FP68800027 PM 1941473 ER PT J AU AHMED, AR KURGIS, BS ROGERS, RS AF AHMED, AR KURGIS, BS ROGERS, RS TI CICATRICIAL PEMPHIGOID SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Review ID EPIDERMOLYSIS-BULLOSA-ACQUISITA; LINEAR IGA DISEASE; BRUNSTING-PERRY; IMMUNOSUPPRESSIVE THERAPY; RHEUMATOID-ARTHRITIS; IMMUNOFLUORESCENCE; ANTIBODIES; AZATHIOPRINE; DERMATOSIS; DIAGNOSIS AB Cicatricial pemphigoid is a subepidermal blistering disease that involves the mucous membranes and the skin. The oral cavity and the eye are most frequently involved. The clinical course is of long duration, and often there is significant scarring that can have devastating sequelae. The majority of the patients are elderly. The disease is characterized by the in vivo deposition of an anti-basement membrane zone antibody. The anti-basement membrane zone antibody cannot be detected in the circulation by routine laboratory techniques. The pathogenesis is poorly understood, and the cause is not known. Cicatricial pemphigoid may remain localized to the oral cavity or the eye or the skin (Brunsting-Perry variety), or it may be generalized. It rarely occurs in children, and it may be drug induced. Efforts must be made to differentiate cicatricial pemphigoid from bullous pemphigoid, epidermolysis bullosa acquisita, linear IgA bullous disease, and other vesiculobullous diseases. Early recognition and treatment can improve the prognosis and avoid surgical intervention. Topical therapy is beneficial and expedites healing. Intralesional corticosteroids are effective and can help reduce the dose of systemic steroids. Most patients require systemic corticosteroid therapy. Dapsone is also useful in treating cicatricial pemphigoid, especially in patients in whom systemic steroids are ineffective or in whom they have to be discontinued because of side effects. Immunosuppressive agents (azathioprine or cyclosphosphamide) are indicated in patients with progressive disease. Occasionally both drugs may be needed. C1 HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,CAMBRIDGE,MA 02138. BAKERSFIELD DERMATOL & SKIN CANC MED GRP,BAKERSFIELD,MN. MAYO CLIN & MAYO FDN,DEPT DERMATOL,ROCHESTER,MN 55905. RP AHMED, AR (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NEI NIH HHS [1R01 EY08379-01] NR 94 TC 110 Z9 112 U1 0 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD JUN PY 1991 VL 24 IS 6 BP 987 EP 1001 DI 10.1016/0190-9622(91)70159-Y PN 1 PG 15 WC Dermatology SC Dermatology GA FN423 UT WOS:A1991FN42300013 PM 1869688 ER PT J AU SHAPIRO, SM BERSOHN, MM LAKS, MM AF SHAPIRO, SM BERSOHN, MM LAKS, MM TI IN SEARCH OF THE HOLY-GRAIL - THE STUDY OF DIASTOLIC VENTRICULAR-FUNCTION BY THE USE OF DOPPLER ECHOCARDIOGRAPHY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CONGESTIVE HEART-FAILURE; CANINE LEFT-VENTRICLE; CARDIOMYOPATHY; RELAXATION C1 UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,W LOS ANGELES VET AFFAIRS MED CTR,TORRANCE,CA 90509. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. NR 11 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN PY 1991 VL 17 IS 7 BP 1517 EP 1519 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FQ229 UT WOS:A1991FQ22900011 PM 2033183 ER PT J AU LEIFER, D COLE, DG KOWALL, NW AF LEIFER, D COLE, DG KOWALL, NW TI NEUROPATHOLOGIC ASYMMETRIES IN THE BRAIN OF A PATIENT WITH A UNILATERAL STATUS EPILEPTICUS SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE STATUS EPILEPTICUS; AUTOPSY; HIPPOCAMPUS; CEREBELLUM; IMMUNOHISTOCHEMISTRY ID HUMAN TEMPORAL-LOBE; ENKEPHALIN-LIKE IMMUNOREACTIVITY; HUMAN HIPPOCAMPAL-FORMATION; CROSSED CEREBELLAR ATROPHY; CALCIUM-BINDING PROTEIN; RAT HIPPOCAMPUS; SYNAPTIC REORGANIZATION; MONOCLONAL-ANTIBODY; ALZHEIMERS-DISEASE; SUBSTANCE-P AB Autopsy study of a patient who died after an episode of prolonged unilateral status epilepticus revealed neuronal loss in the hippocampus on the epileptic side, with gliosis confined to the CA1 and CA3 fields. There was loss of the parvalbumin-immunoreactive gamma-aminobutyric acid (GABA)-ergic interneurons in the hippocampus on that side. There was also loss of the normal laminar pattern of substance P staining with increased substance P immunoreactivity in the supragranular plexus on that side. Met-enkephalin immunoreactivity was also increased in the outer molecular layer of the dentate gyrus on the epileptic side. Mossy fibers on the epileptic side stained more strongly with the Hicks' silver stain and with antibodies against glutamate and taurine, but less intensely with antibodies against calbindin. In the contralateral cerebellum, there was Purkinje cell loss, injury to the remaining Purkinje cells, and increased prominence of the Bergmann glia. Our observations show that prolonged unilateral seizure activity can be associated with specific histochemical changes in the human hippocampus. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP LEIFER, D (reprint author), CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115, USA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NICHD NIH HHS [CHD00888]; NINDS NIH HHS [NS10828, NS25588] NR 51 TC 24 Z9 24 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD JUN PY 1991 VL 103 IS 2 BP 127 EP 135 DI 10.1016/0022-510X(91)90155-Z PG 9 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FU029 UT WOS:A1991FU02900001 PM 1715386 ER PT J AU YU, JS HAYASHI, T SEBOUN, E SKLAR, RM DOOLITTLE, TH HAUSER, SL AF YU, JS HAYASHI, T SEBOUN, E SKLAR, RM DOOLITTLE, TH HAUSER, SL TI FOS RNA ACCUMULATION IN MULTIPLE-SCLEROSIS WHITE MATTER TISSUE SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Article DE PROTO-ONCOGNENE; ASTROCYTE; INVIVO RNA EXPRESSION ID CENTRAL NERVOUS-SYSTEM; TUMOR NECROSIS FACTOR; C-FOS; GROWTH-FACTOR; PROTO-ONCOGENE; ASTROCYTES; EXPRESSION; BRAIN; INDUCTION; CELLS AB In order to better characterize the molecular events that accompany lesion development in multiple sclerosis (MS), we studied the accumulation of RNA specific to the nuclear proto-oncogenes c-fos and c-myb in post mortem white matter brain tissue. RNA was prepared from plaque and periplaque regions of 6 different MS brains, from "normal" white matter regions of 3 MS brains and from 6 normal control samples. Quantitation of specific RNA corresponding to each proto-oncogene was performed by Northern blot hybridization and by scanning densitometry. Results indicate a 2-fold increase in c-fos RNA in MS white matter, compared to control tissue. No c-myb signal was identified in any sample. In situ hybridization studies confirmed the selective upregulation of c-fos RNA levels in MS tissue, and suggested that glial cells and not inflammatory cells were responsible for the enhanced c-fos signal. These results suggest that persistent glial cell activation is present within chronic MS lesions irrespective of whether the lesions are active (e.g., inflammatory) or inactive. RP YU, JS (reprint author), MASSACHUSETTS GEN HOSP,NEUROIMMUNOL UNIT,WARREN 352,32 FRUIT ST,BOSTON,MA 02114, USA. RI Hauser, Stephen/J-2978-2016 FU NINDS NIH HHS [NS26799] NR 48 TC 7 Z9 7 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD JUN PY 1991 VL 103 IS 2 BP 209 EP 215 DI 10.1016/0022-510X(91)90166-5 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FU029 UT WOS:A1991FU02900012 PM 1715387 ER PT J AU LAMURAGLIA, GM VLAHAKES, GJ MONCURE, AC BREWSTER, DC BUCKLEY, MJ DAGGETT, WM PALACIOS, I CAMBRIA, R AKINS, CW TORCHIANA, DF ABBOTT, WM AUSTEN, WG AF LAMURAGLIA, GM VLAHAKES, GJ MONCURE, AC BREWSTER, DC BUCKLEY, MJ DAGGETT, WM PALACIOS, I CAMBRIA, R AKINS, CW TORCHIANA, DF ABBOTT, WM AUSTEN, WG TI THE SAFETY OF INTRAAORTIC BALLOON PUMP CATHETER INSERTION THROUGH SUPRAINGUINAL PROSTHETIC VASCULAR BYPASS GRAFTS SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 17TH ANNUAL MEETING OF THE NEW ENGLAND SOC FOR VASCULAR SURGERY CY SEP 13-14, 1990 CL NEWPORT, RI SP NEW ENGLAND SOC VASC SURG ID INTRA-AORTIC BALLOON; DACRON AORTOFEMORAL GRAFTS; SURGICAL TECHNIQUES; COMPLICATIONS; COUNTERPULSATION; PLACEMENT; PUNCTURE AB To determine the safety of intraaortic balloon pump catheter insertion for critical coronary ischemia through suprainguinal prosthetic bypass grafts, we examined our experience of 19 intraaortic balloon pumps placed through grafts in 17 patients by means of surgical exposure (8) or the percutaneous (11) approach. Fourteen intraaortic balloon pumps were placed through matured grafts at a time remote (2 to 13 years; mean, 7 years) from their vascular bypass surgery. Five were inserted through nonmatured grafts during the same hospitalization as their vascular reconstructive surgery (1 to 12 days; mean, 4 days). One patient, a day after an aortoiliac bypass, died during an urgent, surgical intraaortic balloon pump insertion for cardiogenic shock. All other patients had prompt reversal of their cardiac ischemia. Decreased limb perfusion developed during use of the intraaortic balloon pump in three patients, all of whom had their intraaortic balloon pump placed percutaneously through mature grafts. Two of these required surgical thrombectomy. Ten intraaortic balloon pump insertions in eight patients survived the hospitalization and were followed for a mean of 24 months (range, 2 weeks to 64 months). No localized groin or graft infections were identified. No bleeding complications or pseudoaneurysms occurred. Thus in patients with unstable, severe, cardiac disease, intraaortic balloon pumps can be safely placed through indwelling suprainguinal bypass grafts. C1 MASSACHUSETTS GEN HOSP,GEN SURG SERV,CARDIAC SURG UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAMURAGLIA, GM (reprint author), MASSACHUSETTS GEN HOSP,GEN SURG SERV,VASC SURG UNIT,BOSTON,MA 02114, USA. NR 16 TC 4 Z9 4 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JUN PY 1991 VL 13 IS 6 BP 830 EP 837 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA FQ231 UT WOS:A1991FQ23100008 PM 1828091 ER PT J AU DABROWSKI, CE SCHAFFER, PA AF DABROWSKI, CE SCHAFFER, PA TI HERPES-SIMPLEX VIRUS TYPE-1 ORIGIN-SPECIFIC BINDING-PROTEIN - ORIS-BINDING PROPERTIES AND EFFECTS OF CELLULAR PROTEINS SO JOURNAL OF VIROLOGY LA English DT Article ID DNA-REPLICATION ORIGIN; ADENOVIRUS ORIGIN; GENE-PRODUCTS; T-ANTIGEN; WILD-TYPE; IDENTIFICATION; SEQUENCE; REQUIREMENTS; ACTIVATION; INVITRO AB The herpes simplex virus type 1 (HSV-1) origin of replication, oriS, contains three highly homologous sequences, sites I, II, and III. The HSV-1 origin-binding protein (OBP), the product of the UL9 gene, has been shown to bind specifically to sites I and II. In this study, gel shift analysis was used to characterize interactions between site I DNA and proteins in infected and uninfected cell extracts. The formation of two protein-DNA complexes, bands A and B, was demonstrated with infected cell extracts, and one predominant protein-DNA complex, band M, was identified with mock-infected extracts. Protein interactions with the highly homologous site II and III DNAs were also characterized. Incubation of infected cell extracts with the lower-affinity site II DNA as a probe resulted in the appearance of two protein-DNA complexes with mobilities identical to those of the A and B complexes, while incubation with site III DNA resulted in the formation of a single complex with the mobility of band B; no A-like band was observed. Incubation of high concentrations of partially purified OBP with site I DNA resulted in the formation of two novel complexes, bands 9-1 and 9-2. Addition of uninfected or HSV-1-infected cell extracts to the purified OBP-site I DNA mix significantly enhanced the formation of complex 9-1. The enhanced formation of complex 9-1 by uninfected cell extracts implicates a cellular factor or factors in the formation or stabilization of the OBP-site I DNA complex. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [CA08749]; NIAID NIH HHS [AI28537] NR 48 TC 34 Z9 34 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1991 VL 65 IS 6 BP 3140 EP 3150 PG 11 WC Virology SC Virology GA FM165 UT WOS:A1991FM16500045 PM 1851874 ER PT J AU MANDAVILLI, U SCHMIDT, J RATTNER, DW WATSON, WT WARSHAW, AL AF MANDAVILLI, U SCHMIDT, J RATTNER, DW WATSON, WT WARSHAW, AL TI CONTINUOUS COMPLETE COLLECTION OF UNCONTAMINATED URINE IN CONSCIOUS RODENTS SO LABORATORY ANIMAL SCIENCE LA English DT Article ID URETER; RATS AB We describe a novel technique for complete and continuous bladder urine collection in conscious unrestrained rats. After urethral ligation, a silastic catheter is placed through a flexible steel tether, tunneled subcutaneously from the posterior neck area to a suprapubic incision, and inserted and fixed into the exposed urinary bladder. The catheter drains by gravity into a dependent collecting vessel protected from contamination by feces or food. RP MANDAVILLI, U (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 7 TC 18 Z9 18 U1 0 U2 0 PU AMER ASSOC LABORATORY ANIMAL SCIENCE PI CORDOVA PA 70 TIMBERCREEK DR, SUITE 5, CORDOVA, TN 38018 SN 0023-6764 J9 LAB ANIM SCI JI Lab. Anim. Sci. PD JUN PY 1991 VL 41 IS 3 BP 258 EP 261 PG 4 WC Veterinary Sciences; Zoology SC Veterinary Sciences; Zoology GA GF778 UT WOS:A1991GF77800009 PM 1658466 ER PT J AU ELNER, SG STRIETER, RM ELNER, VM ROLLINS, BJ DELMONTE, MA KUNKEL, SL AF ELNER, SG STRIETER, RM ELNER, VM ROLLINS, BJ DELMONTE, MA KUNKEL, SL TI MONOCYTE CHEMOTACTIC PROTEIN GENE-EXPRESSION BY CYTOKINE-TREATED HUMAN RETINAL-PIGMENT EPITHELIAL-CELLS SO LABORATORY INVESTIGATION LA English DT Article DE RETINAL PIGMENT EPITHELIUM, INTERLEUKIN 1-BETA, TUMOR NECROSIS FACTOR-ALPHA ID TUMOR NECROSIS FACTOR; VASCULAR ENDOTHELIAL-CELLS; SENILE MACULAR DEGENERATION; ACTIVATING FACTOR MCAF; PROLIFERATIVE VITREORETINOPATHY; SYMPATHETIC OPHTHALMIA; DERMAL FIBROBLASTS; GROWTH-FACTOR; GIANT-CELLS; INTERLEUKIN-1 AB Inflammation involving the retina and choroid is a common clinical problem, but the mechanisms that elicit and maintain ocular inflammation remain poorly understood. Interposed between the sensory retina and the systemic blood circulation within the choroid is the neural-derived retinal pigment epithelium (RPE), which forms part of the blood-retina barrier. The RPE is actively phagocytic and shares several features with mononuclear phagocytes of bone marrow origin, including the production of a neutrophil chemotactic factor, interleukin 8, after stimulation with interleukin 1-beta-(IL-1-beta) or tumor necrosis factor alpha-(TNF-alpha). Because monocyte-derived macrophages are present in retinal lesions of many common and blinding diseases, we monitored human RPE cells or monocyte chemotactic protein (MCP) mRNA expression and activity following cytokine stimulation. Cultured human RPE cells were left unstimulated or exposed to recombinant human IL-1-beta, TNF-alpha, or lipopolysaccharide. MCP mRNA expression in RPE cells and biologically active MCP in RPE cell supernatants were present 1 hour after stimulation and maintained for 24 hours. Conditioned media from RPE cells stimulated with 20 ng/ml of IL-1-beta or TNF-alpha for 24 hours contained biologically active monocyte chemotactic activity that rose rapidly from baseline levels over 4 hours and plateaued over the subsequent 20 hours. RPE chemotactic activity was dose dependent using concentrations of these cytokines ranging from 20 pg/ml to 20 ng/ml of 4-hour assays. Time- and concentration-dependent expression of RPE cell MCP mRNA was also found in the same cultures. Peak MCP mRNA expression occurred after 8 hours of stimulation with IL-1-beta or TNF-alpha. Maximal steady-state MCP mRNA expression occurred at 20 ng/ml for IL-1-beta. Immunohistochemical staining using specific anti-MCP antibodies resulted in distinctive RPE cell staining, confirming the presence of MCP in human RPE cells. These findings demonstrate that cytokine-stimulated RPE cells may evoke or augment mononuclear phagocyte-mediated ocular inflammation by synthesizing MCP. C1 UNIV MICHIGAN,SCH MED,DEPT PATHOL,BOX 0602,1301 CATHERINE,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,KELLOGG EYE CTR,DEPT OPHTHALMOL,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-31963, HL35276]; NIDDK NIH HHS [DK-38149] NR 49 TC 129 Z9 132 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0023-6837 J9 LAB INVEST JI Lab. Invest. PD JUN PY 1991 VL 64 IS 6 BP 819 EP 825 PG 7 WC Medicine, Research & Experimental; Pathology SC Research & Experimental Medicine; Pathology GA FQ918 UT WOS:A1991FQ91800011 PM 2046333 ER PT J AU CANELLOS, GP ROSENBERG, W AF CANELLOS, GP ROSENBERG, W TI WILL DOXORUBICIN-CONTAINING REGIMENS REPLACE MOPP AND ITS VARIANTS SO LEUKEMIA LA English DT Article; Proceedings Paper CT 2ND VICENZA INTERNATIONAL WORKSHOP OF HEMATOLOGY : NEW INSIGHTS IN LYMPHOMAS CY MAY 29-31, 1991 CL VICENZE, ITALY SP ITALIAN SOC HEMATOL ID ADVANCED HODGKINS-DISEASE; TERM FOLLOW-UP; COMBINATION CHEMOTHERAPY; PROGNOSTIC FACTORS; RADIATION-THERAPY; ABVD; RADIOTHERAPY; ETOPOSIDE; RECURRENT; LEUKEMIA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. OI Rosenberg, William/0000-0002-2732-2304 NR 32 TC 0 Z9 0 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD JUN PY 1991 VL 5 SU 1 BP 50 EP 52 PG 3 WC Oncology; Hematology SC Oncology; Hematology GA GH798 UT WOS:A1991GH79800012 PM 1890866 ER PT J AU ROSEN, BR BELLIVEAU, JW BUCHBINDER, BR MCKINSTRY, RC PORKKA, LM KENNEDY, DN NEUDER, MS FISEL, CR ARONEN, HJ KWONG, KK WEISSKOFF, RM COHEN, MS BRADY, TJ AF ROSEN, BR BELLIVEAU, JW BUCHBINDER, BR MCKINSTRY, RC PORKKA, LM KENNEDY, DN NEUDER, MS FISEL, CR ARONEN, HJ KWONG, KK WEISSKOFF, RM COHEN, MS BRADY, TJ TI CONTRAST AGENTS AND CEREBRAL HEMODYNAMICS SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article; Proceedings Paper CT MEETING/WORKSHOP ON FUTURE DIRECTIONS IN MRI OF DIFFUSION AND MICROCIRCULATION CY JUN 07-08, 1990 CL BETHESDA, MD SP SOC MAGNET RESONANCE MED, BERLEX, BRUKER, GE, MED SYST, PICKER INT, SALUTAR, SQUIBB DIAGNOST, TOSHIBA INT ID EMISSION COMPUTED-TOMOGRAPHY; BLOOD-BRAIN-BARRIER; MEAN TRANSIT-TIME; DRUG DELIVERY; VOLUME; FLOW; SUSCEPTIBILITY; RAT; CHEMOTHERAPY; ENHANCEMENT C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSEN, BR (reprint author), MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,DEPT RADIOL,BOSTON,MA 02114, USA. RI Kennedy, David/H-3627-2012; Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [P01-CA48729, R01-CA40303]; NHLBI NIH HHS [R01-HL39870] NR 50 TC 213 Z9 215 U1 1 U2 9 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD JUN PY 1991 VL 19 IS 2 BP 285 EP 292 DI 10.1002/mrm.1910190216 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FQ243 UT WOS:A1991FQ24300015 PM 1881317 ER PT J AU AMIEL, D GELBERMAN, R HARWOOD, F SIEGEL, D AF AMIEL, D GELBERMAN, R HARWOOD, F SIEGEL, D TI FIBRONECTIN IN HEALING FLEXOR TENDONS SUBJECTED TO IMMOBILIZATION OR EARLY CONTROLLED PASSIVE MOTION SO MATRIX LA English DT Article DE FIBRONECTIN; FLEXOR TENDON; IMMOBILIZATION; WOUND HEALING ID CONNECTIVE-TISSUE; PLASMA FIBRONECTIN; COLLAGEN; REPAIR; IMMUNOASSAY AB The medial and lateral forepaw flexor tendons of 20-adult mongrel dogs (n = 40) were transected and repaired with a modified Kessler suture. Post-operatively the dogs were subjected either to immobilization or early controlled passive digital motion. Sacrifices were at 3, 7, 10 and 17 days. The tendons of the contralateral limbs were left intact and used as controls. Urea-heparin-extracted fibronectin was quantitated by competitive ELISA in the tendons and sheaths at the four post-injury/repair time periods. In both groups (controlled passive motion and immobilization), fibronectin concentrations were higher in the injured tissues than in control tissues. However, peak fibronectin concentration (7-days post-injury/repair) was approximately twice as high in the controlled passive motion tissues as in the immobilized tissues. It was concluded, therefore, that, relative to early controlled passive motion, early immobilization depresses the accumulation of tissue fibronectin during the early stages of healing following injury. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP AMIEL, D (reprint author), UNIV CALIF SAN DIEGO,DIV ORTHOPAED & REHABIL,9506 GILMAN DR,LA JOLLA,CA 92093, USA. FU NIAMS NIH HHS [AR38159, AR33097] NR 19 TC 19 Z9 20 U1 0 U2 1 PU GUSTAV FISCHER VERLAG PI STUTTGART PA WOLLGRASWEG 49, D-70599 STUTTGART, GERMANY SN 0934-8832 J9 MATRIX JI Matrix PD JUN PY 1991 VL 11 IS 3 BP 184 EP 189 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FN854 UT WOS:A1991FN85400005 PM 1870449 ER PT J AU SASAKI, AW DOSKOW, J MACLEOD, CL ROGERS, MB GUDAS, LJ WILKINSON, MF AF SASAKI, AW DOSKOW, J MACLEOD, CL ROGERS, MB GUDAS, LJ WILKINSON, MF TI THE ONCOFETAL GENE PEM ENCODES A HOMEODOMAIN AND IS REGULATED IN PRIMORDIAL AND PRE-MUSCLE STEM-CELLS SO MECHANISMS OF DEVELOPMENT LA English DT Article DE ONCOFETAL; HOMEOBOX; EMBRYONAL STEM CELL; MUSCLE DEVELOPMENT ID EMBRYONAL CARCINOMA-CELLS; RETINOIC ACID; MESSENGER-RNA; VISCERAL ENDODERM; HOMEOBOX GENES; 10T1/2 CELLS; DIFFERENTIATION; EXPRESSION; PROTEIN; DOMAIN AB The oncofetal gene, Pem, is expressed in a stage specific manner during murine ontogeny. The carboxy terminal portion of the predicted Pem protein has significant similarity to homeodomains of the Drosophila prd family. The Pem gene is expressed in undifferentiated embryonal stem (ES) and embryonal carcinoma (EC) cell lines. Pem mRNA is induced 35-fold in ES cells differentiated in the absence of retinoic acid. Pem mRNA is increased in EC cells differentiated towards parietal or visceral endoderm, consistent with the abundant Pem expression in embryonic yolk sac. In 10T mesenchymal stem cells committed to muscle cell differentiation, Pem mRNA expression is dramatically increased. The elevation in Pem expression preceded the induction of the muscle master regulatory gene, myoD. We conclude that the Pem gene encodes a candidate transcription factor which is developmentally regulated. C1 UNIV CALIF SAN DIEGO,CTR CANC,DEPT MED,CANC BIOL PROGRAM,SAN DIEGO,CA 92103. OREGON HLTH SCI UNIV,DEPT MICROBIOL & IMMUNOL,PORTLAND,OR 97201. VET ADM MED CTR,PORTLAND,OR 97207. OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA39036, CA37778]; NIGMS NIH HHS [GM-39586] NR 46 TC 38 Z9 41 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0925-4773 J9 MECH DEVELOP JI Mech. Dev. PD JUN PY 1991 VL 34 IS 2-3 BP 155 EP 164 DI 10.1016/0925-4773(91)90052-8 PG 10 WC Developmental Biology SC Developmental Biology GA FZ472 UT WOS:A1991FZ47200008 PM 1680379 ER PT J AU LAUFFER, RB AF LAUFFER, RB TI IRON STORES AND THE INTERNATIONAL VARIATION IN MORTALITY FROM CORONARY-ARTERY DISEASE SO MEDICAL HYPOTHESES LA English DT Article ID LOW-DENSITY LIPOPROTEIN; LIVER-STORAGE IRON; REPERFUSION INJURY; FREE-RADICALS; HEART; DEFEROXAMINE; CANCER; RISK; CHOLESTEROL; METABOLISM AB Possible roles for iron in coronary artery disease (CAD) have emerged, including contributions to atherogenesis and/or the vulnerability of the myocardium to ischemia/reperfusion events. The value of hepatic storage iron as a potential risk factor for CAD was evaluated independently and in combination with various lipoprotein indices using CAD mortality data from 11 countries along with available data on liver iron stores. CAD mortality rates were found to be best correlated with the liver iron-serum cholesterol product in both men (r = 0.72) and, more importantly, in both genders combined (r = 0.74). It was also found that estimated CAD incidence could be related in a non-linear fashion to iron-cholesterol values in a simple normal distribution model where all subjects above a threshold value of iron-cholesterol were assumed to have CAD. Hepatic iron values thus appear to be useful in describing the differences in CAD due to both diet (and/or culture) and sex. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAUFFER, RB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,NUCL MAGNET RESONANCE SECT,BAKER 2,BOSTON,MA 02114, USA. NR 38 TC 34 Z9 34 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JUN PY 1991 VL 35 IS 2 BP 96 EP 102 DI 10.1016/0306-9877(91)90030-3 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FT512 UT WOS:A1991FT51200007 PM 1890983 ER PT J AU LAUFFER, RB AF LAUFFER, RB TI EXERCISE AS PREVENTION - DO THE HEALTH BENEFITS DERIVE IN PART FROM LOWER IRON LEVELS SO MEDICAL HYPOTHESES LA English DT Article ID LOW-DENSITY LIPOPROTEIN; REPERFUSION INJURY; FERRITIN SYNTHESIS; HYDROGEN-PEROXIDE; PHYSICAL-FITNESS; DEFEROXAMINE; DISEASE; HEART; PATHOGENESIS; INFLAMMATION AB The mechanism by which exercise, a key component of modern preventative medicine, protects man from strikingly different diseases such as heart disease and cancer, is largely a mystery. It is proposed that exercise-induced reductions in iron levels, either through iron loss or enhanced iron storage, could be responsible for some of the beneficial effects. Possible roles for iron in coronary artery disease and cancer have recently emerged, particularly as a catalyst for oxygen free radical-induced tissue damage. The iron hypothesis is consistent with the graded reductions in mortality observed as a function of fitness level, and it is the first unified mechanism which can explain the reductions in both heart disease and cancer. If confirmed, preventative medicine in the future will need to include close monitoring of iron levels and, possibly, occasional blood donation for those with moderately high iron stores. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAUFFER, RB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,NUCL MAGNET RESONANCE SECT,BAKER 2,BOSTON,MA 02114, USA. NR 35 TC 23 Z9 22 U1 0 U2 2 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PD JUN PY 1991 VL 35 IS 2 BP 103 EP 107 DI 10.1016/0306-9877(91)90031-S PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FT512 UT WOS:A1991FT51200008 PM 1890967 ER PT J AU CINCOTTA, AH SCHILLER, BC MEIER, AH AF CINCOTTA, AH SCHILLER, BC MEIER, AH TI BROMOCRIPTINE INHIBITS THE SEASONALLY OCCURRING OBESITY, HYPERINSULINEMIA, INSULIN RESISTANCE, AND IMPAIRED GLUCOSE-TOLERANCE IN THE SYRIAN-HAMSTER, MESOCRICETUS-AURATUS SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article ID DEPENDENT DIABETES-MELLITUS; BODY-FAT DISTRIBUTION; GOLDEN-HAMSTER; TEMPORAL SYNERGISM; LIPID-METABOLISM; RISK-FACTORS; PHOTOPERIODIC CONTROL; CIRCADIAN VARIATION; PROLACTIN PERMITS; FUNDULUS-GRANDIS C1 HARVARD UNIV, SCH MED, DEPT DERMATOL, BOSTON, MA 02115 USA. LOUISIANA STATE UNIV, DEPT ZOOL & PHYSIOL, BATON ROUGE, LA 70803 USA. RP CINCOTTA, AH (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. NR 53 TC 51 Z9 51 U1 1 U2 2 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0026-0495 EI 1532-8600 J9 METABOLISM JI Metab.-Clin. Exp. PD JUN PY 1991 VL 40 IS 6 BP 639 EP 644 DI 10.1016/0026-0495(91)90057-4 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FN658 UT WOS:A1991FN65800015 PM 1865827 ER PT J AU ROLLINS, BJ SUNDAY, ME AF ROLLINS, BJ SUNDAY, ME TI SUPPRESSION OF TUMOR-FORMATION INVIVO BY EXPRESSION OF THE JE GENE IN MALIGNANT-CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID CHEMOATTRACTANT PROTEIN-1 MCP-1; GROWTH STIMULATORY ACTIVITY; ACTIVATING FACTOR MCAF; MOUSE CHROMOSOME-11; SEQUENCE SIMILARITY; CHEMOTACTIC FACTOR; PLATELET FACTOR-4; NECROSIS FACTOR; CYTOKINE GENES; PURIFICATION AB The early growth response gene JE encodes a monocyte chemoattractant, MCP-1. The JE/MCP-1 protein attracts and stimulates human monocytes and induces monocyte-mediated inhibition of tumor cell growth in vitro. Expression of human or murine JE/MCP-1 in Chinese hamster ovary (CHO) cells completely suppressed their ability to form tumors in nude mice. Coinjection of JE/MCP-1-expressing cells with nonexpressing CHO cells or with HeLa cells also prevented tumor formation. Since JE/MCP-1 expression had no discernible effect on the transformed phenotype of these cells in vitro, the suppressive effect depends on host animal factors. These factors are likely to be components of the inflammatory response, because JE/MCP-1-expressing cells elicited a predominantly monocytic infiltrate at the site of injection. Our results suggest that JE/MCP-1 protein may be useful in cancer therapy. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROLLINS, BJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA53091]; NHLBI NIH HHS [HL/CA44984] NR 37 TC 221 Z9 224 U1 1 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 JUN PY 1991 VL 11 IS 6 BP 3125 EP 3131 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200024 PM 2038321 ER PT J AU MUNDSCHAU, LJ FALLER, DV AF MUNDSCHAU, LJ FALLER, DV TI BALB/C-3T3 FIBROBLASTS RESISTANT TO GROWTH-INHIBITION BY BETA INTERFERON EXHIBIT ABERRANT PLATELET-DERIVED GROWTH-FACTOR, EPIDERMAL GROWTH-FACTOR, AND FIBROBLAST GROWTH-FACTOR SIGNAL TRANSDUCTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DOUBLE-STRANDED-RNA; C-MYC SUPPRESSION; ALPHA-INTERFERON; GAMMA-INTERFERON; GENE-EXPRESSION; CELLS RESISTANT; 3T3 CELLS; INDUCTION; FOS; DIFFERENTIATION AB Several lines of evidence now exist to suggest an interaction between the platelet-derived growth factor (PDGF) growth-stimulatory signal transduction pathway and the beta interferon (IFN-beta) growth-inhibitory signal transduction pathway. The most direct examples are inhibition of PDGF-mediated gene induction and mitogenesis by IFN-beta and the effects of activators and inhibitors of the IFN-inducible double-stranded RNA-dependent eIF2 kinase on expression of PDGF-inducible genes. To further investigate the nature of this PDGF/IFN-beta interaction, we selected BALB/c-3T3 cells for resistance to growth inhibition by IFN-beta and analyzed the phenotypes of resulting clonal lines (called IRB cells) with respect to PDGF signal transduction. Although selected only for IFN resistance, the IRB cells were found to be defective for induction of growth-related genes c-fos, c-myc, and JE in response to PDGF. This block to signal transduction was not due to loss or inactivation of PDGF receptors, as immunoprecipitation of PDGF receptors with antiphosphotyrosine antibodies showed them to be present at equal levels in the BALB/c-3T3 and IRB cells and to be autophosphorylated normally in response to PDGF. Furthermore, treatment with other peptide growth factors (PDGF-AA, fibroblast growth factor, and epidermal growth factor) also failed to induce c-fos, c-myc, or JE expression in IRB cells. All of these growth factors, however, were able to induce another early growth-related gene, Egr-1. The block to signaling was not due to a defect in inositol phosphate metabolism, as PDGF treatment induced normal calcium mobilization and phosphotidylinositol-3-kinase activation in these cells. Activation of protein kinase C by phorbol esters did induce c-fos, c-myc, and JE in IRB cells, indicating that signaling pathways distal to this enzyme remained intact. We have previously shown that IFN-inducible enzyme activities, including double-stranded RNA-dependent eIF2 kinase and 2',5'-oligoadenylate synthetase, are normal in IRB cells. The finding that the induction of multiple growth-related genes by several independent growth factors is inhibited in these IFN-resistant cells suggests that there is a second messenger common to both growth factor and IFN signaling pathways and that this messenger is defective in these cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT HEMATOL & ONCOL,44 BINNEY ST,BOSTON,MA 02115. NR 28 TC 16 Z9 16 U1 0 U2 0 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 JUN PY 1991 VL 11 IS 6 BP 3148 EP 3154 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200027 PM 1645446 ER PT J AU HENDRICKSON, EA LIU, VF WEAVER, DT AF HENDRICKSON, EA LIU, VF WEAVER, DT TI STRAND BREAKS WITHOUT DNA REARRANGEMENT IN V(D)J RECOMBINATION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID LIGHT-CHAIN GENES; PRE-B CELLS; SITE-SPECIFIC RECOMBINATION; COMBINED IMMUNE-DEFICIENCY; SIGNAL SEQUENCES; SCID MICE; SEGMENTS; DEFECT; HEAVY; SUBSTRATE AB Somatic gene rearrangement of immunoglobulin and T-cell receptor genes [V(D)J recombination] is mediated by pairs of specific DNA sequence motifs termed signal sequences. In experiments described here, retroviral vectors containing V(D)J rearrangement cassettes in which the signal sequences had been altered were introduced into wild-type and scid (severe combined immune deficiency) pre-B cells and used to define intermediates in the V(D)J recombination pathway. The scid mutation has previously been shown to deleteriously affect the V(D)J recombination process. Cassettes containing a point mutation in one of the two signal sequences inhibited rearrangement in wild-type cells. In contrast, scid cells continued to rearrange these cassettes with the characteristic scid deletional phenotype. Using these mutated templates, we identified junctional modifications at the wild-type signal sequences that had arisen from strand breaks which were not associated with overall V(D)J rearrangements. Neither cell type was able to rearrange constructs which contained only a single, nonmutated, signal sequence. In addition, scid and wild-type cell lines harboring cassettes with mutations in both signal sequences did not undergo rearrangement, suggesting that at least one functional signal sequence was required for all types of V(D)J recombination events. Analysis of these signal sequence mutations has provided insights into intermediates in the V(D)J rearrangement pathway in wild-type and scid pre-B cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NICHD NIH HHS [5F32HD07034]; NIGMS NIH HHS [GM39312] NR 31 TC 33 Z9 33 U1 0 U2 0 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 JUN PY 1991 VL 11 IS 6 BP 3155 EP 3162 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200028 PM 2038323 ER PT J AU SEGATTO, O LONARDO, F WEXLER, D FAZIOLI, F PIERCE, JH BOTTARO, DP WHITE, MF DIFIORE, PP AF SEGATTO, O LONARDO, F WEXLER, D FAZIOLI, F PIERCE, JH BOTTARO, DP WHITE, MF DIFIORE, PP TI THE JUXTAMEMBRANE REGIONS OF THE EPIDERMAL GROWTH-FACTOR RECEPTOR AND GP185ERBB-2 DETERMINE THE SPECIFICITY OF SIGNAL TRANSDUCTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID STIMULATES TYROSINE PHOSPHORYLATION; PHOSPHOLIPASE-C-GAMMA; PDGF BETA-RECEPTOR; PROTEIN KINASE-C; EGF RECEPTOR; MITOGENIC RESPONSE; INSULIN-RECEPTOR; 3T3 CELLS; THREONINE; ERBB-2 AB The epidermal growth factor receptor (EGFR) and gp185erbB-2 are closely related tyrosine kinases. Despite extensive sequence and structural homology, these two receptors display quantitative and qualitative differences in their ability to couple with mitogenic signalling pathways. By using chimeric molecules between EGFR and erbB-2, we found that the determinants responsible for the specificity of mitogenic signal transduction are located in the amino-terminal half of the tyrosine kinase domain of either receptor. In the EGFR, mutational analysis within this subdomain revealed that deletion of residues 660 to 667 impaired receptor mitogenic activity without affecting its tyrosine kinase properties. This sequence is therefore likely to contribute to the specificity of substrate recognition by the EGFR kinase. C1 NCI,MOLEC & CELLULAR BIOL LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. RI Bottaro, Donald/F-8550-2010; Di Fiore, Pier Paolo/K-2130-2012 OI Bottaro, Donald/0000-0002-5057-5334; Di Fiore, Pier Paolo/0000-0002-2252-0950 FU NIDDK NIH HHS [DK38712] NR 46 TC 51 Z9 51 U1 0 U2 4 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 JUN PY 1991 VL 11 IS 6 BP 3191 EP 3202 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200032 PM 1674818 ER PT J AU PRICE, BD CALDERWOOD, SK AF PRICE, BD CALDERWOOD, SK TI CA2+ IS ESSENTIAL FOR MULTISTEP ACTIVATION OF THE HEAT-SHOCK FACTOR IN PERMEABILIZED CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Note ID DNA-BINDING; HSP70 GENE; PROTEIN; MECHANISMS; GENISTEIN; INHIBITOR; SEQUENCE; ELEMENT; INVITRO; CALCIUM AB We have developed a novel permeabilized-cell system to study transcription mechanisms. In permeabilized cells, heat-induced activation of the heat shock factor and transcription of the hsp70 gene require Ca2+. Activation involves at least two steps: Ca2+-and heat-dependent activation of heat shock factor binding and a second step, prior to transcription of hsp70, that requires ATP and is sensitive to genistein, a protein kinase inhibitor. RP PRICE, BD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R29CA44940]; PHS HHS [R0147407] NR 21 TC 115 Z9 119 U1 0 U2 0 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 JUN PY 1991 VL 11 IS 6 BP 3365 EP 3368 PG 4 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200050 PM 2038338 ER PT J AU BARTEL, DP DOUDNA, JA USMAN, N SZOSTAK, JW AF BARTEL, DP DOUDNA, JA USMAN, N SZOSTAK, JW TI TEMPLATE-DIRECTED PRIMER EXTENSION CATALYZED BY THE TETRAHYMENA RIBOZYME SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Note ID RNA-POLYMERASE MODEL; INTRONS; ORIGIN; WORLD; SITE; LIFE AB The Tetrahymena ribozyme has been shown to catalyze an RNA polymerase-like reaction in which an RNA primer is extended by the sequential addition of pN nucleotides derived from GpN dinucleotides, where N = A, C, or U. Here, we show that this reaction is influenced by the presence of a template; bases that can form Watson-Crick base pairs with a template add as much as 25-fold more efficiently than mismatched bases. A mutant enzyme with an altered guanosine binding site can catalyze template-directed primer extension with all four bases when supplied with dinucleotides of the form 2-aminopurine-pN. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. FU NIAID NIH HHS [T32 AIO 7245] NR 28 TC 31 Z9 31 U1 1 U2 3 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 JUN PY 1991 VL 11 IS 6 BP 3390 EP 3394 PG 5 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM852 UT WOS:A1991FM85200055 PM 2038341 ER PT J AU RUBIN, E KHARBANDA, S GUNJI, H KUFE, D AF RUBIN, E KHARBANDA, S GUNJI, H KUFE, D TI ACTIVATION OF THE C-JUN PROTOONCOGENE IN HUMAN MYELOID-LEUKEMIA CELLS TREATED WITH ETOPOSIDE SO MOLECULAR PHARMACOLOGY LA English DT Note ID DNA TOPOISOMERASE-II; HAMSTER OVARY CELLS; TRANSCRIPTIONAL REGULATION; PROTO-ONCOGENE; BINDING PROTEINS; GENE-EXPRESSION; XENOPUS OOCYTES; P34CDC2 KINASE; FOS; INDUCTION AB The epipodophyllotoxin etoposide is an inhibitor of topoisomerase II. The effects of this agent on gene expression, particularly the transcriptional induction of genes implicated in growth control, are unknown. The present results demonstrate that etoposide induces expression of the c-jun protooncogene in HL-60 myeloid leukemia cells. This induction of c-jun expression was maximal at 3 hr and was transient. Similar findings were obtained in the human U-937 myeloid leukemia cell line. Nuclear run-on assays demonstrated that the induction of c-jun expression by etoposide is regulated at the transcriptional level. The results further demonstrate that etoposide-induced c-jun expression occurs in association with the appearance of c-fos transcripts. Moreover, the c-jun gene is induced by etoposide during periods of oligonucleosomal DNA cleavage, which is characteristic of programmed cell death. These findings suggest that transcriptional induction of c-jun expression represents a signaling pathway activated in the cellular response to etoposide-induced DNA damage. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [CA-29431, CA-42802] NR 42 TC 98 Z9 99 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JUN PY 1991 VL 39 IS 6 BP 697 EP 701 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FQ961 UT WOS:A1991FQ96100002 PM 1904980 ER PT J AU LEVY, DI SUCHER, NJ LIPTON, SA AF LEVY, DI SUCHER, NJ LIPTON, SA TI GLUTATHIONE PREVENTS N-METHYL-D-ASPARTATE RECEPTOR-MEDIATED NEUROTOXICITY SO NEUROREPORT LA English DT Article DE EXCITOTOXICITY; GLUTATHIONE; NMDA RECEPTOR; GLYCINE CO-AGONIST SITE; MAMMALIAN CENTRAL NEURONS; GLUTAMATE NEUROTOXICITY; RETINAL GANGLION CELLS ID RETINAL GANGLION-CELLS; AMINO-ACID RECEPTORS; GLUTAMATE TOXICITY; RAT; NEURONS; ANTAGONISTS; MODULATION; INHIBITION; RESPONSES AB N-METHYL-D-ASPARTATE (NMDA) antagonists afford possible therapeutic modalities for stroke, trauma, and various neurodegenerative conditions thought to be mediated by excessive stimulation of NMDA receptors in the brain. To date, however, no drug has been demonstrated to be a safe NMDA antagonist at a dosage necessary for neuroprotection. In the present study, we use an invitro preparation to show that glutathione is capable of attenuating neuronal damage mediated by NMDA receptor activation. Both oxidized and reduced glutathione are protective, and an extracellular mechanism of action on the NMDA receptor-channel complex is suggested. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,ENDERS BLDG,SUITE 361,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [R01 EY05477] NR 17 TC 57 Z9 57 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD JUN PY 1991 VL 2 IS 6 BP 345 EP 347 DI 10.1097/00001756-199106000-00011 PG 3 WC Neurosciences SC Neurosciences & Neurology GA FV633 UT WOS:A1991FV63300011 PM 1832987 ER PT J AU EZZEDDINE, ZD MARTUZA, RL PLATIKA, D SHORT, MP MALICK, A CHOI, B BREAKEFIELD, XO AF EZZEDDINE, ZD MARTUZA, RL PLATIKA, D SHORT, MP MALICK, A CHOI, B BREAKEFIELD, XO TI SELECTIVE KILLING OF GLIOMA-CELLS IN CULTURE AND INVIVO BY RETROVIRUS TRANSFER OF THE HERPES-SIMPLEX VIRUS THYMIDINE KINASE GENE SO NEW BIOLOGIST LA English DT Article DE BRAIN TUMORS; GANCICLOVIR; GENE TRANSFER; GLIOMA; RETROVIRUS; THYMIDINE KINASE; VIRUS VECTORS ID MALIGNANT GLIOMAS; RADIATION-THERAPY; TRANSGENIC MICE; BRAIN; RADIOTHERAPY; TUMORS; GLIOBLASTOMA; EXPRESSION; SURVIVAL; PATTERNS C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,CTR NEUROSCI,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NIDDK NIH HHS [2K12DK01410-06]; NINDS NIH HHS [NS24279] NR 44 TC 248 Z9 253 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 1043-4674 J9 NEW BIOL PD JUN PY 1991 VL 3 IS 6 BP 608 EP 614 PG 7 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA GK721 UT WOS:A1991GK72100012 PM 1655012 ER PT J AU CARLIN, A WALKER, WA AF CARLIN, A WALKER, WA TI RAPID DEVELOPMENT OF VITAMIN-K DEFICIENCY IN AN ADOLESCENT BOY RECEIVING TOTAL PARENTERAL-NUTRITION FOLLOWING BONE-MARROW TRANSPLANTATION SO NUTRITION REVIEWS LA English DT Review ID REQUIREMENTS; INFANTS AB In this case report the development of a vitamin K deficiency in a neutropenic adolescent receiving parenteral nutrition following bone marrow transplantation is described. The parenteral nutrition solution did not provide vitamin K and the patient had been receiving oral antibiotics prior to and during use of the intravenous feeding. Oral intake was minimal. Standard adult oral and intravenous multivitamin preparations for use in individuals older than 11 years do not routinely contain this vitamin. The function of vitmain K and causes for development of a deficiency are reviewed. Recommended intakes and guidelines for supplementation are also discussed. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. RP CARLIN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 16 TC 8 Z9 8 U1 0 U2 1 PU INT LIFE SCIENCES INST PI LAWRENCE PA 810 EAST 10TH ST SUBSCRIPTION OFFICE, LAWRENCE, KS 66044 SN 0029-6643 J9 NUTR REV JI Nutr. Rev. PD JUN PY 1991 VL 49 IS 6 BP 179 EP 183 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA FP315 UT WOS:A1991FP31500003 PM 1904566 ER PT J AU MAIDEN, MFJ TANNER, A AF MAIDEN, MFJ TANNER, A TI IDENTIFICATION OF ORAL YEASTS BY POLYACRYLAMIDE-GEL ELECTROPHORESIS SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE ORAL YEAST; CANDIDA-ALBICANS; SDS-PAGE; IDENTIFICATION AB Protein profiles of sonicated cells for 9 species of yeasts isolated from oral samples were obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and visualized with a silver stain. The profiles obtained on 12% acrylamide gels were distinct, and characteristic for 6 species of Candida, and Torulopsis glabrata, Yarrowia lipolytica, and Saccharomyces cerevisiae. Using this method, 79 fresh isolates of yeasts from saliva samples were identified; 58 as Candida albicans, 9 as Candida parapsilosis, 1 as Candida tropicalis, and 11 as T. glabrata. SDS-PAGE offers a rapid, convenient alternative or adjunct to yeast identification systems based on carbohydrate assimilation tests. RP MAIDEN, MFJ (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE 03488] NR 0 TC 8 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 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD JUN PY 1991 VL 6 IS 3 BP 187 EP 190 DI 10.1111/j.1399-302X.1991.tb00475.x PG 4 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA FQ080 UT WOS:A1991FQ08000010 PM 1945503 ER PT J AU REDDY, MS BRUCH, JM JEFFCOAT, MK WILLIAMS, RC AF REDDY, MS BRUCH, JM JEFFCOAT, MK WILLIAMS, RC TI CONTRAST ENHANCEMENT AS AN AID TO INTERPRETATION IN DIGITAL SUBTRACTION RADIOGRAPHY SO ORAL SURGERY ORAL MEDICINE ORAL PATHOLOGY ORAL RADIOLOGY AND ENDODONTICS LA English DT Article ID PERIODONTAL BONE-LESIONS; STANDARDIZED RADIOGRAPHS; DENTAL RADIOGRAPHY; DIAGNOSIS; GEOMETRY AB An initial study was performed to demonstrate the feasibility of pseudocolor contrast enhancement technique in digital subtraction radiography (DSR). DSR is an electronic image processing technique that has been shown to be of greater diagnostic value in the detection of small periodontal bone lesions than conventional radiography. Pseudocolor enhancement involves selectively assigning a unique color to each shade of gray present in a black-and-white subtracted image. Two image enhancement techniques were developed and tested in a phantom system consisting of extracted teeth set in blocks of plaster mixed with sawdust to simulate trabecular bone. It was found that experimentally induced periodontal lesions were more readily detected by the average clinician in both types of enhanced subtraction images than unenhanced subtractions. Furthermore, both enhancement techniques were of significantly greater diagnostic value for lesions smaller than 1.0 mm (p < 0.001). The technique that colored an isolated area of interest was significantly more diagnostic at all depths tested (p < 0.001 at 0.5 and 1.0 mm, and p < 0.05 at 0.5 mm). Contrast enhancement may be a significant aid to the average clinician for the interpretation of DSR and the detection of small periodontal defects. C1 MASSACHUSETTS GEN HOSP,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA 02114. HARVARD UNIV,SCH DENT SCI,DEPT PERIODONTOL,CAMBRIDGE,MA 02138. RP REDDY, MS (reprint author), UNIV ALABAMA,SCH DENT,DEPT PERIODONT,UNIV ALABAMA STN,SISDB 412,BIRMINGHAM,AL 35294, USA. NR 14 TC 28 Z9 28 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1079-2104 J9 ORAL SURG ORAL MED O JI Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. PD JUN PY 1991 VL 71 IS 6 BP 763 EP 769 DI 10.1016/0030-4220(91)90289-O PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FR495 UT WOS:A1991FR49500022 PM 2062529 ER PT J AU VECSEI, L BEAL, MF AF VECSEI, L BEAL, MF TI COMPARATIVE BEHAVIORAL AND NEUROCHEMICAL STUDIES WITH STRIATAL KAINIC ACID-LESIONED OR QUINOLINIC ACID-LESIONED RATS SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE BEHAVIOR; GABA; KAINIC ACID; QUINOLINIC ACID; RATS; SUBSTANCE-P ID HUNTINGTONS-DISEASE; BARREL ROTATION; SOMATOSTATIN; CHOREA; BRAIN; INJECTIONS; GLUTAMATE; NEURONS; MODEL AB In the present studies the effects of kainic acid (KA)- or quinolinic acid (QA)-induced striatal lesions were compared in different behavioral tests in rats. Both KA- and QA-lesioned animals had ipsilateral barrel-rotation (BR). The KA-lesioned rats, however, had contralateral, while the QA-lesioned rats had both ipsi- and contralateral turning activity. The KA-lesioned animals showed increased open-field activity as well as increased percentage of entries, and time spent in the open arms of Montgomery's conflict test. Learning of an active avoidance response was strongly inhibited by both striatal QA- or KA-induced striatal lesions. The QA-lesioned animals showed less pronounced behavioral changes than KA-lesioned animals in most of the tests, and had a smaller loss of body weight. There was no significant difference in the extent of the KA- and QA-induced substance P (SP) and GABA depletions in striatum, however, the depletions with QA lesions were slightly greater. These findings show that KA-induced striatal lesions produce more pronounced behavioral effects than QA lesions of similar size. It is possible that the differential effects of KA versus QA on striatal interneurons may result in its more marked behavioral effects. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Vecsei, Laszlo/B-2066-2010 OI Vecsei, Laszlo/0000-0001-8037-3672 FU PHS HHS [16367] NR 41 TC 37 Z9 37 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0091-3057 J9 PHARMACOL BIOCHEM BE JI Pharmacol. Biochem. Behav. PD JUN PY 1991 VL 39 IS 2 BP 473 EP 478 DI 10.1016/0091-3057(91)90211-J PG 6 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA FZ846 UT WOS:A1991FZ84600037 PM 1719569 ER PT J AU PARRISH, JA WILSON, BC AF PARRISH, JA WILSON, BC TI CURRENT AND FUTURE-TRENDS IN LASER MEDICINE SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article; Proceedings Paper CT SPECIAL SYMP AT THE 18TH ANNUAL MEETING OF THE AMERICAN SOC FOR PHOTOBIOLOGY : LASERS IN MEDICINE CY JUN, 1990 CL VANCOUVER, CANADA SP AMER SOC PHOTOBIOL ID CLINICAL-APPLICATIONS; THERAPY; SURGERY AB In this overview, a number of the major current, and possible future developments in laser medicine are explored. In therapeutic applications, particular emphasis is given to obtaining selectivity in tissue targets and interaction mechanisms in order to achieve specific biological effects. This includes spatial confinement of thermal damage by pulsed laser irradiation and targetting by exogenous photothermal or photochemical chromophores. The potential for diagnostic applications of lasers in medicine is illustrated primarily by various in vivo spectroscopic techniques. Both therapeutic and diagnostic applications will rely increasingly on the development of total systems in which lasers will form only one, albeit an essential, part. Numerous scientific and technical problems need to be solved in order to realize the full clinical potential of the many new concepts in laser medicine. The impetus for such progress will come from integrated, multidisciplinary collaborations between medical, scientific and industrial groups. C1 HAMILTON REG CANC CTR,HAMILTON L8V 1C3,ONTARIO,CANADA. MCMASTER UNIV,HAMILTON L8V 1C3,ONTARIO,CANADA. ONTARIO LASER & LIGHTWAVE RES CTR,TORONTO M5S 1A7,ONTARIO,CANADA. RP PARRISH, JA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 28 TC 22 Z9 23 U1 1 U2 1 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD JUN PY 1991 VL 53 IS 6 BP 731 EP 738 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FN605 UT WOS:A1991FN60500002 PM 1886931 ER PT J AU WATANABE, S ANDERSON, RR BRORSON, S DALICKAS, G FUJIMOTO, JG FLOTTE, TJ AF WATANABE, S ANDERSON, RR BRORSON, S DALICKAS, G FUJIMOTO, JG FLOTTE, TJ TI COMPARATIVE-STUDIES OF FEMTOSECOND TO MICROSECOND LASER-PULSES ON SELECTIVE PIGMENTED CELL INJURY IN SKIN SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article; Proceedings Paper CT SPECIAL SYMP AT THE 18TH ANNUAL MEETING OF THE AMERICAN SOC FOR PHOTOBIOLOGY : LASERS IN MEDICINE CY JUN, 1990 CL VANCOUVER, CANADA SP AMER SOC PHOTOBIOL ID OPTICAL PULSES; PHOTOTHERMOLYSIS; RADIATION; DAMAGE; TARGET; NM AB Threshold radiant exposures for grossly apparent immediate whitening and ultrastructural alterations of melanosomes in black guinea pig skin were determined for a series of red visible laser pulses ranging from 4 x 10(-4) to 6.5 x 10(-14) S. Threshold exposures for melanosomal injury were found to be independent of pulsewidth when the pulsewidths were below the estimated thermal relaxation time of melanosomes. Threshold radiant exposures for melanosomal injury were found to increase when the pulsewidths were approximately equal to or above the thermal relaxation time of melanosomes. At longer pulse durations, fracturing of melanosomes was not observed despite the longer exposures necessary for injury. Instead, perimelanosomal vacuoles were noted. These findings are consistent with the theory of selective photothermolysis and provide evidence for the thermal initiation of melanosomal disruption. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MIT,DEPT ELECT ENGN,BOSTON,MA. MIT,ELECTR RES LAB,BOSTON,MA. FU NIGMS NIH HHS [2-RO1-GM35459-05] NR 11 TC 43 Z9 43 U1 0 U2 2 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD JUN PY 1991 VL 53 IS 6 BP 757 EP 762 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FN605 UT WOS:A1991FN60500006 PM 1886935 ER PT J AU JACQUES, SL MCAULIFFE, DJ AF JACQUES, SL MCAULIFFE, DJ TI THE MELANOSOME - THRESHOLD TEMPERATURE FOR EXPLOSIVE VAPORIZATION AND INTERNAL ABSORPTION-COEFFICIENT DURING PULSED LASER IRRADIATION SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article; Proceedings Paper CT SPECIAL SYMP AT THE 18TH ANNUAL MEETING OF THE AMERICAN SOC FOR PHOTOBIOLOGY : LASERS IN MEDICINE CY JUN, 1990 CL VANCOUVER, CANADA SP AMER SOC PHOTOBIOL ID HUMAN-SKIN; MELANIN; ORGANELLE; CELLS; NM AB The explosive vaporization of melanosomes in situ in skin during pulsed laser irradiation (pulse duration <1-mu-s) is observed as a visible whitening of the superficial epidermal layer due to stratum corneum disruption. In this study, the ruby laser (694 nm) was used to determine the threshold radiant exposure, HO (J/cm2), required to elicit whitening for in vitro black (Negroid) human skin samples which were pre-equilibrated at an initial temperature, T(i), of 0, 20, or 50-degrees-C. A plot of H0 vs T(i) yields a straight line whose x-intercept indicates the threshold temperature of explosive vaporization to be 112 +/- 7-degrees-C (SD, N = 3). The slope, partial H(O)/partial T(i), specifies the internal absorption coefficient, mu-a, within the melanosome: mu-a = -rho-C/(slope(1 + 7.1R(d))), where rho-C is the product of density and specific heat, and R(d) is the total diffuse reflectance from the skin. A summary of the absorption spectrum (mu-a) for the melanosome interior (351-1064 nm) is presented based on H(O) data from this study and the literature. The in vivo absorption spectrum (380-820 nm) for human epidermal melanin was measured by an optical fiber spectrophotometer and is compared with the melanosome spectrum. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02139. RP JACQUES, SL (reprint author), UNIV TEXAS,MD ANDERSON CANC CTR,LASER BIOL RES LAB,1515 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. FU NIADDK NIH HHS [AM25395-08] NR 17 TC 157 Z9 160 U1 0 U2 4 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD JUN PY 1991 VL 53 IS 6 BP 769 EP 775 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FN605 UT WOS:A1991FN60500008 PM 1886936 ER PT J AU IKEDA, ER SCHENKMAN, ML RILEY, PO HODGE, WA AF IKEDA, ER SCHENKMAN, ML RILEY, PO HODGE, WA TI INFLUENCE OF AGE ON DYNAMICS OF RISING FROM A CHAIR SO PHYSICAL THERAPY LA English DT Article DE AGING; GERIATRICS; KINESIOLOGY BIOMECHANICS, GENERAL; MOVEMENT ID TO-STAND MOVEMENT; NORMAL RANGE; MOTION; FORCES; JOINT; HIP AB This article describes the sit-to-stand movement in nine healthy elderly adults, ages 61 to 74 years, and compares peak joint angles, torques, and velocities of 11 body segments with data collected from nine young women, ages 25 to 36 years. The subjects in this study rose from a chair under a controlled protocol. An optoelectronic system, two force plates, and two computers were used for data collection and processing. The data are described in relationship to three phases of the task previously described for the young subjects' data. Percentages of difference were calculated for the torques and the velocities. Independent t tests were conducted on maximum angles achieved and total joint excursions. Consistency between groups was demonstrated in the duration of each phase, as well as the body kinematics and kinetics occurring within each phase. There was little difference in maximum torques or velocities. Maximum angles of head-to-trunk extension, head-to-ground flexion, head-to-trunk excursion, and trunk-to-pelvis flexion were significantly different between groups. The differences in head position demonstrated between these two groups may have clinical implications for loss of balance during this task in older patients. C1 MASSACHUETTES GEN HOSP,INST HLTH PROFESS,PROGRAM PHYS THERAPY,BOSTON,MA 02108. MIT,DEPT MECH ENGN,NEWMAN LAB,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BIOMOT LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ORTHOPAED,BOSTON,MA 02114. RP IKEDA, ER (reprint author), UNIV MONTANA,DEPT PHYS THERAPY,026 MCGILL HALL,MISSOULA,MT 59812, USA. RI Riley, Patrick/B-3053-2009 NR 33 TC 90 Z9 96 U1 0 U2 9 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 JUN PY 1991 VL 71 IS 6 BP 473 EP 481 PG 9 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA FP577 UT WOS:A1991FP57700010 PM 2034710 ER PT J AU MAY, JW AF MAY, JW TI UPPER EYELID BLEPHAROPLASTY - REPLY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Letter RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,DIV PLAST & RECONSTRUCT SURG,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUN PY 1991 VL 87 IS 6 BP 1141 EP 1142 DI 10.1097/00006534-199106000-00031 PG 2 WC Surgery SC Surgery GA FP126 UT WOS:A1991FP12600024 ER PT J AU NEYFAKH, AA BIDNENKO, VE CHEN, LB AF NEYFAKH, AA BIDNENKO, VE CHEN, LB TI EFFLUX-MEDIATED MULTIDRUG RESISTANCE IN BACILLUS-SUBTILIS - SIMILARITIES AND DISSIMILARITIES WITH THE MAMMALIAN SYSTEM SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE BMR GENE; BACTERIAL RESISTANCE; MEMBRANE TRANSPORT; GENE AMPLIFICATION ID P-GLYCOPROTEIN; ESCHERICHIA-COLI; AMPLIFICATION; TRANSPORT; MEMBRANE; DNA AB Bacillus subtilis cells selected for their resistance to rhodamine 6G demonstrated a multidrug-resistance (MDR) phenotype resembling that of mammalian MDR cells. Like MDR in mammalian cells, MDR in bacteria was mediated by the efflux of the drugs from the cells. The bacterial multidrug efflux system transported similar drugs and was sensitive to similar inhibitors as the mammalian multidrug transporter, P-glycoprotein. The gene coding for the bacterial multidrug transporter, like the P-glycoprotein gene in mammalian MDR cells, was amplified in the resistant bacteria. On the other hand, the bacterial multidrug transporter showed no sequence similarity to P-glycoprotein but exhibited an obvious homology to tetracycline efflux pumps and carbohydrate-ion symporters. These results show that the transport of structurally unrelated molecules can be mediated by members of different families of membrane transporters. C1 MV LOMONOSOV STATE UNIV,BELOZERSKY LAB MOLEC BIOL & BIOORGAN CHEM,MOSCOW 117234,USSR. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MOSCOW GENET & SELECT IND MICROORGANISMS INST,MOSCOW,USSR. NR 19 TC 265 Z9 278 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 JUN PY 1991 VL 88 IS 11 BP 4781 EP 4785 DI 10.1073/pnas.88.11.4781 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FP087 UT WOS:A1991FP08700046 PM 1675788 ER PT J AU FREEMAN, M EKKEL, Y ROHRER, L PENMAN, M FREEDMAN, NJ CHISOLM, GM KRIEGER, M AF FREEMAN, M EKKEL, Y ROHRER, L PENMAN, M FREEDMAN, NJ CHISOLM, GM KRIEGER, M TI EXPRESSION OF TYPE-I AND TYPE-II BOVINE SCAVENGER RECEPTORS IN CHINESE-HAMSTER OVARY CELLS - LIPID DROPLET ACCUMULATION AND NONRECIPROCAL CROSS COMPETITION BY ACETYLATED AND OXIDIZED LOW-DENSITY-LIPOPROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ATHEROSCLEROSIS; FOAM CELLS; LIGAND BINDING ID HERITABLE HYPERLIPIDEMIC RABBIT; MOUSE PERITONEAL-MACROPHAGES; OXIDATIVELY MODIFIED LDL; ATHEROSCLEROTIC LESIONS; MEDIATED ENDOCYTOSIS; ENDOTHELIAL-CELLS; SERUM-ALBUMIN; CHOLESTEROL DEPOSITION; CULTURED-CELLS; SMOOTH-MUSCLE AB Type I and type II scavenger receptors, which have been implicated in the development of atherosclerosis and other macrophage-associated functions, differ only by the presence in the type I receptor of an extracellular cysteine-rich C-terminal domain. Stable Chinese hamster ovary (CHO) cell transfectants expressing high levels of either the type I or type II bovine scavenger receptors have been generated. Type I and type II receptors in these cells mediated high-affinity saturable endocytosis of both I-125-labeled acetylated low density lipoprotein (LDL) and I-125-labeled oxidized LDL with the distinctive broad ligand specificity characteristic of scavenger receptors. After incubation for 2 days with acetylated LDL, the transfected cell accumulated oil red O-staining lipid droplets reminiscent of those in macrophage foam cells, whereas untransfected CHO cells did not. Thus, macrophage-specific gene products other than the scavenger receptor are not required for modified-LDL-induced intracellular lipid accumulation. In transfected cells, acetylated LDL efficiently competed for both its own endocytosis and that of oxidized LDL. In contrast, oxidized LDL competed effectively for its own endocytosis but only poorly for that of acetylated LDL. This nonreciprocal cross competition suggests that these ligands may bind to nonidentical but interacting sites on a single receptor. Results were similar for transfectants expressing either type I or type II scavenger receptors. Therefore, the nonreciprocal cross competition previously reported for cultured peritoneal macrophages may not be the result of differences between the type I and type II receptors. The nonreciprocal cross competition seen in the transfected CHO cells differs from that previously observed with cultured macrophages. C1 MIT,DEPT BIOL,E25-236,CAMBRIDGE,MA 02139. CLEVELAND CLIN FDN,RES INST,DEPT VASC CELL BIOL & ATHEROSCLEROSIS,CLEVELAND,OH 44195. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NHLBI NIH HHS [HL29582, HL41484] NR 54 TC 201 Z9 203 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 11 BP 4931 EP 4935 DI 10.1073/pnas.88.11.4931 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FP087 UT WOS:A1991FP08700077 PM 2052575 ER PT J AU MARGOSSIAN, SS KRUEGER, JW SELLERS, JR CUDA, G CAULFIELD, JB NORTON, P SLAYTER, HS AF MARGOSSIAN, SS KRUEGER, JW SELLERS, JR CUDA, G CAULFIELD, JB NORTON, P SLAYTER, HS TI INFLUENCE OF THE CARDIAC MYOSIN HINGE REGION ON CONTRACTILE ACTIVITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SUBFRAGMENT-2; MOTILITY; SARCOMERE SHORTENING; MYOCYTES ID MUSCLE; FORCE; SUBFRAGMENT-2; ACTIN; INVITRO; ALPHA; THROMBOSPONDIN; MYOFIBRILS; ANTIBODIES; FILAMENTS AB The participation of cardiac myosin hinge in contractility was investigated by in vitro motility and ATPase assays and by measurements of sarcomere shortening. The effect on contractile activity was analyzed using an antibody directed against a 20-amino acid peptide within the hinge region of myosin. This antibody bound specifically at the hinge at a distance of 55 nm from the S1/S2 junction, was specific to human, dog, and rat cardiac myosins, did not crossreact with gizzard or skeletal myosin, and had no effect on ATPase activity of purified S1 and myofibrils. However, it completely suppressed the movement of actin filaments in in vitro motility assays and reduced active shortening of sarcomeres of skinned cardiac myocytes by half. Suppression of motion by the antihinge antibody may reflect a mechanical constraint imposed by the antibody upon the mobility of the S2 region of myosin. The results suggest that the steps in the mechanochemical energy transduction can be separately influenced through S2. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. NHLBI,MOLEC CARDIOL LAB,BETHESDA,MD 20892. UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MONTEFIORE MED CTR,DEPT MED & PHYSIOL BIOPHYS,BRONX,NY 10467. RP MARGOSSIAN, SS (reprint author), MONTEFIORE MED CTR,DEPT BIOCHEM & ORTHOPED RES,ORTHOPED RES LABS,111 E 210TH ST,BRONX,NY 10467, USA. RI Cuda, Giovanni/F-5359-2012 OI Cuda, Giovanni/0000-0001-6313-1866 FU NHLBI NIH HHS [HL-26569, HL23125, HL37412] NR 33 TC 26 Z9 26 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 11 BP 4941 EP 4945 DI 10.1073/pnas.88.11.4941 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FP087 UT WOS:A1991FP08700079 PM 1828886 ER PT J AU LAFORGIA, S MORSE, B LEVY, J BARNEA, G CANNIZZARO, LA LI, F NOWELL, PC BOGHOSIANSELL, L GLICK, J WESTON, A HARRIS, CC DRABKIN, H PATTERSON, D CROCE, CM SCHLESSINGER, J HUEBNER, K AF LAFORGIA, S MORSE, B LEVY, J BARNEA, G CANNIZZARO, LA LI, F NOWELL, PC BOGHOSIANSELL, L GLICK, J WESTON, A HARRIS, CC DRABKIN, H PATTERSON, D CROCE, CM SCHLESSINGER, J HUEBNER, K TI RECEPTOR PROTEIN-TYROSINE PHOSPHATASE-GAMMA IS A CANDIDATE TUMOR SUPPRESSOR GENE AT HUMAN-CHROMOSOME REGION 3P21 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHROMOSOME DELETIONS TRANSLOCATIONS; LOSS OF HETEROZYGOSITY; TYROSINE PHOSPHORYLATION DEPHOSPHORYLATION; SOMATIC CELL HYBRIDS ID RENAL-CELL CARCINOMA; LUNG-CANCER; HOMOZYGOUS DELETION; DNA-SEQUENCE; SHORT ARM; FAMILY; CLONING; LOCUS; D3S3 AB PTPG, the gene for protein-tyrosine phosphatase-gamma (PTP-gamma), maps to a region of human chromosome 3, 3p21, that is frequently deleted in renal cell carcinoma and lung carcinoma. One of the functions of protein-tyrosine phosphatases is to reverse the effect of protein-tyrosine kinases, many of which are oncogenes, suggesting that some protein-tyrosine phosphatase genes may act as tumor suppressor genes. A hallmark of tumor suppressor genes is that they are deleted in tumors in which their inactivation contributes to the malignant phenotype. In this study, one PTP-gamma allele was lost in 3 of 5 renal carcinoma cell lines and 5 of 10 lung carcinoma tumor samples tested. Importantly, one PTP-gamma allele was lost in three lung tumors that had not lost flanking loci. PTP-gamma mRNA was expressed in kidney cell lines and lung cell lines but not expressed in several hematopoietic cell lines tested. Thus, the PTP-gamma gene has characteristics that suggest it as a candidate tumor suppressor gene at 3p21. C1 RHONE POULENC RORER CENT RES,KING OF PRUSSIA,PA 19406. NYU MED CTR,DEPT PHARMACOL,NEW YORK,NY 10016. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. NCI,HUMAN CARCINOGENESIS LAB,BETHESDA,MD 20892. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. ELEANOR ROOSEVELT INST,DENVER,CO 80206. RP LAFORGIA, S (reprint author), TEMPLE UNIV,HLTH SCI CTR,SCH MED,FELS INST CANC RES & MOLEC BIOL,PHILADELPHIA,PA 19140, USA. FU NCI NIH HHS [CA39860, CA21124, CA42232] NR 26 TC 232 Z9 233 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 11 BP 5036 EP 5040 DI 10.1073/pnas.88.11.5036 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FP087 UT WOS:A1991FP08700098 PM 1711217 ER PT J AU AHMED, AR WAGNER, R KHATRI, K NOTANI, G AWDEH, Z ALPER, CA YUNIS, EJ AF AHMED, AR WAGNER, R KHATRI, K NOTANI, G AWDEH, Z ALPER, CA YUNIS, EJ TI MAJOR HISTOCOMPATIBILITY COMPLEX HAPLOTYPES AND CLASS-II GENES IN NON-JEWISH PATIENTS WITH PEMPHIGUS VULGARIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HLA; EXTENDED HAPLOTYPES; AUTOIMMUNITY ID INHERITED STRUCTURAL POLYMORPHISM; HLA; COMPLOTYPES; DISEASE AB Previous studies demonstrated that HLA-DR4 was markedly increased among Ashkenazi Jewish patients with pemphigus vulgaris (PV), almost entirely as the common Jewish extended haplotype [HLA-B38, SC21, DR4, DQw8] or as the haplotype HLA-B35, SC31, DR4, DQw8, and that HLA-DR4, DQw8 was distributed among patients in a manner consistent with dominant expression of a class II (D-region or D-region-linked) susceptibility gene. In the present study of major histocompatibility complex (MHC) haplotypes in 25 non-Jewish PV patients, DR4, DQw8 was found in 12 of the patients and DRw6, DQw5 was found in 15. Only 3 patients had neither. Only 1 of the DR4, DQw8 haplotypes was [HLA-B38, SC21, DR4, DQw8] and 2 were HLA-B35, SC31, DR4, DQw8; most were the presumed fragments (SC31, DR4, DQw8) or (SC21, DR4, DQw8) or DR4, DQw8 with some other complotype. Of the patients with DRw6, DQw5, all were DRw14, DQw5, and 6 had a rare Caucasian haplotype, HLA-Bw55, SB45, DRw14, DQw5. Four of 6 of these were found in patients of Italian extraction, as was the 1 normal example. The non-Jewish patients were of more Southern European extraction than our controls. This suggests that there are two major MHC susceptibility alleles in American patients with PV. The more ancient apparently arose on a haplotype in the Jews, HLA-B38(35), SC21(SC31), DR4, DQw8, and spread to other populations largely as D-region segments. The other arose in or near Italy on the haplotype HLA-Bw55, SB45, DRw14, DQw5 and has also partially fragmented so that many patients carry only DRw14, DQw5. The available data do not permit the specific localization of either the DR4, DQw8- or the DRw14, DQw5-linked susceptibility genes. C1 AMER RED CROSS,BLOOD SERV,NE REG,DEDHAM,MA 02026. HARVARD UNIV,SCH DENT MED,DEPT ORAL PATHOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP AHMED, AR (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 29583]; NICHD NIH HHS [HD 17461]; NIDDK NIH HHS [DK 26844] NR 29 TC 105 Z9 111 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 11 BP 5056 EP 5060 DI 10.1073/pnas.88.11.5056 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FP087 UT WOS:A1991FP08700102 PM 1675792 ER PT J AU CLAYTON, LK DADAMIO, L HOWARD, FD SIEH, M HUSSEY, RE KOYASU, S REINHERZ, EL AF CLAYTON, LK DADAMIO, L HOWARD, FD SIEH, M HUSSEY, RE KOYASU, S REINHERZ, EL TI CD3-ETA AND CD3-ZETA ARE ALTERNATIVELY SPLICED PRODUCTS OF A COMMON GENETIC-LOCUS AND ARE TRANSCRIPTIONALLY AND OR POSTTRANSCRIPTIONALLY REGULATED DURING T-CELL DEVELOPMENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE T-CELL RECEPTOR; SIGNAL TRANSDUCTION; LYMPHOID DIFFERENTIATION; THYMIC SELECTION ID ANTIGEN RECEPTOR; ZETA-CHAIN; MOUSE CHROMOSOME-1; MOLECULAR-CLONING; ETA-CHAIN; EXPRESSION; COMPLEX; IDENTIFICATION; DEFINITION; FRAGMENTS AB The CD3-eta subunit of the T-cell receptor is thought to subserve an important role in signal transduction and possibly T-cell development. Herein we characterize the organization of the mouse CD3-eta gene and show that it is part of one gene locus that also encodes CD3-zeta on chromosome 1. The NH2-terminal sequence of CD3-zeta and CD3-eta, which share the same leader peptide and are identical through amino acid 122 of each mature protein, is encoded by exons 1-7. However, exons 8 and 9 are differentially spliced to give rise to CD3-zeta and CD3-eta: exons 1-8 encode CD3-zeta and exons 1-7 plus 9 encode CD3-eta. RNase protection analysis with RNA from a variety of fetal, neonatal, and adult cell types indicates that expression of both gene products is T-lineage-restricted. Importantly, expression of CD3-zeta and CD3-eta mRNA appears before or on day 16 of fetal gestation. Expression is apparently coordinate since no cell types tested express CD3-zeta or CD3-eta alone. The steady-state level of CD3-zeta mRNA is greater-than-or-equal-to 40-60 times that of CD3-eta mRNA. In immature CD4+CD8+CD3low double-positive thymocytes and CD4+CD8-CD3high or CD4-CD8+ CD3 high single-positive thymocytes, the respective steady-state CD3-zeta and CD3-eta mRNA levels are equivalent, whereas the amount of receptor-associated CD3-zeta and CD3-eta proteins in double-positive thymocytes is almost-equal-to 10 times less than in single-positive thymocytes. Nevertheless, the CD3-zeta/CD3-eta protein ratio remains constant in all populations (40-60:1). Furthermore, discordance between mRNA and protein levels for CD3-zeta and CD3-eta is also observed in splenic T cells. Thus, post-transcriptional and/or transcriptional regulatory mechanisms control CD3-zeta and CD3-eta expression during T-cell development. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP CLAYTON, LK (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115, USA. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 NR 34 TC 61 Z9 64 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 12 BP 5202 EP 5206 DI 10.1073/pnas.88.12.5202 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FR448 UT WOS:A1991FR44800029 PM 1828894 ER PT J AU CLARK, MA OZGUR, LE CONWAY, TM DISPOTO, J CROOKE, ST BOMALASKI, JS AF CLARK, MA OZGUR, LE CONWAY, TM DISPOTO, J CROOKE, ST BOMALASKI, JS TI CLONING OF A PHOSPHOLIPASE-A2-ACTIVATING PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ANTISENSE DNA; LEUKOTRIENE; ARACHIDONIC ACID ID BOVINE ENDOTHELIAL-CELLS; DIGLYCERIDE LIPASE; HUMAN-PLATELETS; CULTURED-CELLS; RELEASE; PHOSPHOLIPASES; BRADYKININ; LEUKOTRIENE-D4; COMPLEMENTARY; ARACHIDONATE AB Recently we have described the isolation and biochemical characterization of a phospholipase A2-activating protein (PLAP). We have cloned this protein and found it to be expressed as a 2.5-kilobase mRNA. The steady-state levels of PLAP mRNA are induced in smooth muscle and endothelial cells following treatment with leukotriene D4. The increased message levels coincide with increased amounts of PLAP. Synthetic antisense DNA was used to block the synthesis of PLAP and this treatment effectively blocked the activation of phospholipase A2 and the increased generation of prostanoids in smooth muscle and endothelial cells treated with leukotriene D4. C1 WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. SCHERING PLOUGH CORP,RES,BLOOMFIELD,NJ 07003. MED COLL PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19129. RP CLARK, MA (reprint author), SK&F LABS,KING OF PRUSSIA,PA 19479, USA. NR 40 TC 131 Z9 132 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN PY 1991 VL 88 IS 12 BP 5418 EP 5422 DI 10.1073/pnas.88.12.5418 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FR448 UT WOS:A1991FR44800073 PM 2052621 ER PT J AU ALBERT, MS LAFLECHE, G AF ALBERT, MS LAFLECHE, G TI NEUROIMAGING IN ALZHEIMERS-DISEASE SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID CEREBRAL BLOOD-FLOW; EMISSION COMPUTED-TOMOGRAPHY; MULTI-INFARCT DEMENTIA; WHITE MATTER DISORDER; ADRDA WORK GROUP; MAGNETIC-RESONANCE; SENILE DEMENTIA; DIFFERENTIAL-DIAGNOSIS; CLINICAL-DIAGNOSIS; VASCULAR DEMENTIA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP ALBERT, MS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,CNY-6,BOSTON,MA 02114, USA. FU NIA NIH HHS [P01-AG04953] NR 94 TC 6 Z9 6 U1 4 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD JUN PY 1991 VL 14 IS 2 BP 443 EP 459 PG 17 WC Psychiatry SC Psychiatry GA HL470 UT WOS:A1991HL47000016 PM 2062727 ER PT J AU BIEDERMAN, J ROSENBAUM, JF BOLDUC, EA FARAONE, SV HIRSHFELD, DR AF BIEDERMAN, J ROSENBAUM, JF BOLDUC, EA FARAONE, SV HIRSHFELD, DR TI A HIGH-RISK STUDY OF YOUNG-CHILDREN OF PARENTS WITH PANIC DISORDER AND AGORAPHOBIA WITH AND WITHOUT COMORBID MAJOR DEPRESSION SO PSYCHIATRY RESEARCH LA English DT Article DE PANIC DISORDER; AGORAPHOBIA; DEPRESSION; CHILDREN; COMORBIDITY ID ATTENTION DEFICIT DISORDER; LA-TOURETTES SYNDROME; ANXIETY DISORDERS; BEHAVIORAL-INHIBITION; GENETIC-RELATIONSHIP; MULTIPLE THRESHOLDS; GENERAL-POPULATION; ANXIOUS CHILDREN; PHOBIC NEUROSIS; FAMILY HISTORY AB Using family study methodology and psychiatric assessments by blind raters, this study tested hypotheses about patterns of familial association between anxiety and depressive disorders among high risk children of clinically referred parents. The study design contrasted five groups of children defined by the presence or absence in a parent of (1) panic disorder and agoraphobia (PDAG) without comorbid major depressive disorder (MDD) (n = 14); (2) comorbid PDAG plus MDD (PDAG + MDD) (n = 25); (3) MDD without comorbid PDAG (n = 12); (4) other psychiatric disorders (n = 23); and (5) normal comparisons (n = 47). While the PDAG and PDAG + MDD groups had similarly elevated rates of anxiety disorders and MDD, offspring of MDD parents had an elevated rate of MDD but not of anxiety disorders. Among children of parents with PDAG + MDD, the presence of an anxiety disorder did not significantly increase the risk for MDD in the same child. Thus, anxiety and MDD did not cosegregate among children of PDAG parents. These findings indicate that parental PDAG, either alone or comorbidly with MDD, increases the risk for both anxiety and depressive disorders in offspring. In the absence of PDAG, however, parental MDD does not appear to place children at risk for anxiety disorders. These findings are most consistent with the hypothesis that PDAG and PDAG + MDD share common familial etiologic factors while MDD alone is an independent disorder. More studies are needed to confirm these preliminary findings as well as to identify mediating factors that influence the transition from childhood to adult anxiety disorders. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,BOSTON,MA 02114. VET ADM MED CTR,PSYCHIAT SERV,BROCKTON,MA 02401. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 68 TC 112 Z9 113 U1 4 U2 8 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUN PY 1991 VL 37 IS 3 BP 333 EP 348 DI 10.1016/0165-1781(91)90068-Z PG 16 WC Psychiatry SC Psychiatry GA FX278 UT WOS:A1991FX27800011 PM 1891513 ER PT J AU FAVA, M LITTMAN, A HALPERIN, P PRATT, E DREWS, FR OLESHANSKY, M KNAPIK, J THOMPSON, C BIELENDA, C AF FAVA, M LITTMAN, A HALPERIN, P PRATT, E DREWS, FR OLESHANSKY, M KNAPIK, J THOMPSON, C BIELENDA, C TI PSYCHOLOGICAL AND BEHAVIORAL BENEFITS OF A STRESS TYPE-A BEHAVIOR REDUCTION PROGRAM FOR HEALTHY MIDDLE-AGED ARMY OFFICERS SO PSYCHOSOMATICS LA English DT Article ID DISEASE; POPULATION AB Twenty army officers who participated in a stress/type A behavior reduction program and a comparison group of 17 officer nonparticipants volunteered to undergo a battery of psychological and behavioral tests before and after the program. Following the program, participants displayed a significantly greater reduction in average daily caloric intake and levels of perceived stress, anxiety, hostility, depression, psychological distress, and type A behavior as compared to the officers who did not participate in it. Given the fact that most of these psychological and behavioral factors have been found in previous studies to be related to an increased risk for coronary artery disease, it seems that the changes reported by the participants in the program are potentially healthful. C1 USA,COLL WAR,CARLISLE,PA. MASSACHUSETTS GEN HOSP,DEPT PREVENT MED,BOSTON,MA 02114. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT ACC-815,BOSTON,MA 02114, USA. NR 15 TC 17 Z9 17 U1 2 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SUM PY 1991 VL 32 IS 3 BP 337 EP 342 PG 6 WC Psychiatry; Psychology SC Psychiatry; Psychology GA FU214 UT WOS:A1991FU21400012 PM 1882025 ER PT J AU MUELLER, PR AF MUELLER, PR TI METALLIC ENDOPROSTHESES - BOON OR BUST SO RADIOLOGY LA English DT Editorial Material DE BILE DUCTS, INTERVENTIONAL PROCEDURE; BILE DUCTS, NEOPLASMS; BILE DUCTS, STENOSIS OR OBSTRUCTION; EDITORIALS; GALLBLADDER, NEOPLASMS; INTERVENTIONAL PROCEDURES, COMPLICATIONS ID MALIGNANT BILIARY OBSTRUCTION; STENTS; STRICTURES; EXPERIENCE; MANAGEMENT; DRAINAGE; COMPLICATIONS RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 32 Z9 32 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 JUN PY 1991 VL 179 IS 3 BP 603 EP 605 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM910 UT WOS:A1991FM91000003 PM 2027958 ER PT J AU WILLETT, CG SHELLITO, PC RODKEY, GV WOOD, WC AF WILLETT, CG SHELLITO, PC RODKEY, GV WOOD, WC TI PREOPERATIVE IRRADIATION FOR TETHERED RECTAL-CARCINOMA SO RADIOTHERAPY AND ONCOLOGY LA English DT Note DE TETHERED RECTAL CARCINOMA ID CANCER; RADIATION AB Twenty-eight patients with resectable but tethered rectal carcinomas were treated with preoperative irradiation (EBRT) and surgical resection. The 5-year actuarial disease-free survival and local control rates of these 28 patients were 66 and 76%, respectively. Two patients have developed local failure only, 2 patients concurrent local failures and distant metastases, and 4 patients distant metastases only. All local failures occurred in areas of tumor adherence to unresectable structures (sacrum, pelvic side wall). Patients with tethered rectal tumors are at risk for local failure despite preoperative irradiation and surgical resection. To improve local control in this subset of patients, an intraoperative radiation therapy (IORT) boost is given to areas of tumor adherence at resection following EBRT. C1 MASSACHUSETTS GEN HOSP,CTR CANC,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,DIV SURG ONCOL,BOSTON,MA 02114. RP WILLETT, CG (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,RADIAT MED SERV,BOSTON,MA 02114, USA. NR 5 TC 18 Z9 18 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0167-8140 J9 RADIOTHER ONCOL JI Radiother. Oncol. PD JUN PY 1991 VL 21 IS 2 BP 141 EP 142 DI 10.1016/0167-8140(91)90087-W PG 2 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FX199 UT WOS:A1991FX19900011 PM 1866465 ER PT J AU ROSOW, C ECKHARDT, WF AF ROSOW, C ECKHARDT, WF TI THE PHARMACOLOGY OF CARDIOPULMONARY BYPASS SO SEMINARS IN ANESTHESIA LA English DT Article ID PLASMA-PROTEIN BINDING; CARDIAC-SURGERY; PHARMACOKINETICS; FENTANYL; DISPOSITION; HYPOTHERMIA; INFUSION; KINETICS; SEQUESTRATION; PANCURONIUM C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ANESTHESIA SERV,BOSTON,MA 02114. NR 40 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0277-0326 J9 SEMIN ANESTH JI Semin. Anesth. PD JUN PY 1991 VL 10 IS 2 BP 122 EP 128 PG 7 WC Anesthesiology SC Anesthesiology GA FQ845 UT WOS:A1991FQ84500007 ER PT J AU MUELLER, PR DAWSON, SL AF MUELLER, PR DAWSON, SL TI UPDATE ON LASER ANGIOPLASTY - EDITORIAL SO SEMINARS IN INTERVENTIONAL RADIOLOGY LA English DT Editorial Material RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DIV HEAD ABDOMINAL IMAGING & INTERVENT RADIOL,BOSTON,MA 02114, USA. 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 0739-9529 J9 SEMIN INTERVENT RAD JI Semin. Interv. Radiol. PD JUN PY 1991 VL 8 IS 2 BP 87 EP 87 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FN939 UT WOS:A1991FN93900001 ER PT J AU HIRSCH, MS AF HIRSCH, MS TI CYTOMEGALOVIRUS AND ITS ROLE IN THE PATHOGENESIS OF ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT SYMP ON PATHOGENESIS OF HUMAN CYTOMEGALOVIRUS-ASSOCIATED DISEASES CY APR 05-07, 1990 CL IRVINE, CA ID VIRUS TYPE-1; INFECTION; MONONUCLEOSIS; GENE; HIV; IMMUNOSUPPRESSION; SUBSETS; RETINA; REGION; AIDS RP HIRSCH, MS (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT INFECT DIS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA12464, CA35020] NR 23 TC 14 Z9 14 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 JUN PY 1991 VL 23 IS 3 SU 3 BP 118 EP 121 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA FQ909 UT WOS:A1991FQ90900024 PM 1648813 ER PT J AU LAWRENCE, MB SPRINGER, TA AF LAWRENCE, MB SPRINGER, TA TI LEUKOCYTES ROLL ON A SELECTIN AT PHYSIOLOGICAL FLOW-RATES - DISTINCTION FROM AND PREREQUISITE FOR ADHESION THROUGH INTEGRINS SO CELL LA English DT Article ID INCREASED SURFACE EXPRESSION; GRANULE MEMBRANE-PROTEIN; WEIBEL-PALADE BODIES; NEUTROPHIL ADHERENCE; INTERCELLULAR-ADHESION; ENDOTHELIAL-CELLS; BLOOD-FLOW; TRANSENDOTHELIAL MIGRATION; VASCULAR ENDOTHELIUM; CULTURED ENDOTHELIUM AB Rolling of leukocytes on vascular endothelial cells, an early event in inflammation, can be reproduced in vitro on artificial lipid bilayers containing purified CD62, a selectin also named PADGEM and GMP-140 that is inducible on endothelial cells. Neutrophils roll onthis selectin under flow conditions similar to those found in postcapillary venules. Adhesion of resting or activated neutrophils through the integrins LFA-1 and Mac-1 to ICAM-1 in a lipid bilayer does not occur at physiologic shear stresses; however, static incubation of activated neutrophils allows development of adhesion that is greater than 100-fold more shear resistant than found on CD62. Addition of a chemoattractant to activate LFA-1 and Mac-1 results in the arrest of neutrophils rolling on bilayers containing both CD62 and ICAM-1. Thus, at physiologic shear stress, rolling on a selectin is a prerequisite for activation-induced adhesion strengthening through integrins. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAWRENCE, MB (reprint author), HARVARD UNIV,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 31799] NR 68 TC 1893 Z9 1911 U1 3 U2 54 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAY 31 PY 1991 VL 65 IS 5 BP 859 EP 873 DI 10.1016/0092-8674(91)90393-D PG 15 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FP516 UT WOS:A1991FP51600016 PM 1710173 ER PT J AU BENNER, SA ELLINGTON, AD AF BENNER, SA ELLINGTON, AD TI RNA WORLD SO SCIENCE LA English DT Letter ID EVOLUTION; PROTOGENOTE; PROGENOTE; MOLECULES; PLACE C1 MASSACHUSETTS GEN HOSP, DEPT MOLEC BIOL, BOSTON, MA 02114 USA. RP BENNER, SA (reprint author), SWISS FED INST TECHNOL, ORGAN CHEM LAB, CH-8092 ZURICH, SWITZERLAND. NR 21 TC 3 Z9 3 U1 0 U2 3 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 EI 1095-9203 J9 SCIENCE JI Science PD MAY 31 PY 1991 VL 252 IS 5010 BP 1232 EP 1232 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FN857 UT WOS:A1991FN85700006 PM 1718033 ER PT J AU BLACK, PM AF BLACK, PM TI BRAIN-TUMORS .2. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID CENTRAL NERVOUS-SYSTEM; PRIMITIVE NEUROECTODERMAL TUMORS; THERAPY-ONCOLOGY-GROUP; RADIATION-THERAPY; PITUITARY-ADENOMAS; ACOUSTIC NEUROMAS; MALIGNANT GLIOMAS; POSTOPERATIVE RADIOTHERAPY; MENINGEAL CARCINOMATOSIS; PETROCLIVAL MENINGIOMAS C1 BRIGHAM & WOMENS HOSP,BRAIN TUMOR GRP,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP BLACK, PM (reprint author), BRIGHAM & WOMENS HOSP,NEUROSURG SERV,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 118 TC 151 Z9 151 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 30 PY 1991 VL 324 IS 22 BP 1555 EP 1564 DI 10.1056/NEJM199105303242205 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA FN051 UT WOS:A1991FN05100005 PM 2027359 ER PT J AU PODOLSKY, DK FERRUCCI, JT ELLIS, DS MARK, EJ PASTERNACK, MS HUANG, PL LEWANDROWSKI, KB DOWLING, WJ GOLDFINGER, SE AF PODOLSKY, DK FERRUCCI, JT ELLIS, DS MARK, EJ PASTERNACK, MS HUANG, PL LEWANDROWSKI, KB DOWLING, WJ GOLDFINGER, SE TI A 15-YEAR-OLD BOY WITH FEVER OF UNKNOWN ORIGIN, SEVERE ANEMIA, AND PORTAL-VEIN THROMBOSIS - APPENDICITIS WITH PERIAPPENDICITIS AND FOREIGN-BODY GIANT-CELL REACTION CONSISTENT WITH PRIOR RUPTURE - PYLEPHLEBITIS WITH THROMBOSIS, ACUTE AND CHRONIC TRIADITIS, AND CHOLANGITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ULTRASONOGRAPHIC DIAGNOSIS; UNDETERMINED ORIGIN; CHILDREN C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PODOLSKY, DK (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. NR 11 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 MAY 30 PY 1991 VL 324 IS 22 BP 1575 EP 1584 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA FN051 UT WOS:A1991FN05100007 ER PT J AU FINN, SF SWARTZ, KJ BEAL, MF AF FINN, SF SWARTZ, KJ BEAL, MF TI 2-CHLOROADENOSINE ATTENUATES NMDA, KAINATE, AND QUISQUALATE TOXICITY SO NEUROSCIENCE LETTERS LA English DT Article DE 2-CHLOROADENOSINE; N-METHYL-D-ASPARTATE; KAINATE; QUISQUALATE ID DEPOLARIZATION-INDUCED RELEASE; KAINIC ACID; CYCLIC-AMP; ADENOSINE-TRIPHOSPHATE; EVOKED-POTENTIALS; CEREBRAL-CORTEX; RAT; SLICES; INHIBITION; GLUTAMATE AB Excitatory amino acid (EAA)-induced cell death in the striatum is dependent upon intact glutamatergic afferents arising from the cerebral cortex. Through a mechanism possibly related to inhibition of glutamate release, adenosine receptor agonists attenuate EAA induced toxicity in the rat striatum. In the present study, we examined whether 2-chloroadenosine (2CLA), a stable adenosine analog, protects against toxicity induced by kainate (KA), quisqualate (QUIS), N-methyl-D-aspartate (NMDA), and ibotenate (IBO). In vivo intrastriatal injections of 2CLA (50 nmol) with each EAA tested provided a partial but significant protective effect versus injection of the EAA alone, as measured by striatal concentrations of gamma-aminobutyric acid (GABA) and substance P-like immunoreactivity (SP-LI). These results show that 2CLA attenuates both NMDA- and non-NMDA-mediated neuronal cell death. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. FU DS NIH HHS [NINDS 16367]; NINDS NIH HHS [NS 10828-14A] NR 37 TC 23 Z9 23 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAY 27 PY 1991 VL 126 IS 2 BP 191 EP 194 DI 10.1016/0304-3940(91)90551-4 PG 4 WC Neurosciences SC Neurosciences & Neurology GA FQ078 UT WOS:A1991FQ07800023 PM 1922933 ER PT J AU CHOI, EJ TOSCANO, DG RYAN, JA RIEDEL, N TOSCANO, WA AF CHOI, EJ TOSCANO, DG RYAN, JA RIEDEL, N TOSCANO, WA TI DIOXIN INDUCES TRANSFORMING GROWTH FACTOR-ALPHA IN HUMAN KERATINOCYTES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID HUMAN EPIDERMAL KERATINOCYTES; SQUAMOUS-CELL CARCINOMAS; FACTOR-RECEPTOR; SIGNAL TRANSDUCTION; TERMINAL DIFFERENTIATION; FACTOR BINDING; TGF-ALPHA; 2,3,7,8-TETRACHLORODIBENZO-PARA-DIOXIN; TCDD; INDUCTION AB 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental toxicant, is a tumor promoter that induces hyperplasia in epithelia cells. Exposure of cultured human keratinocytes to TCDD, resulted in a time-dependent dioxin-specific Ah receptor-mediated release of transforming growth factor-alpha (TGF-alpha) into the culture medium. Cultures exposed to TCDD showed a rate of TGF-alpha secretion into the medium of about 30 fmol/ml/day, as well as a 3- to 6-fold increase in TGF-alpha mRNA expression. Increased production of TGF-alpha in human keratinocytes exposed to TCDD demonstrates a modulation of autocrine regulation in those cells. These results suggest that induction of TGF-alpha could be an important part of the mechanism of dioxin-mediated toxicity and tumor promotion. C1 UNIV MINNESOTA, DIV ENVIRONM & OCCUPAT HLTH, ENVIRONM TOXICOL PROGRAM, BOX 197, MINNEAPOLIS, MN 55455 USA. MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. BOSTON UNIV, SCH MED, DEPT MED, BOSTON, MA 02118 USA. FU NIEHS NIH HHS [ES-02866] NR 68 TC 111 Z9 115 U1 0 U2 1 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 MAY 25 PY 1991 VL 266 IS 15 BP 9591 EP 9597 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM459 UT WOS:A1991FM45900041 PM 2033054 ER PT J AU STANDIFORD, TJ KUNKEL, SL PHAN, SH ROLLINS, BJ STRIETER, RM AF STANDIFORD, TJ KUNKEL, SL PHAN, SH ROLLINS, BJ STRIETER, RM TI ALVEOLAR MACROPHAGE-DERIVED CYTOKINES INDUCE MONOCYTE CHEMOATTRACTANT PROTEIN-1 EXPRESSION FROM HUMAN PULMONARY TYPE-II-LIKE EPITHELIAL-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-NECROSIS-FACTOR; NEUTROPHIL CHEMOTACTIC FACTOR; FACTOR GENE-EXPRESSION; ACTIVATING FACTOR MCAF; HUMAN-LUNG CARCINOMA; GROWTH FACTOR-BETA; HUMAN-FIBROBLASTS; ENDOTHELIAL-CELLS; SECRETION; LINE AB Many acute and chronic lung diseases are characterized by the presence of increased numbers of activated macrophages. These macrophages are derived predominantly from newly recruited peripheral blood monocytes and may play a role in the amplification and perpetuation of an initial lung insult. The process of inflammatory cell recruitment is poorly understood, although the expression of inflammatory cell-specific chemoattractants and subsequent generation of chemotactic gradients is likely involved. Although immune cells such as macrophages and lymphocytes are known to generate several inflammatory cell chemoattractants, parenchymal cells can also synthesize and secrete a number of bioactive factors. We now demonstrate the generation of significant monocyte chemotactic activity from tumor necrosis factor (TNF)-alpha and interleukin (IL)-1-beta-treated pulmonary type II-like epithelial cells (A549). The predominant inducible monocyte chemotaxin had an estimated molecular mass of approximately 14-15 kDa and was neutralized by specific antibody to human monocyte chemotactic protein-1 (MCP-1). Induction of activity was accompanied by increases in steady-state mRNA level for MCP-1. These data are consistent with the induction of MCP-1 expression from A549 cells by TNF and IL-1. MCP-1 production from A549 cells could be induced by lipopolysaccharide (LPS)-stimulated alveolar macrophage (AM)-conditioned media, but not by LPS alone. The inducing activity in AM-conditioned media was neutralized with specific antibodies to IL-1-beta, but not TNF-alpha. Our findings suggest that the alveolar epithelium can participate in inflammatory cell recruitment via the production of MCP-1 and that cytokine networking between contiguous alveolar macrophages and the pulmonary epithelium may be essential for parenchymal cell MCP-1 expression. C1 UNIV MICHIGAN,SCH MED,DEPT INTERNAL MED,DIV PULM & CRIT CARE MED,BOX 0360,3916 TAUBMAN CTR,ANN ARBOR,MI 48109. UNIV MICHIGAN,SCH MED,DEPT PATHOL,ANN ARBOR,MI 48109. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Phan, Sem/A-7033-2009; OI Phan, Sem/0000-0002-3711-2159 FU NHLBI NIH HHS [HL02401, HL31693, HL35276] NR 49 TC 272 Z9 276 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 MAY 25 PY 1991 VL 266 IS 15 BP 9912 EP 9918 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM459 UT WOS:A1991FM45900085 PM 2033076 ER PT J AU CHU, HM FISCHER, WH OSBORNE, TF COMB, MJ AF CHU, HM FISCHER, WH OSBORNE, TF COMB, MJ TI NF-I PROTEINS FROM BRAIN INTERACT WITH THE PROENKEPHALIN CAMP INDUCIBLE ENHANCER SO NUCLEIC ACIDS RESEARCH LA English DT Article ID NUCLEAR FACTOR-I; CULTURED CHROMAFFIN CELLS; DNA-BINDING PROTEINS; CYCLIC-AMP; ENKEPHALIN BIOSYNTHESIS; ACTIVATES TRANSCRIPTION; CATALYTIC SUBUNIT; GENE-EXPRESSION; PROMOTER; PURIFICATION AB A short region of the human proenkephalin promoter has been shown previously to mediate transcriptional regulation in response to activation of the cAMP, TPA, and Ca+ + dependent intracellular signalling pathways. Two adjacent DNA elements, CRE-1 and CRE-2, are essential for this regulation although neither element alone is sufficient for inducible expression. The CRE-2 element consists of overlapping binding sites for the transcription factors AP-1 and AP-4. The CRE-1 element has been shown to interact with a DNA binding factor called ENKTF-1. Here we characterize proteins from bovine brain which bind the CRE-1 element of the human proenkephalin gene. Interactions between proteins binding the CRE-1 and CRE-2 elements are characterized in vitro using affinity purified DNA binding proteins. We demonstrate that CRE-1 binding proteins from bovine brain consist of three different polypeptides each belonging to the NF-1 family of transcription factors. Point mutation analysis of the contacts of these proteins with the CRE-1 element indicate that NF-1 proteins contact the inducible enhancer at the sequence [GRAPHICS] which overlaps the CRE-1 element (underlined) defined by in vivo point mutation analysis. Cotransfection of one of the three NF-1 proteins purified from bovine brain, NF-1/Red1, together with a proenkephalin/bacterial chloramphenicol acetyl transferase (CAT) fusion gene repressed protein kinase A or forskolin stimulated CAT expression. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROBIOL LAB,PROGRAM NEUROSCI,BOSTON,MA 02114. SALK INST BIOL STUDIES,LA JOLLA,CA 92037. UNIV CALIF IRVINE,DEPT MOLEC BIOL & BIOCHEM,IRVINE,CA 92715. FU NIDA NIH HHS [DA 05706-01] NR 33 TC 43 Z9 44 U1 0 U2 1 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 MAY 25 PY 1991 VL 19 IS 10 BP 2721 EP 2728 DI 10.1093/nar/19.10.2721 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP319 UT WOS:A1991FP31900023 PM 1828294 ER PT J AU TROFATTER, JA GUSELLA, JF HAINES, JL AF TROFATTER, JA GUSELLA, JF HAINES, JL TI DINUCLEOTIDE REPEAT POLYMORPHISM AT THE DEBRISOQUINE 4-HYDROXYLASE (CYP2D) LOCUS SO NUCLEIC ACIDS RESEARCH LA English DT Note RP TROFATTER, JA (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02129, USA. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [F32 HG-00016, R01 HG-00317, R01 HG-00324] NR 2 TC 8 Z9 8 U1 0 U2 2 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAY 25 PY 1991 VL 19 IS 10 BP 2802 EP 2802 DI 10.1093/nar/19.10.2802-a PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FP319 UT WOS:A1991FP31900061 PM 2041763 ER PT J AU SPIES, T DEMARS, R AF SPIES, T DEMARS, R TI RESTORED EXPRESSION OF MAJOR HISTOCOMPATIBILITY CLASS-I MOLECULES BY GENE-TRANSFER OF A PUTATIVE PEPTIDE TRANSPORTER SO NATURE LA English DT Article ID HLA-B ANTIGENS; LYMPHOBLASTOID CELLS; T-CELLS; MHC; COMPLEX; REGION; DETERMINANT; BINDING; PROTEIN; PATHWAY AB CYTOTOXIC T lymphocytes recognize antigen-derived peptides bound to major histocompatibility complex (MHC) class I molecules with which they assemble in the endoplasmic reticulum or in an undefined subcompartment 1-10. There is genetic evidence that the peptides that are products of cytosolic protein degradation are transported into this compartment by a peptide supply factor (PSF), encoded in the MHC class II region 11. Like the corresponding genes RING4, HAM1 and mtp1 (refs 12-14), PSF is related to the multidrug-resistance family of transporters 11 and may be a peptide pump, as translocation of peptides across membranes must occur independently of the secretory pathway 15. There is, however, no functional evidence for this role so far. Here we report gene transfer experiment showing that expression of PSF complementary DNA in the human lymphoblastoid cell line mutant 721.134 (refs 11, 16, 17) restores normal levels of surface HLA-A2 and -B5. No similar effect was observed in 721.174 mutant cells, in which a homozygous deletion includes PSF among several other closely linked genes 11. At least one of these genes may therefore also be required for PSF function. C1 UNIV WISCONSIN,GENET LAB,MADISON,WI 53706. RP SPIES, T (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115, USA. NR 25 TC 410 Z9 411 U1 1 U2 3 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAY 23 PY 1991 VL 351 IS 6324 BP 323 EP 324 DI 10.1038/351323a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FM976 UT WOS:A1991FM97600063 PM 2034277 ER PT J AU BARTON, NW BRADY, RO DAMBROSIA, JM DIBISCEGLIE, AM DOPPELT, SH HILL, SC MANKIN, HJ MURRAY, GJ PARKER, RI ARGOFF, CE GREWAL, RP YU, KT AF BARTON, NW BRADY, RO DAMBROSIA, JM DIBISCEGLIE, AM DOPPELT, SH HILL, SC MANKIN, HJ MURRAY, GJ PARKER, RI ARGOFF, CE GREWAL, RP YU, KT TI REPLACEMENT THERAPY FOR INHERITED ENZYME DEFICIENCY - MACROPHAGE-TARGETED GLUCOCEREBROSIDASE FOR GAUCHERS-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CELLS; GENE AB Background and Methods. Gaucher's disease, the most prevalent of the sphingolipid storage disorders, is caused by a deficiency of the enzyme glucocerebrosidase (glucosylceramidase). Enzyme replacement was proposed as a therapeutic strategy for this disorder in 1966. To assess the clinical effectiveness of this approach, we infused macrophage-targeted human placental glucocerebrosidase (60 IU per kilogram of body weight every 2 weeks for 9 to 12 months) into 12 patients with type 1 Gaucher's disease who had intact spleens. The frequency of infusions was increased to once a week in two patients (children) during part of the trial because they had clinically aggressive disease. Results. The hemoglobin concentration increased in all 12 patients, and the platelet count in 7. Serum acid phosphatase activity decreased in 10 patients during the trial, and the plasma glucocerebroside level in 9. Splenic volume decreased in all patients after six months of treatment, and hepatic volume in five. Early signs of skeletal improvements were seen in three patients. The enzyme infusions were well tolerated, and no antibody to the exogenous enzyme developed. Conclusions. Intravenous administration of macrophage-targeted glucocerebrosidase produces objective clinical improvement in patients with type 1 Gaucher's disease. The hematologic and visceral responses to enzyme replacement develop more rapidly than the skeletal response. C1 NINCDS,BIOMETRY & FIELD STUDIES BRANCH,BETHESDA,MD 20892. NIDDKD,LIVER DIS SECT,BETHESDA,MD. NIH,CTR CLIN,DEPT DIAGNOST RADIOL,BETHESDA,MD 20892. NIH,CTR CLIN,DEPT CLIN PATHOL,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. RP BARTON, NW (reprint author), NINCDS,DEV & METAB NEUROL BRANCH,BLDG 10,RM 3D04,BETHESDA,MD 20892, USA. OI Kaneski, Christine/0000-0003-1453-2502 NR 30 TC 851 Z9 873 U1 2 U2 31 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 23 PY 1991 VL 324 IS 21 BP 1464 EP 1470 DI 10.1056/NEJM199105233242104 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA FM460 UT WOS:A1991FM46000004 PM 2023606 ER PT J AU BLACK, PM AF BLACK, PM TI MEDICAL PROGRESS - BRAIN-TUMORS .1. SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID GROWTH-FACTOR RECEPTOR; POSITRON EMISSION TOMOGRAPHY; HUMAN GLIOBLASTOMA; RADIATION-THERAPY; L-3-IODO-ALPHA-METHYL TYROSINE; INTRACRANIAL TUMORS; HUMAN ASTROCYTOMAS; RECURRENT GLIOMAS; MALIGNANT GLIOMA; NATIONAL SURVEY C1 BRIGHAM & WOMENS HOSP,BRAIN TUMOR GRP,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP BLACK, PM (reprint author), BRIGHAM & WOMENS HOSP,NEUROSURG SERV,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 101 TC 195 Z9 203 U1 0 U2 6 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 23 PY 1991 VL 324 IS 21 BP 1471 EP 1476 DI 10.1056/NEJM199105233242105 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA FM460 UT WOS:A1991FM46000005 PM 1822669 ER PT J AU BLACKMORE, PF MOJSOV, S EXTON, JH HABENER, JF AF BLACKMORE, PF MOJSOV, S EXTON, JH HABENER, JF TI ABSENCE OF INSULINOTROPIC GLUCAGONLIKE PEPTIDE-I(7-37) RECEPTORS ON ISOLATED RAT-LIVER HEPATOCYTES SO FEBS LETTERS LA English DT Article DE GLUCAGONLIKE PEPTIDE-I; HEPATOCYTE RECEPTOR; PANCREATIC B-CELL; INSULINOTROPIC; CYCLIC AMP ID CYCLIC-AMP LEVELS; PEPTIDE-I; GENE-EXPRESSION; CA-2+ FLUXES; PANCREAS; RELEASE; GLUCONEOGENESIS; PHOSPHORYLASE; INTESTINE AB The effects of glucagon and the glucagon-like peptide GLP-1(7-37) were compared in rat liver hepatocytes. Glucagon elevated cAMP, elevated intracellular free calcium ([Ca2+]i), activated phosphorylase and stimulated gluconeogenesis, whereas GLP-1(7-37) was without effect on any of these parameters. GLP-1(7-37) did not block any of the actions of glucagon. The glucagon analog, des His1[Glu9] glucagon amide, was a partial agonist in liver, but also was an effective antagonist of glucagon actions in liver but not those of GLP-1(7-37) in islet B cells. It was concluded that in the rat, GLP-1(7-37) is a potent insulin secretagogue [1] but is without effect on liver. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED, HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB, BOSTON, MA 02114 USA. VANDERBILT UNIV, MED CTR, SCH MED, HOWARD HUGHES MED INST, NASHVILLE, TN 37232 USA. RP BLACKMORE, PF (reprint author), EASTERN VIRGINIA MED SCH, DEPT PHARMACOL, POB 1980, NORFOLK, VA 23501 USA. FU NIDDK NIH HHS [DK30834] NR 28 TC 42 Z9 43 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 EI 1873-3468 J9 FEBS LETT JI FEBS Lett. PD MAY 20 PY 1991 VL 283 IS 1 BP 7 EP 10 DI 10.1016/0014-5793(91)80541-A PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FP194 UT WOS:A1991FP19400003 PM 1645298 ER PT J AU BLUM, HE GALUN, E VONWEIZSACKER, F WANDS, JR AF BLUM, HE GALUN, E VONWEIZSACKER, F WANDS, JR TI INHIBITION OF HEPATITIS-B VIRUS BY ANTISENSE OLIGODEOXYNUCLEOTIDES SO LANCET LA English DT Letter RP BLUM, HE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MGH CANC CTR,BOSTON,MA 02129, USA. NR 5 TC 53 Z9 54 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 MAY 18 PY 1991 VL 337 IS 8751 BP 1230 EP 1230 DI 10.1016/0140-6736(91)92907-J PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FM261 UT WOS:A1991FM26100053 PM 1673773 ER PT J AU WEAVER, D ALBANESE, C COSTANTINI, F BALTIMORE, D AF WEAVER, D ALBANESE, C COSTANTINI, F BALTIMORE, D TI RETRACTION - ALTERED REPERTOIRE OF ENDOGENOUS IMMUNOGLOBULIN GENE-EXPRESSION IN TRANSGENIC MICE CONTAINING A REARRANGED MU-HEAVY CHAIN GENE SO CELL LA English DT Letter C1 WHITEHEAD INST,CAMBRIDGE,MA 02142. COLUMBIA UNIV,DEPT HUMAN GENET & DEV,NEW YORK,NY 10027. ROCKEFELLER UNIV,NEW YORK,NY 10021. RP WEAVER, D (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 1 TC 3 Z9 3 U1 1 U2 6 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAY 17 PY 1991 VL 65 IS 4 BP 536 EP 536 DI 10.1016/0092-8674(91)90085-D PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM037 UT WOS:A1991FM03700003 PM 2032282 ER PT J AU ROCK, KL GAMBLE, S ROTHSTEIN, L GRAMM, C BENACERRAF, B AF ROCK, KL GAMBLE, S ROTHSTEIN, L GRAMM, C BENACERRAF, B TI DISSOCIATION OF BETA-2-MICROGLOBULIN LEADS TO THE ACCUMULATION OF A SUBSTANTIAL POOL OF INACTIVE CLASS-I MHC HEAVY-CHAINS ON THE CELL-SURFACE SO CELL LA English DT Article ID RESTRICTED T-CELLS; HISTOCOMPATIBILITY MOLECULES; ANTIGEN PRESENTATION; DENOVO SYNTHESIS; LYMPHOMA-CELLS; MOUSE LYMPHOMA; LYMPHOCYTES-T; RECOGNITION; PEPTIDES; BINDING AB A large pool of free class I heavy chains is detected in situ on the plasma membrane of living cells. These chains are present on cells of different MHC genotypes and appear to exist under physiological conditions in vivo. These molecules arise from the dissociation of previously assembled class I heterodimers at the cell surface. The ratio of intact to dissociated heterodimers is strongly affected by the occupancy of the peptide-binding site of the class I molecule. Upon dissociation of the heterodimer, the class I molecule is functionally inactive. These finding may help to explain why class I molecules on the cell surface are unreceptive to binding peptides yet readily associated with peptides in the presence of exogenous beta-2-microglobulin. These results have implications for understanding the distinct functions of class I versus class II molecules and how the immunological identify of cells is preserved. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROCK, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115, USA. FU PHS HHS [A120248] NR 49 TC 155 Z9 155 U1 1 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAY 17 PY 1991 VL 65 IS 4 BP 611 EP 620 DI 10.1016/0092-8674(91)90093-E PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FM037 UT WOS:A1991FM03700011 PM 2032286 ER PT J AU WILSON, BE SUN, S OZTURK, M WANDS, JR AF WILSON, BE SUN, S OZTURK, M WANDS, JR TI STABILITY OF MONOCLONAL ANTIBODY-DEFINED EPITOPES SO JOURNAL OF IMMUNOLOGICAL METHODS LA English DT Article DE CELL SURFACE ANTIGEN; EPITOPE; MONOCLONAL ANTIBODY ID DIFFERENTIAL SCANNING CALORIMETRY; HUMAN HEPATOCELLULAR-CARCINOMA; THERMAL-DENATURATION; IMMUNOHISTOCHEMICAL TECHNIQUES; ENZYMATIC CATALYSIS; STRUCTURAL-CHANGES; IMMUNOGLOBULIN-E; PROTEIN; ANTIGENS; 100-DEGREES-C AB Epitope instability can limit the applications of monoclonal antibody (mAb) technology in laboratory and clinical research. We exposed a group of representative antigens on human hepatocellular carcinoma (HCC) cells to physiochemical insults to study epitope stability as measured by mAb immunoreactivity. Each epitope was found to have a unique pattern of instability which serves to biophysically characterize the antigen and defines the conditions to which the antigen can be exposed during laboratory and clinical investigations. Individual antigens were found to be unstable within a surprisingly well defined window of solvent polarities while being stable on either side of that window. Several antigens were observed to be unstable when exposed to transient changes in pH. When a critical temperature between 42-degrees-C and 65-degrees-C was achieved, epitopes which were thermosensitive underwent a sudden loss in immunoreactivity. This critical temperature was found to be pH dependent. The effects of polarity, pH, and temperature on epitope stability are consistent with changes in protein structural conformation. In addition, we found that certain fixatives cause a time and concentration dependent loss of epitope immunoreactivity. This study provides a rapid and easy determination of monoclonal antibody-defined epitope stability; the results of which serve to guide further studies on the antigen and to characterize the antigen on the basis of its unique physiochemical stability. C1 MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC HEPATOL LAB,7TH FLOOR,MGH E,149 13TH ST,BOSTON,MA 02129. HARVARD UNIV SCH MED,DEPT MED,BOSTON,MA 02114. RI ozturk, mehmet/G-3330-2014 FU NCI NIH HHS [CA-3571]; NIAAA NIH HHS [AA-02666, AA-01862] NR 37 TC 5 Z9 5 U1 0 U2 1 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 MAY 17 PY 1991 VL 139 IS 1 BP 55 EP 64 DI 10.1016/0022-1759(91)90351-F PG 10 WC Biochemical Research Methods; Immunology SC Biochemistry & Molecular Biology; Immunology GA FN935 UT WOS:A1991FN93500007 PM 1710252 ER PT J AU SIDDIQUE, T FIGLEWICZ, DA PERICAKVANCE, MA HAINES, JL ROULEAU, G JEFFERS, AJ SAPP, P HUNG, WY BEBOUT, J MCKENNAYASEK, D DENG, G HORVITZ, HR GUSELLA, JF BROWN, RH ROSES, AD AF SIDDIQUE, T FIGLEWICZ, DA PERICAKVANCE, MA HAINES, JL ROULEAU, G JEFFERS, AJ SAPP, P HUNG, WY BEBOUT, J MCKENNAYASEK, D DENG, G HORVITZ, HR GUSELLA, JF BROWN, RH ROSES, AD TI LINKAGE OF A GENE CAUSING FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS TO CHROMOSOME-21 AND EVIDENCE OF GENETIC-LOCUS HETEROGENEITY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID MOTOR NEURON DISEASE; COMMITTEE; MAPS AB Background. Amyotrophic lateral sclerosis is a progressive neurologic disorder that commonly results in paralysis and death. Despite more than a century of research, no cause of, cure for, or means of preventing this disorder has been found. In a minority of cases, it is familial and inherited as an autosomal dominant trait with age-dependent penetrance. In contrast to the sporadic form of amyotrophic lateral sclerosis, the familial form provides the opportunity to use molecular genetic techniques to localize an inherited defect. Furthermore, such studies have the potential to discover the basic molecular defect causing motor-neuron degeneration. Methods and Results. We evaluated 23 families with familial amyotrophic lateral sclerosis for linkage of the gene causing this disease to four DNA markers on the long arm of chromosome 21. Multipoint linkage analyses demonstrated linkage between the gene and these markers. The maximum lod score - 5.03 - was obtained 10 centimorgans distal (telomeric) to the DNA marker D21S58. There was a significant probability (P < 0.0001) of genetic-locus heterogeneity in the families. Conclusions. The localization of a gene causing familial amyotrophic lateral sclerosis provides a means of isolating this gene and studying its function. Insight gained from understanding the function of this gene may be applicable to the design of rational therapy for both the familial and sporadic forms of the disease. C1 MCGILL UNIV,CTR RES NEUROSCI,MONTREAL H3A 2T5,QUEBEC,CANADA. DUKE UNIV,MED CTR,DURHAM,NC 27710. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SIDDIQUE, T (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT NEUROL,SEARLE 11-543,303 E CHICAGO AVE,CHICAGO,IL 60611, USA. RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [P0-NS-21442, NS-20012, P0-NS-26630] NR 22 TC 354 Z9 354 U1 2 U2 8 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 16 PY 1991 VL 324 IS 20 BP 1381 EP 1384 DI 10.1056/NEJM199105163242001 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA FL125 UT WOS:A1991FL12500001 PM 2020294 ER PT J AU COSIMI, AB RUBIN, RH AF COSIMI, AB RUBIN, RH TI POSTTRANSPLANTATION LYMPHOPROLIFERATIVE DISORDER AND OKT3 SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID RENAL-ALLOGRAFT REJECTION; ANTI-THYMOCYTE GLOBULIN; MONOCLONAL-ANTIBODY; CLINICAL-TRIAL; RECIPIENTS; INTERFERON; INFECTION; VIRUS RP COSIMI, AB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 16 PY 1991 VL 324 IS 20 BP 1438 EP 1438 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FL125 UT WOS:A1991FL12500021 ER PT J AU BAKSHI, R DUCATMAN, AM HOCHBERG, FH AF BAKSHI, R DUCATMAN, AM HOCHBERG, FH TI GLIOBLASTOMAS IN NEW-ENGLAND OPHTHALMOLOGISTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID BRAIN-TUMORS; MORTALITY; PAPOVAVIRUS; CANCER; JC C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP BAKSHI, R (reprint author), SUNY BUFFALO,SCH MED,BUFFALO,NY 14201, USA. NR 10 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 16 PY 1991 VL 324 IS 20 BP 1440 EP 1441 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FL125 UT WOS:A1991FL12500026 PM 1850499 ER PT J AU STEIN, PD ALAVI, A GOTTSCHALK, A HALES, CA SALTZMAN, HA VREIM, CE WEG, JG AF STEIN, PD ALAVI, A GOTTSCHALK, A HALES, CA SALTZMAN, HA VREIM, CE WEG, JG TI USEFULNESS OF NONINVASIVE DIAGNOSTIC-TOOLS FOR DIAGNOSIS OF ACUTE PULMONARY-EMBOLISM IN PATIENTS WITH A NORMAL CHEST RADIOGRAPH SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article AB The value of bedside examination and noninvasive tests in the diagnosis of acute pulmonary embolism (PE) among patients with a normal chest radiograph was investigated. Normal chest radiographs were present in 20 of 260 patients (8%) with acute PE and in 113 of 642 (18%) with suspected acute PE, in whom the diagnosis was excluded. A partial pressure of oxygen in arterial blood less-than-or-equal-to 70 mm Hg in a dyspneic patient with a normal chest radiograph was more often seen among patients with PE (9 of 17, 53%) than among patients in whom PE was excluded (18 of 93, 19%; p < 0.01). However, no combinations of blood gases, signs and symptoms were strictly diagnostic. High probability ventilation/perfusion scans among patients with a normal chest radiograph were indicative of PE in only 6 of 9 patients (67%). Among patients with low-probability ventilation/perfusion scans, 8 of 47 (17%) had PE. This study showed that the combination of dyspnea and hypoxia in a patient with a normal chest radiograph is a useful clue to the diagnosis of PE. Although intuition suggested that ventilation/perfusion scans would yield better results in patients with a normal chest radiograph, the ability to diagnose PE by ventilation/perfusion scans in this subset of patients was not enhanced, except by a reduction of the percentage of patients with intermediate probability scans. C1 UNIV PENN,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NHLBI,BETHESDA,MD 20892. MICHIGAN STATE UNIV,E LANSING,MI 48824. DUKE UNIV,DURHAM,NC 27706. UNIV MICHIGAN,DETROIT,MI. RP STEIN, PD (reprint author), HENRY FORD HOSP,INST HEART & VASC,2799 W GRAND BLVD,DETROIT,MI 48202, USA. FU NHLBI NIH HHS [N01-HR-34007, N01-HR-34009, N01-HR-34008] NR 4 TC 47 Z9 47 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAY 15 PY 1991 VL 67 IS 13 BP 1117 EP 1120 DI 10.1016/0002-9149(91)90875-L PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FL100 UT WOS:A1991FL10000014 PM 2024602 ER PT J AU BERSON, EL ROSNER, B SANDBERG, MA WEIGELDIFRANCO, C DRYJA, TP AF BERSON, EL ROSNER, B SANDBERG, MA WEIGELDIFRANCO, C DRYJA, TP TI OCULAR FINDINGS IN PATIENTS WITH AUTOSOMAL DOMINANT RETINITIS-PIGMENTOSA AND RHODOPSIN, PROLINE-347-LEUCINE SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CHROMOSOME-3; GENE AB We studied the ocular findings in eight unrelated patients with a form of autosomal dominant retinitis pigmentosa and the same cytosine-to-thymine transition in the second nucleotide of codon 347 of the rhodopsin gene. This mutation, detected in leukocyte DNA, corresponds to a substitution of leucine for proline in amino acid 347 of the rhodopsin protein, and, therefore, we designated this form of retinitis pigmentosa as rhodopsin, proline-347-leucine. On average, these patients had significantly smaller visual field areas and smaller electroretinogram amplitudes than 140 unrelated patients of comparable age with dominant retinitis pigmentosa without this mutation. The findings in eight relatives with this mutation from three of these families are presented to provide examples of the variability that exists in the clinical severity of this disease. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. RP BERSON, EL (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY02014, EY00169] NR 15 TC 99 Z9 100 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAY 15 PY 1991 VL 111 IS 5 BP 614 EP 623 PG 10 WC Ophthalmology SC Ophthalmology GA FK067 UT WOS:A1991FK06700014 PM 2021172 ER PT J AU LIN, CW SHULOK, JR KIRLEY, SD CINCOTTA, L FOLEY, JW AF LIN, CW SHULOK, JR KIRLEY, SD CINCOTTA, L FOLEY, JW TI LYSOSOMAL LOCALIZATION AND MECHANISM OF UPTAKE OF NILE BLUE PHOTOSENSITIZERS IN TUMOR-CELLS SO CANCER RESEARCH LA English DT Article ID LIVING CELLS; ACRIDINE-DYES; HELA-CELLS; MITOCHONDRIAL; RHODAMINE-123; ACCUMULATION; PHOTOLYSIS; AGENTS; LINES; PH AB Nile blue derivatives have been shown to be potentially effective photosensitizers for photodynamic therapy of malignant tumors. Results of a previous study suggested that the high accumulation of these dyes in cells may be the result of dye aggregation, partition in membrane lipids, and/or sequestration in subcellular organelles. In this report, results of studies are presented from an investigation of the subcellular localization and mechanism of accumulation of these dyes in cells in vitro. A video-enhanced fluorescence microscopy was used, and a punctate pattern of fluorescence was seen, most of which was localized in the perinuclear region with extracellular dye concentrations between 1 to 100 nM. These particles resembled characteristic particles identified by standard lysosomal dyes. At higher dye concentrations (1-mu-M or above), fluorescence in the perinuclear region was too intense to resolve into discrete cellular structures, while fluorescence in other cellular structures including mitochondria and cytomembranes was visible. At even higher dye concentrations (10-100-mu-M), Nile blue derivatives were seen with a light microscope as blue particles, the size and location of which resembled the punctate fluorescence described above. Results which further suggest that the lysosome is the main site of dye localization include (a) histochemical staining of dye-loaded cells with the lysosomal marker enzyme acid phosphatase, which showed similar localization of the enzyme-staining and dye-containing particles, (b) phototreatment of dye-loaded cells which obliterated the majority of the acid phosphatase-stained particles, and (c) treatments with agents affecting the membrane pH gradient reduced the uptake and enhanced the efflux of dyes, while agents that alter cellular membrane potentials had no effect on dye accumulation. The uptake of the dyes was partially inhibited by inhibitors of oxidative phosphorylation indicating that at least part of the process is energy dependent. These findings, together with previous results showing that the cellular uptake of these dyes is highly concentrative and proportional to the extracellular dye concentration over a wide range, are consistent with the hypothesis that the dyes are mainly localized in the lysosomes via an ion-trapping mechanism. Results of the present study also suggest that the lysosomes may be an intracellular target for photodynamic killing of tumor cells mediated by Nile blue photosensitizers and that lysosomotropic photosensitization may be a strategy for effective and selective destruction of tumor cells. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. ROWLAND INST SCI INC,CAMBRIDGE,MA 02142. RP LIN, CW (reprint author), MASSACHUSETTS GEN HOSP,UROL RES LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 32259] NR 45 TC 73 Z9 74 U1 2 U2 4 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 15 PY 1991 VL 51 IS 10 BP 2710 EP 2719 PG 10 WC Oncology SC Oncology GA FK910 UT WOS:A1991FK91000033 PM 2021950 ER PT J AU MASTERSON, ME BAREST, G CHUI, CS DOPPKE, KP EPPERSON, RD HARMS, WB KRIPPNER, KE MOHAN, R SLESSINGER, ED SONTAG, MR URIE, MM WALLACE, RE WONG, JW AF MASTERSON, ME BAREST, G CHUI, CS DOPPKE, KP EPPERSON, RD HARMS, WB KRIPPNER, KE MOHAN, R SLESSINGER, ED SONTAG, MR URIE, MM WALLACE, RE WONG, JW TI INTERINSTITUTIONAL EXPERIENCE IN VERIFICATION OF EXTERNAL PHOTON DOSE CALCULATIONS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE EXTERNAL PHOTON TREATMENT PLANNING; DOSE CALCULATIONS; ALGORITHM ACCURACY ID CARCINOMA AB Under the auspices of NCI contracts, four institutions have collaborated to assess the accuracy of the pixel-based dose calculation methods they employ for external photon treatment planning. The approach relied on comparing calculations using each group's algorithm with measurements in phantoms of increasing complexity. The first set of measurements consisted of ionization chamber measurements in water phantoms in normally incident square fields, an elongated field, a wedged field, a blocked field, and an obliquely incident beam. The second group of measurements was carried out using thermoluminescent dosimeters in phantoms designed to investigate the effects of surface curvature, high density heterogeneities, and low density heterogeneities. The final study tested the entire treatment planning system, including CT data conversion, in an anthropomorphic phantom. Overall, good agreement between calculation and measurements was found for all algorithms. Regions in which discrepancies were observed are pointed out, areas for algorithm improvement are identified and the clinical import of algorithm accuracy is discussed. C1 FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MASTERSON, ME (reprint author), UNIV PENN,SCH MED,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47696, N01 CM-47695] NR 17 TC 19 Z9 19 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 37 EP 58 PG 22 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100005 PM 2032896 ER PT J AU DRZYMALA, RE MOHAN, R BREWSTER, L CHU, J GOITEIN, M HARMS, W URIE, M AF DRZYMALA, RE MOHAN, R BREWSTER, L CHU, J GOITEIN, M HARMS, W URIE, M TI DOSE-VOLUME HISTOGRAMS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE DOSE-VOLUME HISTOGRAMS; RADIATION THERAPY; COMPUTERIZED TREATMENT PLANNING ID RADIATION; THERAPY AB A plot of a cumulative dose-volume frequency distribution, commonly known as a dose-volume histogram (DVH), graphically summarizes the simulated radiation distribution within a volume of interest of a patient which would result from a proposed radiation treatment plan. DVHs show promise as tools for comparing rival treatment plans for a specific patient by clearly presenting the uniformity of dose in the target volume and any hot spots in adjacent normal organs or tissues. However, because of the loss of positional information in the volume(s) under consideration, it should not be the sole criterion for plan evaluation. DVHs can also be used as input data to estimate tumor control probability (TCP) and normal tissue complication probability (NTCP). The sensitivity of TCP and NTCP calculations to small changes in the DVH shape points to the need for an accurate method for computing DVHs. We present a discussion of the methodology for generating and plotting the DVHs, some caveats, limitations on their use and the general experience of four hospitals using DVHs. C1 MEM MED CTR,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DRZYMALA, RE (reprint author), WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,510 S KINGSHIGHWAY BLVD,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 17 TC 161 Z9 165 U1 2 U2 11 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 71 EP 78 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100007 PM 2032898 ER PT J AU URIE, MM GOITEIN, M DOPPKE, K KUTCHER, JG LOSASSO, T MOHAN, R MUNZENRIDER, JE SONTAG, M WONG, JW AF URIE, MM GOITEIN, M DOPPKE, K KUTCHER, JG LOSASSO, T MOHAN, R MUNZENRIDER, JE SONTAG, M WONG, JW TI THE ROLE OF UNCERTAINTY ANALYSIS IN TREATMENT PLANNING SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-DIMENSIONAL TREATMENT PLANNING; PHOTON BEAM ANALYSIS; UNCERTAINTY ANALYSIS ID COMPUTED-TOMOGRAPHY; RADIATION-THERAPY; DOSE CALCULATIONS; X-RAYS; DENSITY; SYSTEM AB The role of uncertainty analysis in 3-D treatment planning systems was addressed by four institutions which contracted with NCI to evaluate high energy photon external beam treatment planning. Treatment plans were developed at eight disease sites and the effects of uncertainties assessed in a number of experiments. Uncertainties which are patient-site specific included variations in the delineation of target volumes and normal tissues and the effects of positional uncertainties due to physiological motion and setup nonreproducibility. These were found to have a potentially major impact on the doses to the target volumes and to critical normal tissues which could result in significantly altered probabilities of tumor control and normal tissue complications. Other uncertainties, such as the conversion of CT data to electron densities, heterogeneities and dose calculation algorithms' weaknesses, are related to physical processes. The latter was noted to have the greatest potential contribution to uncertainty in some sites. A third category of uncertainty related to the treatment machine, the consequences of compensator misregistration, are exclusive to the site and the treatment portal. Because conventional treatment planning systems have not incorporated uncertainty analysis, tools and techniques had to be devised for this work; further development in this area is needed. Many of the analyses could not have been done without full 3-D capabilities of the planning systems, and it can be anticipated that the availability of uncertainty analysis in these systems which allow nontraditional beam arrangements will be of great value. C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP URIE, MM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 25 TC 74 Z9 75 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 91 EP 107 PG 17 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100009 PM 1903372 ER PT J AU EMAMI, B LYMAN, J BROWN, A COIA, L GOITEIN, M MUNZENRIDER, JE SHANK, B SOLIN, LJ WESSON, M AF EMAMI, B LYMAN, J BROWN, A COIA, L GOITEIN, M MUNZENRIDER, JE SHANK, B SOLIN, LJ WESSON, M TI TOLERANCE OF NORMAL TISSUE TO THERAPEUTIC IRRADIATION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE NORMAL TISSUE TOLERANCE; 3-DIMENSIONAL TREATMENT PLANNING; VOLUME EFFECTS; IRRADIATION ID INDUCED HEART-DISEASE; RADIATION-INDUCED PERICARDITIS; TOTAL-BODY IRRADIATION; THORACIC SPINAL-CORD; HODGKINS-DISEASE; COMPUTED-TOMOGRAPHY; MANTLE IRRADIATION; FIELD IRRADIATION; SMALL BOWEL; X-RAYS AB The importance of knowledge on tolerance of normal tissue organs to irradiation by radiation oncologists cannot be overemphasized. Unfortunately, current knowledge is less than adequate. With the increasing use of 3-D treatment planning and dose delivery, this issue, particularly volumetric information, will become even more critical. As a part of the NCI contract NO1 CM-47316, a task force, chaired by the primary author, was formed and an extensive literature search was carried out to address this issue. In this manuscript we present the updated information on tolerance of normal tissues of concern in the protocols of this contract, based on available data, with a special emphasis on partial volume effects. Due to a lack of precise and comprehensive data base, opinions and experience of the clinicians from four universities involved in the contract have also been contributory. Obviously, this is not and cannot be a comprehensive work, which is beyond the scope of this contract. C1 MEM MED CTR,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,DEPT RADIAT THERAPY,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV CALIF BERKELEY LAWRENCE BERKELEY LAB,DIV RES MED & RADIAT BIOPHYS,BERKELEY,CA 94720. RP EMAMI, B (reprint author), WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,4939 AUDUBON AVE,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 197 TC 2113 Z9 2208 U1 10 U2 78 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 109 EP 122 PG 14 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100010 PM 2032882 ER PT J AU BURMAN, C KUTCHER, GJ EMAMI, B GOITEIN, M AF BURMAN, C KUTCHER, GJ EMAMI, B GOITEIN, M TI FITTING OF NORMAL TISSUE TOLERANCE DATA TO AN ANALYTIC-FUNCTION SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE TISSUE TOLERANCES; PARAMETERS; TREATMENT PLANNING; RADIOTHERAPY ID VOLUME AB During external beam radiotherapy, normal tissues are irradiated along with the tumor. Radiation therapists try to minimize the dose to normal tissues while delivering a high dose to the target volume. Often this is difficult and complications arise due to irradiation of normal tissues. These complications depend not only on the dose but also on volume of the organ irradiated. Lyman (4) has suggested a four-parameter empirical model which can be used to represent normal tissue response under conditions of uniform irradiation to whole and partial volumes as a function of the dose and volume irradiated. In this paper, Lyman's model has been applied to a compilation of clinical tolerance data developed by Emami et al. (1). The four parameters to characterize the tissue response have been determined and graphical representations of the derived probability distributions are presented. The model may, therefore, be used to interpolate clinical data to provide estimated normal tissue complication probabilities for any combination of dose and irradiated volume for the normal tissues and end points considered. C1 WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BURMAN, C (reprint author), MEM MED CTR,1275 YORK AVE,SPRINGFIELD,IL 62781, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 6 TC 740 Z9 767 U1 1 U2 12 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 123 EP 135 PG 13 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100011 PM 2032883 ER PT J AU KUTCHER, GJ BURMAN, C BREWSTER, L GOITEIN, M MOHAN, R AF KUTCHER, GJ BURMAN, C BREWSTER, L GOITEIN, M MOHAN, R TI HISTOGRAM REDUCTION METHOD FOR CALCULATING COMPLICATION PROBABILITIES FOR 3-DIMENSIONAL TREATMENT PLANNING EVALUATIONS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-D TREATMENT PLANNING; COMPLICATION PROBABILITY CALCULATIONS; TREATMENT PLANNING EVALUATION; SCORING ID DOSE-VOLUME HISTOGRAMS; RADIATION-THERAPY; OPTIMIZATION; RADIOTHERAPY; MODELS AB New tools are needed to help in evaluating 3-D treatment plans because of the large volume of data. One technique which may prove useful is the application of complication probability calculations. A method of calculating complication probabilities for inhomogeneously irradiated normal tissues is presented in this paper. The method uses clinical estimates of tolerance doses for a few discreet conditions of uniform partial organ irradiation, an empirical fit of a continuous function to these data, and a technique (the effective volume method) for transforming nonuniform dose-volume histograms into equivalent uniform histograms. The behavior of the effective volume histogram reduction method for various boundary conditions is reviewed. The use of complication probabilities in evaluating treatment plans is presented, using examples from an NCI 3-D treatment planning contract. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KUTCHER, GJ (reprint author), MEM MED CTR,1275 YORK AVE,SPRINGFIELD,IL 62781, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 20 TC 347 Z9 354 U1 1 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 137 EP 146 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100012 PM 2032884 ER PT J AU MUNZENRIDER, JE BROWN, AP CHU, JCH COIA, LR DOPPKE, KP EMAMI, B KUTCHER, GJ MOHAN, R PURDY, JA SHANK, B SIMPSON, JR SOLIN, LJ URIE, MM AF MUNZENRIDER, JE BROWN, AP CHU, JCH COIA, LR DOPPKE, KP EMAMI, B KUTCHER, GJ MOHAN, R PURDY, JA SHANK, B SIMPSON, JR SOLIN, LJ URIE, MM TI NUMERICAL SCORING OF TREATMENT PLANS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-D TREATMENT PLANNING; PLAN EVALUATION; OPTIMIZATION; NUMERICAL SCORING; DOSE-VOLUME HISTOGRAM; TUMOR CONTROL PROBABILITY; NORMAL TISSUE COMPLICATION PROBABILITY ID BEAM RADIATION-THERAPY; OPTIMIZATION AB This is a report on numerical scoring techniques developed for the evaluation of treatment plans as part of a four-institution study of the role of 3-D planning in high energy external beam photon therapy. A formal evaluation process was developed in which plans were assessed by a clinician who displayed dose distributions in transverse, sagittal, coronal, and arbitrary oblique planes, viewed dose-volume histograms which summarized dose distributions to target volumes and the normal tissues of interest, and reviewed dose statistics which characterized the volume dose distribution for each plan. In addition, tumor control probabilities were calculated for each biological target volume and normal tissue complication probabilities were calculated for each normal tissue defined in the agreed-upon protocols. To score a plan, the physician assigned a score for each normal tissue to reflect possible complications; for each target volume two separate scores were assigned, one representing the adequacy of tumor coverage, the second the likelihood of a complication. After scoring each target and normal tissue individually, two summary scores were given, one for target coverage, the second reflecting the impact on all normal tissues. Finally, each plan was given an overall rating (which could include a downgrading of the plan if the treatment was judged to be overly complex). C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 30 TC 43 Z9 44 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 147 EP 163 PG 17 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100013 PM 1903371 ER PT J AU GOITEIN, M AF GOITEIN, M TI THE CLINICAL 3-DIMENSIONAL TREATMENT PLANNING STUDIES - A PROLOGUE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GOITEIN, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 165 EP 167 PG 3 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100014 ER PT J AU KUTCHER, GJ FUKS, Z BRENNER, H BROWN, AP BURMAN, C CHENG, E COIA, L KRIPPNER, K MANOLIS, JM MOHAN, R SIMPSON, JR URIE, M VIKRAM, B WALLACE, R AF KUTCHER, GJ FUKS, Z BRENNER, H BROWN, AP BURMAN, C CHENG, E COIA, L KRIPPNER, K MANOLIS, JM MOHAN, R SIMPSON, JR URIE, M VIKRAM, B WALLACE, R TI 3-DIMENSIONAL PHOTON TREATMENT PLANNING FOR CARCINOMA OF THE NASOPHARYNX SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE NASOPHARYNX; TREATMENT PLANNING; 3-DIMENSIONAL PLANNING ID RADIOTHERAPY AB The role of 3-D treatment planning for carcinoma of the nasopharynx was assessed in a four institution study. Two patients were worked up and had an extensive number of CT scans on which target volumes and normal tissues were defined. Treatment planning was then performed using state of the art dose planning systems for these patients to assess the value of the new technology. In general, it was demonstrated that multi-field conformal plans could achieve good tumor dose coverage, while at the same time reducing normal tissue doses, compared to standard treatment planning techniques. The role of inhomogeneity corrections, beam energy, and the use of CT vs. simulation films for defining target volumes were also discussed. In addition, techniques to evaluate 3-D plans for the nasopharynx were considered, and some analysis of this problem is presented in this paper. C1 CHAIM SHEBA MED CTR,TEL HAFHOMER HOSP,IL-52621 TEL HASHOMER,ISRAEL. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BETH ISRAEL MED CTR,DEPT RADIAT ONCOL,NEW YORK,NY 10003. RP KUTCHER, GJ (reprint author), MEM MED CTR,1275 YORK AVE,SPRINGFIELD,IL 62781, USA. FU NCI NIH HHS [N01 CM-47695, N01 CM-47696, N01 CM-47316] NR 15 TC 37 Z9 37 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 169 EP 182 PG 14 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100015 PM 2032886 ER PT J AU COIA, L GALVIN, J SONTAG, M BLITZER, P BRENNER, H CHENG, E DOPPKE, K HARMS, W HUNT, M MOHAN, R MUNZENRIDER, J SIMPSON, J AF COIA, L GALVIN, J SONTAG, M BLITZER, P BRENNER, H CHENG, E DOPPKE, K HARMS, W HUNT, M MOHAN, R MUNZENRIDER, J SIMPSON, J TI 3-DIMENSIONAL PHOTON TREATMENT PLANNING IN CARCINOMA OF THE LARYNX SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-DIMENSIONAL TREATMENT PLANNING; TISSUE INHOMOGENEITY CORRECTIONS; LARYNX CARCINOMA ID RADIATION-THERAPY; CANCER AB The role of three-dimensional (3-D) treatment planning in the definitive treatment of carcinoma of the larynx with radiation was evaluated at four institutions as part of an NCI contract. A total of 30 different treatment approaches were devised for two patients with larynx cancer. CT scans were obtained for both patients and various treatment planning tools were employed to optimize beam arrangements and to evaluate the resulting dose distribution. The effect on dose distribution of a number of factors was also examined: 1) the use of dose calculation algorithms which correct for tissue inhomogeneties, 2) the variation of the CT numbers used for inhomogeneity corrections to simulate inaccuracies in the knowledge of the CT numbers, and 3) the modification of beam energy. A multitude of data was used in plan evaluation and a numberical score was given to each plan to estimate the tumor control probability and the normal tissue complication probability. We found 3-D treatment planning to be of potential value in optimizing treatment plans in larynx cancer. Improved target coverage was achieved when complete information describing 3-D geometry of the anatomy was utilized. In some cases, the treatment planning tools employed, such as the beam's eye view, helped devise novel beam arrangements which were useful alternatives to standard techniques. We found little effect of change in CT number on dose distributions. A comparison between dose distributions calculated with tissue inhomogeneity corrections to those calculated without this correction showed little difference. We did find some improvement in the dose to the primary tumor volume at lower beam energies, but with an increased larynx volume potentially receiving doses above tolerance. C1 FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. RP COIA, L (reprint author), UNIV PENN,SCH MED,PHILADELPHIA,PA 19104, USA. FU NCI NIH HHS [N01 CM-47695, N01 CM-47696, N01 CM-47316] NR 18 TC 15 Z9 15 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 183 EP 192 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100016 PM 2032887 ER PT J AU SOLIN, LJ CHU, JCH SONTAG, MR BREWSTER, L CHENG, E DOPPKE, K DRZYMALA, RE HUNT, M KUSKE, R MANOLIS, JM MCCORMICK, B MUNZENRIDER, JE AF SOLIN, LJ CHU, JCH SONTAG, MR BREWSTER, L CHENG, E DOPPKE, K DRZYMALA, RE HUNT, M KUSKE, R MANOLIS, JM MCCORMICK, B MUNZENRIDER, JE TI 3-DIMENSIONAL PHOTON TREATMENT PLANNING OF THE INTACT BREAST SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE BREAST CANCER; RADIATION THERAPY; COMPUTED TOMOGRAPHY; TREATMENT PLANNING; PHOTONS ID RADIATION-THERAPY; CANCER; CT; IRRADIATION; CARCINOMA; TRIAL; BEAM AB Three-dimensional treatment planning for the intact breast was performed on two patients who had undergone CT scanning. A total of 38 treatment plans were evaluated. Multiple plans were evaluated for each patient including plans with and without inhomogeneity corrections, plans using varying photon energies of Co-60, 4 MV, 6 MV, 10 MV, and 15 MV, and three-dimensionally unconstrained plans. Increased hot spots were appreciated in the central axis plane when lung inhomogeneity corrections were used. Additional hot spots were appreciated in off-axis planes towards the cephalad and caudad aspects of the target volume because of lung inhomogeneity corrections and changes in the breast contour. The use of Co-60 was associated with an increase in the magnitude and volume of hot spots, whereas the use of higher energy photons such as 10 MV and 15 MV was associated with an unacceptable target coverage at shallow depths. Therefore, for the two patients studied, the use of a medium energy photon beam (such as from a 6 MV linear accelerator) appeared to be the energy of choice for treatment of the intact breast. The three-dimensionally unconstrained plans were able to improve slightly upon the standard plans, particularly with relationship of dose to normal tissue structures. Areas for future research were identified, including the use of tissue compensators. C1 WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MEM MED CTR,DEPT RADIAT THERAPY,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. MEM MED CTR,DEPT MED PHYS,SPRINGFIELD,IL 62781. MASSACHUSETTS GEN HOSP,DEPT RADIAT THERAPY,BOSTON,MA 02114. RP SOLIN, LJ (reprint author), FOX CHASE CANC INST,DEPT RADIAT ONCOL,7701 BURHOLME AVE,PHILADELPHIA,PA 19111, USA. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 29 TC 59 Z9 70 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 193 EP 203 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100017 PM 2032888 ER PT J AU BROWN, AP URIE, MM BAREST, G CHENG, E COIA, L EMAMI, BN GALVIN, J KUTCHER, J MANOLIS, J WONG, JW YAHALOM, J AF BROWN, AP URIE, MM BAREST, G CHENG, E COIA, L EMAMI, BN GALVIN, J KUTCHER, J MANOLIS, J WONG, JW YAHALOM, J TI 3-DIMENSIONAL PHOTON TREATMENT PLANNING FOR HODGKINS-DISEASE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-DIMENSIONAL RADIOTHERAPY; HODGKINS DISEASE ID RADIATION-THERAPY; STAGE-II; RADIOTHERAPY AB A multi-institutional study was undertaken using computerized planning systems to develop three-dimensional (3-D) radiotherapy plans for Hodgkin's disease (H.D.). Two patients, the first afflicted with bulky stage II disease and another one with early stage I H.D., were studied. Three main categories of plan were produced for each patient: a) a traditional plan which modelled a conventional mantle treatment on the 3-D system, b) a 3-D standard plan where anterior and posterior fields were designed to cover 3-D target volumes, and c) a 3-D unconstrained plan where innovational techniques were employed. Three-dimensional planning provides information about the dose distribution throughout the large volume irradiated in patients with H.D. that is not available with conventional mantle planning. The use of 3-D techniques resulted in improved tumor coverage, but by allowing for uncertainties such as motion, the doses to normal tissues tended to be higher. The use of unorthodox beam arrangements introduced added complexities, and further increased the lung doses. The most even dose distributions were obtained by incorporating compensating filters into anterior fields. Clinicians showed wide variations in their assessment of the plans, possible reasons for which are addressed in this paper. In addition, calculated probabilities from models of tumor control and normal tissue damage are also presented. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. FU NCI NIH HHS [N01 CM0-47695, N01 CM-47316, N01 CM-47696] NR 26 TC 14 Z9 14 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 205 EP 215 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100018 PM 2032889 ER PT J AU EMAMI, B PURDY, JA MANOLIS, J BAREST, G CHENG, E COIA, L DOPPKE, K GALVIN, J LOSASSO, T MATTHEWS, J MUNZENRIDER, J SHANK, B AF EMAMI, B PURDY, JA MANOLIS, J BAREST, G CHENG, E COIA, L DOPPKE, K GALVIN, J LOSASSO, T MATTHEWS, J MUNZENRIDER, J SHANK, B TI 3-DIMENSIONAL TREATMENT PLANNING FOR LUNG-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE LUNG CANCER; TREATMENT PLANNING; 3-DIMENSIONAL; RADIATION THERAPY ID COMPUTED-TOMOGRAPHY; CARCINOMA; DENSITY AB The experience of four institutions involved in a three-dimensional treatment planning contract (NCI) for lung cancer is described. It was found that three-dimensional treatment planning has a significant potential for optimization of treatment plans for radiotherapy of lung cancer both for tumor coverage and sparing of critical normal tissues within the complex anatomy of the human thorax. Evaluation tools, such as dose-volume histograms, and three-dimensional isodose displays, such as multiple plane views, surface dose displays, etc., were found to be extremely valuable in evaluation and comparison of these complex plans. It is anticipated that with further developments in three-dimensional simulation and treatment delivery systems, major progress towards uncomplicated local regional control of lung cancer may be forthcoming. C1 MEM MED CTR,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP EMAMI, B (reprint author), WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,4939 AUBUDON AVE,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [N01 CM-47695, N01 CM-47696, N01 CM-47316] NR 18 TC 47 Z9 49 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 217 EP 227 PG 11 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100019 PM 2032890 ER PT J AU MUNZENRIDER, JE DOPPKE, KP BROWN, AP BURMAN, C CHENG, E CHU, J CHUI, C DRZYMALA, RE GOITEIN, M MANOLIS, JM NORI, D SIMPSON, JR SOLIN, L URIE, MM AF MUNZENRIDER, JE DOPPKE, KP BROWN, AP BURMAN, C CHENG, E CHU, J CHUI, C DRZYMALA, RE GOITEIN, M MANOLIS, JM NORI, D SIMPSON, JR SOLIN, L URIE, MM TI 3-DIMENSIONAL TREATMENT PLANNING FOR PARAAORTIC NODE IRRADIATION IN PATIENTS WITH CERVICAL-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CERVIX CANCER; PARAAORTIC NODES; NORMAL TISSUE TOLERANCE; SMALL BOWEL; LARGE BOWEL; KIDNEY; SPINAL CORD; 3-DIMENSIONAL PLANNING ID EXTENDED-FIELD IRRADIATION; UTERINE CERVIX; CARCINOMA; METASTASES; RADIATION AB Three-dimensional treatment planning has been used by four cooperating centers to prepare and analyze multiple treatment plans on two cervix cancer patients. One patient had biopsy-proven and CT-demonstrable metastasis to the para-aortic nodes, while the other was at high risk for metastatic involvement of para-aortic nodes. Volume dose distributions were analyzed, and an attempt was made to define the role of 3-D treatment planning to the para-aortic region, where moderate to high doses (50-66 Gy) are required to sterilize microscopic and gross metastasis. Plans were prepared using the 3-D capabilities for tailoring fields to the target volumes, but using standard field arrangements (3-D standard), and with full utilization of the 3-D capabilities (3-D unconstrained). In some but not all 3-D unconstrained plans, higher doses were delivered to the large nodal volume and to the volume containing gross nodal disease than in plans analyzed but not prepared with full 3-D capability (3-D standard). The small bowel was the major dose limiting organ. Its tolerance would have been exceeded in all plans which prescribed 66 Gy to the gross nodal mass, although some reduction in small bowel near-maximum dose was achieved in the 3-D unconstrained plans. All plans were able to limit doses to other normal organs to tolerance levels or less, with significant reductions seen in doses to spinal cord, kidneys, and large bowel in the 3-D unconstrained plans, as compared to the 3-D standard plans. A high probability of small bowel injury was detected in one of four 3-D standard plans prescribed to receive 50 Gy to the large para-aortic nodal volume; the small bowel dose was reduced to an acceptable level in the corresponding 3-D unconstrained plan. An optimum beam energy for treating this site was not identified, with plans using 4, 6, 10, 15, 18, and 25 MV photons all being equally acceptable. Attempts to deliver moderate or high doses (50-66 Gy) to this region should be made only after careful analysis of the plan with techniques similar to those employed in this study. C1 WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MEM MED CTR,SPRINGFIELD,IL 62781. FU NCI NIH HHS [N01 CM-47316, N01 CM-47695, N01 CM-47696] NR 25 TC 8 Z9 8 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 229 EP 242 PG 14 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100020 PM 2032891 ER PT J AU SIMPSON, JR PURDY, JA MANOLIS, JM PILEPICH, MV BURMAN, C FORMAN, J FUKS, Z CHENG, E CHU, J MATTHEWS, J MOHAN, R SOLIN, L TEPPER, J URIE, M AF SIMPSON, JR PURDY, JA MANOLIS, JM PILEPICH, MV BURMAN, C FORMAN, J FUKS, Z CHENG, E CHU, J MATTHEWS, J MOHAN, R SOLIN, L TEPPER, J URIE, M TI 3-DIMENSIONAL TREATMENT PLANNING CONSIDERATIONS FOR PROSTATE-CANCER SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE PROSTATE CANCER; TREATMENT PLANNING; 3-DIMENSIONAL; RADIATION THERAPY ID CARCINOMA AB Over 300 treatment plans for a total of eight disease sites based on 3-D treatment planning considerations utilizing serial CT delineated target volumes were generated by four institutions as part of an NCI supported contract to both assess the current state-of-the-art capabilities and point directions for future efforts. Two patients with stage C prostate cancer were evaluated with protocol plans which required treatment of the prostate to 70 Gy and the pelvic lymph nodes to 46 Gy. When full 3-D target definition and multiple beam arrangements were employed, all institutions were able to submit plans which scored higher on tumor coverage and had lower normal tissue complication scores compared to traditional plans. The 3-D plans using standard beam arrangements, however, were often rated as highly as the 3-D unconstrained plans due to the multiple beam arrangements already selected to optimize standard plans at most institutions. For this site, heterogeneity corrections, beam energy changes and changes in CT number did not substantially change plan scores. C1 MEM MED CTR,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SIMPSON, JR (reprint author), WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,4939 AUDUBON AVE,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [N01 CM-47696, N01 CM-47695, N01 CM-47316] NR 8 TC 23 Z9 23 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 243 EP 252 PG 10 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100021 PM 2032892 ER PT J AU SHANK, B LOSASSO, T BREWSTER, L BURMAN, C CHENG, E CHU, JCH DRZYMALA, RE MANOLIS, J PILEPICH, MV SOLIN, LJ TEPPER, JE URIE, MM AF SHANK, B LOSASSO, T BREWSTER, L BURMAN, C CHENG, E CHU, JCH DRZYMALA, RE MANOLIS, J PILEPICH, MV SOLIN, LJ TEPPER, JE URIE, MM TI 3-DIMENSIONAL TREATMENT PLANNING FOR POSTOPERATIVE TREATMENT OF RECTAL-CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE 3-DIMENSIONAL TREATMENT PLANNING; DOSE-VOLUME HISTOGRAMS; BEAMS EYE VIEW; RECTAL CARCINOMA ID PREOPERATIVE IRRADIATION; RADIOTHERAPY; ADENOCARCINOMA; RADIATION AB The role of three-dimensional (3-D) treatment planning for postoperative radiation therapy was evaluated for rectal carcinoma as part of an NCI contract awarded to four institutions. It was found that the most important contribution of 3-D planning for this site was the ability to plan and localize target and normal tissues at all levels of the treatment volume, rather than using the traditional method of planning with only a single central transverse slice and simulation films. There was also a slight additional improvement when there were no constraints on the types of plans (i.e., when noncoplanar beams were used). Inhomogeneity considerations were not important at this site under the conditions of planning, i.e., with energies > 4 MV and multiple fields. Higher beam energies (15-25 MV) were preferred by a small margin over lower energies (down to 4 MV). The beam's eye view and dose-volume histograms were found quite useful as planning tools, but it was clear that work should continue on better 3-D displays and improved means of translating such plans to the treatment area. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. MEM MED CTR,SPRINGFIELD,IL 62781. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FOX CHASE CANC INST,PHILADELPHIA,PA 19111. WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. FU NCI NIH HHS [N01 CM-47316, N01 CM-47696, N01 CM-47695] NR 22 TC 11 Z9 13 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY 15 PY 1991 VL 21 IS 1 BP 253 EP 265 PG 13 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FM941 UT WOS:A1991FM94100022 PM 2032894 ER PT J AU WILLIAMS, WV KIEBEREMMONS, T WEINER, DB RUBIN, DH GREENE, MI AF WILLIAMS, WV KIEBEREMMONS, T WEINER, DB RUBIN, DH GREENE, MI TI CONTACT RESIDUES AND PREDICTED STRUCTURE OF THE REOVIRUS TYPE 3-RECEPTOR INTERACTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ANTIRECEPTOR ANTIBODY; MAMMALIAN REOVIRUS; CELL RECEPTORS; HEMAGGLUTININ; ATTACHMENT; BINDING; GLYCOPROTEINS; INHIBITION; IDIOTYPE; DOMAINS AB Sequence similarity between the reovirus type 3 hemagglutinin (HA3) and a anti-idiotypic monoclonal antibody (87.92.6) has been shown to define the site of interaction with a neutralizing (idiotypic) monoclonal antibody (9B.G5) and the cellular receptor for the virus. A synthetic peptide (V(L) peptide) derived from the anti-idiotypic sequence inhibits viral binding to the receptor. In this study, variants of the V(L) peptide were utilized to probe specific amino acid residues involved in binding the neutralizing antibody and the receptor. These studies indicate that the - OH groups of several residues are involved in contacting the reovirus type 3 receptor, including Tyr49, Ser50, Ser52, and Thr53 in the anti-idiotypic sequence, corresponding to Tyr326, Ser327, Ser329, and Ser325 in HA3, respectively. In contrast, only Ser50 of the anti-idiotypic sequence, corresponding to Ser327 of HA3, significantly altered neutralizing antibody binding. Additional studies implicate sialic acid as a potential reovirus type 3 receptor on some cells. This includes inhibition of binding of reovirus type 3 and 87.92.6 to L cells by heavily sialylated glycoproteins. Sialic acid was therefore utilized as a candidate receptor to analyze potential interaction schemes with HA3/87.92.6. Sequence similarity to other immunoglobulin structures with similar sequences allowed modeling of the three-dimensional structure of these epitopes. These structures, in combination with peptide studies, allow the development of a model of the interaction of these epitopes with sialic acid, which serves as a reovirus type 3 receptor. These models reveal that similar amino acid residues and side-chain geometries may be utilized by the reovirus type 3 and influenza hemagglutinins in their interactions with cell-surface receptors. C1 UNIV PENN,SCH MED,DEPT PATHOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MICROBIOL,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,DEPT MED,PHILADELPHIA,PA. WISTAR INST,PHILADELPHIA,PA 19104. RP WILLIAMS, WV (reprint author), UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104, USA. RI Weiner, David/H-8579-2014 NR 22 TC 36 Z9 36 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1991 VL 266 IS 14 BP 9241 EP 9250 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM038 UT WOS:A1991FM03800087 PM 1709165 ER PT J AU LUCCHESI, PA SWEADNER, KJ AF LUCCHESI, PA SWEADNER, KJ TI POSTNATAL CHANGES IN NA,K-ATPASE ISOFORM EXPRESSION IN RAT CARDIAC VENTRICLE - CONSERVATION OF BIPHASIC OUABAIN AFFINITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID (NA+ + K+)-ATPASE; SPONTANEOUSLY HYPERTENSIVE RATS; BINDING-SITES; CATALYTIC SUBUNIT; NA+,K+-ATPASE ACTIVITY; DEVELOPMENTAL-CHANGES; NA+/K+-ATPASE; HEART-MUSCLE; ISOZYME; MYOCYTES AB The cardiac glycoside sensitivity of the rat heart changes during postnatal maturation and in response to certain pathological conditions. The Na,K-ATPase is thought to be the receptor for cardiac glycosides, and there are three isozymes of its catalytic (alpha) subunit with different cardiac glycoside affinities: alpha-1 (low affinity) and alpha-2 and alpha-3 (high affinity). We examined the developmental expression of the alpha-subunit isozymes in rat ventricular membrane preparations by immunoblotting with isozyme-specific antibodies. The alpha-1 isozyme was present throughout all stages of maturation. A developmental switch from alpha-3 to alpha-2 occurred between 14 and 21 days after birth. Measurements of [H-3]ouabain binding and inhibition of Na,K-ATPase activity indicated that alpha-2 and alpha-3 should make equivalent contributions to ion pump capacity; in both neonatal and adult preparations, ouabain interacted with a single class of high-affinity binding sites (K(D) = 15 or 40 nM, respectively; B(max) = 4-5 pmol/mg protein), and at low concentrations produced a similar degree of Na,K-ATPase inhibition (25%). The results indicate that the developmental difference in cardiac glycoside sensitivity cannot be explained by quantitative differences in the proportion of high-affinity isozymes of the Na,K-ATPase. The switch from alpha-3 to alpha-2 coincides with other major changes in cardiac electrophysiology and calcium metabolism. C1 MASSACHUSETTS GEN HOSP,WELLMAN 4,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RI Lucchesi, Pamela/E-3558-2011 FU NHLBI NIH HHS [HL08110, HL36271] NR 51 TC 126 Z9 127 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1991 VL 266 IS 14 BP 9327 EP 9331 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM038 UT WOS:A1991FM03800100 PM 1851176 ER PT J AU DANG, LH ROCK, KL AF DANG, LH ROCK, KL TI STIMULATION OF LYMPHOCYTES-B THROUGH SURFACE IG RECEPTORS INDUCES LFA-1 AND ICAM-1-DEPENDENT ADHESION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HELPER T-CELLS; MAJOR HISTOCOMPATIBILITY COMPLEX; ANTIGEN-PRESENTING CELLS; SOLUBLE-PROTEIN ANTIGENS; IMMUNE-RESPONSE; PROLIFERATIVE RESPONSE; COGNATE INTERACTIONS; MURINE LYMPHOCYTES; MOLECULE-1 ICAM-1; MOUSE LYMPHOCYTES AB Engagement of the surface Ig receptor with anti-IgM antibodies stimulates murine B lymphocytes to markedly increase their expression of the cell adhesion molecules ICAM-1 and LFA-1. Stimulated B cells display increased homotypic adhesiveness and form spontaneous heterotypic conjugates with T lymphocytes. This latter T-B cell interaction is further enhanced if T cells have been previously activated with phorbol esters. In all cases, the formation of cell-cell conjugates is dependent on LFA-1-ICAM-1-mediated interactions as assessed in mAb blocking experiments. B lymphocytes stimulated with anti-IgM display a marked increase in binding to ICAM-1-transfected L cells. This cell-cell interaction is inhibited by anti-LFA-1 mAb binding to the B lymphocyte. Together, these results demonstrate that there is an induction of both ICAM-1 and LFA-1 on stimulated B cells and a corresponding increase in the adhesiveness of these cells. These findings suggest that Ag binding to the surface Ig receptor could prepare a B lymphocyte for subsequent interaction with a T lymphocyte. This provides insight into how efficient T-B collaboration may occur between very infrequent Ag-specific lymphocytes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-20248] NR 50 TC 78 Z9 78 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 MAY 15 PY 1991 VL 146 IS 10 BP 3273 EP 3279 PG 7 WC Immunology SC Immunology GA FL836 UT WOS:A1991FL83600002 PM 1673979 ER PT J AU MCGREW, JT ROCK, KL AF MCGREW, JT ROCK, KL TI ISOLATION, EXPRESSION, AND SEQUENCE OF THE TAP/LY-6A.2 CHROMOSOMAL GENE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL-ACTIVATING PROTEIN; BONE-MARROW CELLS; MONOCLONAL-ANTIBODY; MULTIGENE FAMILY; LY-6 LOCUS; T-CELLS; CDNA CHARACTERIZATION; LYMPHOCYTES-T; ANTIGEN; TAP AB The murine Ly-6 locus controls the expression of a number of genes. One of the products of the Ly-6 locus, Ly-6A.2, has been implicated in the process of T cell activation. We have identified the chromosomal sequences encoding the Ly-6A.2 molecule using very stringent hybridization and washing conditions. We confirmed that this gene encoded the Ly-6A.2 molecule by transfection studies using a cell line genetically negative for the Ly-6A.2 gene as a DNA recipient. Sequence analysis showed that the Ly-6A.2 gene is made up of four exons. The start site of transcription was determined by primer extension analysis. The first exon does not contain protein coding sequences. The structure of the Ly-6A.2 gene supports previous speculation that various Ly-6 RNA can be generated by alternate splicing events. The Ly-6A.2 chromosomal gene is closely related to the previously characterized Ly-6C.1 chromosomal gene in the intron, exon, and 5' flanking regions. This analysis indicates that these genes have arisen as a consequence of gene duplication. Although endogenous Ly-6A.2 and Ly-6C genes are IFN responsive, only the latter contains a clearly identifiable IFN responsive element. A transfected Ly-6A.2 chromosomal gene that contains 3.9 kb of 5'-untranslated sequence is IFN responsive. However, a shorter chromosomal clone containing only 940 bp of 5' sequence is constitutively expressed in transfectants but does not respond to IFN. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [T32 CA 09130-15]; NIGMS NIH HHS [R01 GM 38515] NR 47 TC 18 Z9 19 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 MAY 15 PY 1991 VL 146 IS 10 BP 3633 EP 3638 PG 6 WC Immunology SC Immunology GA FL836 UT WOS:A1991FL83600051 PM 1709198 ER PT J AU ANDREWS, NC FALLER, DV AF ANDREWS, NC FALLER, DV TI A RAPID MICROPREPARATION TECHNIQUE FOR EXTRACTION OF DNA-BINDING PROTEINS FROM LIMITING NUMBERS OF MAMMALIAN-CELLS SO NUCLEIC ACIDS RESEARCH LA English DT Note C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP ANDREWS, NC (reprint author), CHILDRENS HOSP MED CTR,DEPT PEDIAT,BOSTON,MA 02115, USA. OI Andrews, Nancy/0000-0003-0243-4462 NR 2 TC 2160 Z9 2184 U1 2 U2 18 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 MAY 11 PY 1991 VL 19 IS 9 BP 2499 EP 2499 DI 10.1093/nar/19.9.2499 PG 1 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FM145 UT WOS:A1991FM14500041 PM 2041787 ER PT J AU BADER, H ROSOWSKY, A AF BADER, H ROSOWSKY, A TI 1ST USE OF THE TAYLOR PTERIDINE SYNTHESIS AS A ROUTE TO POLYGLUTAMATE DERIVATIVES OF ANTIFOLATES .45. SO JOURNAL OF ORGANIC CHEMISTRY LA English DT Article ID GAMMA-GLUTAMYL METABOLITES; H35 HEPATOMA-CELLS; DIHYDROFOLATE-REDUCTASE; BIOLOGICAL EVALUATION; N-10-PROPARGYL-5,8-DIDEAZAFOLIC ACID; THYMIDYLATE SYNTHASE; FOLATE ANALOGS; FOLIC-ACID; METHOTREXATE; INHIBITION AB The di- through penta-gamma-L-glutamates of 2-desamino-2-methylaminopterin, a new antifolate with a novel mechanism of action requiring gamma-polyglutamylation for biological activity, were prepared. alpha-tert-Butyl gamma-methyl L-glutamate was condensed with 4-nitrobenzoyl chloride, the methyl ester selectively hydrolyzed with base, and the product condensed with di-tert-butyl L-glutamate to obtain tri-tert-butyl N-(4-nitrobenzoyl)-gamma-L-glutamyl-L-glutamate. Reduction of the nitro group followed by reaction with 2-amino-5-(chloromethyl)-pyrazine-3-carbonitrile yielded tri-tert-butyl [4-[[(2-amino-3-cyanopyrazin-5-yl)methyl]amino]benzoyl]-L-gamma-glutamyl-L-glutamate, which was heated with acetamidine acetate to form tri-tert-butyl N-[4-[[(4-amino-2-methylpteridine-6-yl)methyl]amino]benzoyl]-gamma-L-glutamyl-L-glutamate. Removal of the ester groups with trifluoroacetic acid then gave 2-desamino-2-methylaminopterin diglutamate. A similar sequence was employed to convert esterified oligomers with three, four, and five glutamyl residues to 2-desamino-2-methylaminopterin tri-, tetra-, and pentaglutamate. This is the first example of the preparation of the polyglutamates of an antifolate via the Taylor pteridine synthesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 23 TC 7 Z9 7 U1 1 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-3263 J9 J ORG CHEM JI J. Org. Chem. PD MAY 10 PY 1991 VL 56 IS 10 BP 3386 EP 3391 DI 10.1021/jo00010a038 PG 6 WC Chemistry, Organic SC Chemistry GA FL744 UT WOS:A1991FL74400038 ER PT J AU EZEKOWITZ, RAB WILLIAMS, DJ KOZIEL, H ARMSTRONG, MYK WARNER, A RICHARDS, FF ROSE, RM AF EZEKOWITZ, RAB WILLIAMS, DJ KOZIEL, H ARMSTRONG, MYK WARNER, A RICHARDS, FF ROSE, RM TI UPTAKE OF PNEUMOCYSTIS-CARINII MEDIATED BY THE MACROPHAGE MANNOSE RECEPTOR SO NATURE LA English DT Article ID INVITRO; ZYMOSAN; PHAGOCYTOSIS AB HUMAN exposure to Pneumocystis carinii is common 1,2 but, in the absence of acquired 3 or genetic 4 dysfunction of either cellular or humoral immunity, exposure rarely leads to illness. Although alveolar macrophages can degrade P. carinii 5,6, macrophage receptors involved in P. carinii recognition have not been clearly defined. Characterization of a predominant surface glycoprotein of the high mannose type 7,8 led us to investigate the role of the macrophage mannose receptor in this process. We report here that binding and uptake of cultured rat P. carinii by human and rat alveolar macrophages is reduced by 90% in the presence of competitive inhibitors of mannose receptor activity and by adherence of alveolar macrophages to mannan-coated surfaces. Further, only those COS cells transfected with the human macrophage mannose receptor complementary DNA that express surface mannose receptors bind and ingest P. carinii. These studies establish that the macrophage mannose receptor is sufficient for uptake of P. carinii and emphasize the role of the alveolar macrophage in first-line host defence against P. carinii. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MACARTHUR CTR MOLE PARASITOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT INTERNAL MED,PULM & CRIT CARE SECT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT EPIDEMIOL & PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,DIV PULM & CRIT CARE MED,BOSTON,MA 02215. HARVARD UNIV,SCH PUBL HLTH,DEPT RESP BIOL,BOSTON,MA 02115. RP EZEKOWITZ, RAB (reprint author), CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 21 TC 338 Z9 342 U1 3 U2 8 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAY 9 PY 1991 VL 351 IS 6322 BP 155 EP 158 DI 10.1038/351155a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FL035 UT WOS:A1991FL03500054 PM 1903183 ER PT J AU JELLINEK, MS MURPHY, JM BISHOP, S POITRAST, F QUINN, D AF JELLINEK, MS MURPHY, JM BISHOP, S POITRAST, F QUINN, D TI PROTECTING SEVERELY ABUSED AND NEGLECTED CHILDREN - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 LUMEN VITAE,BOSTON,MA 02108. RP JELLINEK, MS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 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 MAY 9 PY 1991 VL 324 IS 19 BP 1367 EP 1367 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FK186 UT WOS:A1991FK18600014 ER PT J AU HARRIS, WH AF HARRIS, WH TI JOINT-REPLACEMENT SURGERY - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID THROMBOSIS RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 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 MAY 9 PY 1991 VL 324 IS 19 BP 1368 EP 1368 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FK186 UT WOS:A1991FK18600017 ER PT J AU REERS, M SMITH, TW CHEN, LB AF REERS, M SMITH, TW CHEN, LB TI J-AGGREGATE FORMATION OF A CARBOCYANINE AS A QUANTITATIVE FLUORESCENT INDICATOR OF MEMBRANE-POTENTIAL SO BIOCHEMISTRY LA English DT Article ID RED-BLOOD-CELLS; MITOCHONDRIA; PROBES; RHODAMINE-123; MECHANISM; VESICLES AB The spectral properties of a novel membrane potential sensitive probe (JC-1) were characterized in aqueous buffers and in isolated cardiac mitochondria. JC-1 is a carbocyanine with a delocalized positive charge. It formed under favorable conditions a concentration-dependent fluorescent nematic phase consisting of J-aggregates. When excited at 490 nm, the monomers exhibited an emission maximum at 527 nm and J-aggregates at 590 nm. Increasing concentrations of JC-1 above a certain concentration caused a linear rise in the J-aggregate fluorescence, while the monomer fluorescence remained constant. The membrane potential of energized mitochondria (negative inside) promoted a directional uptake of JC-1 into the matrix, also with subsequent formation of J-aggregates. The J-aggregate fluorescence was sensitive to transient membrane potential changes induced by ADP and to metabolic inhibitors of oxidative phosphorylation. The J-aggregate fluorescence was found to be pH independent within the physiological pH range of 7.15-8.0 and could be linearly calibrated with valinomycin-induced K+ diffusion potentials. The advantage of JC-1 over rhodamines and other carbocyanines is that its color altered reversibly from green to red with increasing membrane potentials. This can be exploited for imaging live mitochondria on the stage of a microscope. C1 BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. HARVARD UNIV, DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. FU NHLBI NIH HHS [HL19259]; NIGMS NIH HHS [GM38318] NR 23 TC 682 Z9 688 U1 4 U2 44 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAY 7 PY 1991 VL 30 IS 18 BP 4480 EP 4486 DI 10.1021/bi00232a015 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK814 UT WOS:A1991FK81400015 PM 2021638 ER PT J AU GOUELI, SA HANTEN, JA AHMED, K AF GOUELI, SA HANTEN, JA AHMED, K TI MODULATION OF COFACTOR REQUIREMENT FOR THE ACTIVATION OF PROTEIN-KINASE-C BY HEPARIN - POSSIBLE EFFECT AT THE REGULATORY DOMAIN SO FEBS LETTERS LA English DT Article DE PROTEIN KINASE-C; HEPARIN; PHOSPHORYLATION; REGULATORY DOMAIN ID PURIFICATION; SUBSTRATE; ISOZYMES; CALCIUM AB Heparin was found to stimulate the phosphorylation of histone H1 but not protamine sulfate catalyzed by Ca2+/phospholipid-dependent protein kinase (protein kinase C or PKC). The effect of heparin on histone H1 phosphorylation appeared to be due to an increase in phosphatidylserine affinity of PKC activation in the presence of heparin. This effect of heparin was abolished when trypsinized, cofactor-independent, PKC was employed to phosphorylate histone H1. These studies suggest that heparin acts at the regulatory domain of PKC, and emphasize the importance of the negative charge in influencing the accessibility of the substrate to PKC action. C1 US DEPT VET AFFAIRS,MED CTR,1 VET DR,MINNEAPOLIS,MN 55417. UNIV MINNESOTA,SCH MED,CELLULAR & MOLEC BIOCHEM LAB 151,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,SCH MED,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. FU NCI NIH HHS [CA-15062, R01 CA015062] NR 13 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD MAY 6 PY 1991 VL 282 IS 2 BP 445 EP 448 DI 10.1016/0014-5793(91)80533-9 PG 4 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA FM908 UT WOS:A1991FM90800054 PM 2037060 ER PT J AU ROTHENBERG, PL LANE, WS KARASIK, A BACKER, J WHITE, M KAHN, CR AF ROTHENBERG, PL LANE, WS KARASIK, A BACKER, J WHITE, M KAHN, CR TI PURIFICATION AND PARTIAL SEQUENCE-ANALYSIS OF PP185, THE MAJOR CELLULAR SUBSTRATE OF THE INSULIN-RECEPTOR TYROSINE KINASE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH FACTOR-I; SODIUM DODECYL-SULFATE; DIMENSIONAL GEL-ELECTROPHORESIS; POLYACRYLAMIDE GELS; PROTEIN-KINASE; RAT ADIPOCYTES; ENDOGENOUS SUBSTRATE; INTACT-CELLS; STIMULATES PHOSPHORYLATION; AFFINITY-CHROMATOGRAPHY AB Insulin stimulates the tyrosine phosphorylation of a 185-kDa putative cytosolic substrate protein (pp185) in diverse cell types. After intravenous insulin infusion into the live intact rat, pp185 and the 95-kDa insulin receptor beta-subunit were the major proteins that tyrosine phosphorylated in liver, skeletal muscle, and adipose tissue. Both proteins were maximally phosphorylated within 30 s andboth increased in phosphotyrosine content in parallel with increasing insulin dose. However, pp185 tyrosine phosphorylation was transient, with almost complete dephosphorylation within 2-3 min despite continued insulin stimulation. To identify pp185 directly, we purified pp185 from insulin-stimulated rat liver, using a denaturation-based extraction procedure that blocks endogenous protein phosphatases and thus allows a high yield, single step isolation of phosphotyrosyl proteins by anti-phosphotyrosine antibody immunoaffinity absorption. From 50 rat livers, 50-100 pmol of pp185 was isolated. Edman degradation of seven internal tryptic peptide fragments of pp185 yielded novel amino acid sequences, indicating that pp185 is a new protein. Antipeptide antibodies were raised which specifically recognize a single, 185-kDa insulin-stimulated phosphotyrosyl protein in liver, skeletal muscle, adipose tissue, and several cultured cell lines. These results indicate that pp185 is expressed in a variety of insulin-responsive tissues is the major protein rapidly tyrosine phosphorylated under physiological conditions in the intact animal, and also provide a route for cloning the pp185 gene and elucidating the function of pp185 in insulin signal transduction. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIBET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOL,PROT MICROCHEM FACIL,CAMBRIDGE,MA 02138. NR 88 TC 199 Z9 200 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 MAY 5 PY 1991 VL 266 IS 13 BP 8302 EP 8311 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK441 UT WOS:A1991FK44100055 PM 2022647 ER PT J AU MOHAN, PS SPIRO, RG AF MOHAN, PS SPIRO, RG TI CHARACTERIZATION OF HEPARAN-SULFATE PROTEOGLYCAN FROM CALF LENS CAPSULE AND PROTEOGLYCANS SYNTHESIZED BY CULTURED LENS EPITHELIAL-CELLS - COMPARISON WITH OTHER BASEMENT-MEMBRANE PROTEOGLYCANS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ENDOTHELIAL-CELLS; CORE PROTEIN; MOUSE-TUMOR; IDENTIFICATION; COMPONENTS; LAMININ; CHROMATOGRAPHY; PRECURSOR; ADHESION; CHAINS AB After extraction with 4 M guanidinium chloride and purification by DEAE-cellulose chromatography, the heparan sulfate proteoglycan (HSPG) of calf anterior lens capsule was found to consist of two immunologically related components (M(r) = 340,000 and 250,000) which upon deglycosylation with trifluoromethanesulfonic acid yielded core proteins with M(r) values of 170,000 and 145,000. The heparan sulfate chains were uniform in size (M(r) = 14,000) and manifested a clustering of sulfate groups in a peripheral domain. From the decrease in M(r) observed after heparitinase digestion, it could be estimated that 6 and 11 glycosaminoglycan chains were present in the M(r) = 250,000 and 340,000 components respectively. The occurrence of N-linked oligosaccharides was evident from the size difference of the heparitinase- and trifluoromethane-sulfonic acid-treated proteoglycans (approximately 20 kDa), as well as from the presence of a substantial number of mannose residues; furthermore, interaction of the capsule proteoglycan with Bandeiraea simplicifolia I suggested that these carbohydrate units contains terminal alpha-D-Gal groups. Cultured lens epithelial cells deposited a single [S-35]sulfate-labeled proteoglycan into their matrix (M(r) = 400,000) which was immunologically related to the lens capsule proteoglycan and contained only heparan sulfate chains. In addition to this component, the medium from these cells contained an immunologically unrelated HSPG (M(r) = 150,000) as well as a chondroitin sulfate proteoglycan (M(r) = 240,000). Examination of bovine glomeruli indicated that, in addition to the previously described 200-kDa HSPG, an immunologically related 350-kDa component was also present. This size heterogeneity, which is comparable to that seen in the lens capsule, is most readily attributable to proteolytic processing of a precursor molecule. Studies with polyclonal antibodies demonstrated only limited cross-reactivities between the Engelbreth-Holms-Swarm proteoglycan and the components from lens capsule and glomerular basement membrane; since even the latter two differed somewhat in their antigenic sites, it would appear that cell- and species-dictated genetic differences as well as post-translational events contribute to the diversity observed in basement membrane HSPGs. C1 JOSLIN DIABET CTR,ELLIOTT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 17325] NR 39 TC 37 Z9 37 U1 1 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1991 VL 266 IS 13 BP 8567 EP 8575 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA FK441 UT WOS:A1991FK44100091 PM 2022669 ER PT J AU DAVIS, S LU, ML LO, SH LIN, S BUTLER, JA DRUKER, BJ ROBERTS, TM AN, Q CHEN, LB AF DAVIS, S LU, ML LO, SH LIN, S BUTLER, JA DRUKER, BJ ROBERTS, TM AN, Q CHEN, LB TI PRESENCE OF AN SH2 DOMAIN IN THE ACTIN-BINDING PROTEIN TENSIN SO SCIENCE LA English DT Article ID SMOOTH-MUSCLE VINCULIN; PHOSPHOLIPASE C-II; TYROSINE KINASES; FOCAL ADHESIONS; ALPHA-ACTININ; SARCOMA-VIRUS; CELLS; PHOSPHORYLATION; SIMILARITY; INVITRO AB The molecular cloning of the complementary DNA coding for a 90-kilodalton fragment of tensin, an actin-binding component of focal contacts and other submembraneous cytoskeletal structures, is reported. The derived amino acid sequence revealed the presence of a Src homology 2 (SH2) domain. This domain is shared by a number of signal transduction proteins including nonreceptor tyrosine kinases such as Abl, Fps, Src, and Src family members, the transforming protein Crk, phospholipase C-gamma-l, PI-3 (phosphatidylinositol) kinase, and guanosine triphosphatase-activating protein (GAP). Like the SH2 domain found in Src, Crk, and Abl, the SH2 domain of tensin bound specifically to a number of phosphotyrosine-containing proteins from v-src-transformed cells. Tensin was also found to be phosphorylated on tyrosine residues. These findings suggest that by possessing both actin-binding and phosphotyrosine-binding activities and being itself a target for tyrosine kinases, tensin may link signal transduction pathways with the cytoskeleton. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. JOHNS HOPKINS UNIV,DEPT BIOPHYS,BALTIMORE,MD 21218. FU NIGMS NIH HHS [GM 22289, GM 38318] NR 42 TC 209 Z9 210 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAY 3 PY 1991 VL 252 IS 5006 BP 712 EP 715 DI 10.1126/science.1708917 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FK185 UT WOS:A1991FK18500051 PM 1708917 ER PT J AU SMITH, DB SACKNOFF, R MARK, EJ HUANG, PL PETTIT, CK HARRIS, NL FIENBERG, R AMREIN, PC AF SMITH, DB SACKNOFF, R MARK, EJ HUANG, PL PETTIT, CK HARRIS, NL FIENBERG, R AMREIN, PC TI A 70-YEAR-OLD MAN WITH WALDENSTROMS MACROGLOBULINEMIA FOLLOWED BY RECURRENT LYMPHADENOPATHY AND FEVER - LARGE-CELL LYMPHOMA, IMMUNOBLASTIC-PLASMACYTOID TYPE, EVOLVING FROM SMALL-CELL LYMPHOCYTIC-PLASMACYTOID LYMPHOMA (RICHTERS SYNDROME) - WALDENSTROMS MACROGLOBULINEMIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID NON-HODGKINS LYMPHOMA; DIFFUSE HISTIOCYTIC LYMPHOMA; MALIGNANT-LYMPHOMA; MILIARY TUBERCULOSIS; PLEURAL EFFUSIONS; LEUKEMIA; DISEASE; FEATURES C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SMITH, DB (reprint author), MASSACHUSETTS GEN HOSP,MED,BOSTON,MA 02114, USA. NR 60 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 MAY 2 PY 1991 VL 324 IS 18 BP 1267 EP 1277 PG 11 WC Medicine, General & Internal SC General & Internal Medicine GA FJ823 UT WOS:A1991FJ82300008 ER PT J AU EAGLE, KA AF EAGLE, KA TI MEDICAL DECISION-MAKING IN PATIENTS WITH CHEST PAIN SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID CORONARY-CARE UNIT; MYOCARDIAL-INFARCTION; INTENSIVE-CARE; PREDICTIVE INSTRUMENT; EMERGENCY RP EAGLE, KA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 TC 13 Z9 13 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 2 PY 1991 VL 324 IS 18 BP 1282 EP 1283 DI 10.1056/NEJM199105023241811 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FJ823 UT WOS:A1991FJ82300011 PM 2014041 ER PT J AU SHIPP, MA STEFANO, GB SCHARRER, B REINHERZ, EL AF SHIPP, MA STEFANO, GB SCHARRER, B REINHERZ, EL TI CD10 (CALLA, COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN) NEUTRAL ENDOPEPTIDASE 24.11 (NEP, ENKEPHALINASE) - MOLECULAR-STRUCTURE AND ROLE IN REGULATING MET-ENKEPHALIN MEDIATED INFLAMMATORY RESPONSES SO ADVANCES IN NEUROIMMUNOLOGY LA English DT Review ID AMINO-ACID SEQUENCE; HUMAN-NEUTROPHILS; OPIOID NEUROPEPTIDES; DOWN-REGULATION; BETA-ENDORPHIN; GUINEA-PIG; MEMBRANE; METALLOENDOPEPTIDASE; PEPTIDES; CLONING AB CD10 (common acute lymphoblastic leukemia antigen, CALLA) is a 100 kDa cell surface glycoprotein (Brown et al., 1975; Ritz et al., 1980; Metzgar et al., 1981; Cossman et al., 1983; Graves et al., 1983; Shipp et al., 1988, 1989), expressed by acute lymphoblastic leukemias (Brown et al., 1975; Ritz et al., 1980), normal lymphoid progenitors (Greaves et al., 1983), mature polymorphonuclear leukocytes (Cossman et al., 1983) and certain non-hematopoietic cells (Metzgar et al., 1981). Molecular cloning and expression studies have shown that CD10 is the zinc metalloprotease, neutral endopeptidase 24.11 (NEP, "enkephalinase") (LeTarte et al., 1988; Shipp et al., 1988, 1989). CD10/NEP hydrolyzes a number of naturally occurring peptides including the endogenous opioid pentapeptides met- and leu- enkephalin. Hence, the enzyme in brain has been termed "enkephalinase" (Malfroy et al., 1978). In invertebrate organisms such as the mollusc M. edulis, met-enkephalin triggers inflammatory responses by inducing morphological changes, directed migration, and aggregation of hemocytes (Stefano et al., 1989a,b). We recently found that M. edulis hemocytes express a CD10/NEP related structure and that abrogation of CD10/NEP enzymatic activity reduces the amount of met-enkephalin required for hemocyte activation by five orders of magnitude (Shipp et al., 1990). Human CD10+ polymorphonuclear leukocytes are similarly responsive to met-enkephalin and inhibition of CDIO/NEP enzymatic activity dramatically potentiates met-enkephalin effects in these cells (Shipp et al., 1990). Therefore, CD10/NEP related structures modulate enkephalin-mediated inflammatory responses in organisms that are approximately 500 million years divergent in evolution (Meglitsch, 1967). These results suggest that in hematopoietic, and perhaps other cells, enkephalin signals are regulated via co-expression of cell surface opioid receptors and the CD10/NEP hydrolytic enzyme and that CD10/NEP functions to down-regulate induced responses to peptide hormones that are CD10/NEP substrates. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. SUNY COLL OLD WESTBURY,MULTIDISCIPLINARY CTR STUDY AGING,OLD WESTBURY,NY 11568. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT ANAT & STRUCT BIOL,BRONX,NY 10461. RP SHIPP, MA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,BOSTON,MA 02115, USA. NR 41 TC 5 Z9 5 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0960-5428 J9 ADV NEUROIMMUNOL JI Adv. Neuroimmunol. PD MAY PY 1991 VL 1 IS 2 BP 139 EP 149 DI 10.1016/S0960-5428(06)80218-4 PG 11 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA GQ142 UT WOS:A1991GQ14200004 ER PT J AU CONWAY, B TOMFORD, W MANKIN, HJ HIRSCH, MS SCHOOLEY, RT AF CONWAY, B TOMFORD, W MANKIN, HJ HIRSCH, MS SCHOOLEY, RT TI RADIOSENSITIVITY OF HIV-1 - POTENTIAL APPLICATION TO STERILIZATION OF BONE ALLOGRAFTS SO AIDS LA English DT Letter ID HUMAN IMMUNODEFICIENCY VIRUS; GAMMA-IRRADIATION; INACTIVATION C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPED,BOSTON,MA 02114. OTTAWA GEN HOSP,DIV INFECT DIS,OTTAWA K1H 8L6,ONTARIO,CANADA. RP CONWAY, B (reprint author), MASSACHUSETTS GEN HOSP,DEPT INFECT DIS,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA37461, CA12464]; NIAMS NIH HHS [AR21896] NR 12 TC 32 Z9 32 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0269-9370 J9 AIDS JI Aids PD MAY PY 1991 VL 5 IS 5 BP 608 EP 609 DI 10.1097/00002030-199105000-00029 PG 2 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA FR017 UT WOS:A1991FR01700029 PM 1863419 ER PT J AU CHAMBERS, RF TERADA, M KUFE, D OHNO, T AF CHAMBERS, RF TERADA, M KUFE, D OHNO, T TI SHAKING HIV-1 INFECTED-CELLS INDICATES NOVEL BEHAVIOR OF MN STRAIN SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; HTLV-III; ANTIBODIES; PREVALENCE; CD4 AB The shaking method of harvesting human immunodeficiency virus type 1 (HIV-1) is a powerful method of obtaining high titer, highly infective virus solutions. In this method infected cells are suspended in a small volune of liquid and the mixture is shaken. Viral infectivity, measured by tissue culture infective dose (TCID-50) studies, rises faster than virus titer, as measured by reverse transcriptase levels. It is postulated that this disproportionate increase in infectivity results from improved infectivity for the virus particles obtained from shaking the infected cells. Of the five strains of HIV-1 studied (IIIB, AL1212, 906, RJ4029, and MN), one strain, MN, behaved differently than the others. Upon shaking, its virus titer increased 18-fold, as opposed to the 5-10 fold increase demonstrated by the other strains. These results may indicate that MN virions are retained more on the surface of the infected cells, rather than budding off into the surrounding medium, than other HIV-1 strains. In support of this theory it was found that ratios of immunofluorescence assay scores to reverse transcriptase levels were higher for MN than for other strains. C1 JIKEI UNIV,TOKYO,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP CHAMBERS, RF (reprint author), NISSIN MOLEC BIOL INST,20 OVERLAND ST,BOSTON,MA 02215, USA. NR 12 TC 6 Z9 6 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1991 VL 7 IS 5 BP 459 EP 463 DI 10.1089/aid.1991.7.459 PG 5 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA FT600 UT WOS:A1991FT60000006 PM 1714747 ER PT J AU LERNER, MH DELUCA, SA AF LERNER, MH DELUCA, SA TI MEDIASTINAL GRANULOMA SECONDARY TO HISTOPLASMOSIS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Mediastinal granuloma is one of the many potential clinical manifestations of infection with Histoplasma capsulatum. Plain radiographs, computed tomography and magnetic resonance imaging can help identify intrathoracic adenopathy, calcification, and compression or invasion of vital structures. RP LERNER, MH (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD MAY PY 1991 VL 43 IS 5 BP 1649 EP 1651 PG 3 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA FK649 UT WOS:A1991FK64900012 PM 2021101 ER PT J AU SAKAI, T TOGUCHIDA, J OHTANI, N YANDELL, DW RAPAPORT, JM DRYJA, TP AF SAKAI, T TOGUCHIDA, J OHTANI, N YANDELL, DW RAPAPORT, JM DRYJA, TP TI ALLELE-SPECIFIC HYPERMETHYLATION OF THE RETINOBLASTOMA TUMOR-SUPPRESSOR GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SUSCEPTIBILITY GENE; HEREDITARY RETINOBLASTOMA; DNA METHYLATION; OSTEO-SARCOMA; DETERMINES METHYLATION; LINKAGE ANALYSIS; RB GENE; EXPRESSION; MUTATION; POLYMORPHISMS AB Inactivation of the retinoblastoma gene appears to have a fundamental role in the genesis of retinoblastoma, osteosarcoma, and other malignant tumors. The gene is generally inactivated because of loss-of-function mutations, although epigenetic phenomena, such as hypermethylation of the promoter region, could possibly have the same effect. We investigated the methylation pattern at the 5' end of the retinoblastoma gene, including its promoter region and exon 1, in DNA purified from 56 primary retinoblastomas. We found five tumors with evidence for hypermethylation, all from unilateral, simplex patients. No methylation abnormalities were detected in DNA purified from the leukocytes from these patients. It is interesting that in one of these tumors the hypermethylation was confined to one allele. There were no mutations in a 1,306-bp sequence including the hypermethylated region that might account for the allele-specific hypermethylation. We believe that the hypermethylation of the retinoblastoma gene that we found in these tumors corresponds to the allelic inactivation of the gene, and we speculate that erroneous hypermethylation without alteration of nucleotide sequence occasionally plays a role in the genesis of this cancer. If this is true, then retinoblastomas with hypermethylation might be treatable with chemotherapeutic agents that interfere with methylation of DNA. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. FU NEI NIH HHS [EY05321, EY07573] NR 36 TC 370 Z9 385 U1 0 U2 7 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAY PY 1991 VL 48 IS 5 BP 880 EP 888 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA FK897 UT WOS:A1991FK89700007 PM 1673287 ER PT J AU CLINKINGBEARD, C LAWRENCE, D SHENKER, Y AF CLINKINGBEARD, C LAWRENCE, D SHENKER, Y TI EFFECT OF VARYING POTASSIUM INTAKE ON ATRIAL NATRIURETIC HORMONE-INDUCED SUPPRESSION OF ALDOSTERONE SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Note DE ATRIAL NATRIURETIC HORMONE; ALDOSTERONE; POTASSIUM INTAKE; RENIN-ANGIOTENSIN SYSTEM AB To further assess the mechanism of atrial natriuretic hormone (ANH) induced suppression of aldosterone, we infused 0.5 pmol/kg/min Ser-Tyr28 human ANH over 2 h under three dietary conditions: low salt (LS), low potassium (LK), and high potassium (HK). The diets were consumed for 3 days before each study day. After 3 days of LK diet, blood pressure was slightly higher than under the other conditions. Serum potassium on LK was significantly lower than on HK (3.8 +/- 0.1 upsilon 4.3 +/- 0.2). The ANH infusion did not cause any changes in blood pressure or urinary sodium and potassium excretion. Urine volume increased with ANH infusion under all diet conditions. Plasma renin activity and plasma angiotensin II levels were significantly lower on LK than on LS or HK, probably reflecting sodium retention. Increase in plasma ANH levels of about 75% (well within normal range) suppressed all hormonal parameters on LS and HK diets, but had no significant effect on LK diet. The pattern of aldosterone changes closely followed the changes in the renin-angiotensin system. We conclude that under various physiologic conditions ANH suppresses aldosterone predominantly through suppression of renin. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705. FU NCRR NIH HHS [RR-03186]; NIDDK NIH HHS [R29-DK-39444] NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD MAY PY 1991 VL 4 IS 5 BP 456 EP 459 PN 1 PG 4 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FK921 UT WOS:A1991FK92100012 PM 1829901 ER PT J AU DOMINGUES, RC TAVERAS, JM REIMER, P ROSEN, BR AF DOMINGUES, RC TAVERAS, JM REIMER, P ROSEN, BR TI FORAMEN MAGNUM CHOROID-PLEXUS PAPILLOMA WITH DROP METASTASES TO THE LUMBAR SPINE SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article RP DOMINGUES, RC (reprint author), MASSACHUSETTS GEN HOSP,NMR CTR,BOSTON,MA 02129, USA. NR 8 TC 35 Z9 35 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD MAY-JUN PY 1991 VL 12 IS 3 BP 564 EP 565 PG 2 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA FJ904 UT WOS:A1991FJ90400042 PM 2058519 ER PT J AU TITUS, MND GALL, NG YERXA, EJ ROBERSON, TA MACK, W AF TITUS, MND GALL, NG YERXA, EJ ROBERSON, TA MACK, W TI CORRELATION OF PERCEPTUAL PERFORMANCE AND ACTIVITIES OF DAILY LIVING IN STROKE PATIENTS SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article DE ASSESSMENT PROCESS; OCCUPATIONAL THERAPY; CEREBROVASCULAR DISORDERS; PERCEPTUAL DISORDERS; SELF CARE ID CONSTRUCTIONAL APRAXIA; CEREBRAL LESIONS; REHABILITATION C1 AUDIE L MURPHY MEM VET ADM MED CTR,REHABIL MED,SAN ANTONIO,TX 78284. UNIV SO CALIF,DEPT OCCUPAT THERAPY,LOS ANGELES,CA 90089. NO CALIF CTR REHABIL,SACRAMENTO,CA. UNIV SO CALIF,DEPT PREVENT MED,LOS ANGELES,CA 90089. RP TITUS, MND (reprint author), SAN ANTONIO WARM SPRINGS REHABIL HOSP,OCCUPAT THERAPY,5101 MED DR,SAN ANTONIO,TX 78229, USA. NR 56 TC 31 Z9 31 U1 0 U2 1 PU AMER OCCUPATION THERAPY ASSN PI ROCKVILLE PA 1383 PICCARD DRIVE PO BOX ROCKVILLE, MD 20850-4375 SN 0272-9490 J9 AM J OCCUP THER JI Am. J. Occup. Ther. PD MAY PY 1991 VL 45 IS 5 BP 410 EP 418 PG 9 WC Rehabilitation SC Rehabilitation GA FH399 UT WOS:A1991FH39900004 PM 2048622 ER PT J AU KIVELA, T VIRTANEN, I MARCUS, DM OBRIEN, JM CARPENTER, JL BRAUNER, E TARKKANEN, A ALBERT, DM AF KIVELA, T VIRTANEN, I MARCUS, DM OBRIEN, JM CARPENTER, JL BRAUNER, E TARKKANEN, A ALBERT, DM TI NEURONAL AND GLIAL PROPERTIES OF A MURINE TRANSGENIC RETINOBLASTOMA MODEL SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID SUSCEPTIBILITY GENE; TRILATERAL RETINOBLASTOMA; INTERMEDIATE FILAMENTS; BILATERAL RETINOBLASTOMA; HUMAN RETINA; PRODUCT; DIFFERENTIATION; IDENTIFICATION; SYNAPTOPHYSIN; PROTEINS AB Antigenic properties of a murine transgenic model for hereditary retinoblastoma, induced by a chimeric gene coding for Simian virus 40 large T antigen, an oncogene that inactivates the retinoblastoma susceptibility gene product, were studied by immunohistochemistry. All transgenic mice develop bilateral intraocular retinal tumors in the inner nuclear layer with Homer Wright-like rosettes, and one quarter develop midbrain tumors resembling trilateral retinoblastoma. Cell lines TE-1 and TM-1 were established from intraocular and metastatic tumors, respectively. Intraocular tumors reacted with antibodies to neuron-specific enolase and synaptophysin, while vimentin, glial fibrillary acidic, and S-100 proteins were detected only in reactive glia derived from adjacent retina. The midbrain tumors showed weak reactivity to synaptophysin, and they blended with reactive astrocytes positive for glial markers. The tumors were negative for cytokeratins. Finally both derived cell lines expressed synaptophysin and individual neurofilament triplet proteins in immunofluorescence and Western blotting, supporting their essentially neuronal nature. The antigenic profile resembles human retinoblastoma, but differences in morphology and antigen distribution suggest a more close relationship to neurons of the inner nuclear layer than to photoreceptor cells. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DAVID G COGAN EYE PATHOL LAB,BOSTON,MA 02114. ANGELL MEM ANIM HOSP,DEPT PATHOL & MED,BOSTON,MA. UNIV HELSINKI,DEPT OPHTHALMOL,SF-00100 HELSINKI 10,FINLAND. UNIV HELSINKI,DEPT ANAT,SF-00100 HELSINKI 10,FINLAND. RI Kivela, Tero/C-9241-2009 OI Kivela, Tero/0000-0003-1198-4394 FU NEI NIH HHS [EYO1917] NR 48 TC 20 Z9 21 U1 1 U2 1 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAY PY 1991 VL 138 IS 5 BP 1135 EP 1148 PG 14 WC Pathology SC Pathology GA FK717 UT WOS:A1991FK71700010 PM 1708946 ER PT J AU FLETCHER, JA PINKUS, GS WEIDNER, N MORTON, CC AF FLETCHER, JA PINKUS, GS WEIDNER, N MORTON, CC TI LINEAGE-RESTRICTED CLONALITY IN BIPHASIC SOLID TUMORS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID PULMONARY HAMARTOMA; ESTROGEN-RECEPTOR; FIBROADENOMA; TISSUE; GROWTH; CHROMOSOMES; CARCINOMA; LEUKEMIA; BREAST; CELLS AB Cytogenetic analysis of two pulmonary chondroid hamartomas and nine breast adenofibromas revealed clonal chromosome aberrations in both hamartomas and in four breast tumors. To determine lineage of the cells with chromosome aberrations, a combined immunohistochemical/cytogenetic approach was developed that enabled simultaneous ascertainment of cytogenetic aberrations and immunohistochemical features in individual cells. Immunohistochemical/cytogenetic evaluation of one harmartoma and two adenofibromas demonstrated that neoplastic proliferation, in each case, was confined to the mesenchymal (stromal) component, whereas epithelial cells appeared to be reactive. Cytogenetically abnormal short-term cultures of the remaining hamartoma and another of the breast adenofibromas were composed entirely of mesenchymal elements, indicating mesenchymal clonality in those tumors as well. Our findings support redesignation of pulmonary chondroid hamartomas as 'pulmonary chondromas' and suggest that carcinomas developing within fibroadenomas arise from reactive epithelial proliferation. Combined immunohistochemical/cytogenetic analysis might be useful in the development of novel therapeutic approaches that selectively target neoplastic populations within solid tumors. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL 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 28 TC 76 Z9 76 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 MAY PY 1991 VL 138 IS 5 BP 1199 EP 1207 PG 9 WC Pathology SC Pathology GA FK717 UT WOS:A1991FK71700016 PM 1708947 ER PT J AU GUTMANN, EJ NILES, JL MCCLUSKEY, RT BROWN, D AF GUTMANN, EJ NILES, JL MCCLUSKEY, RT BROWN, D TI LOSS OF ANTIGENS ASSOCIATED WITH THE APICAL ENDOCYTOTIC PATHWAY IN PROXIMAL TUBULES FROM RATS WITH HEYMANN NEPHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID EXPERIMENTAL MEMBRANOUS NEPHROPATHY; ANTIBODY-MEDIATED INJURY; EPITHELIAL-CELLS; BRUSH-BORDER; COATED PITS; IMMUNOELECTRON MICROSCOPY; INDUCED REDISTRIBUTION; PATHOGENIC ANTIGEN; IMMUNE-COMPLEXES; KIDNEY AB In addition to the glomerular lesions associated with Heymann nephritis, a rat model of human membranous nephritis, proximal tubule damage, and a perturbation of proximal tubule function also have been reported to occur in this disease. The aim of the present study was to examine in more detail the nature of the apical plasma membrane damage in proximal tubules using specific antibodies directed against clathrin, gp330, and a proton-pumping adenosine triphosphatase, all of which are components of the apical endocytotic apparatus of these epithelial cells. Immunocytochemical studies revealed a marked reduction in staining for all three antigens in proximal tubules from rats with active Heymann nephritis. Furthermore endocytotic uptake of intravenously injected FITC-dextran was considerably lower in diseased animals than in normal rats. Gp330 and rat IgG were identified as components of the luminal debris that accumulated during the course of Heymann nephritis. These results show that perturbation of proximal tubule endocytosis occurs in Heymann nephritis together with a loss of three apical antigens that are normally localized on membrane domains associated with the apical endocytotic pathway in these cells. The results also suggest that antibody-antigen complexes may be shed from the plasma membrane in both the glomerulus and the proximal tubule in this disease. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MED SERV,RENAL UNIT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-18729, DK-38452, DK-07540] NR 46 TC 9 Z9 9 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 MAY PY 1991 VL 138 IS 5 BP 1243 EP 1255 PG 13 WC Pathology SC Pathology GA FK717 UT WOS:A1991FK71700020 PM 1708948 ER PT J AU SHIBA, E LINDON, JN KUSHNER, L MATSUEDA, GR HAWIGER, J KLOCZEWIAK, M KUDRYK, B SALZMAN, EW AF SHIBA, E LINDON, JN KUSHNER, L MATSUEDA, GR HAWIGER, J KLOCZEWIAK, M KUDRYK, B SALZMAN, EW TI ANTIBODY-DETECTABLE CHANGES IN FIBRINOGEN ADSORPTION AFFECTING PLATELET ACTIVATION ON POLYMER SURFACES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MONOCLONAL ANTIBODIES; POLYALKYL METHACRYLATE POLYMERS ID RECEPTOR RECOGNITION DOMAINS; CARBOXY-TERMINAL SEGMENT; VON WILLEBRAND FACTOR; GAMMA-CHAIN; INDUCED THROMBOSIS; ALPHA-CHAIN; ADHESION; BINDING; PLASMA; SITE AB Reactivity of platelets with an artificial surface exposed to whole blood is correlated with the concentration of adsorbed fibrinogen detectable by antifibrinogen antibodies. To examine the effect on platelets of the organization (distribution, orientation, conformation) of fibrinogen adsorbed on a hydrophobic surface, we studied the binding of polyclonal and monoclonal antifibrinogen antibodies to polyalkyl methacrylate polymers previously exposed to purified fibrinogen solution or diluted plasma and compared the results with platelet retention in methacrylate bead columns. There was an increase in platelet retention following diluted plasma pretreatment, which was eliminated by a polyclonal antibody against fibrinogen or against a gamma-(395-411) peptide from fibrinogen and was reduced by monoclonal antibodies (4A5, 4-2) against other COOH-terminal gamma-chain epitopes. Monoclonal antibody 10E5 against the fibrinogen receptor GpIIb/IIIa totally inhibited platelet retention in the bead columns. Our data suggest that different methacrylate polymers induce different changes in adsorbed fibrinogen, which may interfere with its interaction with platelets, and that platelet retention in a methacrylate bead column involves interaction of the COOH-terminal end of the gamma-chain of adsorbed fibrinogen with platelet GpIIb/IIIa receptors. C1 BETH ISRAEL HOSP,BOSTON,MA 02215. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NEW YORK BLOOD CTR,NEW YORK,NY 10021. FU NHLBI NIH HHS [HL-37610, HL-28015, HL-25066] NR 42 TC 48 Z9 48 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAY PY 1991 VL 260 IS 5 BP C965 EP C974 PN 1 PG 10 WC Physiology SC Physiology GA FM776 UT WOS:A1991FM77600009 PM 2035620 ER PT J AU THOMAS, JD NEWELL, JB CHOONG, CYP WEYMAN, AE AF THOMAS, JD NEWELL, JB CHOONG, CYP WEYMAN, AE TI PHYSICAL AND PHYSIOLOGICAL DETERMINANTS OF TRANSMITRAL VELOCITY - NUMERICAL-ANALYSIS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE ECHOCARDIOGRAPHY; DOPPLER; DIASTOLIC FUNCTION; MATHEMATICAL MODEL; COMPUTER SIMULATION; COMPLIANCE; RELAXATION; VENTRICULAR FILLING ID VENTRICULAR DIASTOLIC FUNCTION; 3-DIMENSIONAL COMPUTATIONAL METHOD; PRESSURE-VOLUME RELATION; CANINE LEFT-VENTRICLE; DOPPLER ECHOCARDIOGRAPHY; MITRAL-VALVE; FILLING DYNAMICS; FLUID-DYNAMICS; LEFT ATRIAL; BLOOD-FLOW AB The Doppler transmitral velocity curve is commonly used to assess left ventricular diastolic function. Recent investigations, however, relating Doppler mitral indexes to ventricular compliance, relaxation, and preload have been inconclusive and at times contradictory. We used a mathematical formulation to study the physical and physiological determinants of the transmitral velocity pattern for exponential chamber pressure-volume relationships with active ventricular relaxation (2,187 combinations investigated). We showed that transmitral velocity is fundamentally affected by two principal physical determinants, the transmitral pressure difference and the net atri-oventricular compliance, as well as the impedance characteristics of the mitral valve. These physical determinants in turn are specified by the compliance and relaxation parameters of physiological interest. We found that the peak mitral velocity is most strongly related to initial left atrial pressure but lowered by prolonged relaxation, low atrial and ventricular compliance, and systolic dysfunction. Peak acceleration varies directly with atrial pressure and inversely with the time constant of isovolumic relaxation, with little influence of compliance, whereas the mitral deceleration rate is approximately valve area divided by atrioventricular compliance. We then used these data to suggest possible strategies for improved analysis of noninvasive data (Doppler indexes, planimetered valve area, and isovolumic relaxation time) to estimate ventricular compliance and relaxation and atrial pressure. RP THOMAS, JD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NONINVAS CARDIAC LAB,0 EMERSON PL,SUITE 2F,BOSTON,MA 02114, USA. NR 47 TC 82 Z9 82 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAY PY 1991 VL 260 IS 5 BP H1718 EP H1730 PN 2 PG 13 WC Physiology SC Physiology GA FM778 UT WOS:A1991FM77800043 ER PT J AU BIEDERMAN, J NEWCORN, J SPRICH, S AF BIEDERMAN, J NEWCORN, J SPRICH, S TI COMORBIDITY OF ATTENTION-DEFICIT HYPERACTIVITY DISORDER WITH CONDUCT, DEPRESSIVE, ANXIETY, AND OTHER DISORDERS SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Review ID MINIMAL BRAIN-DYSFUNCTION; CO-MORBIDITY; FOLLOW-UP; CHILDHOOD HYPERACTIVITY; PSYCHIATRIC STATUS; TOURETTES SYNDROME; CLINICAL CHARACTERISTICS; GENERAL-POPULATION; BEHAVIOR DISORDERS; REFERRED CHILDREN AB Objective: Attention deficit hyperactivity disorder is a heterogeneous disorder of unknown etiology. Little is known about the comorbidity of this disorder with disorders other than conduct. Therefore, the authors made a systematic search of the psychiatric and psychological literature for empirical studies dealing with the comorbidity of attention deficit hyperactivity disorder with other disorders. Data Collection: The search terms included hyperactivity, hyperkinesis, attention deficit disorder, and attention deficit hyperactivity disorder, cross-referenced with antisocial disorder (aggression, conduct disorder, antisocial disorder), depression (depression, mania, depressive disorder, bipolar), anxiety (anxiety disorder, anxiety), learning problems (learning, learning disability, academic achievement), substance abuse (alcoholism, drug abuse), mental retardation, and Tourette's disorder. Findings: The literature supports considerable comorbidity of attention deficit hyperactivity disorder with conduct disorder, oppositional defiant disorder, mood disorders, anxiety disorders, learning disabilities, and other disorders, such as mental retardation, Tourette's syndrome, and borderline personality disorder. Conclusions: Subgroups of children with attention deficit hyperactivity disorder might be delineated on the basis of the disorder's comorbidity with other disorders. These subgroups may have differing risk factors, clinical courses, and pharmacological responses. Thus, their proper identification may lead to refinements in preventive and treatment strategies. Investigation of these issues should help to clarify the etiology, course, and outcome of attention deficit hyperactivity disorder. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT ACC725,FRUIT ST,BOSTON,MA 02114, USA. OI Newcorn, Jeffrey /0000-0001-8993-9337 NR 118 TC 962 Z9 976 U1 14 U2 208 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAY PY 1991 VL 148 IS 5 BP 564 EP 577 PG 14 WC Psychiatry SC Psychiatry GA FJ317 UT WOS:A1991FJ31700002 PM 2018156 ER PT J AU TORRY, DS FAULK, WP MCINTYRE, JA AF TORRY, DS FAULK, WP MCINTYRE, JA TI TROPHOBLAST IMMUNITY IN HUMAN-PREGNANCY DEFINED BY ANTIIDIOTYPE SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Article DE REPRODUCTION; PLACENTA; ANTIBODY; IMMUNOREGULATION ID INTRAVENOUS GAMMA-GLOBULIN; SECONDARY ABORTER SERA; CLASS-I HLA; IMMUNOGLOBULIN CLASS; SUBCLASS RESPONSES; CHORIONIC VILLI; ANTIGENS; AUTOANTIBODIES; EXPRESSION; ANTIBODY AB Successful reproduction in mammals requires the mother to immunologically accept genetically disparate tissues. Allotypic trophoblast antigens (TLX) are thought to be responsible for influencing maternal acceptance of the feto-placental graft, and faulty regulation of immunity to TLX antigens has been associated with recurrent pregnancy losses. In this report, rabbit antiidiotype (RAb2) was produced to a human TLX antibody (Ab1). This RAb2 detected TLX cross-reactive idiotypes (CRI) on antitrophoblast IgG from women with normal and abnormal pregnancies. These findings support an hypothesis that women respond immunologically to allotypic trophoblast antigens, and that idiotype-antiidiotype regulation of this response is characteristic of normal pregnancy. C1 METHODIST HOSP INDIANA,CTR REPROD & TRANSPLANTAT IMMUNOL,1701 N SENATE BLVD,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR MOLEC CARCINOGENESIS,BOSTON,MA 02115. NR 33 TC 11 Z9 11 U1 0 U2 2 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 MAY PY 1991 VL 25 IS 4 BP 181 EP 184 PG 4 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA GH653 UT WOS:A1991GH65300008 PM 1786088 ER PT J AU CHEW, FS DISLER, DG AF CHEW, FS DISLER, DG TI CHONDROSARCOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 2 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 MAY PY 1991 VL 156 IS 5 BP 1016 EP 1016 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH751 UT WOS:A1991FH75100025 PM 2017923 ER PT J AU YOUNG, RH GILKS, CB SCULLY, RE AF YOUNG, RH GILKS, CB SCULLY, RE TI MUCINOUS TUMORS OF THE APPENDIX ASSOCIATED WITH MUCINOUS TUMORS OF THE OVARY AND PSEUDOMYXOMA PERITONEI - A CLINICOPATHOLOGICAL ANALYSIS OF 22 CASES SUPPORTING AN ORIGIN IN THE APPENDIX SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE OVARY; MUCINOUS TUMOR; APPENDIX MUCINOUS TUMOR; PSEUDOMYXOMA PERITONEI; MUCINOUS CYSTADENOMA; MUCINOUS CYSTADENOMA OF BORDERLINE MALIGNANCY ID BORDERLINE MALIGNANCY; EPITHELIAL TUMORS; CYSTADENOCARCINOMA; CYSTADENOMAS; CARCINOMAS; NEOPLASMS; MUCOCELES; BENIGN AB Twenty-two cases in which mucinous tumors of the appendix were associated with mucinous tumors of the ovary are reported. The patients ranged from 23 to 83 (average 49) years of age and usually presented with increasing abdominal girth. The appendiceal and ovarian tumors were synchronous in 21 cases. Laparotomy typically disclosed large cystic ovarian tumors that averaged 16 cm in diameter and were usually multilocular, an appendix that was usually dilated and covered with mucus, and abundant intra-abdominal mucus. The ovarian tumors were bilateral in seven cases. The ovarian and appendiceal tumors were typically similar histologically, with features similar to those of ovarian mucinous cyst-adenomas and cystadenomas of borderline malignancy. In most of the ovarian tumors, mucin dissected through the ovarian stroma (so-called pseudomyxoma ovarii). Eight of the 20 patients with follow-up information were well when last seen, but the duration of follow-up was 3 years or less in six of them. Two patients died of pseudomyxoma peritonei 4 and 5.5 years after presentation. One patient died of a myocardial infarct shortly after laparotomy for recurrent pseudomyxoma peritonei at 11 years. The remaining patients had definite or probable recurrent or residual disease but were alive at the time of the last follow-up information. The typical synchronous presentation of the ovarian and appendiceal tumors, their histologic similarity, the frequency of bilaterality of the ovarian tumors, the predominance of right-sided ovarian involvement, and the usual presence of mucin and atypical mucinous cells on the ovarian surfaces all point toward the probable secondary nature of the ovarian tumors. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 60 TC 221 Z9 226 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAY PY 1991 VL 15 IS 5 BP 415 EP 429 DI 10.1097/00000478-199105000-00001 PG 15 WC Pathology; Surgery SC Pathology; Surgery GA FH203 UT WOS:A1991FH20300001 PM 2035736 ER PT J AU MAYTIN, EV LEVIN, EN ANDERSON, RR AF MAYTIN, EV LEVIN, EN ANDERSON, RR TI A LASER DENSITOMETER FOR SELECTIVE SPOT ANALYSIS ON DOT BLOTS AND 2-DIMENSIONAL GEL AUTORADIOGRAMS SO ANALYTICAL BIOCHEMISTRY LA English DT Article ID TWO-DIMENSIONAL GELS; COMPUTER-ANALYSIS; ELECTROPHORESIS; PROTEINS C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP MAYTIN, EV (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,WELLMAN 2,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5T32ARO7098-15] NR 17 TC 6 Z9 6 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 0003-2697 J9 ANAL BIOCHEM JI Anal. Biochem. PD MAY 1 PY 1991 VL 194 IS 2 BP 284 EP 294 DI 10.1016/0003-2697(91)90231-H PG 11 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA FJ174 UT WOS:A1991FJ17400009 PM 1862932 ER PT J AU MCKEE, MD AOBA, T MORENO, EC AF MCKEE, MD AOBA, T MORENO, EC TI MORPHOLOGY OF THE ENAMEL ORGAN IN THE MINIATURE SWINE SO ANATOMICAL RECORD LA English DT Article ID RAT INCISOR AMELOBLASTS; SECRETORY AMELOBLASTS; FINE-STRUCTURE; AUTORADIOGRAPHIC EVIDENCE; ELECTRON-MICROSCOPY; MATURATION PATTERN; FREEZE-FRACTURE; MATURING ENAMEL; GOLGI-APPARATUS; STAINING METHOD AB In recent years, the dentition of the pig has been increasingly used as a model for the study of amelogenesis. Indeed, much of our current knowledge on enamel formation derives from biochemical and physicochemical analyses of the organic and inorganic components, respectively, of porcine enamel. As an extension of this previous work, and as the first step in our attempt to correlate known enamel matrix and mineral changes with adjacent enamel organ morphology, the present study was undertaken to provide a description of the morphological events occurring in the enamel organ during porcine amelogenesis. Two-week-old miniature swine (minipigs) were fixed by vascular perfusion with glutaraldehyde, the deciduous teeth present at this age were embedded in Epon resin and sectioned, and the cells of the enamel organ at each of the various developmental stages of amelogenesis were examined by light and transmission electron microscopy. In many respects, the morphology of the porcine enamel organ was similar to that previously described in other mammalian species. On the other hand, several particularities were noted and these are discussed in the context of available data correlating cell ultrastructure with putative function during enamel formation. C1 FORSYTH DENT CTR,DEPT PHYS CHEM,BOSTON,MA 02115. FU NIDCR NIH HHS [DE07623, DE03187] NR 75 TC 5 Z9 6 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0003-276X J9 ANAT REC JI Anat. Rec. PD MAY PY 1991 VL 230 IS 1 BP 97 EP 113 DI 10.1002/ar.1092300110 PG 17 WC Anatomy & Morphology SC Anatomy & Morphology GA FH961 UT WOS:A1991FH96100008 PM 2064032 ER PT J AU ALI, HH SHORTEN, G AF ALI, HH SHORTEN, G TI NERVE-STIMULATION AND RESIDUAL NEUROMUSCULAR BLOCK SO ANESTHESIOLOGY LA English DT Letter ID NEOSTIGMINE; RECOVERY C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. RP ALI, HH (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 4 TC 1 Z9 1 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 MAY PY 1991 VL 74 IS 5 BP 956 EP 957 DI 10.1097/00000542-199105000-00034 PG 2 WC Anesthesiology SC Anesthesiology GA FJ905 UT WOS:A1991FJ90500034 PM 2021220 ER PT J AU MARTYN, JAJ HOGUE, CW AF MARTYN, JAJ HOGUE, CW TI RESISTANCE TO D-TUBOCURARINE FOLLOWING DENERVATION - REPLY SO ANESTHESIOLOGY LA English DT Letter ID MUSCLE C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. WASHINGTON UNIV SCH MED,ANESTHESIOL,ST LOUIS,MO 63110. RP MARTYN, JAJ (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02114, USA. NR 7 TC 2 Z9 2 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 MAY PY 1991 VL 74 IS 5 BP 960 EP 961 DI 10.1097/00000542-199105000-00040 PG 2 WC Anesthesiology SC Anesthesiology GA FJ905 UT WOS:A1991FJ90500040 ER PT J AU HALLER, C DHADLY, M AF HALLER, C DHADLY, M TI THE TUMOR LYSIS SYNDROME SO ANNALS OF INTERNAL MEDICINE LA English DT Letter RP HALLER, C (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 9 Z9 9 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 MAY 1 PY 1991 VL 114 IS 9 BP 808 EP 809 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA FJ117 UT WOS:A1991FJ11700019 PM 2012365 ER PT J AU RISKIND, PN MASSACESI, L DOOLITTLE, TH HAUSER, SL AF RISKIND, PN MASSACESI, L DOOLITTLE, TH HAUSER, SL TI THE ROLE OF PROLACTIN IN AUTOIMMUNE DEMYELINATION - SUPPRESSION OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS BY BROMOCRIPTINE SO ANNALS OF NEUROLOGY LA English DT Article ID MULTIPLE-SCLEROSIS; LYMPHOCYTE-T; RATS; PREGNANCY; CYCLOSPORINE; THYROTROPIN; RECEPTORS; HORMONE AB Several lines of evidence suggest that the anterior pituitary hormone prolactin has a stimulatory role on immune function and that pharmacological suppression of prolactin secretion with the dopamine-agonist bromocriptine suppresses both humoral and cellular immunity. Here, we describe the effects of prolactin-suppression on the course of experimental allergic encephalomyelitis in female Lewis rats. Initiation of continuous bromocriptine treatment before immunization reduced both the severity and incidence of clinical signs of acute experimental allergic encephalomyelitis. Experimental allergic encephalomyelitis-immunized rats experienced a threefold rise in basal prolactin levels on day 4 after immunization and maintained elevated prolactin levels on day 10, before the onset of neurological signs of experimental allergic encephalomyelitis. Bromocriptine treatment reduced prolactin levels to those of shamimmunized rats. In vivo bromocriptine pretreatment inhibited splenic lymphocyte proliferative responses in vitro to the immunizing antigen and to concanavalin A. Moreover, bromocriptine therapy was protective when initiated 1 week after the initial immunization and was also effective in suppression of late disease. These results indicate that (1) prolactin levels are elevated after immunization and before the onset of experimental allergic encephalomyelitis, (2) bromocriptine inhibits both prolactin secretion and the severity of acute experimental allergic encephalomyelitis, and (3) inhibition is also present when treatment is begun after sensitization, suggesting an effect of prolactin on the effector limb of the immune response during experimental allergic encephalomyelitis. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RI Hauser, Stephen/J-2978-2016; OI Massacesi, Luca/0000-0001-5083-372X NR 36 TC 84 Z9 85 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAY PY 1991 VL 29 IS 5 BP 542 EP 547 DI 10.1002/ana.410290514 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FK274 UT WOS:A1991FK27400013 PM 1859183 ER PT J AU ROHRICH, RJ EHRLICHMAN, RJ MAY, JW AF ROHRICH, RJ EHRLICHMAN, RJ MAY, JW TI SENSATE PALM OF HAND FREE FLAP FOR FOREARM LENGTH PRESERVATION IN NONREPLANTABLE FOREARM AMPUTATION - LONG-TERM FOLLOW-UP SO ANNALS OF PLASTIC SURGERY LA English DT Article AB In traumatic proximal forearm amputation where replantation is not possible, "spare parts" from the amputated segment can be used to maintain adequate length or successful use of a below-elbow prosthesis. Two patients with long-term follow-up are presented in whom forearm length was preserved with the use of a sensate palmar skin free flap. C1 UNIV TEXAS,SW MED CTR,DEPT PLAST & RECONSTRUCT SURG,DALLAS,TX 75230. LAHEY CLIN FDN,MED CTR,BURLINGTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PLAST & RECONSTRUCT SURG,BOSTON,MA 02114. PARKLAND MEM HOSP & AFFILIATED INST,DALLAS,TX 75235. NR 10 TC 8 Z9 8 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD MAY PY 1991 VL 26 IS 5 BP 469 EP 473 DI 10.1097/00000637-199105000-00011 PG 5 WC Surgery SC Surgery GA FL405 UT WOS:A1991FL40500012 PM 1952722 ER PT J AU GRILLO, HC AF GRILLO, HC TI DILEMMAS IN CARDIOTHORACIC SURGICAL EDUCATION SO ANNALS OF THORACIC SURGERY LA English DT Editorial Material RP GRILLO, HC (reprint author), MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114, USA. NR 4 TC 6 Z9 6 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD MAY PY 1991 VL 51 IS 5 BP 809 EP 811 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA FK133 UT WOS:A1991FK13300021 PM 2025087 ER PT J AU TAYLOR, CR STERN, RS AF TAYLOR, CR STERN, RS TI MAGNITUDE AND DURATION OF UV-B-INDUCED TOLERANCE SO ARCHIVES OF DERMATOLOGY LA English DT Article ID SKIN; PROTECTION; SUNBURN AB Using repeated minimal erythema dose (MED) testing, we investigated the magnitude and duration of tolerance to short-wave UV radiation in the B range (UV-B) in 37 patients with psoriasis who received at lease 12 UV-B phototherapy treatments. Without substantial erythema developing, half of the patients received UV-B doses in excess of 13 times their pretreatment MED dose and a fourth received UV-B doses in excess of 28 times their pretreatment MED dose. On average, tolerance faded to about half that present at the last UV-B treatment in 3 weeks. Six weeks after therapy was stopped, most posttreatment MEDs were less than twice the pretreatment MED. The magnitude of tolerance achieved and the rate of decay did not vary with skin type. Our findings indicate that repeated exposures to suberythemal or mildly erythematous doses of UV-B can induce exceptional degrees of tolerance to UV-B radiation. The duration of this increase in tolerance is, however, short. C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS,DEPT DERMATOL,BOSTON,MA 02114. NR 18 TC 10 Z9 10 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAY PY 1991 VL 127 IS 5 BP 673 EP 677 DI 10.1001/archderm.127.5.673 PG 5 WC Dermatology SC Dermatology GA FL673 UT WOS:A1991FL67300007 PM 2024985 ER PT J AU DESTRO, M DAMICO, DJ GRAGOUDAS, ES BROCKHURST, RJ PINNOLIS, MK ALBERT, DM TOPPING, TM PULIAFITO, CA AF DESTRO, M DAMICO, DJ GRAGOUDAS, ES BROCKHURST, RJ PINNOLIS, MK ALBERT, DM TOPPING, TM PULIAFITO, CA TI RETINAL MANIFESTATIONS OF NEUROFIBROMATOSIS - DIAGNOSIS AND MANAGEMENT SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID VONRECKLINGHAUSEN NEUROFIBROMATOSIS; ASSOCIATION; HAMARTOMA; DISEASE AB Five patients presented with vision-threatening retinal tumors and systemic signs of neurofibromatosis, including neurofibromatosis type 1 (four patients) and familial cafe-au-lait spots (one patient). These tumors included large retinal astrocytic hamartomas, multiple retinal capillary hemangiomas, and combined hamartomas of the retina and retinal pigment epithelium, which resulted in rubeotic glaucoma, vitreous hemorrhage, and retinal detachment. Surgical therapy included retinal cryopexy, xenon and argon photocoagulation, scleral buckling, and pars plana vitrectomy with excisional retinal biopsy. Retinal tumors may result in marked visual loss in patients with neurofibromatosis, and vitreoretinal surgery may restore useful vision in some of these patients. C1 HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. RP DESTRO, M (reprint author), HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, RETINA SERV, 243 CHARLES ST, BOSTON, MA 02114 USA. NR 22 TC 43 Z9 45 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 330 N WABASH AVE, STE 39300, CHICAGO, IL 60611-5885 USA SN 0003-9950 EI 1538-3601 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAY PY 1991 VL 109 IS 5 BP 662 EP 666 PG 5 WC Ophthalmology SC Ophthalmology GA FL409 UT WOS:A1991FL40900028 PM 1902661 ER PT J AU KURODA, T DOODY, DP DONAHOE, PK AF KURODA, T DOODY, DP DONAHOE, PK TI ABERRANT COLONIC EXPRESSION OF MHC CLASS II ANTIGENS IN HIRSCHSPRUNGS-DISEASE SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF SURGERY LA English DT Article DE CLASS II ANTIGEN; CYTOTOXIC SUPPRESSOR T-CELL; HIRSCHSPRUNGS DISEASE; MAJOR HISTOCOMPATIBILITY COMPLEX (MHC); NATURAL KILLER CELL AB The major histocompatibility complex (MHC) Class I and II cell surface antigens responsible for the recognition of self vs non-self were studied in patients with documented Hirschsprung's disease. Monoclonal antibodies reactive with monomorphic determinants of human lymphocyte antigen (HLA)-A,B,C (Class I) and HLA-DR (Class II) were used to demonstrate immunohistochemically the expression of MHC antigens in 27 biopsy specimens from a variety of colorectal disorders. The rectal specimens examined from patients with Hirschsprung's disease showed an unexpected, marked elevation of Class II antigens with abnormal localization in the mucosa and lamina propria. This ectopic expression was not seen in any portion of the small or large bowel of patients who did not have Hirschsprung's disease. Furthermore, proximal normal colon of children with Hirschsprung's disease failed to show increased expression of Class II antigen. In an attempt to better define the effector arm at a cellular level, the distribution of helper T cells (CD4+), cytotoxic/suppressor T cells (CD8+) and natural killer cells (NK; CD16+) was examined in 5 cases. In Hirschsprung's disease, rectal infiltration of CD8+ and CD16+ cells was found, but not CD4+ cells. Ectopic expression of Class II antigen with increased numbers of rectal T cells and NK cells suggested that an early immunologic event may be causal in Hirschsprung's disease. C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT SURG,PEDIAT SURG RES LAB,32 FRUIT ST,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL SCIENCE PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON VICTORIA 3053, AUSTRALIA SN 0004-8682 J9 AUST NZ J SURG JI Aust. N. Z. J. Surg. PD MAY PY 1991 VL 61 IS 5 BP 373 EP 379 DI 10.1111/j.1445-2197.1991.tb00238.x PG 7 WC Surgery SC Surgery GA FK823 UT WOS:A1991FK82300011 PM 1827250 ER PT J AU BACKER, JM KING, GL AF BACKER, JM KING, GL TI REGULATION OF RECEPTOR-MEDIATED ENDOCYTOSIS BY PHORBOL ESTERS SO BIOCHEMICAL PHARMACOLOGY LA English DT Review ID PROTEIN-KINASE-C; EPIDERMAL GROWTH-FACTOR; HUMAN LYMPHOCYTES-T; SURFACE TRANSFERRIN RECEPTOR; HUMAN INTERLEUKIN-2 RECEPTOR; HUMAN ERYTHROLEUKEMIC CELLS; VASCULAR ENDOTHELIAL-CELLS; FACTOR-II RECEPTOR; INSULIN-RECEPTOR; TYROSINE KINASE RP BACKER, JM (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK-08126, DK-36433] NR 142 TC 37 Z9 37 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 MAY 1 PY 1991 VL 41 IS 9 BP 1267 EP 1277 DI 10.1016/0006-2952(91)90097-O PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FF426 UT WOS:A1991FF42600002 PM 1850281 ER PT J AU PAMPORI, NA AGRAWAL, AK WAXMAN, DJ SHAPIRO, BH AF PAMPORI, NA AGRAWAL, AK WAXMAN, DJ SHAPIRO, BH TI DIFFERENTIAL-EFFECTS OF NEONATALLY ADMINISTERED GLUTAMATE ON THE ULTRADIAN PATTERN OF CIRCULATING GROWTH-HORMONE REGULATING EXPRESSION OF SEX-DEPENDENT FORMS OF CYTOCHROME-P450 SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID MONOSODIUM GLUTAMATE; STEROID-METABOLISM; P-450 FORMS; RAT-LIVER; SECRETION; MICE; RADIOIMMUNOASSAY; SOMATOSTATIN; ASPARTATE; LESIONS AB Neonatal male rats were treated with monosodium glutamate (MSG) at either 0.5, 1.0, 2.0, 3.0 or 4.0 mg/g body weight on alternate days during the first 9 days of life. As adults, rats were catheterized to obtain unstressed, serial blood samples for the determination of ultradian patterns of circulating growth hormone. In addition, the levels of drug-metabolizing enzymes (i.e. hexobarbital hydroxylase, cytochromes P450 and b5, NADPH-cytochrome P450 reductase and ethoxyresorufin O-deethylase) as well as sex-dependent forms of cytochrome P450 [i.e. male-dependent cytochromes P450 2c (IIC11), 2a (IIIA2) and RLM2 (IIA2) and female-dependent cytochromes P450 2d (IIC12) and 3 (IIA1)] and/or their catalytic activities were measured in the hepatic microsomes of the treated rats. The results demonstrated a dose-dependent, graded response to MSG treatment. As the dose of MSG increased from 0.5 to 4.0 mg, there was a concurrent decline in the amplitudes of the characteristically masculine, episodic bursts of growth hormone, until at the highest dose (4 mg), the pulses were no longer detectable. Associated with this dose-dependent alteration in the ultradian pattern of growth hormone secretion was a measurable change in the activities of the sex-dependent hepatic enzymes. As the pulse heights of the hormone declined to 10-20% of their normal amplitudes, the levels of the male-dependent enzymes (i.e. the drug-metabolizing enzymes, as well as the male forms of cytochrome P450 and their specific steroid hydroxylases) were maintained, and in some cases, exceeded the levels normally found in males. However, as the hormone pulse heights declined, there appeared an accompanying increase in the activities of some of the female-dependent enzymes. Finally, with the loss of all detectable levels of circulating growth hormone, the normal masculine profile of hepatic enzymes was reversed to an apparently normal (with the exception of cytochrome P450 2d) feminine profile. Summarizing, the results indicate that (1) neonatal administration of MSG can produce dose-dependent, graded, long-term developmental defects in the ultradian rhythm of circulating growth hormone and associated sex-dependent hepatic enzymes, and (2) while the male-dependent hepatic enzymes can be maintained at normal or even higher levels in the face of an up to 90% reduction in the pulse heights of plasma growth hormone, the activities of the female-dependent enzymes may begin to increase. C1 UNIV PENN,SCH VET MED,DEPT ANIM BIOL,BIOCHEM LABS,3800 SPRUCE ST,PHILADELPHIA,PA 19104. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NICHD NIH HHS [HD-16358]; NIDDK NIH HHS [R01 DK033765, DK-33765] NR 41 TC 38 Z9 39 U1 0 U2 3 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 MAY 1 PY 1991 VL 41 IS 9 BP 1299 EP 1309 DI 10.1016/0006-2952(91)90101-A PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FF426 UT WOS:A1991FF42600006 PM 2018562 ER PT J AU YOST, RW GRAUVICKEL, SJ CANTWELL, R BOMALASKI, JS HUDSON, AP AF YOST, RW GRAUVICKEL, SJ CANTWELL, R BOMALASKI, JS HUDSON, AP TI YEAST MITOCHONDRIA (SACCHAROMYCES-CEREVISIAE) CONTAIN CA2+-INDEPENDENT PHOSPHOLIPASE-A1 AND PHOSPHOLIPASE-A2 ACTIVITIES - EFFECT OF RESPIRATORY STATE SO BIOCHEMISTRY INTERNATIONAL LA English DT Article ID ENZYME-ACTIVITIES; RAT-HEART; PURIFICATION; HYDROLYSIS; LIPIDS; DNA C1 MED COLL PENN,DEPT MED,PHILADELPHIA,PA 19129. MED COLL PENN,DEPT MICROBIOL IMMUNOL,PHILADELPHIA,PA 19129. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. RP YOST, RW (reprint author), DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. FU NIAMS NIH HHS [AR39382] NR 29 TC 8 Z9 8 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 0158-5231 J9 BIOCHEM INT PD MAY PY 1991 VL 24 IS 2 BP 199 EP 208 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA GC121 UT WOS:A1991GC12100001 PM 1930243 ER PT J AU DUNN, JCY TOMPKINS, RG YARMUSH, ML AF DUNN, JCY TOMPKINS, RG YARMUSH, ML TI LONG-TERM INVITRO FUNCTION OF ADULT HEPATOCYTES IN A COLLAGEN SANDWICH CONFIGURATION SO BIOTECHNOLOGY PROGRESS LA English DT Article AB In an effort to reconstruct the cellular polarity normally found in the liver, adult rat hepatocytes were sandwiched between two layers of hydrated rat tail tendon collagen matrix. Functionally, sandwiched hepatocytes maintained the secretion of albumin, transferrin, fibrinogen, bile acids, and urea for at least 6 weeks, whereas cells cultured on a single layer of collagen gel ceased such secretion in 1-2 weeks. After 1 week of culture on a single layer of collagen gel, hepatocytes could still recover these lost functions when a second layer of collagen gel was applied. The exact nature of the substrate for constructing the sandwich system appeared to be unimportant as long as it allowed cellular attachment. Hepatocytes cultured in the sandwich system appeared to maintain a distribution of actin filaments similar to the in vivo state, whereas cells cultured on a single layer of collagen gel showed abnormal formation of stress fibers. These studies suggest that simple manipulations of the configuration of extracellular elements can dramatically alter the behavior of cultured hepatocytes. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. FU NIDDK NIH HHS [DK-01746, DK-41709] NR 0 TC 463 Z9 472 U1 1 U2 28 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD MAY-JUN PY 1991 VL 7 IS 3 BP 237 EP 245 DI 10.1021/bp00009a007 PG 9 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA FQ997 UT WOS:A1991FQ99700007 PM 1367596 ER PT J AU HENDERSON, IC AF HENDERSON, IC TI RAPPORTEURS REPORT - TREATMENT AND RESPONSE SO BREAST CANCER RESEARCH AND TREATMENT LA English DT Editorial Material ID BREAST-CANCER; ENDOCRINE AB During earlier sessions of this conference it was observed that the incidence of breast cancer has, in the past, been lower in Japan than in the West, and in addition, the average survival of Japanese women with breast cancer, especially postmenopausal women, has been longer. In this session, the possibility that these observed differences in survival were due to differences in treatment or in response to treatment was discussed. RP HENDERSON, IC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CTR BREAST EVALUAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6806 J9 BREAST CANCER RES TR JI Breast Cancer Res. Treat. PD MAY PY 1991 VL 18 SU 1 BP S157 EP S158 DI 10.1007/BF02633549 PG 2 WC Oncology SC Oncology GA FM811 UT WOS:A1991FM81100032 ER PT J AU NG, SF WAXMAN, DJ AF NG, SF WAXMAN, DJ TI N,N',N''-TRIETHYLENETHIOPHOSPHORAMIDE (THIO-TEPA) OXYGENATION BY CONSTITUTIVE HEPATIC P450 ENZYMES AND MODULATION OF DRUG-METABOLISM AND CLEARANCE INVIVO BY P450-INDUCING AGENTS SO CANCER RESEARCH LA English DT Article ID HIGH-DOSE THIOTEPA; PLASMA PHARMACOKINETICS; HORMONAL-REGULATION; PHASE-I; EXPRESSION; CYCLOPHOSPHAMIDE; IDENTIFICATION; ACTIVATION AB The cancer chemotherapeutic drug N,N',N"-triethylenethiophosphoramide (thio-TEPA) is oxidatively desulfurated to yield the active metabolite N,N',N"-triethylenephosphoramide (TEPA) in a reaction catalyzed by the phenobarbital-inducible rat liver P450 enzyme IIB1. In the current study, the role of constitutively expressed P450 enzymes in thio-TEPA metabolism was studied using purified P450s, isolated liver microsomes, and intact rats. Metabolism of thio-TEPA (100-mu-M) to TEPA by uninduced adult female and male rat liver microsomes proceeded at initial rates of 0.10 and 0.28 nmol TEPA formed/min/mg microsomal protein, respectively. Although these rates are low compared to those catalyzed by phenobarbital-induced liver microsomes (3.5 nmol TEPA/min/mg), they are sufficient to contribute to the systemic metabolism of this drug. Thio-TEPA metabolism catalyzed by uninduced female liver microsomes was approximately 70% inhibitable by antibodies selectively reactive with P450 IIC6. For the uninduced male liver microsomes, which exhibit a severalfold higher rate of thio-TEPA metabolism, enzyme activity was only 15-20% inhibitable by these antibodies but was 80-85% inhibited by an anti-P450 IIC6 monoclonal antibody cross-reactive with P450 IIC11, which is expressed only in the males. Consistent with these observations, purified P450s IIC11 and IIC6 both oxidized thio-TEPA in reconstituted systems (turnover, 1.1 and 0.3 min-1 P450(-1), respectively, at 100-mu-M substrate), while several other constitutive hepatic P450s exhibited significantly lower or undetectable activities (turnover, less-than-or-equal-to 0.15 min-1 P450(-1). Metabolism of thio-TEPA by purified P450 IIC11 was associated with a time-dependent inactivation of the cytochrome analogous to that previously shown to accompany thio-TEPA metabolism catalyzed by P450 IIB1. Depletion of hepatic P450 IIC11 by cisplatin treatment of adult male rats led to a 70% reduction of TEPA formation catalyzed by the isolated liver microsomes, suggesting that cisplatin may influence thio-TEPA pharmacokinetics when these two drugs are given in combination. The extent to which hepatic P450s contribute to thio-TEPA metabolism and clearance in vivo was assessed by monitoring thio-TEPA and TEPA pharmacokinetics in rats that exhibit widely differing rates of microsomal thio-TEPA metabolism, i.e., uninduced female and male rats, and male rats treated with the P450 IIB1 inducers clofibrate and phenobarbital. In accord with the microsomal activities, conversion of thio-TEPA to TEPA was less extensive and thio-TEPA elimination slower in female than in male rats. Clofibrate and phenobarbital both accelerated thio-TEPA clearance by increasing metabolism to TEPA; this was evidenced by a 4-fold increase in the peak plasma level of the oxo-metabolite in the inducer-pretreated animals. These findings demonstrate that liver P450 enzymes have a major impact on thio-TEPA metabolism and clearance and further suggest ways in which thio-TEPA pharmacokinetics might be modulated in vivo to achieve improved therapeutic effects. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JF-525,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 31 TC 35 Z9 36 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 1 PY 1991 VL 51 IS 9 BP 2340 EP 2345 PG 6 WC Oncology SC Oncology GA FJ821 UT WOS:A1991FJ82100017 PM 1707751 ER PT J AU TAICHMAN, DB DJAFFAR, I TEIXIDO, J ARUFFO, A CYBULSKY, MI LONGENECKER, BM RICE, GE BEVILACQUA, MP AF TAICHMAN, DB DJAFFAR, I TEIXIDO, J ARUFFO, A CYBULSKY, MI LONGENECKER, BM RICE, GE BEVILACQUA, MP TI TUMOR-CELL SURFACE ALPHA-4-BETA-1 INTEGRIN MEDIATES ADHESION TO VASCULAR ENDOTHELIUM - DEMONSTRATION OF AN INTERACTION WITH THE N-TERMINAL DOMAINS OF INCAM-110/VCAM-1 SO CELL REGULATION LA English DT Article ID NECROSIS FACTOR; HUMAN-MELANOMA; MONOCLONAL-ANTIBODY; MALIGNANT-MELANOMA; RECEPTOR; VLA-4; IDENTIFICATION; FIBRONECTIN; MOLECULE-1; METASTASIS AB Hematogenous metastasis involves adhesive interactions between blood-borne tumor cells and the vessel wall. By the use of in vitro assays, the adhesion of human melanoma, osteosarcoma, and kidney carcinoma (but not colon carcinoma) cell lines was shown to involve thecytokine-inducible endothelial cell surface protein inducible cell adhesion molecule 110 (INCAM-110) and the alpha-4-beta-1 integrin, molecules normally involved in endothelial-leukocyte interactions. Tumor adhesion to human endothelial cell monolayers was increased 1.9- to 8.2-fold by endothelial activation with the cytokine tumor necrosis factor (TNF) and inhibited by the anti-INCAM-110 monoclonal antibody (mAb) E1/6. Each of these tumor cells expressed members of the beta-1 integrin family of adhesion molecules, and antibodies to the alpha-4 and beta-1 integrin subunits inhibited tumor-endothelial adhesion (48-87% inhibition). A cDNA encompassing the three N-terminal Ig-like domains of vascular cell adhesion molecule 1 (VCAM-1) encoded a protein recognized by the anti-INCAM-110 mAb E1/6 and, when captured onto plastic, supported melanoma cell adhesion by an alpha-4 integrin-dependent mechanism. In contrast to mAb E1/6, a second anti-INCAM-110 mAb Hu8/4 neither inhibited adhesion to activated endothelium nor bound the first three Ig-like domains of INCAM-110/VCAM-1. These data indicate that the adherence of several human tumors to activated endothelium is mediated by an interaction of alpha-4-beta-1 integrin and the N-terminal Ig-like domains of endothelial INCAM-110/VCAM-1. Tumor acquisition of the alpha-4 integrin subunit and endothelial expression of INCAM-110 may affect the frequency and distribution of metastasis. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. UNIV ALBERTA,DEPT IMMUNOL,EDMONTON T6G 2H7,ALBERTA,CANADA. RP TAICHMAN, DB (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV VASC RES,BOSTON,MA 02115, USA. RI Teixido, Joaquin/J-8543-2014 OI Teixido, Joaquin/0000-0002-3177-4151 FU NHLBI NIH HHS [HL-07727, HL-36028]; NIGMS NIH HHS [GM-38903] NR 47 TC 125 Z9 127 U1 0 U2 2 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1044-2030 J9 CELL REGUL PD MAY PY 1991 VL 2 IS 5 BP 347 EP 355 PG 9 WC Cell Biology SC Cell Biology GA FM945 UT WOS:A1991FM94500002 PM 1716464 ER PT J AU Misson, JP Austin, CP Takahashi, T Cepko, CL Caviness, VS AF Misson, Jean-Paul Austin, Christopher P. Takahashi, Takao Cepko, Constance L. Caviness, Verne S., Jr. TI The Alignment of Migrating Neural Cells in Relation to the Murine Neopallial Radial Glial Fiber System SO CEREBRAL CORTEX LA English DT Article AB The direction of neural cell migration in relation to the pattern of alignment of adjacent radial glial fibers has been studied in the developing neopallium of embryonic days 16-18 mouse embryos. The radial glial fibers were stained with RC2, a monoclonal antibody selective for cells of astroglial lineage in the developing murine brain. Migrating neural cells were stained histochemically with 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-gal) following retroviral transduction of the gene encoding beta-galactosidase into proliferating progenitors on E13. The leading processes and, generally, the somata of migrating neurons were found to be aligned in parallel with the radial glial fibers, despite substantial variations in the patterns of alignment of the fiber fascicles. The set of observations is consistent with the hypothesis that neural cell migration is supported by radial glial fibers. C1 [Misson, Jean-Paul; Austin, Christopher P.; Takahashi, Takao; Caviness, Verne S., Jr.] Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA. [Misson, Jean-Paul] Univ Liege, Sch Med, Lab Physiol & Dev Neurobiol, B-4000 Liege, Belgium. [Cepko, Constance L.] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA. RP Takahashi, T (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Neurol, Boston, MA 02114 USA. FU Charles A. King Trust; Massachusetts General Hospital; Foundation Princesse Marie-Christine; NATO [27B85BE]; NIH [NS 12005, NS 23021] FX We wish to thank Miyuki Yamamoto and Anne Boiteau for the RC2 antibody, Chris Walsh for the virus stocks, Margaretha Jacobson for technical and photographic assistance, and Ginny Tosney for editing the manuscript. J.-P.M. was a Frank Boas Scholar at Harvard University and was supported by a Charles A. King Trust Fellowship, and C.P.A. was supported by the Massachusetts General Hospital. This work was supported by the Foundation Princesse Marie-Christine, by NATO Grant 27B85BE to J.-P.M., and by NIH Grants NS 12005 to V.S.C. and NS 23021 to C.L.C. NR 39 TC 125 Z9 126 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 1047-3211 J9 CEREB CORTEX JI Cereb. Cortex PD MAY PY 1991 VL 1 IS 3 BP 221 EP 229 DI 10.1093/cercor/1.3.221 PG 9 WC Neurosciences SC Neurosciences & Neurology GA V19BH UT WOS:000208047400002 PM 1668365 ER PT J AU ONEILL, AV JOHNSON, DC AF ONEILL, AV JOHNSON, DC TI TRANSITION FROM EXERCISE TO REST - VENTILATORY AND ARTERIAL BLOOD-GAS RESPONSES SO CHEST LA English DT Article AB The mechanisms leading to rapid changes in arterial blood gas values soon after exercise ends have not been well established. To further study these phenomena, we exercised seven normal male volunteers to exhaustion on a cycle ergometer with a 25-W/min ramped protocol measuring arterial blood gas values, and breath-by-breath gas exchange from rest to exercise and through 15 minutes of recovery. Arterial Po-2 (PaO2) increased from 108 mm Hg at peak exercise to 125 mm Hg at 2 minutes of recovery. There was a smaller rise in calculated alveolar Po-2 (PaO2) from 121 to 128 mm Hg over the same period. Arterial P(CO2) (PaCO2) fell from 35.0 mm Hg to 31.9 mm Hg. The gas exchange ratio R rose from 1.21 to 1.52, after having peaked at 1.68 at 1 minute. The alveolar-arterial O2 gradient (P[A-a]O2) fell from 12.3 mm Hg at peak exercise to 3.2 mm Hg at 2 minutes. Following exercise, the rise in R is related to a more rapid fall in O2 uptake than in CO2 output, and the fall in P(A-a)O2 is probably related to improved V/Q relationships and to a rise in mixed venous PO2. We conclude that the rise in PaO2 in the recovery period after progressive nonsteady state exercise is due to several factors, including a fall in P(A-a)O2 and a rise in P(A)O2 due primarily to an elevation of R and also to a fall in PaCO2. C1 MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL07354, HL-01166] NR 14 TC 2 Z9 2 U1 0 U2 2 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAY PY 1991 VL 99 IS 5 BP 1145 EP 1150 DI 10.1378/chest.99.5.1145 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA FK421 UT WOS:A1991FK42100020 PM 1902160 ER PT J AU SYSTROM, DM FRAGOSO, CV KANAREK, DJ KAZEMI, HY AF SYSTROM, DM FRAGOSO, CV KANAREK, DJ KAZEMI, HY TI AMMONIUM ION AND THE ANAEROBIC THRESHOLD IN MAN SO CHEST LA English DT Article ID HUMAN SKELETAL-MUSCLE; AMINO-ACIDS; EXERCISE; LACTATE; DOGS; METABOLISM; STATE AB To determine if ammonium ion plays a role in the lactate and ventilatory thresholds of incremental exercise, we investigated the effects on blood lactate and ventilation of NH4+ - buffering by monosodium glutamate. Six normal volunteers underwent intravenous loading with MSG, 9 g, in a randomized, double-blind, saline placebo controlled crossover study. Four of the six subjects had a > 10 percent fall in peak (NH4+) following MSG (37 +/- 2.0 vs 25 +/- 4.3-mu-g/dl, p = 0.003, PLB vs MSG). When MSG blunted the rise in venous (NH4+) during exercise, uncoupling of the LT and VT was observed. Specifically, with suppression of peak exercise (NH4+) by MSG, the LT was delayed (r = -0.84, p = 0.03), the VT was earlier (r = 0.86, p = 0.02), and the VO2 difference between the LT and VT widened (r = -0.90, p = 0.02). We conclude that NH4+ plays a role in determining the LT and VT of incremental exercise and that the VT may not be exclusively dependent on blood lactate. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. FU NCRR NIH HHS [MO 1RR01066-11S2]; NHLBI NIH HHS [HL07354, HL 29493] NR 35 TC 5 Z9 5 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAY PY 1991 VL 99 IS 5 BP 1197 EP 1202 DI 10.1378/chest.99.5.1197 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA FK421 UT WOS:A1991FK42100030 PM 2019178 ER PT J AU PUOPOLO, PR POTHIER, ME VOLPICELLI, SA FLOOD, JG AF PUOPOLO, PR POTHIER, ME VOLPICELLI, SA FLOOD, JG TI SINGLE PROCEDURE FOR DETECTION, CONFIRMATION, AND QUANTIFICATION OF BENZODIAZEPINES IN SERUM BY LIQUID-CHROMATOGRAPHY WITH PHOTODIODE-ARRAY DETECTION SO CLINICAL CHEMISTRY LA English DT Note DE CHROMATOGRAPHY; REVERSED-PHASE; TOXICOLOGY; ABUSED DRUGS ID MASS-SPECTROMETRY; TRICYCLIC ANTIDEPRESSANTS; ULTRAVIOLET-SPECTRA; BLOOD-SAMPLES; DRUG ANALYSIS; MULTICHANNEL; PLASMA; CYCLOBENZAPRINE; IDENTIFICATION; INTERFERENCE AB We developed a reversed-phase chromatographic procedure for detecting benzodiazepines and other drugs in serum. A liquid-liquid extraction step with hexane/ethyl acetate isolates the drugs from serum; absolute recoveries are generally > 85%. Reconstituted extracts are chromatographed on a 4-mu-m (particle size) C18 column; 14 drugs and an internal standard (flunitrazepam) are separated in 8 min. Peak detection, purity checking, and identification are performed with a computerized photodiode-array detector. Run-to-run imprecision (CV) for many benzodiazepines is < 3%. In a study of 126 specimens from Emergency Department patients, the procedure showed excellent agreement with a gas-chromatographic method involving either mass-spectrometric or flame-ionization detection. This single procedure provides rapid and accurate detection, quantification, and confirmation of benzodiazepines in serum. C1 MASSACHUSETTS GEN HOSP,CHEM LAB,GRAY 5,BOSTON,MA 02114. NR 27 TC 28 Z9 28 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 MAY PY 1991 VL 37 IS 5 BP 701 EP 706 PG 6 WC Medical Laboratory Technology SC Medical Laboratory Technology GA FL981 UT WOS:A1991FL98100016 PM 2032323 ER PT J AU HARRIS, WH MULROY, RD MALONEY, WJ BURKE, DW CHANDLER, HP ZALENSKI, EB AF HARRIS, WH MULROY, RD MALONEY, WJ BURKE, DW CHANDLER, HP ZALENSKI, EB TI INTRAOPERATIVE MEASUREMENT OF ROTATIONAL STABILITY OF FEMORAL COMPONENTS OF TOTAL HIP-ARTHROPLASTY SO CLINICAL ORTHOPAEDICS AND RELATED RESEARCH LA English DT Article AB High out-of-plane forces acting on the hip joint can produce important rotational micromotion of the femoral component. This micromotion at the prosthesis interface may be detrimental to the stability of the implant. In cementless femoral implants this could prevent bone ingrowth, and in the cemented component this could cause generation of particulate debris, lysis, and loosening. The introduction of the torque wrench micrometer for assessment of intraoperative femoral component stability can quantify the initial stability of primary cementless femoral components and critically evaluate the stability (at either the initial or revision arthroplasty) of both cemented and cementless femoral components. It allows the surgeon to produce a known torque in the direction and magnitude of the out-of-plane forces that load the hip in vivo. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HARRIS, WH (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114, USA. NR 15 TC 30 Z9 30 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 MAY PY 1991 IS 266 BP 119 EP 126 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA FK401 UT WOS:A1991FK40100019 PM 2019039 ER PT J AU TAUBER, J DELAMAZA, MS FOSTER, CS AF TAUBER, J DELAMAZA, MS FOSTER, CS TI SYSTEMIC CHEMOTHERAPY FOR OCULAR CICATRICIAL PEMPHIGOID SO CORNEA LA English DT Article DE CHEMOTHERAPY; CICATRICIAL PEMPHIGOID; SIDE EFFECTS; DAPSONE; CYCLOPHOSPHAMIDE; AZATHIOPRINE; CONJUNCTIVA AB The records of 105 patients treated with three different chemotherapeutic agents for ocular cicatricial pemphigoid (OCP) were reviewed to compare long-term efficacies, side effects, and tolerance of different regimens. For the entire group, OCP progressed in 6% of eyes in 10% of patients (follow-up 35 months). More than half of the treatment failures occurred in patients intolerant of chemotherapy. Diaminodiphenylsulfone (DAP), as initial agent, failed to control disease in 2% of patients, compared with 8% after cyclophosphamide (CYC) and 9% after azathioprine (AZA) (p < 0.05). Stratification of results revealed that DAP was the most effective initial agent for modestly active OCP, whereas CYC was the most effective initial choice for highly active cases. In patients treated with a single agent exclusively for 10 months or more, failure to control disease occurred in 4% of DAP, 4% of CYC, and 15% of AZA patients (p < 0.01). Recommendations for a sequential approach to chemotheraphy for OCP are presented. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. FU NEI NIH HHS [EY 06008, EY 06052] NR 0 TC 96 Z9 97 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD MAY PY 1991 VL 10 IS 3 BP 185 EP 195 DI 10.1097/00003226-199105000-00001 PG 11 WC Ophthalmology SC Ophthalmology GA FJ475 UT WOS:A1991FJ47500001 PM 2055022 ER PT J AU FAUSTMAN, D SCHOENFELD, D ZIEGLER, R AF FAUSTMAN, D SCHOENFELD, D ZIEGLER, R TI LYMPHOCYTE-T CHANGES LINKED TO AUTOANTIBODIES - ASSOCIATION OF INSULIN AUTOANTIBODIES WITH CD4+CD45R+ LYMPHOCYTE SUBPOPULATION IN PREDIABETIC SUBJECTS SO DIABETES LA English DT Article ID ISLET-CELL ANTIBODIES; I DIABETES-MELLITUS; HELPER-INDUCER; PROTEIN-A; BB/W RAT; SUBSETS; ANTIGEN; ASSAY; DIFFERENTIATION; ACTIVATION AB The onset of insulin-dependent (type I) diabetes is predictable before hyperglycemia by the presence of islet cell autoantibodies (ICAs) and competitive insulin autoantibodies (CIAAs). CIAA+ICA+ first-degree relatives of individuals with type I diabetes have increased numbers of CD4 cells bearing the CD45R antigen and reciprocal depressions of the CD4 cells bearing the CD29 determinant. In addition, depressed CD4/CD8 ratios are present. In this study, we investigated the correlation between autoantibody levels and T-lymphocyte changes in the prediabetic state. The data demonstrate a clear linear relationship between rising CIAA levels, a marker of disease rate, and rising elevations in the CD4+CD45R+/CD4+CD29+ ratio in 37 CIAA+ICA+ and CIAA+ICA- relatives (r = 0.93). In marked contrast, the degree of CD4/CD8 depression found in individuals with prediabetes or long-term diabetes failed to correlate with either CIAA (r = 0.32) or ICA (r = 0.29) levels. The investigation of T-lymphocyte changes in siblings of individuals with type I diabetes with different stable autoantibody patterns (CIAAs and/or ICAs), and thus varying risks for diabetes, revealed differences in the prediabetic groups. Fifteen CIAA+ICA- relatives with high CIAA levels (> 80 nU/ml) had high CD4+CD45R+/CD4+CD29+ ratios (P = 0.03) and depressed CD4/CD8 ratios (P = 0.008). In contrast, CIAA+ICA- relatives with low CIAA levels (39-80 nU/ml), and thus low risk of diabetes, had no alteration in their CD4/CD8 ratio (P = 0.75) or CD4+CD45R+/CD4+CD29+ ratio (P = 0.33). Nineteen CIAA-ICA+ siblings with a predicted intermediate risk for diabetes showed heterogeneity in the presence of T-lymphocyte abnormalities. No statistically significant trend was observed in the peripheral T-lymphocyte composition with all CIAA-ICA+ relatives combined. This study links the magnitude of the well-described CIAA production to the magnitude of altered numbers of T lymphocytes bearing the CD45R+ and CD29+ antigens in the prediabetic stage. We conclude that prediabetic relatives prone to frank hyperglycemia represent a heterogeneous population now definable by autoantibody production and the newly described T-lymphocyte changes. This study represents an initial delineation of a link between abnormal alterations in the humoral and cellular immune response. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR BIOSTAT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RP FAUSTMAN, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP E,SCH MED,DIABET UNIT,13TH ST,BOSTON,MA 02129, USA. NR 45 TC 32 Z9 33 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 MAY PY 1991 VL 40 IS 5 BP 590 EP 597 DI 10.2337/diabetes.40.5.590 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FL179 UT WOS:A1991FL17900010 PM 1827080 ER PT J AU FIELDS, SM KOELLER, JM AF FIELDS, SM KOELLER, JM TI IDARUBICIN - A 2ND-GENERATION ANTHRACYCLINE SO DICP-THE ANNALS OF PHARMACOTHERAPY LA English DT Article ID PHASE-II TRIAL; ADVANCED BREAST-CANCER; CELL LUNG-CANCER; ACUTE MYELOID-LEUKEMIA; NON-LYMPHOBLASTIC-LEUKEMIA; ADVANCED COLORECTAL-CARCINOMA; INTERMEDIATE-DOSE CYTARABINE; ACUTE MYELOGENOUS LEUKEMIA; COOPERATIVE GROUP GIMEMA; RELAPSED ACUTE LEUKEMIAS AB Because of its in vitro activity in leukemic cell lines and Phase I studies of acute leukemia, Phase II and III clinical trials with idarubicin hydrochloride were conducted in patients with acute lymphocytic leukemia or acute nonlymphocytic leukemia. In the Phase III comparative trials between the combinations of idarubicin and cytarabine and daunorubicin hydrochloride and cytarabine, the idarubicin/cytarabine combination resulted in significantly greater complete remission rates and longer overall survival in two of three studies conducted in the US. As a result, the Food and Drug Administration approved intravenous idarubicin with a Class 1A rating in September 1990 for use in combination with other antileukemic drugs (e.g., cytarabine) for the treatment of acute myelogenous leukemia in adults. The recommended dose of idarubicin is 12 mg/m2 daily for three days by slow intravenous injection in combination with cytarabine. Although idarubicin causes myelosuppression similar to that described with daunorubicin, the incidence of cardiotoxicity in animal models is lower. Idarubicin also has the advantages of oral administration, but the oral formulation of the drug remains investigational. The use of idarubicin in pediatric patients also remains to be established. C1 UNIV TEXAS,HLTH SCI CTR,DIV PHARM,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. UNIV TEXAS,CLIN,AUSTIN,TX 78712. AUDIE L MURPHY MEM VET ADM MED CTR,ONCOL CLIN,SAN ANTONIO,TX 78284. NR 103 TC 13 Z9 13 U1 0 U2 2 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 0012-6578 J9 DICP ANN PHARMAC PD MAY PY 1991 VL 25 IS 5 BP 505 EP 517 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FL571 UT WOS:A1991FL57100013 PM 2068836 ER PT J AU BERNARDS, R AF BERNARDS, R TI N-MYC DISRUPTS PROTEIN KINASE-C-MEDIATED SIGNAL TRANSDUCTION IN NEUROBLASTOMA SO EMBO JOURNAL LA English DT Article DE N-MYC; NEUROBLASTOMA; PROTEIN KINASE; SIGNAL TRANSDUCTION ID IMMUNOGLOBULIN ENHANCER-BINDING; KAPPA-B; NEURO-BLASTOMA; EGF RECEPTOR; EXPRESSION; PHOSPHORYLATION; AMPLIFICATION; ONCOGENE; FAMILY; CELLS AB In neuroblastoma, amplification of the N-myc gene is closely correlated with increased metastatic ability. The mechanism by which N-myc acts to increase neuroblastoma malignancy is poorly understood as yet. It is shown here that transfection of N-myc in a neuroblastoma cell line causes suppression of one isoform of protein kinase C, named-delta, and induction of an unusual type of protein kinase C, named-zeta. N-myc-transfected neuroblastoma cells were found to be blocked in the activation of both c-fos mRNA and the NF-chi-B transcription factor by phorbol ester. Introduction of a protein kinase C expression vector in N-myc transfected neuroblastoma cells restored inducibility of both c-fos and NF-chi-B by phorbol ester. These observations indicate that changes in protein kinase C gene expression significantly alter the response of N-myc-amplified neuroblastomas to a variety of external signals. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP BERNARDS, R (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,149 13TH ST,BOSTON,MA 02129, USA. OI Bernards, Rene/0000-0001-8677-3423 NR 37 TC 62 Z9 62 U1 0 U2 0 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 MAY PY 1991 VL 10 IS 5 BP 1119 EP 1125 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ822 UT WOS:A1991FJ82200012 PM 1902412 ER PT J AU VASIOS, G MADER, S GOLD, JD LEID, M LUTZ, Y GAUB, MP CHAMBON, P GUDAS, L AF VASIOS, G MADER, S GOLD, JD LEID, M LUTZ, Y GAUB, MP CHAMBON, P GUDAS, L TI THE LATE RETINOIC ACID INDUCTION OF LAMININ-B1 GENE-TRANSCRIPTION INVOLVES RAR BINDING TO THE RESPONSIVE ELEMENT SO EMBO JOURNAL LA English DT Article DE F9 CELLS; RETINOIC ACID RECEPTOR; RAR; RARE; RAR-ALPHA, RAR-BETA AND RAR-GAMMA ID MOUSE TERATOCARCINOMA CELLS; THYROID-HORMONE; ESTROGEN-RECEPTOR; NEURONAL DIFFERENTIATION; NUCLEAR RECEPTORS; AMINO-ACIDS; STEM-CELLS; EXPRESSION; CARCINOMA; CLONING AB Transcription of the murine laminin B1 (LB1) gene is induced by retinoic acid (RA), but responds only 24-28 h after RA treatment in F9 EC cells. Here we have shown by gel retardation assay that all three retinoic acid receptors (RARs) alpha, beta and gamma expressed in Cos cells can bind directly to the previously characterized retinoic acid response element (RARE) of the LB1 promoter, albeit with a weaker affinity than to the RAR-beta gene RARE. Three stereo-aligned TGACC-like motifs are crucial for this binding. Interestingly, the capacity of RAR-alpha, -beta, and -gamma to bind the LB1 RARE appears to be differentially modulated by factor(s) present in HeLa cells infected with RAR-expressing vaccinia virus vectors. Analyses of LB1 RARE mutants provide a strong correlation between RA-inducibility in vivo and efficiency of RAR binding in vitro. Thus, RARs can participate directly in transcriptional induction of the LB1 gene, even though this induction is cycloheximide sensitive and RARs are present in F9 cells prior to RA addition. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CNRS,CNRS,GENET MOLEC EUCARYOTES LAB,INSERM,U184,F-67085 STRASBOURG,FRANCE. HARVARD UNIV,SCH MED,CELL & DEV BIOL PROGRAM,BOSTON,MA 02115. FU NCI NIH HHS [1F32CA08451, 2T32CA09361]; NICHD NIH HHS [R01HD24319] NR 50 TC 137 Z9 138 U1 1 U2 2 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 MAY PY 1991 VL 10 IS 5 BP 1149 EP 1158 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ822 UT WOS:A1991FJ82200015 PM 1850696 ER PT J AU WHITCOMB, RW SCHNEYER, AL ROSER, JF HUGHES, JP AF WHITCOMB, RW SCHNEYER, AL ROSER, JF HUGHES, JP TI CIRCULATING ANTAGONIST OF LUTEINIZING-HORMONE IN ASSOCIATION WITH INFERTILITY IN STALLIONS SO ENDOCRINOLOGY LA English DT Article ID LEYDIG TUMOR-CELLS; MONOCLONAL-ANTIBODY; GONADOTROPIN; SECRETION; LH; PATTERNS AB Using a LH radioligand receptor assay (RRA) previously validated for use in serum and an equine monoclonal RIA, we have distinguished a subset of subfertile stallions with an elevated RRA/RIA ratio. After purification of the active moiety by anion exchange chromatography and immunoprecipitation with the equine LH (eLH) monoclonal antibody, RRA activity remained in the supernatant. This activity was also recognized by a polyclonal LH antibody (GDN 15) with wide cross-species recognition. This active fraction was further purified by gel filtration chromatography and shown to displace labeled eLH in a dose-dependent fashion in the RRA with an inhibition slope of 2.8 compared with a slope of 1.1 for native eLH. This fraction also inhibited the LH-stimulated steroidogenesis of Leydig cells in vitro in a dose-dependent fashion, but had no effect on basal (minus LH) steroid production. Polyacrylamide gel electrophoresis and electroelution of this material demonstrated RRA activity in a fraction with a mol wt between 45-66 kDa. We conclude that this substance 1) competitively inhibited binding of eLH and hCG to the LH receptor, 2) antagonized LH-stimulated steroidogenesis in vitro, and 3) may represent a LH isoform found in association with infertility in these animals. C1 UNIV CALIF DAVIS,SCH VET MED,DEPT ANIM SCI,DAVIS,CA 95616. UNIV CALIF DAVIS,SCH VET MED,DEPT REPROD,DAVIS,CA 95616. RP WHITCOMB, RW (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BHX-5,BOSTON,MA 02114, USA. FU FDA HHS [FD-U-000523-1]; NICHD NIH HHS [HD-15788, HD-25941] NR 18 TC 9 Z9 9 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 MAY PY 1991 VL 128 IS 5 BP 2497 EP 2502 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FJ396 UT WOS:A1991FJ39600038 PM 2019262 ER PT J AU GOODFRIEND, TL BALL, DL ELLIOTT, ME MORRISON, AR EVENSON, MA AF GOODFRIEND, TL BALL, DL ELLIOTT, ME MORRISON, AR EVENSON, MA TI FATTY-ACIDS ARE POTENTIAL ENDOGENOUS REGULATORS OF ALDOSTERONE SECRETION SO ENDOCRINOLOGY LA English DT Article ID LIQUID-CHROMATOGRAPHIC ANALYSIS; ANGIOTENSIN-II; GLOMERULOSA CELLS; HYPERTENSION; RECEPTORS; CORTICOSTERONE AB Adrenal glomerulosa cells washed with delipidated albumin produced increased amounts of aldosterone in response to angiotensin-II (AII) or (Bu)2cAMP. Albumin treatment also increased binding of I-125-labeled AII to high affinity binding sites on adrenal cells. Lipid extracts of albumin solutions that were used to wash cells inhibited AII binding and aldosterone responses by washed glomerulosa cells. Chromatographic fractionation and mass spectroscopic analysis indicated that the inhibitors removed from cells by albumin were long chain fatty acids. Exogenous fatty acids not only inhibited AII binding, but they inhibited basal aldosterone production and increments in aldosterone caused by AII or dbcAMP, suggesting an effect on postreceptor steps in aldosteronogenesis. The most potent and most abundant fatty acids removed from adrenal cells were oleic, linoleic, and arachidonic. These fatty acids inhibited at micromolar concentrations in the absence of albumin and at somewhat higher concentrations in its presence. Cells that had been washed, then inhibited by exogenous oleic acid in vitro, were restored to their enhanced responsiveness by a second albumin wash, making it unlikely that cell damage is the mechanism of inhibition by fatty acids. Responses of fasciculata cells were not potentiated by albumin washes, and cortisol production was less sensitive than aldosterone production to exogenous fatty acids. Binding of ANP to glomerulosa cells was not affected by albumin or fatty acids. These results combined with clinical correlations make it plausible that unesterified fatty acids are naturally occurring regulators of the adrenal glomerulosa. Insulin's ability to lower plasma levels of fatty acids may be one way that it causes sodium retention. C1 UNIV WISCONSIN,SCH MED,DEPT MED,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PHARMACOL,MADISON,WI 53705. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. RP GOODFRIEND, TL (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,2500 OVERLOOK TERR,MADISON,WI 53705, USA. NR 27 TC 40 Z9 40 U1 0 U2 1 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAY PY 1991 VL 128 IS 5 BP 2511 EP 2519 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FJ396 UT WOS:A1991FJ39600040 PM 2019263 ER PT J AU CUNNINGHAM, LA SHORT, MP VIELKIND, U BREAKEFIELD, XO BOHN, MC AF CUNNINGHAM, LA SHORT, MP VIELKIND, U BREAKEFIELD, XO BOHN, MC TI SURVIVAL AND DIFFERENTIATION WITHIN THE ADULT-MOUSE STRIATUM OF GRAFTED RAT PHEOCHROMOCYTOMA CELLS (PC12) GENETICALLY MODIFIED TO EXPRESS RECOMBINANT BETA-NGF SO EXPERIMENTAL NEUROLOGY LA English DT Article ID NERVE GROWTH-FACTOR; SENILE DEMENTIA; BRAIN; NEURONS; LINE; RETROVIRUS; RESPONSES; CULTURES C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP CUNNINGHAM, LA (reprint author), UNIV ROCHESTER,MED CTR,DEPT NEUROBIOL & ANAT,ROCHESTER,NY 14642, USA. FU NIA NIH HHS [T32AG00107]; NIMH NIH HHS [T32MH18260]; NINDS NIH HHS [KO8NS01252] NR 34 TC 18 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 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD MAY PY 1991 VL 112 IS 2 BP 174 EP 182 DI 10.1016/0014-4886(91)90067-M PG 9 WC Neurosciences SC Neurosciences & Neurology GA FJ614 UT WOS:A1991FJ61400005 PM 1674694 ER PT J AU BLOCH, KD HONG, CC EDDY, RL SHOWS, TB QUERTERMOUS, T AF BLOCH, KD HONG, CC EDDY, RL SHOWS, TB QUERTERMOUS, T TI CDNA CLONING AND CHROMOSOMAL ASSIGNMENT OF THE ENDOTHELIN-2 GENE - VASOACTIVE INTESTINAL CONTRACTOR PEPTIDE IS RAT ENDOTHELIN-2 SO GENOMICS LA English DT Article ID VASOCONSTRICTOR PEPTIDE; HUMAN GENOME; C-FOS; EXPRESSION; CELLS; ORGANIZATION; MITOGENESIS; FAMILY; DNA C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIAC UNIT,BOSTON,MA 02114. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT HUMAN GENET,BUFFALO,NY 14263. RP BLOCH, KD (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115, USA. RI Hong, Charles/C-9989-2010 FU NHLBI NIH HHS [5 T32 HL07208-13]; NIGMS NIH HHS [GM 20454] NR 21 TC 119 Z9 121 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 MAY PY 1991 VL 10 IS 1 BP 236 EP 242 DI 10.1016/0888-7543(91)90505-9 PG 7 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA FK408 UT WOS:A1991FK40800030 PM 1840558 ER PT J AU LAMURAGLIA, MV MEISTER, M DIBONA, N AF LAMURAGLIA, MV MEISTER, M DIBONA, N TI TRACHEAL RESECTION AND RECONSTRUCTION - INDICATIONS, SURGICAL-PROCEDURE, AND POSTOPERATIVE CARE SO HEART & LUNG LA English DT Article AB Nursing management of the patient undergoing tracheal resection and reconstruction is not well described in the literature. Over the last 25 years, nurses in the respiratory surgical intensive care unit at Massachusetts General Hospital in Boston have cared for more than 600 patients who have undergone this procedure. Using a diagnostic format, we have developed a plan of care for this patient population. In this article, the etiology of tracheal obstruction, its diagnosis and surgical correction, and nursing care of the patient after tracheal resection and reconstruction are presented. RP LAMURAGLIA, MV (reprint author), MASSACHUSETTS GEN HOSP,RESP SURG INTENS CARE UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 0 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 0147-9563 J9 HEART LUNG JI Heart Lung PD MAY PY 1991 VL 20 IS 3 BP 245 EP 254 PG 10 WC Cardiac & Cardiovascular Systems; Nursing; Respiratory System SC Cardiovascular System & Cardiology; Nursing; Respiratory System GA FN317 UT WOS:A1991FN31700007 PM 2032861 ER PT J AU SCHENKER, S MADDREY, WC AF SCHENKER, S MADDREY, WC TI SUBLIMINAL DRUG-DRUG INTERACTIONS - USERS AND THEIR PHYSICIANS TAKE NOTICE SO HEPATOLOGY LA English DT Editorial Material ID ACETAMINOPHEN-INDUCED HEPATOTOXICITY; CHRONIC ETHANOL-CONSUMPTION; CARBON-TETRACHLORIDE; LIVER-INJURY; ALCOHOL; RAT; CYTOCHROME-P-450; POTENTIATION; TOXICITY; METABOLISM C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SW MED SCH,DALLAS,TX 75235. RP SCHENKER, S (reprint author), UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284, USA. FU NIAAA NIH HHS [R01 AA07514] NR 39 TC 5 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD MAY PY 1991 VL 13 IS 5 BP 995 EP 998 PG 4 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA FM340 UT WOS:A1991FM34000029 PM 2030003 ER PT J AU ANDERSON, RJ DUCHIN, KL GORE, RD HERMAN, TS MICHAELS, RS NICHOLA, PS NOLEN, TM WOLFSON, P WOMBOLT, DG ZUSMAN, R AF ANDERSON, RJ DUCHIN, KL GORE, RD HERMAN, TS MICHAELS, RS NICHOLA, PS NOLEN, TM WOLFSON, P WOMBOLT, DG ZUSMAN, R TI ONCE-DAILY FOSINOPRIL IN THE TREATMENT OF HYPERTENSION SO HYPERTENSION LA English DT Article DE ESSENTIAL HYPERTENSION; FOSINOPRIL; ANGIOTENSIN CONVERTING ENZYME INHIBITORS; DIURETIC THERAPY ID ANGIOTENSIN-CONVERTING-ENZYME; INHIBITOR AB This multicenter, dose-ranging study evaluated the antihypertensive effectiveness of once-daily administration of fosinopril sodium in 220 patients with supine diastolic blood pressure of 95-115 mm Hg. After a 4-week placebo period, patients were randomly assigned to double-blind therapy with either placebo or 10, 40, or 80 mg fosinopril once daily for 4 weeks. If treatment goals were not met, chlorthalidone 25 mg/day was added for weeks 5 to 8. Thereafter, patients could enter the long-term, open-label phase and receive 10-80 mg/day fosinopril plus chlorthalidone, if needed. After 4 weeks of monotherapy, the average decreases in supine diastolic blood pressure were 9% (10 mg), 11.5% (40 mg), and 12.5% (80 mg) compared with 6% in the placebo group. After 8 weeks, the average decreases, with or without diuretic therapy, were 12.5-18.2%, compared with 10.8% with placebo. Blood pressure continued to be well controlled, and the patients showed no evidence of tachyphylaxis or tolerance through 12-15 months of treatment. Fosinopril was well tolerated. During the short-term phase, no patient withdrew because of adverse events possibly related to fosinopril; during the long-term phase, nine of 148 patients (6.1%) withdrew for that reason. In patients with mild-to-moderate hypertension, once-daily fosinopril (40 and 80 mg) provided significant antihypertensive effects with or without diuretic therapy. The 10 mg dose was effective in some patients and may be considered a starting dose. C1 HENRY FORD HOSP,DEARBORN,MI. COLUMBIANA CLIN,COLUMBIANA,AL. NEPHROL ASSOCIATES TIDEWATER,NORFOLK,VA. SQUIBB PHARMACEUT RES INST,PRINCETON,NJ. VET ADM MED CTR,BUFFALO,NY. CHICAGO COLL OSTEOPATH MED,CHICAGO,IL 60615. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV COLORADO,DENVER,CO 80202. PROVIDENCE MED CTR,PORTLAND,OR 97213. NR 14 TC 25 Z9 26 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD MAY PY 1991 VL 17 IS 5 BP 636 EP 642 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA FL208 UT WOS:A1991FL20800006 PM 1827086 ER PT J AU URANO, M MAJIMA, H MILLER, R KAHN, J AF URANO, M MAJIMA, H MILLER, R KAHN, J TI CYTOTOXIC EFFECT OF 1,3 BIS (2-CHLOROETHYL)-N-NITROSOUREA AT ELEVATED-TEMPERATURES - ARRHENIUS PLOT ANALYSIS AND TUMOR RESPONSE SO INTERNATIONAL JOURNAL OF HYPERTHERMIA LA English DT Article DE BCNU; THERMOCHEMOTHERAPY; FSA-II TUMOR CELLS; BLEOMYCIN; CISPLATINUM; 5FU; CYTOXAN ID CHINESE-HAMSTER CELLS; MURINE FIBRO-SARCOMA; CYTO-TOXICITY; THERMAL ENHANCEMENT; HYPERTHERMIA; BLEOMYCIN; THERMOCHEMOTHERAPY; CHEMOTHERAPY; INVITRO; BCNU AB The effect of hyperthermia on the cytotoxicity of 1,3-bis-(2-chloroethyl)-N-nitrosourea (BCNU) was investigated in vitro and in vivo. Tumour cells were early-generation isotransplants of a spontaneous C3Hf/Sed mouse fibrosarcoma, FSa-II. For in vitro studies, single cell suspensions containing 1.0 x 10(6) cells/ml were treated in a water bath where a desired temperature was maintained by a constant-temperature circulator. Cell survival was determined by lung colony assay immediately thereafter. For in vivo studies the tumour cell suspensions were transplanted into the dorsal site of the C3Hf/Sed mouse foot. Tumours were treated by immersing animal feet into a constant-temperature water bath when tumours reached an average diameter of 4 mm (35 mm3). The tumour growth (TG) time or the time for one-half of the treated tumours to reach 1000 mm3 from initial treatment day was used as an endpoint. BCNU dose-cell survival curve at 37-degrees-C was exponential with a D0 of 1.1-mu-g/ml. Dose-cell survival curves at 37-43-degrees-C were determined as a function of treatment time at pH 6.7 and 7.4. BCNU of 1-mu-g/ml was added immediately before treatment. The slope of the survival curve became steeper with increasing temperature, indicating that the cytotoxic effect of BCNU was enhanced by hyperthermia. The Arrhenius plot analysis showed that activation energies at pH 6.7 and 7.4 were 53 and 51 kcal/M, respectively (no significant difference). Of interest in this analysis was that the Arrhenius plot did not show a breaking point which has been observed for other agents. Further investigation demonstrated that the decomposition of BCNU, which has been reported to be essential for production of reactive intermediates, occurred in aqueous medium at elevated temperatures. The magnitude of this decomposition depended on treatment temperature. As a result, preheated BCNU became less cytotoxic with an increase in preheating temperatures. The activation energy for this decomposition was about one-half of the activation energy for BCNU cytotoxicity. Studies in vivo indicated that the effect of BCNU was enhanced with increasing temperatures, and the enhancement was greatest when BCNU was administered i.p. immediately before hyperthermia. A glucose dose of 5 g/kg administered i.p. 60 min before hyperthermia further enhanced the antitumour effect of BCNU. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. RP URANO, M (reprint author), UNIV KENTUCKY,MED CTR,DEPT RADIAT MED,LEXINGTON,KY 40536, USA. FU NCI NIH HHS [CA26350] NR 30 TC 16 Z9 17 U1 0 U2 0 PU TAYLOR & FRANCIS LTD PI LONDON PA ONE GUNDPOWDER SQUARE, LONDON, ENGLAND EC4A 3DE SN 0265-6736 J9 INT J HYPERTHER JI Int. J. Hyperthermia PD MAY-JUN PY 1991 VL 7 IS 3 BP 499 EP 510 DI 10.3109/02656739109005014 PG 12 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FW960 UT WOS:A1991FW96000009 PM 1919145 ER PT J AU HOLDEN, SA TEICHER, BA HERMAN, TS AF HOLDEN, SA TEICHER, BA HERMAN, TS TI EFFECT OF ENVIRONMENTAL-CONDITIONS (PH, OXYGENATION, AND TEMPERATURE) ON MISONIDAZOLE CYTOTOXICITY AND RADIOSENSITIZATION INVITRO AND INVIVO IN FSAIIC FIBROSARCOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE MISONIDAZOLE; HYPERTHERMIA; PH; COMBINED MODALITY TREATMENT; HYPOXIA; RADIOSENSITIZATION ID MOUSE MAMMARY-CARCINOMA; MURINE TUMOR; CYTO-TOXICITY; ELEVATED-TEMPERATURES; CELL-SURVIVAL; FIBRO-SARCOMA; HOECHST 33342; HYPERTHERMIA; RADIATION; RO-07-0582 AB The effect of pH on misonidazole-induced cell killing at normal and elevated temperatures and on radiosensitization by misonidazole at 37-degrees-C was assessed in FSaIIC fibrosarcoma cells in vitro. At doses of 5-500-mu-M for 1 hr, misonidazole was 1.5- to 2-fold more toxic toward hypoxic versus euoxic cells at 37-degrees-C and pH 7.40. At 42-degrees-C and 43-degrees-C at pH 7.40, a less than 2-fold increase in cytotoxicity was observed in both normally oxic and hypoxic cells as compared with 37-degrees-C. At pH 6.45 and 37-degrees-C, misonidazole was less cytotoxic toward both euoxic and hypoxic cells than at pH 7.40. Unexpectedly, exposure to misonidazole at 42-degrees-C or 43-degrees-C and pH 6.45 caused no significant increase in cytotoxicity over that attributable to hyperthermia alone. Similarly, the dose modifying effect of misonidazole on single radiation fractions in vitro was also reduced at pH 6.45 versus pH 7.40 (2.60 versus 2.40, p < 0.01). In vivo, treatment of the FSaIIC tumor with misonidazole (1 g/kg) and/or local hyperthermia (43-degrees-C for 30 min to the tumor-bearing limb) in conjunction with radiation (10, 20, or 30 Gy) yielded a radiation dose modifying factor for misonidazole of 1.32, for hyperthermia of 1.38, and for the combination of 2.06 (probably additive). Analysis of the cytotoxicity achieved by these treatments in Hoechst 33342 dye-selected tumor subpopulations demonstrated that, whereas radiation was more toxic toward bright (presumably euoxic) cells, misonidazole, hyperthermia, and the combination were significantly more toxic toward dim (presumably hypoxic) cells. The addition of both hyperthermia and misonidazole to radiation more than overcame the relative resistance of the dim subpopulation to 10 Gy. These results indicate that misonidazole is a reasonable drug for use with hyperthermia and radiation to increase killing of hypoxic cells, but the decrease in cytotoxicity and radiosensitizing abilities of this agent observed under acidotic conditions could reduce the effectiveness of this treatment. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. FU NCI NIH HHS [R01-CA47379]; PHS HHS [R01-36508] NR 57 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY PY 1991 VL 20 IS 5 BP 1031 EP 1038 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FL424 UT WOS:A1991FL42400017 PM 2022503 ER PT J AU ROZENTAL, JM LEVINE, RL MEHTA, MP KINSELLA, TJ LEVIN, AB ALGAN, O MENDOZA, M HANSON, JM SCHRADER, DA NICKLES, RJ AF ROZENTAL, JM LEVINE, RL MEHTA, MP KINSELLA, TJ LEVIN, AB ALGAN, O MENDOZA, M HANSON, JM SCHRADER, DA NICKLES, RJ TI EARLY CHANGES IN TUMOR METABOLISM AFTER TREATMENT - THE EFFECTS OF STEREOTAXIC RADIOTHERAPY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Note DE STEREOTAXIC RADIOTHERAPY; PET; GLIOMA METABOLISM; BRAIN TUMOR ID POSITRON EMISSION TOMOGRAPHY; NERVOUS-SYSTEM TUMORS; CEREBRAL BLOOD-FLOW; GLUCOSE-METABOLISM; BRAIN-TUMOR; LINEAR-ACCELERATOR; MALIGNANT GLIOMAS; PET; CHEMOTHERAPY; PROGNOSIS AB Four patients with intracranial neoplasms, two with malignant gliomas and two with brain metastases, were treated with stereotactic radiotherapy. Patients received between 15 and 27.5 Gray of photon irradiation to the central tumor target point; the 80% isodose line covered the periphery of the tumor as determined by contrast enhanced computed tomography. Patients underwent a sequence of three Positron Emission Tomographic scans using [F-18]-fluorodeoxyglucose (PET-FDG)-a baseline scan the day before treatment, and follow-up scans 1 and 7 days after treatment. Ratios between the maximal tumor regional cerebral metabolic rate for glucose (rCMRGlu) (T*) and the contralateral remote white matter rCMRGlu (RW), that is, the glucose uptake ratio (T*/RW), were calculated. The percent change in ratios relative to each patient's baseline scan were calculated. Ratios increased 25% to 42% 1 day post-radiotherapy, then decreased to between 10% above and 12% below the baseline value 7 days post-radiotherapy. The T*/RW increased acutely after stereotactic radiotherapy in a fashion similar to that previously described following chemotherapy with a complex multi-drug regimen. A common metabolic pathway may underlie the increase in T*/RW after these different treatments. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT NEUROL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT NEUROL SURG,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT RADIOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT HUMAN ONCOL,MADISON,WI 53706. UNIV WISCONSIN,SCH MED,DEPT MED PHYS,MADISON,WI 53706. RP ROZENTAL, JM (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV 127,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. OI mehta, minesh/0000-0002-4812-5713 FU NCI NIH HHS [CA14520, CA47785]; NCRR NIH HHS [RR03186] NR 48 TC 45 Z9 46 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY PY 1991 VL 20 IS 5 BP 1053 EP 1060 PG 8 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FL424 UT WOS:A1991FL42400020 PM 2022505 ER PT J AU CHOI, NC AF CHOI, NC TI CONTROVERSIES IN THE ROLE OF POSTOPERATIVE RADIOTHERAPY IN STAGE-II AND STAGE-IIIA RESECTED NON-SMALL-CELL LUNG-CARCINOMA SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Editorial Material ID LYMPH-NODE METASTASIS; BRONCHOGENIC-CARCINOMA; RADIATION-THERAPY; SURVIVAL; CANCER; IRRADIATION; PULMONARY RP HARVARD UNIV, MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED, DEPT RADIAT THERAPY, DEPT RADIAT MED, BOSTON, MA 02114 USA. NR 36 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0360-3016 EI 1879-355X J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD MAY PY 1991 VL 20 IS 5 BP 1137 EP 1141 PG 5 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA FL424 UT WOS:A1991FL42400033 PM 1850720 ER PT J AU BLUM, HE VONWEIZSACKER, F AF BLUM, HE VONWEIZSACKER, F TI RATIONAL CLINICAL CHEMICAL DIAGNOSIS OF HEPATOBILIARY DISORDERS SO INTERNIST LA German DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 8 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0020-9554 J9 INTERNIST JI Internist PD MAY PY 1991 VL 32 IS 5 BP 239 EP 243 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FN873 UT WOS:A1991FN87300002 PM 1678385 ER PT J AU BLUM, HE VONWEIZSACKER, F AF BLUM, HE VONWEIZSACKER, F TI HBS-AG-NEGATIVE ANTI-HBC/ANTI-HBS-POSITIVE PATIENT SO INTERNIST LA German DT Article ID HEPATITIS-B-VIRUS; POLYMERASE CHAIN-REACTION; CHRONIC LIVER-DISEASE; HEPATOCELLULAR-CARCINOMA; ENZYMATIC AMPLIFICATION; CLINICAL RELEVANCE; MOLECULAR ANALYSES; DNA; SERUM; BIOLOGY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 28 TC 1 Z9 1 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0020-9554 J9 INTERNIST JI Internist PD MAY PY 1991 VL 32 IS 5 BP 262 EP 266 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA FN873 UT WOS:A1991FN87300006 PM 1907949 ER PT J AU HOWARD, MA WARDWELL, S ALBERT, DM AF HOWARD, MA WARDWELL, S ALBERT, DM TI EFFECT OF BUTYRATE AND CORTICOSTEROIDS ON RETINOBLASTOMA INVITRO AND INVIVO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID VITAMIN-D; CELLS; INHIBITION; GROWTH AB The effect of sodium butyrate (NaB) alone and in combination with a glucocorticoid was studied on Y-79 retinoblastoma cells both in vitro and in vivo. Both NaB (0.5 and 4 mM) and hydrocortisone (1-100-mu-M) added separately to cells grown in suspension resulted in a small growth inhibition (< 15%). A marked synergistic effect (75-77% growth inhibition) was observed in vitro when NaB and hydrocortisone were added in combination at all the concentrations tested. With in vivo experiments using the nude mouse model of retinoblastoma, the combination of NaB and methylprednisolone did not inhibit tumor growth. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DAVID G COGAN EYE PATHOL LAB,HOWE LAB,BOSTON,MA 02114. FU NEI NIH HHS [EY01917] NR 9 TC 11 Z9 11 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 MAY PY 1991 VL 32 IS 6 BP 1711 EP 1713 PG 3 WC Ophthalmology SC Ophthalmology GA FM179 UT WOS:A1991FM17900001 PM 2032794 ER PT J AU RONG, BL PAVANLANGSTON, D WENG, QP MARTINEZ, R CHERRY, JM DUNKEL, EC AF RONG, BL PAVANLANGSTON, D WENG, QP MARTINEZ, R CHERRY, JM DUNKEL, EC TI DETECTION OF HERPES-SIMPLEX VIRUS THYMIDINE KINASE AND LATENCY-ASSOCIATED TRANSCRIPT GENE-SEQUENCES IN HUMAN HERPETIC CORNEAS BY POLYMERASE CHAIN-REACTION AMPLIFICATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article ID CHRONIC STROMAL KERATITIS; HUMAN TRIGEMINAL GANGLIA; RNA COMPLEMENTARY; HSV-1 LATENCY; TYPE-1; INFECTION; NEURONS; MICE; DNA; MUTANTS AB Herpes simplex virus (HSV) latency in sensory ganglion neurons is well documented, but the existence of extraneuronal corneal latency is less well defined. To investigate the possibility of extraneuronal latency during ocular HSV infection, corneal specimens from 18 patients with quiescent herpes simplex keratitis (HSK) were obtained at the time of keratoplasty. Polymerase chain reaction (PCR) amplification followed by southern blot hybridization with a radiolabeled oligonucleotide probe was done to detect the presence of HSV-1 genome in these human corneal samples. Two pairs of oligonucleotides from the region of the HSV thymidine kinase (TK) gene and the latency-associated transcript (LAT) gene were used as primers in the PCR amplification. The DNA sequences from either the TK or the LAT gene were identified in 15 of 18 HSK corneas (83%). These results demonstrate that the HSV genome was retained, at least in part, in human corneas during quiescent HSV infection, giving further support to the concept of corneal extraneuronal latency. C1 EYE RES INST,MOLEC VIROL LAB,20 STANIFORD ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. FU NEI NIH HHS [EY05966-03] NR 37 TC 51 Z9 56 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 MAY PY 1991 VL 32 IS 6 BP 1808 EP 1815 PG 8 WC Ophthalmology SC Ophthalmology GA FM179 UT WOS:A1991FM17900014 PM 1851732 ER PT J AU WOLF, GL MISHKIN, MM ROUX, SG HALPERN, EF GOTTLIEB, J ZIMMERMAN, J GILLEN, J THELLMAN, C AF WOLF, GL MISHKIN, MM ROUX, SG HALPERN, EF GOTTLIEB, J ZIMMERMAN, J GILLEN, J THELLMAN, C TI COMPARISON OF THE RATES OF ADVERSE DRUG-REACTIONS - IONIC CONTRAST AGENTS, IONIC AGENTS COMBINED WITH STEROIDS, AND NONIONIC AGENTS SO INVESTIGATIVE RADIOLOGY LA English DT Article DE ADVERSE EFFECTS; CONTRAST MEDIA; IONIC AGENTS; NONIONIC AGENTS; STEROID PREMEDICATION ID MEDIA AB The influence of ionic agents alone, of diatrizoate plus two oral doses of methylprednisolone premedication, and of a nonionic agent (iohexol) upon the frequency and severity of adverse drug reactions (ADRs) was compared in ten hospitals during three separate time periods from 1985 to 1989. Nonionic agents were found to reduce significantly total ADRs; 52 of 8857 patients receiving nonionic agents experienced reactions, versus 263 of 6006 patients for ionics (P < .0001). The frequency of reactions classed as mild (2.9% for ionic agents versus 0.476 for nonionic agents: P < .001), moderate (1.2% versus 0.1%; P < .001), or severe (0.37% versus 0.01%; P < .001), also favored nonionic agents. Steroid premedication provided some protection, but iohexol was significantly better with respect to mild reactions (2.9% versus 0.4%, P < .001), moderate reactions (0.9% versus 0.1%, P < .01), and severe reactions (0.25% versus 0.01%, P < .01). The contrast medium was the greatest risk factor for adverse reaction (odds ratio 7.3), while prior contrast reaction (odds ratio 6.25), and hay fever (odds ratio 2.3) were found to be significant independent risks. We conclude that nonionic agents are safer for intravenous use than ionic agents given alone or with corticosteroid premedication. C1 LONG BEACH MEM MED CTR,LONG BEACH,CA. THOMAS JEFFERSON UNIV,PHILADELPHIA,PA 19107. CONSULTING STATISTICIANS INT,WELLESLEY,MA. PITTSBURGH NMR INST,PITTSBURGH,PA. RP WOLF, GL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 13 TC 72 Z9 74 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 MAY PY 1991 VL 26 IS 5 BP 404 EP 410 DI 10.1097/00004424-199105000-00003 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FH913 UT WOS:A1991FH91300003 PM 2055736 ER PT J AU RODKEY, GV AF RODKEY, GV TI THE AMERICAN-COLLEGE-OF-SURGEONS AND THE AMA SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP RODKEY, GV (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 1 PY 1991 VL 265 IS 17 BP 2194 EP 2194 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA FH877 UT WOS:A1991FH87700029 PM 2013950 ER PT J AU BLOMQUIST, MD BOGGARDS, M HANSON, ICG ROSENBLATT, HM POLLACK, MS HAWKINS, E RITZ, J SHEARER, WT AF BLOMQUIST, MD BOGGARDS, M HANSON, ICG ROSENBLATT, HM POLLACK, MS HAWKINS, E RITZ, J SHEARER, WT TI MONOCLONAL ANTI-T-CELL (T12) ANTIBODY TREATMENT OF GRAFT-VERSUS-HOST DISEASE IN SEVERE COMBINED IMMUNODEFICIENCY - TARGETING OF ANTIBODY AND ACTIVATION OF COMPLEMENT ON CD8+ CYTOTOXIC T-CELL SURFACES SO JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY LA English DT Article ID BONE-MARROW; TRANSPLANTATION; LEUKEMIA; FAILURE AB We report a 6-month-old male child with severe combined immunodeficiency who received an unirradiated blood transfusion and developed acute, severe graft-versus-host disease (GVHD), for which he received monoclonal anti-T cell (anti-T12) antibody treatment. The GVHD was manifested by a confluent maculopapular rash and increased liver function tests and was documented by skin biopsy. Separation of peripheral blood mononuclear cells forming rosettes with sheep red blood cells revealed engrafted T cells having the nonrelated HLA type of the blood donor. The patient was treated with intravenous monoclonal anti-T12 in a dose of 0.3 mg/kg/day for 5 days. An in vivo effect of the anti-T12 was suggested by clinical improvement of his skin rash and return of the liver transaminases to the normal range. Moreover, human complement components, activated C3 and C4, were detected by fluorescence microscopy on the surfaces of the engrafted CD8+ lymphocytes on the skin biopsy specimens. Also, with a biotin-avidin assay, the presence of the anti-T12 was detected on these same cells. These studies document not only the in vivo targeting of monoclonal anti-T12 antibody to cytotoxic T cells producing GVHD but also the activation of complement on these cells. C1 BAYLOR UNIV,DEPT PEDIAT,ALLERGY & IMMUNOL SECT,1 BAYLOR PL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT PATHOL,HOUSTON,TX 77030. BAYLOR UNIV,DEPT MICROBIOL & IMMUNOL,HOUSTON,TX 77030. TEXAS CHILDRENS HOSP,ALLERGY & IMMUNOL SERV,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR BIOL,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCRR NIH HHS [RR-00188] NR 17 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 0091-6749 J9 J ALLERGY CLIN IMMUN JI J. Allergy Clin. Immunol. PD MAY PY 1991 VL 87 IS 5 BP 1029 EP 1033 DI 10.1016/0091-6749(91)90427-P PG 5 WC Allergy; Immunology SC Allergy; Immunology GA FM095 UT WOS:A1991FM09500017 PM 1902852 ER PT J AU CRAIG, WA REDINGTON, J EBERT, SC AF CRAIG, WA REDINGTON, J EBERT, SC TI PHARMACODYNAMICS OF AMIKACIN INVITRO AND IN MOUSE THIGH AND LUNG INFECTIONS SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID TOBRAMYCIN; EFFICACY; MURINE; INVIVO; MICE C1 UNIV WISCONSIN,DEPT MED,MADISON,WI 53705. MERITER HOSP,DEPT PHARM,MADISON,WI 53715. RP CRAIG, WA (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,DEPT MED,MADISON,WI 53705, USA. NR 13 TC 155 Z9 155 U1 2 U2 7 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD MAY PY 1991 VL 27 SU C BP 29 EP 40 PG 12 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FP055 UT WOS:A1991FP05500006 PM 1830302 ER PT J AU PECHERE, JC CRAIG, WA MEUNIER, F AF PECHERE, JC CRAIG, WA MEUNIER, F TI ONCE DAILY DOSING OF AMINOGLYCOSIDE - ONE-STEP FORWARD SO JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY LA English DT Article ID NETILMICIN; GENTAMICIN; APPENDICITIS; COMBINATION; INFECTIONS; TOBRAMYCIN; KINETICS C1 UNIV GENEVA,MED CTR,DEPT MICROBIOL,CH-1211 GENEVA 4,SWITZERLAND. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. INST JULES BORDET,INFECT DIS UNIT,B-1000 BRUSSELS,BELGIUM. INST JULES BORDET,MICROBIOL LAB,B-1000 BRUSSELS,BELGIUM. NR 23 TC 26 Z9 27 U1 0 U2 0 PU W B SAUNDERS CO LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0305-7453 J9 J ANTIMICROB CHEMOTH JI J. Antimicrob. Chemother. PD MAY PY 1991 VL 27 SU C BP 149 EP 152 PG 4 WC Infectious Diseases; Microbiology; Pharmacology & Pharmacy SC Infectious Diseases; Microbiology; Pharmacology & Pharmacy GA FP055 UT WOS:A1991FP05500018 PM 1856144 ER PT J AU CIMA, LG VACANTI, JP VACANTI, C INGBER, D MOONEY, D LANGER, R AF CIMA, LG VACANTI, JP VACANTI, C INGBER, D MOONEY, D LANGER, R TI TISSUE ENGINEERING BY CELL TRANSPLANTATION USING DEGRADABLE POLYMER SUBSTRATES SO JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME LA English DT Article; Proceedings Paper CT SYMP OF TISSUE ENGINEERING CY APR 06-12, 1990 CL KEYSTONE, CO SP UNIV CALIF LOS ANGELES ID EPIDERMAL GROWTH-FACTOR; ANGIOGENESIS INVITRO; EXTRACELLULAR-MATRIX; ARTICULAR-CARTILAGE; ABSORBABLE SUTURES; LIVER-REGENERATION; PRIMARY CULTURES; RAT HEPATOCYTES; GUNN-RATS; CHONDROCYTES AB This paper reviews our research in developing novel matrices for cell transplantation using bioresorbable polymers. We focus on applications to liver and cartilage as paradigms for regeneration of metabolic and structural tissue, but review the approach in the context of cell transplantation as a whole. Important engineering issues in the design of successful devices are the surface chemistry and surface microstructure, which influence the ability of the cells to attach, grow, and function normally; the porosity and macroscopic dimensions, which affect the transport of nutrients to the implanted cells; the shape, which may be necessary for proper function in tissues like cartilage; and the choice of implantation site, which may be dictated by the total mass of the implant and which may influence the dimensions of the device by the available vascularity. Studies show that both liver and cartilage cells can be transplanted in small animals using this approach. C1 MIT, DEPT CHEM ENGN, CAMBRIDGE, MA 02139 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, SURG RES LAB, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT BIOCHEM, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, CAMBRIDGE, MA 02138 USA. CHILDRENS HOSP, SURG RES LAB, CAMBRIDGE, MA USA. NR 80 TC 381 Z9 402 U1 2 U2 38 PU ASME-AMER SOC MECHANICAL ENG PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017 SN 0148-0731 J9 J BIOMECH ENG-T ASME JI J. Biomech. Eng.-Trans. ASME PD MAY PY 1991 VL 113 IS 2 BP 143 EP 151 DI 10.1115/1.2891228 PG 9 WC Biophysics; Engineering, Biomedical SC Biophysics; Engineering GA HP749 UT WOS:A1991HP74900006 PM 1652042 ER PT J AU GOLD, MR STRICHARTZ, GR AF GOLD, MR STRICHARTZ, GR TI USE-DEPENDENT BLOCK OF ATRIAL SODIUM CURRENT BY ETHYLISOPROPYLAMILORIDE SO JOURNAL OF CARDIOVASCULAR PHARMACOLOGY LA English DT Article DE USE-DEPENDENT BLOCK; SODIUM CURRENT; ETHYLISOPROPYLAMILORIDE ID CHICK HEART-CELLS; ION CHANNEL BLOCKADE; LOCAL-ANESTHETICS; PURKINJE-FIBERS; AMILORIDE; INHIBITION; EXCHANGE; BINDING; DRUGS; 20-ALPHA-BENZOATE AB Ethylisopropylamiloride (EIPA) is a potent inhibitor of Na+-H+ exchange in many tissues and is frequently used to study cellular regulation of pH, but the electrophysiologic effects of EIPA on cardiac cells have not been studied previously. The use-dependent effects of EIPA on the sodium current (I(Na)) of cultured embryonic chick atrial myocytes were investigated using standard whole-cell patch-clamp techniques. With 150-ms depolarizations from - 140 to 0 mV, applied at 1-3 Hz in the presence of 10-mu-M EIPA, a decrement in I(Na) was observed. This use-dependent reduction equaled 31 +/- 6% of control I(Na) at steady state during 1-Hz stimulation. Inhibition increased with stimulation rate and with depolarization of the holding potential to - 100 mV, but there was no effect of pulse duration on the EIPA-induced inhibition over the range of 20-500 ms. Moreover, repetitive depolarizations to potentials that did not activate macroscopic current but that did yield pronounced channel inactivation did not result in a decrement in I(Na). The effect of EIPA increased over the concentration range of 1-30-mu-M so that with 3-Hz stimuli steady-state inhibition increased from 3 +/- 1 to 85 +/- 5%. Amiloride, which slows repolarization of the cardiac action potential, was at least 100-fold less potent than EIPA in reducing I(Na). We conclude that EIPA is an "open-channel" blocker of the cardiac sodium current at concentrations comparable to those of many type I antiarrhythmic agents. C1 BRIGHAM & WOMENS HOSP,ANESTHESIA RES LABS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GOLD, MR (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULFINCH BASEMENT,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM 15904] NR 44 TC 19 Z9 19 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0160-2446 J9 J CARDIOVASC PHARM JI J. Cardiovasc. Pharmacol. PD MAY PY 1991 VL 17 IS 5 BP 792 EP 799 DI 10.1097/00005344-199105000-00015 PG 8 WC Cardiac & Cardiovascular Systems; Pharmacology & Pharmacy SC Cardiovascular System & Cardiology; Pharmacology & Pharmacy GA FH070 UT WOS:A1991FH07000015 PM 1713995 ER PT J AU TALAMO, JH STARK, WJ GOTTSCH, JD GOODMAN, DF PRATZER, K CRAVY, TV ENGER, C AF TALAMO, JH STARK, WJ GOTTSCH, JD GOODMAN, DF PRATZER, K CRAVY, TV ENGER, C TI NATURAL-HISTORY OF CORNEAL ASTIGMATISM AFTER CATARACT-SURGERY SO JOURNAL OF CATARACT AND REFRACTIVE SURGERY LA English DT Article DE AGAINST THE RULE; CORNEAL ASTIGMATISM; SUTURE; WITH THE RULE AB Little information on the natural course of corneal astigmatism following cataract surgery exists. We report a prospective, computerized analysis of postoperative astigmatism, based on keratometry measurements, of 137 cases of extracapsular cataract extraction with intraocular lens implantation performed by one surgeon. No sutures were cut postoperatively. Surgery induced 1.44 diopters (D) of with-the-rule astigmatism at one month, which declined at a rate of 0.77 D and 0.35 D per month for the next two months, respectively, with a more gradual decline thereafter. The mean surgically induced astigmatism at the last postoperative visit ranged from 0.29 D at six months (minimum follow-up) to 1.23 D at 48 months; both were against-the-rule. Mean follow-up was 28.92 months. These findings may be technique specific and suggest that (1) corneal curvature continues to change slowly even two to four years postoperatively; (2) most patients develop against-the-rule astigmatism, thus more with-the-rule astigmatism is desirable in the early postoperative period; (3) selective suture removal is necessary only when significantly more than 3.00 D of surgically induced with-the-rule astigmatism is present. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 35 Z9 35 U1 0 U2 0 PU AMER SOC CATARACT REFRACTIVE SURGERY PI FAIRFAX PA 4000 LEGATO RD, SUITE 850, FAIRFAX, VA 22030 SN 0886-3350 J9 J CATARACT REFR SURG JI J. Cataract. Refract. Surg. PD MAY PY 1991 VL 17 IS 3 BP 313 EP 318 PG 6 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA FL031 UT WOS:A1991FL03100006 PM 1861245 ER PT J AU HALL, JE BHATTA, N ADAMS, JM RIVIER, JE VALE, WW CROWLEY, WF AF HALL, JE BHATTA, N ADAMS, JM RIVIER, JE VALE, WW CROWLEY, WF TI VARIABLE TOLERANCE OF THE DEVELOPING FOLLICLE AND CORPUS-LUTEUM TO GONADOTROPIN-RELEASING-HORMONE ANTAGONIST-INDUCED GONADOTROPIN WITHDRAWAL IN THE HUMAN SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID HUMAN MENSTRUAL-CYCLE; HUMAN GRANULOSA-CELLS; STIMULATING-HORMONE; LUTEINIZING-HORMONE; PROGESTERONE SECRETION; NORMAL MEN; SUPPRESSION; LH; PHASE; WOMEN AB To examine the differential sensitivity of the ovary to temporary withdrawal of gonadotropin support at different stages of folliculogenesis and corpus luteum function, GnRH antagonist blockade of gonadotropin secretion was examined in 17 studies using the Nal-Glu GnRH antagonist. A vehicle control, antagonist treatment, and follow-up cycle format was used in each study. A previously determined ED100 dose of the Nal-Glu GnRH antagonist (150-mu-g/kg) or vehicle was administered sc every 24 h for 3 consecutive days in the midfollicular phase (MFP), late follicular phase (LFP), and midluteal phase (MLP). In studies in the MFP (n = 7), the largest follicle was 11 +/- 2 mm (mean +/- SEM), and the mean estradiol (E2) level was 220 +/- 44 pmol/L on the first day of antagonist administration. Administration of the antagonist resulted in a 75 +/- 6% suppression of LH (P < 0.005), no significant change in FSH, and suppression of E2 to the assay detection limit (P < 0.05). Total cycle length was increased compared to that of the vehicle control cycle (37.3 +/- 1.3 vs. 26.3 +/- 1.1 days; P < 0.005) due to prolongation of follicular phase length (P < 0.005) and reinitiation of folliculogenesis. In the LFP (n = 5), the largest follicle was 16 +/- 1 mm (P < 0.05 vs. MFP), and the E2 level was 394 +/- 95 pmol/L (P < 0.05 vs. MFP) on the first day of antagonist administration. Antagonist administration resulted in a 65 +/- 6% suppression of LH (P < 0.05), a 47 +/- 11% decrease in FSH (P < 0.05), and no significant change in E2. Total cycle length was prolonged (32.4 +/- 2.2 vs. 25.6 +/- 0.4 days; P < 0.05) due to an increase in follicular phase length (P < 0.02); however, the prolongation of the follicular phase was significantly less than that of the MFP (8.0 +/- 1.5 vs. 15.1 +/- 0.1 days; P < 0.001), suggesting ovulation from the initial dominant follicle. In studies in the MLP (n = 5), LH, E2, and progesterone decreased to the assay detection limit after antagonist administration, while FSH decreased by 36 +/- 4% (P < 0.05). Menstrual bleeding occurred within 24-48 h of the final Nal-Glu antagonist injection. The total cycle length was decreased after antagonist administration (21.8 +/- 1 vs. 27.8 +/- 1.1 days; P < 0.001), due entirely to luteal phase shortening (7.2 +/- 0.2 vs. 14.0 +/- 0.7 days; P < 0.001) with demise of the corpus luteum. We conclude that 1) the use of an ED100 dose of the Nal-Glu GnRH antagonist for 3 days in normal women results in persistence of the relatively greater suppression of LH compared to FSH previously demonstrated in single dose studies; 2) this degree of gonadotropin deprivation produces different results depending upon the underlying maturation of the dominant follicle or corpus luteum; 3) in the follicular phase, the developing follicle becomes more tolerant to gonadotropin withdrawal as it becomes functionally more mature from the MFP to the LFP; and 4) in the MLP, this degree of gonadotropin withdrawal is not tolerated, and luteolysis occurs. C1 SALK INST BIOL STUDIES, LA JOLLA, CA 92037 USA. RP HALL, JE (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, REPROD ENDOCRINE UNIT, BARTLETT HALL EXTENS 5, BOSTON, MA 02114 USA. FU NCRR NIH HHS [RR-1066]; NICHD NIH HHS [HD-15080, HD-3-2837, U01 HD044417, U54 HD029164, U54 HD028138] NR 32 TC 42 Z9 42 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD MAY PY 1991 VL 72 IS 5 BP 993 EP 1000 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FH996 UT WOS:A1991FH99600008 PM 1902489 ER PT J AU THE, J EBERSOLE, JL AF THE, J EBERSOLE, JL TI RHEUMATOID-FACTOR (RF) DISTRIBUTION IN PERIODONTAL-DISEASE SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Article DE PERIODONTITIS; RHEUMATOID FACTOR (RF); ANTIBODY; ARTHRITIS ID B-CELL ACTIVATION; IMMUNE-COMPLEXES; BACTEROIDES-FRAGILIS; BLOOD-LYMPHOCYTES; SEPTIC ARTHRITIS; IMMUNOGLOBULIN-M; IGG SUBCLASS; ANTIBODIES; SERUM; MOUSE AB This study investigated the occurrence of an autoantibody, IgM rheumatoid factor, that may result from the chronic inflammation noted in periodontal disease and rheumatoid arthritis. In order to detect IgM-RF, a biotinavidin ELISA was developed. This assay was found to be sensitive and accurate by testing a rheumatoid arthritis population. The characteristics of this rheumatoid arthritis group were further determined, such that the total serum immunoglobulin concentrations were slightly elevated although within the normal range for IgM, IgG, and IgA; IgG antibody levels were elevated against oral microorganisms of the genus Capnocytophaga, while elevated IgM antibody levels were noted to Bacteroides species. In a population of 260 subjects of which 171 were periodontal disease patients, 16 of 171 (9.4%) were sero-positive for IgM-RF, of which the predominant disease types were advanced destructive periodontitis and adult periodontitis. For comparison, a random population of seronegative periodontal disease patients was constructed that was matched for sex and approximate age to the seropositive group. The total immunoglobulin levels of the two groups were not significantly different and the means of both were slightly lower than the rheumatoid arthritis group. When the antibody profiles of the two periodontal disease populations were compared it became evident that the RF-positive group showed IgM and IgG antibody that was significantly elevated to Capnocytophaga species and f. nucleatum. Therefore, the chronic inflammation associated with periodontitis appears to increase significantly the formation of IgM-RF; however, there does appear to be a relationship between IgM-RF and elevated antibody to selected oral microorganisms. C1 FORSYTH DENT CTR,DEPT IMMUNOL,BOSTON,MA. HARVARD UNIV,DEPT DENT MED,CAMBRIDGE,MA 02138. FU NIDCR NIH HHS [DE-04881] NR 58 TC 25 Z9 28 U1 1 U2 2 PU PLENUM PUBL CORP PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 SN 0271-9142 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD MAY PY 1991 VL 11 IS 3 BP 132 EP 142 DI 10.1007/BF00918681 PG 11 WC Immunology SC Immunology GA FP236 UT WOS:A1991FP23600003 PM 1890163 ER PT J AU KRAMER, J KATZ, Y ROSEN, FS DAVIS, AE STRUNK, RC AF KRAMER, J KATZ, Y ROSEN, FS DAVIS, AE STRUNK, RC TI SYNTHESIS OF C1 INHIBITOR IN FIBROBLASTS FROM PATIENTS WITH TYPE-I AND TYPE-II HEREDITARY ANGIONEUROTIC-EDEMA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE SYNTHESIS OF C1 INHIBITOR; HEREDITARY ANGIONEUROTIC EDEMA ID FACTOR-B; C1-INHIBITOR SYNTHESIS; GAMMA-INTERFERON; ANGIO-EDEMA; DEFICIENCY; PROTEINS; EXPRESSION; MONOCYTES; PLASMA; CELLS AB Patients with hereditary angioneurotic edema (HANE) have serum levels of functionally active inhibitor of the first component of complement (C1 INH) between 5 and 30% of normal, instead of the 50% expected from the single normal allele. Increases in rates of catabolism have been documented in patients with HANE and certainly account for some of decrease in C1 INH level. A possible role for a decrease in synthesis of C1 INH in producing serum levels of C1 INH below the expected 50% of normal has not been well studied. We studied the synthesis of C1 INH in skin fibroblast lines, which produce easily detectable amounts of C1 INH. In type I HANE cells, C1 INH synthesis was 19.6 +/- 4.0% (mean +/- SD) of normal, much less than the 50% predicted. In type II HANE cells, the total amount of C1 INH synthesis (functional and dysfunctional) was 98.9 +/- 17% of normal; the functional protein comprised 43% of the total. Thus, type II HANE cells synthesized functional C1 INH at a much greater rate than for the type I cells. In both type I and II HANE cells, amounts of steady-state C1 INH mRNA levels paralleled rates of C1 INH synthesis, indicating that control of C1 INH synthesis occurred at pretranslational levels. Both type I and type II fibroblasts synthesized normal amounts of C1r and C1s. These data suggest that the lower than expected amounts of functionally active C1 INH in type I HANE may be due, in part, to a decrease in rate of synthesis of the protein, and that the expressions of the normal C1 INH allele in HANE is influenced by the type of abnormal allele present. C1 WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110. ST LOUIS CHILDRENS HOSP,DIV PULM MED,ST LOUIS,MO 63178. ST LOUIS CHILDRENS HOSP,DIV ALLERGY IMMUNOL,ST LOUIS,MO 63178. CHILDRENS HOSP MED CTR,DIV IMMUNOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV NEPHROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-37591]; NIAID NIH HHS [AI-24836]; NIDDK NIH HHS [DK-26609] NR 24 TC 21 Z9 21 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAY PY 1991 VL 87 IS 5 BP 1614 EP 1620 DI 10.1172/JCI115175 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FK453 UT WOS:A1991FK45300019 PM 1902490 ER PT J AU ANDERSON, RJ BRECKON, R DIXON, BS AF ANDERSON, RJ BRECKON, R DIXON, BS TI ATP RECEPTOR REGULATION OF ADENYLATE-CYCLASE AND PROTEIN-KINASE-C ACTIVITY IN CULTURED RENAL LLC-PK1 CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PURINOCEPTORS; VASOPRESSIN; ADENOSINE TRIPHOSPHATE; CYCLIC AMP ID CORTICAL COLLECTING TUBULE; SIGNAL TRANSDUCTION SYSTEMS; PHOSPHOLIPASE-C; PHOSPHOINOSITIDE TURNOVER; P2Y-PURINERGIC RECEPTOR; GUANINE-NUCLEOTIDES; VASOPRESSIN ACTION; CYCLIC-AMP; ADENOSINE; TRANSPORT AB In cultured intact LLC-PK1 renal epithelial cells, a nonhydrolyzable ATP analogue, ATP-gamma-S, inhibits AVP-stimulated cAMP formation. In LLC-PK1 membranes, several ATP analogues inhibit basal, GTP-, forskolin-, and AVP-stimulated adenylate cyclase activity in a dose-dependent manner. The rank order potency of inhibition by ATP analogues suggests that a P2y type of ATP receptor is involved in this inhibition. The compound ATP-gamma-S inhibits agonist-stimulated adenylate cyclase activity in solubilized and in isobutylmethylxanthine (IBMX) and quinacrine pretreated membranes, suggesting that ATP-gamma-S inhibition occurs independent of AVP and A1 adenosine receptors and of phospholipase A2 activity. The ATP-gamma-S inhibition of AVP-stimulated adenylate cyclase activity is not affected by pertussis toxin but is attenuated by GDP-beta-S, suggesting a possible role for a pertussis toxin insensitive G protein in the inhibition. Exposure of intact LLC-PK cells to ATP-gamma-S results in a significant increase in protein kinase C activity. However, neither of two protein kinase C inhibitors (staurosporine and H-7) prevents ATP-gamma-S inhibition of AVP-stimulated adenylate cyclase activity, suggesting that this inhibition occurs by a protein kinase C independent mechanism. These findings suggest the presence of functional P2y purinoceptors coupled to two signal transduction pathways in cultured renal epithelial cells. The effect of P2y purinoceptors to inhibit AVP-stimulated adenylate cyclase activity may be mediated, at least in part, by a pertussis toxin insensitive G protein. C1 DENVER VET AFFAIRS MED CTR,MED SERV,DENVER,CO 80262. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80262. NR 37 TC 39 Z9 39 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAY PY 1991 VL 87 IS 5 BP 1732 EP 1738 DI 10.1172/JCI115191 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FK453 UT WOS:A1991FK45300035 PM 1850760 ER PT J AU SHERMAN, ML DATTA, R HALLAHAN, DE WEICHSELBAUM, RR KUFE, DW AF SHERMAN, ML DATTA, R HALLAHAN, DE WEICHSELBAUM, RR KUFE, DW TI REGULATION OF TUMOR-NECROSIS-FACTOR GENE-EXPRESSION BY IONIZING-RADIATION IN HUMAN MYELOID-LEUKEMIA CELLS AND PERIPHERAL-BLOOD MONOCYTES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IONIZING RADIATION; TNF; GENE EXPRESSION; TRANSCRIPTION; MONOCYTES ID FACTOR CACHECTIN; FACTOR-ALPHA; FACTOR TNF; MESSENGER-RNA; PHORBOL ESTER; TRANSCRIPTION; ACID; IRRADIATION; INTERFERON; INDUCTION AB Previous studies have demonstrated that ionizing radiation induces the expression of certain cytokines, such as TNF alpha/cachectin. However, there is presently no available information regarding the molecular mechanisms responsible for the regulation of cytokine gene expression by ionizing radiation. In this report, we describe the regulation of the TNF gene by ionizing radiation in human myeloid leukemia cells. The increase in TNF transcripts by x rays was both time- and dose-dependent as determined by Northern blot analysis. Similar findings were obtained in human peripheral blood moncytes. Transcriptional run-on analyses have demonstrated that ionizing radiation stimulates the rate of TNF gene transcription. Furthermore, induction of TNF mRNA was increased in the absence of protein synthesis. In contrast, ionizing radiation had little effect on the half-life of TNF transcripts. These findings indicate that the increase in TNF mRNA observed after irradiation is regulated by transcriptional mechanisms and suggest that production of this cytokine by myeloid cells may play a role in the pathophysiologic effects of ionizing radiation. C1 UNIV CHICAGO,MICHAEL REESE HOSP & MED CTR,CTR RADIAT THERAPY,DEPT RADIAT ONCOL,CHICAGO,IL 60616. RP SHERMAN, ML (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. NR 34 TC 135 Z9 138 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAY PY 1991 VL 87 IS 5 BP 1794 EP 1797 DI 10.1172/JCI115199 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FK453 UT WOS:A1991FK45300043 PM 2022746 ER PT J AU NAKAMURA, H NEMENOFF, RA GRONICH, JH BONVENTRE, JV AF NAKAMURA, H NEMENOFF, RA GRONICH, JH BONVENTRE, JV TI SUBCELLULAR CHARACTERISTICS OF PHOSPHOLIPASE-A2 ACTIVITY IN THE RAT-KIDNEY - ENHANCED CYTOSOLIC, MITOCHONDRIAL, AND MICROSOMAL PHOSPHOLIPASE-A2 ENZYMATIC-ACTIVITY AFTER RENAL ISCHEMIA AND REPERFUSION SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PHOSPHOLIPIDS; ACUTE RENAL FAILURE; ACYL HYDROLASES; CALCIUM; FATTY ACIDS ID FREE CALCIUM-CONCENTRATION; GLOMERULAR MESANGIAL CELLS; ADENOSINE-TRIPHOSPHATE; FATTY-ACIDS; MEMBRANE; INJURY; PURIFICATION; LIVER; ACTIVATION; DAMAGE AB Phospholipase A2 (PLA2) activities in cytosolic, mitochondrial, and microsomal fractions of rat kidneys were characterized under control conditions, after ischemia, and subsequent to ischemia and reperfusion. Two forms of PLA2 activity were present in the cytosolic fraction: a high molecular weight form, active against phosphatidylcholine (PC), and phosphatidylethanolamine (PE), which upon purification has a molecular mass of 110 kD; and a smaller form (M(r) almost-equal-to 14 kD), active against PE. In mitochondrial and microsomal fractions a single form (M(r) almost-equal-to 14 kD), active against both PC and PE, was dominant. Activities in each fraction were optimal at pH 8.5-9.5. Cytosolic PLA2 activity was enhanced when Ca2+ concentration ([Ca2+]) was increased over the range of 10(-7) to 10(-6) M. Mitochondrial PLA2 activity required higher [Ca2+] for activation (> 10(-6) M). After 45 min of ischemia cytosolic PLA2 activity was decreased, whereas mitochondrial and microsomal activities were increased. When ischemia was followed by 1 h of reperfusion, cytosolic, mitochondrial and microsomal activities were enhanced. Ischemia alone did not change the gel filtration chromatography patterns of PLA2 activity, but ischemia and reperfusion resulted in the appearance of a new peak of activity in cytosolic and mitochondrial fractions (M(r) almost-equal-to 2-3 kD). Thus, the rat kidney has multiple forms of PLA, activity, likely representing distinct enzymes, with Ca2+ dependencies suggesting regulation by Ca2+ in vivo. Ischemia and reperfusion result in stable increases of PLA2 activity in each subcellular fraction, perhaps related to covalent modifications of PLA2's, which likely account for membrane phospholipid degradation, and increased tissue levels of unsaturated free fatty acids. C1 MASSACHUSETTS GEN HOSP,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED & ANESTHESIA,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-39249, DK-39773, DK-38452] NR 47 TC 117 Z9 118 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAY PY 1991 VL 87 IS 5 BP 1810 EP 1818 DI 10.1172/JCI115202 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA FK453 UT WOS:A1991FK45300046 PM 2022747 ER PT J AU RAPHAEL, B ANDERSEN, JW SILBER, R OKEN, M MOORE, D BENNETT, J BONNER, H HAHN, R KNOSPE, WH MAZZA, J GLICK, J AF RAPHAEL, B ANDERSEN, JW SILBER, R OKEN, M MOORE, D BENNETT, J BONNER, H HAHN, R KNOSPE, WH MAZZA, J GLICK, J TI COMPARISON OF CHLORAMBUCIL AND PREDNISONE VERSUS CYCLOPHOSPHAMIDE, VINCRISTINE, AND PREDNISONE AS INITIAL TREATMENT FOR CHRONIC LYMPHOCYTIC-LEUKEMIA - LONG-TERM FOLLOW-UP OF AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP RANDOMIZED CLINICAL-TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COMBINATION CHEMOTHERAPY; TOXICITY; THERAPY C1 NYU HOSP,MED CTR,550 1ST AVE,NEW YORK,NY 10016. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. HOSP UNIV PENN,PHILADELPHIA,PA 19104. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. OI Raphael, Bruce/0000-0002-8104-160X FU NCI NIH HHS [CA 16395, CA 23318, CA 21115] NR 26 TC 101 Z9 102 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAY PY 1991 VL 9 IS 5 BP 770 EP 776 PG 7 WC Oncology SC Oncology GA FJ833 UT WOS:A1991FJ83300011 PM 2016618 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 PRIMARY LOCALLY ADVANCED RECTAL AND RECTOSIGMOID CARCINOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COLORECTAL-CANCER; PREOPERATIVE IRRADIATION; RADIOTHERAPY; ADENOCARCINOMA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG & SURG ONCOL,RADIAT MED SERV,BOSTON,MA 02114. UNIV N CAROLINA,SCH MED,CHAPEL HILL,NC 27514. NR 18 TC 130 Z9 131 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 MAY PY 1991 VL 9 IS 5 BP 843 EP 849 PG 7 WC Oncology SC Oncology GA FJ833 UT WOS:A1991FJ83300022 PM 2016628 ER PT J AU ROSENBAUM, JF AF ROSENBAUM, JF TI THE CHANGING HORIZON IN THE TREATMENT OF DEPRESSION AND RELATED DISORDERS - INTRODUCTION SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAY PY 1991 VL 52 SU S BP 3 EP 3 PG 1 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA FQ265 UT WOS:A1991FQ26500001 ER PT J AU ROSENBAUM, JF AF ROSENBAUM, JF TI THE CHANGING HORIZON IN THE TREATMENT OF DEPRESSION SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAY PY 1991 VL 52 SU S BP 63 EP 64 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA FQ265 UT WOS:A1991FQ26500010 ER PT J AU BROWNELL, AL KANO, M MCKINSTRY, RC MOSKOWITZ, MA ROSEN, BR BROWNELL, GL AF BROWNELL, AL KANO, M MCKINSTRY, RC MOSKOWITZ, MA ROSEN, BR BROWNELL, GL TI PET AND MR STUDIES OF EXPERIMENTAL FOCAL STROKE SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE EMISSION COMPUTED TOMOGRAPHY; ANIMAL STUDIES; BRAIN, ISCHEMIA; MAGNETIC RESONANCE IMAGING; METABOLISM, GLUCOSE ID CEREBRAL GLUCOSE-UTILIZATION; RAT-BRAIN; BLOOD-FLOW; ARTERY OCCLUSION; LOCAL CHANGES; INFARCTION; MODEL; METABOLISM; ANESTHESIA; ISCHEMIA AB Positron emission tomography (PET) and MR have been compared with histochemical pathology to show affected tissue areas in rat brain after right middle cerebral artery (MCA) occlusion combined with temporary bilateral common carotid artery occlusion in Long Evans rats. The glucose metabolic rate was 65 +/- 8-mu-mol/100 ml/min in the right cortical gray matter corresponding to the occluded middle cerebral artery territory and 93 +/- 8-mu-mol/100 ml/min in the corresponding (left) normal side. Infarcted tissue showed decreased PET activity and increased signal in MR T2-weighted scans ipsilateral to the MCA occlusion. These regions correspond to a zone of focal infraction identified in coronal tissue sections stained with 3-4-5 triphenyl tetrazolium chloride. This study demonstrates that PET can be used to study glucose utilization in rat stroke model in vivo and noninvasively. C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. RP BROWNELL, AL (reprint author), MASSACHUSETTS GEN HOSP,PHYS RES LAB,BOSTON,MA 02114, USA. RI Moskowitz, Michael/D-9916-2011 FU NCI NIH HHS [CA32873] NR 29 TC 14 Z9 14 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0363-8715 J9 J COMPUT ASSIST TOMO JI J. Comput. Assist. Tomogr. PD MAY-JUN PY 1991 VL 15 IS 3 BP 376 EP 380 DI 10.1097/00004728-199105000-00006 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FM318 UT WOS:A1991FM31800005 PM 2026795 ER PT J AU OOSTERWEGEL, M VANDEWETERING, M DOOIJES, D KLOMP, L WINOTO, A GEORGOPOULOS, K MEIJLINK, F CLEVERS, H AF OOSTERWEGEL, M VANDEWETERING, M DOOIJES, D KLOMP, L WINOTO, A GEORGOPOULOS, K MEIJLINK, F CLEVERS, H TI CLONING OF MURINE TCF-1, A T-CELL SPECIFIC TRANSCRIPTION FACTOR INTERACTING WITH FUNCTIONAL MOTIFS IN THE CD3-EPSILON AND T-CELL RECEPTOR ALPHA ENHANCERS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID DNA-BINDING PROTEIN; GENE-EXPRESSION; PROMOTER; LOCUS; CDNA AB CD3-epsilon-gene expression is confined to the T cell lineage. We have recently identified and cloned a human transcription factor, TCF-1, that binds to a functional element in the T lymphocyte-specific enhancer of CD3-epsilon. In a panel of human cell lines, TCF-1 expression was restricted to T lineage cells. TCF-1 belonged to a novel family of genes that contain the so-called high mobility group 1 (HMG) box. Here we report the cloning of murine TCF-1. Two splice alternatives were identified that were not previously observed in human TCF-1. Murine and human TCF-1 displayed a 95.5% overall amino acid homology. Recombinant murine and human TCF-1 recognized the same sequence motif in the CD3-epsilon enhancer as judged by gel retardation and methylation interference assays. With the murine cDNA clones several aspects of TCF-1 were analyzed. First, deletion analysis revealed that a region of TCF-1 containing the HMG box was sufficient for sequence-specific binding. Second, by high stringency Northern blotting and in situ hybridization, TCF-1 expression was shown to be confined to the thymus and to the T cell areas of the spleen. Third, TCF-1 bound specifically to a functional T cell-specific element in the T cell receptor-alpha (TCR-alpha) enhancer. The T lineage-specific expression and the affinity for functional motifs in the TCR-alpha and CD3-epsilon enhancers imply an important role for TCF-1 in the establishment of the mature T cell phenotype. C1 UNIV HOSP UTRECHT,DEPT CLIN IMMUNOL,POB 85500,3508 GA UTRECHT,NETHERLANDS. STATE UNIV UTRECHT,DEPT CELL BIOL,UTRECHT,NETHERLANDS. HUBRECHT LAB,UTRECHT,NETHERLANDS. UNIV CALIF BERKELEY,DEPT MOLEC & CELL BIOL,DIV IMMUNOL,BERKELEY,CA 94720. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 31 TC 125 Z9 126 U1 0 U2 1 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 MAY 1 PY 1991 VL 173 IS 5 BP 1133 EP 1142 DI 10.1084/jem.173.5.1133 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA FH752 UT WOS:A1991FH75200011 PM 1827138 ER PT J AU SOKOL, SM MCCLOSKEY, M COHEN, NJ ALIMINOSA, D AF SOKOL, SM MCCLOSKEY, M COHEN, NJ ALIMINOSA, D TI COGNITIVE REPRESENTATIONS AND PROCESSES IN ARITHMETIC - INFERENCES FROM THE PERFORMANCE OF BRAIN-DAMAGED SUBJECTS SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-LEARNING MEMORY AND COGNITION LA English DT Article ID MENTAL MULTIPLICATION; PROCEDURAL KNOWLEDGE; TEMPORAL ASPECTS; SIMPLE ADDITION; SINGLE-PATIENT; VERIFICATION; DYSCALCULIA; RETRIEVAL; PATTERNS; SKILL AB In this article, we present data from two brain-damaged patients with calculation impairments in support of claims about the cognitive mechanisms underlying simple arithmetic performance. We first present a model of the functional architecture of the cognitive calculation system based on previous research. We then elaborate this architecture through detailed examination of the patterns of spared and impaired performance of the two patients. From the patients' performance we make the following theoretical claims: that some arithmetic facts are stored in the form of individual fact representations (e.g., 9 x 4 = 36), whereas other facts are stored in the form of a general rule (e.g., 0 x N = 0); that arithmetic fact retrieval is mediated by abstract internal representations that are independent of the form in which problems are presented or responses are given; that arithmetic facts and calculation procedures are functionally independent; and that calculation algorithms may include special-case procedures that function to increase the speed or efficiency of problem solving. We conclude with a discussion of several more general issues relevant to the reported research. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. JOHNS HOPKINS UNIV, BALTIMORE, MD 21218 USA. RP SOKOL, SM (reprint author), MASSACHUSETTS GEN HOSP, INST HLTH PROFESS, NEUROLINGUIST LAB, 15 RIVER ST, BOSTON, MA 02108 USA. FU NINDS NIH HHS [NS21047] NR 75 TC 124 Z9 126 U1 3 U2 5 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0278-7393 EI 1939-1285 J9 J EXP PSYCHOL LEARN JI J. Exp. Psychol.-Learn. Mem. Cogn. PD MAY PY 1991 VL 17 IS 3 BP 355 EP 376 DI 10.1037/0278-7393.17.3.355 PG 22 WC Psychology; Psychology, Experimental SC Psychology GA FK202 UT WOS:A1991FK20200001 PM 1845392 ER PT J AU MCCLOSKEY, M HARLEY, W SOKOL, SM AF MCCLOSKEY, M HARLEY, W SOKOL, SM TI MODELS OF ARITHMETIC FACT RETRIEVAL - AN EVALUATION IN LIGHT OF FINDINGS FROM NORMAL AND BRAIN-DAMAGED SUBJECTS SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-LEARNING MEMORY AND COGNITION LA English DT Article ID MENTAL ADDITION; MULTIPLICATION SKILL; VERIFICATION; NETWORK; MECHANISMS; RECALL AB Retrieval of basic arithmetic facts is a central aspect of almost any arithmetic performance. Furthermore, the arithmetic facts provide an opportunity to study memory processes in the context of a naturally occurring but circumscribed set of facts. This article examines current models of arithmetic fact retrieval in light of previously reported data from normal subjects, as well as the results from brain-damaged patients reported by Sokol, McCloskey, Cohen, and Aliminosa (1991) in the preceding article. The discussion serves to delineate the strengths and limitations of the models and, more generally, to identify important theoretical and empirical issues in the study of arithmetic fact retrieval. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MCCLOSKEY, M (reprint author), JOHNS HOPKINS UNIV,DEPT COGNIT SCI,BALTIMORE,MD 21218, USA. FU NINDS NIH HHS [NS21047] NR 47 TC 95 Z9 95 U1 1 U2 3 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0278-7393 J9 J EXP PSYCHOL LEARN JI J. Exp. Psychol.-Learn. Mem. Cogn. PD MAY PY 1991 VL 17 IS 3 BP 377 EP 397 DI 10.1037/0278-7393.17.3.377 PG 21 WC Psychology; Psychology, Experimental SC Psychology GA FK202 UT WOS:A1991FK20200002 PM 1829472 ER PT J AU LEONG, GB ETH, S SILVA, JA AF LEONG, GB ETH, S SILVA, JA TI THE TARASOFF DILEMMA IN CRIMINAL COURT SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; JURISPRUDENCE; PRIVACY; DOCTOR-PATIENT PRIVILEGE; DUTY TO PROTECT; TESTIMONY; DANGEROUSNESS; CONFIDENTIALITY; PRIVILEGE; ETHICS; PSYCHOTHERAPY AB The duty to protect, or Tarasoff duty, has been conceptualized as arising solely in the context of a clinical setting. A recent California Supreme Court ruling in People nu. Clark adds legal, clinical, and ethical dilemmas to the oftentimes contentious Tarasoff issue. Though the Tarasoff issue is but a minor legal point in Clark, a possible consequence of Clark is that a Tarasoff warning could be deemed nonconfidential and admissible in a criminal trial. Psychoterapists could therefore be testifying in criminal courts as prosecution witnesses. While the possibility of a chilling effect on patients' disclosure of violent ideation in the context of psychotherapy first caused apprehension after the California Supreme Court's 1976 decision in Tarasoff nu. Regents of the University of California, this same Court's ruling in People nu. Clark some 14 years later may ensure that this fear finally becomes realized. C1 UNIV CALIF LOS ANGELES,SCH MED,PSYCHIAT,LOS ANGELES,CA 90024. UNIV SO CALIF,SCH MED,PSYCHIAT,LOS ANGELES,CA 90033. RP LEONG, GB (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,B116A12,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 8 TC 8 Z9 8 U1 0 U2 1 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD MAY PY 1991 VL 36 IS 3 BP 728 EP 735 PG 8 WC Medicine, Legal SC Legal Medicine GA FP610 UT WOS:A1991FP61000019 PM 1856640 ER PT J AU SCHULMAN, KA KINOSIAN, BP JACOBSON, TA GLICK, H EISENBERG, J AF SCHULMAN, KA KINOSIAN, BP JACOBSON, TA GLICK, H EISENBERG, J TI FORMULARY POLICY FOR CHOLESTEROL REDUCTION SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Letter RP SCHULMAN, KA (reprint author), HOSP UNIV PENN, PHILADELPHIA VET AFFAIRS MED CTR, DEPT MED, PHILADELPHIA, PA 19104 USA. OI Jacobson, Terry/0000-0002-9926-2179 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0884-8734 EI 1525-1497 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD MAY-JUN PY 1991 VL 6 IS 3 BP 266 EP 266 DI 10.1007/BF02598978 PG 1 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA FM057 UT WOS:A1991FM05700017 ER PT J AU PERKINS, DL WANG, YS FRUMAN, D SEIDMAN, JG RIMM, IJ AF PERKINS, DL WANG, YS FRUMAN, D SEIDMAN, JG RIMM, IJ TI IMMUNODOMINANCE IS ALTERED IN T-CELL RECEPTOR (BETA-CHAIN) TRANSGENIC MICE WITHOUT THE GENERATION OF A HOLE IN THE REPERTOIRE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID LAMBDA-REPRESSOR; RECOGNITION; MOLECULES; PEPTIDES; PROTEIN AB Despite the tremendous plasticity of the TCR repertoire, T cells recognize a limited number of antigenic sites (frequently a single site, or immunodominant epitope) on a complex protein Ag. Current models suggest that the immunodominant epitope of a complex protein is the processed peptide that binds to the MHC molecule with the highest affinity. Conversely, the inability of the T cell population to recognize a specific epitope, termed a "hole" in the repertoire, can prevent the immunodominance of a peptide despite efficient processing and MHC binding of the peptide. The role of specific TCR alpha- or beta-chains in determining MHC restriction and recognizing specific epitopes is complex and incompletely understood. To evaluate the contribution of each TCR chain to the functional diversity of the T cell repertoire, we investigated in vivo the T cell response to phage lambda-repressor protein in transgenic mice expressing a single rearranged beta-chain gene (C57L-beta mice) in association with the complete germline alpha-chain repertoire. Our results demonstrate that expression of the TCR beta-chain transgene alters the immunodominant epitope recognized by T cells. However, after immunization with the appropriate peptide the transgenic mice can also respond to the nonimmunodominant epitope; thus, the expression of the TCR beta-chain transgene does not create a hole in the repertoire. These data indicate that the primary site, or immunodominant epitope, of an Ag recognized by T cells can be altered by the preimmune TCR repertoire independent of antigen processing and MHC affinity. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP PERKINS, DL (reprint author), BRIGHAM & WOMENS HOSP,IMMUNOGENET & TRANSPLANTAT LAB,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 22 TC 33 Z9 33 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 MAY 1 PY 1991 VL 146 IS 9 BP 2960 EP 2964 PG 5 WC Immunology SC Immunology GA FJ133 UT WOS:A1991FJ13300010 PM 1826701 ER PT J AU MCAULIFFE, DJ BLANK, IH AF MCAULIFFE, DJ BLANK, IH TI EFFECTS OF UVA (320-400 NM) ON THE BARRIER CHARACTERISTICS OF THE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article AB The stratum corneum serves as the major barrier to the entrance of most molecules into the skin. In the studies presented here, the effects of UVA radiation (320-400 nm) on the barrier capacity of human stratum corneum were examined. Penetration of a homologous series of primary alcohols through unirradiated (control) and UVA-irradiated (test) human epidermis was determined in vitro. Permeability constants, k(p), were calculated. Mean ratios of permeability constants for UVA-irradiated and unirradiated epidermis (mean k(p) test)/(mean K(p) control) ranged from 2.3 to 3.0 for methanol and from 2.2 to 2.5 for ethanol. These mean ratios were determined using different pieces of epidermis from the same piece of skin for test and control samples. When k(p) control and k(p) test were determined on the same piece of epidermis on successive days, the ratios (k(p) test/k(p) control) were similar to the mean ratios determined on different pieces of epidermis. For other primary alcohols, propanol, butanol, hexanol, and heptanol, UVA radiation did not alter their permeability constants significantly. Partition coefficients, K(m), were determined for ethanol and heptanol using UVA-irradiated and unirradiated stratum corneum. For ethanol, irradiation resulted in a 1.5 to 2.6 times increase in K(m). For heptanol, irradiation caused no change in K(m). These results demonstrate that the barrier capacity of stratum corneum for small, polar, primary alcohols is diminished (permeability increases) and for higher molecular weight less polar alcohols, is unaffected by small doses of UVA radiation. This increased permeability of small polar alcohols through human skin may be due to enhanced partitioning into UVA-irradiated stratum corneum, which was not apparent for a higher molecular weight less polar alcohol. RP MCAULIFFE, DJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,WELLMAN LABS,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [3R01AR25395] NR 16 TC 28 Z9 28 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAY PY 1991 VL 96 IS 5 BP 758 EP 762 DI 10.1111/1523-1747.ep12471711 PG 5 WC Dermatology SC Dermatology GA FK303 UT WOS:A1991FK30300017 PM 2022882 ER PT J AU KVEDAR, JC DARYANANI, HA BADEN, HP AF KVEDAR, JC DARYANANI, HA BADEN, HP TI CROSS-LINKED COMPONENTS OF THE CUTICLE OF THE CORTEX OF HAIR SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article RP KVEDAR, JC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WARREN 5,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [AR01804-02] NR 5 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAY PY 1991 VL 96 IS 5 BP S84 EP S85 DI 10.1111/1523-1747.ep12472052 PG 2 WC Dermatology SC Dermatology GA FK303 UT WOS:A1991FK30300041 PM 2022892 ER PT J AU SEBREE, L BIANCO, JA SUBRAMANIAN, R WILSON, MA SWANSON, D HEGGE, J TSCHUDY, J PYZALSKI, R AF SEBREE, L BIANCO, JA SUBRAMANIAN, R WILSON, MA SWANSON, D HEGGE, J TSCHUDY, J PYZALSKI, R TI DISCORDANCE BETWEEN ACCUMULATION OF C-14 DEOXYGLUCOSE AND TL-201 IN REPERFUSED MYOCARDIUM SO JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY LA English DT Article DE REPERFUSION; ACUTE; NECROSIS; DEOXYGLUCOSE ID POSITRON EMISSION TOMOGRAPHY; CEREBRAL GLUCOSE-UTILIZATION; ISCHEMIC CELL-DEATH; BLOOD-FLOW; CORONARY-OCCLUSION; CANINE MYOCARDIUM; WAVEFRONT PHENOMENON; METABOLIC OXIDATION; CARDIAC METABOLISM; ARTERY OCCLUSION C1 UNIV WISCONSIN, HOSP & CLIN, DEPT RADIOL, E1-382, 600 HIGHLAND AVE, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT PATHOL, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT MED, MADISON, WI 53792 USA. UNIV WISCONSIN, HOSP & CLIN, DEPT SURG, MADISON, WI 53792 USA. WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53792 USA. FU NHLBI NIH HHS [R01HL33514] NR 55 TC 31 Z9 31 U1 1 U2 1 PU ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD PI LONDON PA 24-28 OVAL RD, LONDON NW1 7DX, ENGLAND SN 0022-2828 EI 1095-8584 J9 J MOL CELL CARDIOL JI J. Mol. Cell. Cardiol. PD MAY PY 1991 VL 23 IS 5 BP 603 EP 616 PG 14 WC Cardiac & Cardiovascular Systems; Cell Biology SC Cardiovascular System & Cardiology; Cell Biology GA FT298 UT WOS:A1991FT29800008 PM 1886139 ER PT J AU LOUIS, DN MEEHAN, SM FERRANTE, RJ HEDLEYWHYTE, ET AF LOUIS, DN MEEHAN, SM FERRANTE, RJ HEDLEYWHYTE, ET TI THE SILVER NUCLEOLAR ORGANIZER REGION TECHNIQUE DISTINGUISHES GLIOSIS FROM LOW-GRADE ASTROCYTOMA SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1991 VL 50 IS 3 BP 290 EP 290 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FK140 UT WOS:A1991FK14000013 ER PT J AU LEE, JM ARRIAGADA, PV HYMAN, BT AF LEE, JM ARRIAGADA, PV HYMAN, BT TI ALZHEIMER NEURONAL CHANGES IN THE BRAIN-STEM MONOAMINE NUCLEI OF NONDEMENTED AGED INDIVIDUALS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1991 VL 50 IS 3 BP 301 EP 301 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FK140 UT WOS:A1991FK14000045 ER PT J AU ARRIAGADA, PV MARZLOFF, KL VANHOESEN, GW HYMAN, BT AF ARRIAGADA, PV MARZLOFF, KL VANHOESEN, GW HYMAN, BT TI PATHOLOGICAL-CHANGES IN THE OLFACTORY-BULB IN AGING AND ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1991 VL 50 IS 3 BP 303 EP 303 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FK140 UT WOS:A1991FK14000050 ER PT J AU DELAMONTE, SM WANDS, JR AF DELAMONTE, SM WANDS, JR TI NEURONAL THREAD PROTEIN - A POTENTIAL MARKER FOR ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1991 VL 50 IS 3 BP 316 EP 316 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FK140 UT WOS:A1991FK14000091 ER PT J AU FERRANTE, RJ KOWALL, NW RICHARDSON, EP AF FERRANTE, RJ KOWALL, NW RICHARDSON, EP TI DENDRITIC PROLIFERATIVE CHANGES PRECEDE CELL-DEATH IN HUNTINGTONS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1991 VL 50 IS 3 BP 318 EP 318 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA FK140 UT WOS:A1991FK14000097 ER PT J AU SEWELL, WF STARR, PA AF SEWELL, WF STARR, PA TI EFFECTS OF CALCITONIN GENE-RELATED PEPTIDE AND EFFERENT NERVE-STIMULATION ON AFFERENT TRANSMISSION IN THE LATERAL LINE ORGAN SO JOURNAL OF NEUROPHYSIOLOGY LA English DT Article ID SUPERIOR OLIVARY COMPLEX; NICOTINIC ACETYLCHOLINE-RECEPTOR; ENKEPHALIN-LIKE IMMUNOREACTIVITY; INNERVATING HAIR-CELLS; GUINEA-PIG ORGAN; XENOPUS-LAEVIS; OLIVOCOCHLEAR NEURONS; IMMUNOELECTRON MICROSCOPY; NEUROACTIVE SUBSTANCES; RNA POLYMORPHISM AB 1. Calcitonin gene-related peptide (CGRP) is a 37-amino acid peptide immunolocalized in efferent fibers innervating hair-cell organs, including the lateral line organ of Xenopus laevis. CGRP, applied in nanomolar concentrations, increased the spontaneous discharge rate in afferent fibers innervating hair cells of the lateral line organ. 2. The increase in spontaneous discharge rate with application of CGRP was associated with an increase in the rate of occurrence of spontaneous excitatory postsynaptic potentials (EPSPs) and with little change in the amplitude of the EPSPs. 3. Prolonged (several hundred seconds) application of CGRP produced an increase in afferent fiber discharge rate that returned to control values in the continued presence of the peptide. 4. Efferent fibers were electrically stimulated to look for a non-cholinergic effect on spontaneous afferent discharge that might be attributed to CGRP. Electrical stimulation of the efferent fibers produced a rapid (100 ms) suppression of discharge rate followed by a rapid (100 ms) increase in discharge rate. However, both the rapid suppression and rapid excitation were likely to be mediated by the release of acetylcholine, because they were blocked by the application of the cholinergic blocking agents curare and atropine as well as by strychnine. 5. In almost one-half of the preparations examined, electrical stimulation of efferent fibers also produced a slowly developing increase in afferent discharge that could persist for several minutes after termination of the shocks. 6. This slow excitation by efferent stimulation was not blocked by concentrations of curare that blocked the rapid effects of efferent stimulation. Thus the slow effect is likely to be mediated by a receptor different from that for the rapid cholinergic effects. One possibility is that the excitation is mediated by the release of CGRP from the efferent nerve fibers. C1 HARVARD UNIV,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP SEWELL, WF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [DC-00767, DC-00119]; PHS HHS [07753] NR 55 TC 40 Z9 40 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 MAY PY 1991 VL 65 IS 5 BP 1158 EP 1169 PG 12 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA FL746 UT WOS:A1991FL74600013 PM 1651373 ER PT J AU JAFAR, JJ TAN, WS CROWELL, RM AF JAFAR, JJ TAN, WS CROWELL, RM TI TISSUE PLASMINOGEN-ACTIVATOR THROMBOLYSIS OF A MIDDLE CEREBRAL-ARTERY EMBOLUS IN A PATIENT WITH AN ARTERIOVENOUS MALFORMATION - CASE-REPORT SO JOURNAL OF NEUROSURGERY LA English DT Article DE TISSUE PLASMINOGEN ACTIVATOR; THROMBOLYSIS; ARTERIOVENOUS MALFORMATION; EMBOLISM; ANGIOGRAPHY ID MYOCARDIAL-INFARCTION; STROKE; COMPLICATIONS; OCCLUSION; THERAPY; TRIAL AB A patient harboring a cerebral arteriovenous malformation (AVM) underwent angiography in an attempt to embolize the AVM. During catheterization (and prior to embolization) he became hemiplegic and aphasic. Angiography revealed a complete middle cerebral artery (MCA) occlusion by an embolus. The patient was treated with recombinant tissue plasminogen activator (t-PA), a thrombolytic agent. Restoration of MCA flow was achieved, and the patient recovered. Immediately after MCA embolus, t-PA infusion may lead to thrombolysis and neurological recovery. The decision-making process as well as the risks associated with the use of t-PA are discussed. C1 UNIV ILLINOIS,DEPT NEUROSURG,CHICAGO,IL 60680. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. RP JAFAR, JJ (reprint author), NYU MED CTR,DEPT NEUROSURG,560 1ST AVE,NEW YORK,NY 10016, USA. NR 28 TC 15 Z9 15 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAY PY 1991 VL 74 IS 5 BP 808 EP 812 DI 10.3171/jns.1991.74.5.0808 PG 5 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FH457 UT WOS:A1991FH45700019 PM 1901602 ER PT J AU PIERI, P FISCHMAN, AJ AHMAD, M MOORE, RH CALLAHAN, RJ STRAUSS, HW AF PIERI, P FISCHMAN, AJ AHMAD, M MOORE, RH CALLAHAN, RJ STRAUSS, HW TI CARDIAC BLOOD-POOL SCINTIGRAPHY IN RATS AND HAMSTERS - COMPARISON OF 5 RADIOPHARMACEUTICALS AND 3 PINHOLE COLLIMATOR APERTURES SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HUMAN-SERUM ALBUMIN; CELLS; INVIVO; TC-99M; VISUALIZATION; INVITRO AB Preclinical evaluation of cardiac drugs may require evaluation of cardiac function in intact animals. To optimize the quality of radionuclide measurements of ventricular function in small animals, a comparison was made of gated blood-pool scans recorded with five blood-pool radiopharmaceuticals (99mTc-labeled human polyclonal IgG, 99mTc-human serum albumin labeled by two methods, and red blood cells radiolabeled with 99mTc via in vivo and in vitro methods) in rats and three pinhole apertures in hamsters. The quality of the radiopharmaceuticals was evaluated by comparing count density ratios (LV/BACKGROUND and LV/LIVER) and ejection fractions recorded with each agent. The edge definition of the left ventricle and count rate performance of the 1-, 2-, and 3-mm apertures was evaluated in hamsters. In general, the images obtained with the radiolabeled cells were superior to those obtained with the labeled proteins and no significant differences between the protein preparations were detected. Left ventricular ejection fractions calculated with all five radiopharmaceuticals were not significantly different. The best quality images were obtained with the 1-mm pinhole collimator. Ejection fraction and acquisition time were inversely related to aperture size. A good compromise between resolution and sensitivity was obtained with the 2-mm pinhole collimator. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,55 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 25 TC 21 Z9 22 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1991 VL 32 IS 5 BP 851 EP 855 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FL183 UT WOS:A1991FL18300026 PM 1850784 ER PT J AU HOOP, B AF HOOP, B TI THE INFILTRATED RADIOPHARMACEUTICAL INJECTION - RISK CONSIDERATIONS SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HOOP, B (reprint author), MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 7 TC 7 Z9 8 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 22090-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 1991 VL 32 IS 5 BP 890 EP 891 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FL183 UT WOS:A1991FL18300038 PM 1902509 ER PT J AU TREADWELL, BV PAVIA, M TOWLE, CA COOLEY, VJ MANKIN, HJ AF TREADWELL, BV PAVIA, M TOWLE, CA COOLEY, VJ MANKIN, HJ TI CARTILAGE SYNTHESIZES THE SERINE PROTEASE INHIBITOR PAI-1 - SUPPORT FOR THE INVOLVEMENT OF SERINE PROTEASES IN CARTILAGE REMODELING SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article DE CARTILAGE; PROTEASES; INHIBITORS; INTERLEUKIN-1; PLASMINOGEN ACTIVATOR ID PLASMINOGEN-ACTIVATOR INHIBITOR-1; ARTICULAR CHONDROCYTES; EXTRACELLULAR-MATRIX; MESSENGER-RNA; II COLLAGEN; PURIFICATION; THROMBOSPONDIN; INTERLEUKIN-1; PROTEOGLYCAN; NEXIN AB The work described here demonstrates the synthesis by human articular cartilage of plasminogen activator inhibitor-1 (PAI-1), a potent inhibitor of the serine protease tissue plasminogen activator (tPA). We also present data demonstrating an increase in PAI-1 messenger ribonucleic acid (mRNA) in chondrocytes exposed to the cytokine interleukin-1 (IL-1). Interestingly, this elevation of steady-state mRNA levels does not appear to result in an increase in synthesis of PAI-1 protein. Northern blot analysis reveals that of the two mRNA species (3.4 kb, 2.4 kb) previously reported for PAI-1, only the larger species (3.4 kb) appears to be synthesized by chrondrocytes. Our data demonstrate the IL-1-stimulated production by cartilage of tissue plasminogen activator. We also show evidence for the presence of plasminogen in cartilage. A scheme is presented indicating the probable importance of the serine proteases (tPA and plasminogen) and PAI-1 in cartilage degradation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TREADWELL, BV (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,JACKSON 11,BOSTON,MA 02114, USA. NR 47 TC 22 Z9 22 U1 0 U2 5 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD MAY PY 1991 VL 9 IS 3 BP 309 EP 316 DI 10.1002/jor.1100090302 PG 8 WC Orthopedics SC Orthopedics GA FF812 UT WOS:A1991FF81200001 PM 1901356 ER PT J AU CUNDY, PJ JOFE, M ZALESKE, DJ EHRLICH, MG MANKIN, HJ AF CUNDY, PJ JOFE, M ZALESKE, DJ EHRLICH, MG MANKIN, HJ TI PHYSEAL RECONSTRUCTION USING TISSUE DONATED FROM EARLY POSTNATAL LIMBS IN A MURINE MODEL SO JOURNAL OF ORTHOPAEDIC RESEARCH LA English DT Article DE PHYSIS; RECONSTRUCTION; TRANSPLANTATION; POSTNATAL TISSUE ID TRANSPLANTS AB Physeal reconstruction was performed in a murine model by transplanting corresponding postnatal tissue from 4-day-old C57B mice to resection defects. The site of the reconstruction, the murine distal femoral epiphysis, is completely cartilaginous and avascular at this stage of development. The tissue transplanted into the defect was demonstrated to have high kinetic activity by its incorporation of titriated thymidine. The physeal reconstruction as performed restored only 25% of normal growth. While transplanting cell populations is feasible, the method will require a great deal of work before clinical application. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,ACC 507,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. ADELAIDE CHILDRENS HOSP INC,ADELAIDE,SA 5006,AUSTRALIA. FU NIAMS NIH HHS [AR39380] NR 12 TC 2 Z9 3 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0736-0266 J9 J ORTHOPAED RES JI J. Orthop. Res. PD MAY PY 1991 VL 9 IS 3 BP 360 EP 366 DI 10.1002/jor.1100090307 PG 7 WC Orthopedics SC Orthopedics GA FF812 UT WOS:A1991FF81200006 PM 2010839 ER PT J AU GUENTER, PA SETTLE, RG PERLMUTTER, S MARINO, PL DESIMONE, GA ROLANDELLI, RH AF GUENTER, PA SETTLE, RG PERLMUTTER, S MARINO, PL DESIMONE, GA ROLANDELLI, RH TI TUBE FEEDING-RELATED DIARRHEA IN ACUTELY ILL PATIENTS SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID VOLATILE FATTY-ACIDS; CLOSTRIDIUM-DIFFICILE; PREVENTION; PECTIN AB Acutely ill patients received tube feeding for an average of 15.8 days and, on average, 35% of those days were spent in the intensive care unit (ICU). Patients were prospectively assigned either a fiber-free formula (FFF-OSMOLITE HN, Ross; n = 50) or a fiber-supplemented (soy polysaccharide 14.4 g/L) formula (FSF = JEVITY, Ross; n = 50). Diarrhea was defined as three or more loose or watery stools per day and occurred in 30% of all patients. Diarrhea developed in 29 (41%) of the 71 patients who received antibiotics during, or within 2 weeks prior to, the feeding period, whereas only 1 (3%) of the 29 patients not receiving antibiotics developed diarrhea (p < 0.005); and this patient developed diarrhea on the day of death. Among the 30 patients with diarrhea, stool Clostridium difficile (CD) toxin was positive in 15 (50%), negative in 11 (37%), and was not measured in four. The mean serum albumin was significantly lower in patients with diarrhea (2.43) than in those without diarrhea (2.75) (p = 0.043). There were no significant differences in age, sex, diagnoses, number of feeding days, and percent ICU days between patients with and without diarrhea. While not statistically significant, patients who received FSF were observed to have a lower incidence of diarrhea, a lower percentage of diarrhea days per total feeding days, and a lower frequency of positive CD toxin assays than patients who received FFF. In this patient population, antibiotic usage was the factor most strongly associated with diarrhea during tube feedings. C1 UNIV PENN,GRAD HOSP,SCH MED,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP GUENTER, PA (reprint author), UNIV PENN,GRAD HOSP,SCH NURSING,PHILADELPHIA,PA 19104, USA. NR 23 TC 87 Z9 95 U1 0 U2 6 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD MAY-JUN PY 1991 VL 15 IS 3 BP 277 EP 280 DI 10.1177/0148607191015003277 PG 4 WC Nutrition & Dietetics SC Nutrition & Dietetics GA FP831 UT WOS:A1991FP83100007 PM 1650854 ER PT J AU SOCRANSKY, SS HAFFAJEE, AD AF SOCRANSKY, SS HAFFAJEE, AD TI MICROBIAL MECHANISMS IN THE PATHOGENESIS OF DESTRUCTIVE PERIODONTAL-DISEASES - A CRITICAL-ASSESSMENT SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article; Proceedings Paper CT 8TH INTERNATIONAL CONF ON PERIODONTAL RESEARCH CY NOV 15-18, 1990 CL SAN ANTONIO, TX SP INT ASSOC DENT RES, PERIODONTAL RES GRP, PROCTER & GAMBLE DE MICROBIAL MECHANISMS; PATHOGENESIS; PERIODONTAL DISEASE ID BACTEROIDES-GINGIVALIS W50; BLACK-PIGMENTED BACTEROIDES; ACTINOMYCES-VISCOSUS T14V; TRYPSIN-LIKE-ENZYME; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS LEUKOTOXIN; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; EXTRACELLULAR MEMBRANE-VESICLES; SALIVA-TREATED HYDROXYAPATITE; FIMBRIA-ASSOCIATED ADHESINS; HUMAN NEUTROPHIL ADHERENCE RP SOCRANSKY, SS (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02847, DE-04881] NR 193 TC 159 Z9 164 U1 0 U2 7 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD MAY PY 1991 VL 26 IS 3 BP 195 EP 212 DI 10.1111/j.1600-0765.1991.tb01646.x PN 2 PG 18 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FU678 UT WOS:A1991FU67800001 PM 1831843 ER PT J AU HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S AF HAFFAJEE, AD SOCRANSKY, SS SMITH, C DIBART, S TI MICROBIAL RISK INDICATORS FOR PERIODONTAL ATTACHMENT LOSS SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Article; Proceedings Paper CT 8TH INTERNATIONAL CONF ON PERIODONTAL RESEARCH CY NOV 15-18, 1990 CL SAN ANTONIO, TX SP INT ASSOC DENT RES, PERIODONTAL RES GRP, PROCTER & GAMBLE DE MICROBIAL RISK INDICATORS; ATTACHMENT LOSS RP HAFFAJEE, AD (reprint author), FORSYTH DENT CTR,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-02847, DE-04881] NR 6 TC 27 Z9 28 U1 1 U2 4 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD MAY PY 1991 VL 26 IS 3 BP 293 EP 296 DI 10.1111/j.1600-0765.1991.tb01662.x PN 2 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA FU678 UT WOS:A1991FU67800017 PM 1831856 ER PT J AU HUSSOIN, S FITZGERALD, GB WICK, MM AF HUSSOIN, S FITZGERALD, GB WICK, MM TI POLYHYDROXYLATED PHENYLACRYLIC ACID-DERIVATIVES AS NEW ANTITUMOR AGENTS SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID MELANOMA-CELLS; DOPAMINE; LEVODOPA; 3,4-DIHYDROXYBENZYLAMINE; TOXICITY; INVITRO AB Preliminary evidence indicates that antitumor agents containing the o-dihydroxybenzene moiety exhibit enhanced antitumor activity toward malignant cells of high oxidative potential, such as melanoma cells. Based on this consideration, 11 hydroxybenzene acrylic acid derivatives of differing redox potential were prepared as potential substrates for the melanoma specific enzyme tyrosinase, that might exhibit general antitumor activity and enhanced cytotoxicity toward melanoma cells. Five of these compounds [alpha-cyano-beta-(4-hydroxyphenyl)-, alpha-cyano-beta-(3,4-dihydroxyphenyl)-, and alpha-cyano-beta-(3,4,5-trihydroxyphenyl)acrylic acid (THPPA), and 3,4-dihydroxy- and 3,4,5-trihydroxybenzalcyanoacetamide] were found to be substrates for tyrosinase with k(m) values from 0.08 to 4.13 mM and V(max) values from 0.18 to 3.02. These data indicate that as the number of hydroxy groups increases, the rate of oxidation increases, and that cyanoamides were faster reacting than corresponding cyanoacids, with dicyanides the least reactive. In contrast, cyanoamides were less effective as substrates than cyanoacids. In vitro studies showed all but two compounds were active against L1210 (IC50 range 21-980-mu-M), SK-MEL-28 (IC50 range 54-950-mu-M), and SK-MEL-30-3 (IC50 range 54-190-mu-M). Only THPPA was active in vivo against L1210 and B-16 melanoma. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. FU NCI NIH HHS [CA24988] NR 16 TC 2 Z9 2 U1 0 U2 0 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD MAY PY 1991 VL 80 IS 5 BP 416 EP 418 DI 10.1002/jps.2600800503 PG 3 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA FL025 UT WOS:A1991FL02500002 PM 1908901 ER PT J AU ORDWAY, GA GAMBARANA, C TEJANIBUTT, SM ARESO, P HAUPTMANN, M FRAZER, A AF ORDWAY, GA GAMBARANA, C TEJANIBUTT, SM ARESO, P HAUPTMANN, M FRAZER, A TI PREFERENTIAL REDUCTION OF BINDING OF I-125 IODOPINDOLOL TO BETA-1 ADRENOCEPTORS IN THE AMYGDALA OF RAT AFTER ANTIDEPRESSANT TREATMENTS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID ADRENERGIC-RECEPTOR BINDING; BEHAVIORAL DESPAIR TEST; SEROTONIN UPTAKE; CEREBRAL-CORTEX; QUANTITATIVE AUTORADIOGRAPHY; BETA-2-ADRENERGIC RECEPTORS; SELECTIVE INHIBITOR; MONOAMINE-OXIDASE; BRAIN; IMIPRAMINE AB This study utilized quantitative receptor autoradiography to examine the effects of repeated administration of antidepressants to rats on the binding of the beta adrenoceptor antagonist, I-125-iodopindolol (I-125-IPIN) to either beta-1 or beta-2 adrenoceptors in various regions of brain. Antidepressants were selected to represent various chemical and pharmacological classes including tricyclic compounds (desipramine and protriptyline), monoamine oxidase inhibitors (clorgyline, phenelzine and tranylcypromine), atypical antidepressants (mianserin and trazodone) and selective inhibitors of the uptake of serotonin (citalopram and sertraline). Additionally, rats were treated with various psychotropic drugs that lack antidepressant efficacy (cocaine, deprenyl, diazepam and haloperidol). Repeated treatment of rats with desipramine, protriptyline, clorgyline, phenelzine, tranylcy-promine or mianserin reduced the binding of I-125-IPIN to beta-1 adrenoceptors in many brain areas. Only in the basolateral and lateral nuclei of the amygdala did all six of these antidepressants significantly reduce I-125-IPIN binding to beta-1 adrenoceptors. In these amygdaloid nuclei, the magnitude of the reduction in the binding of I-125-IPIN caused by each of these drugs was comparable to or greater than the reduction in binding produced in any other region of brain. Reductions of binding of I-125-IPIN after antidepressant treatments were not consistently observed in the cortex, the area of brain examined most often in homogenate binding studies. Only the monoamine oxidase inhibitors caused reductions in the binding of I-125-IPIN to beta-2 adrenoceptors, and this effect was generally localized to the amygdala and hypothalamus. Repeated treatment of rats with citalopram, sertraline, or trazodone or with drugs lacking clinical antidepressant efficacy caused no significant effects on the binding of I-125-IPIN to either subtype of beta adrenoceptor in any region of brain. These results demonstrate that amygdaloid beta-1 adrenoceptors are particularly susceptible to regulation by certain antidepressant treatments and implicate the amygdala as an important site of action for antidepressants with pharmacological activity on noradrenergic neurons. C1 VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT 151E,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PSYCHIAT,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHARMACOL,PHILADELPHIA,PA 19104. FU NIMH NIH HHS [MH09497, MH29094, MH14654] NR 65 TC 90 Z9 90 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD MAY PY 1991 VL 257 IS 2 BP 681 EP 690 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA FM161 UT WOS:A1991FM16100022 PM 1674532 ER PT J AU KOLLIAS, N SAYRE, RM ZEISE, L CHEDEKEL, MR AF KOLLIAS, N SAYRE, RM ZEISE, L CHEDEKEL, MR TI PHOTOPROTECTION BY MELANIN SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY LA English DT Review DE MELANIN; EPIDERMAL MELANIN PIGMENTATION; PHOTOPROTECTION ID UVB-INDUCED ERYTHEMA; SKIN TYPE-V; ULTRAVIOLET-RADIATION; MAMMALIAN MELANOGENESIS; BAND MODEL; PIGMENTATION; TYROSINASE; COLOR; DOPA; PROTECTION AB This paper is an attempt to summarize the current state of information on melanin and epidermal melanin pigmentation (EMP) as photoprotective agents. The chemistry and biochemistry of melanin (the particle) and its interaction, in its various forms, with UV radiation are considered. Methods of attenuation of UV radiation are discussed in terms of structure and chemical constituents. Photoprotection by constitutive and facultative pigmentation is reviewed with minimum erythema dose (MED) as the end point. The issue of acclimatization to UV radiation is discussed in terms of UVB phototherapy for psoriasis. Finally, skin cancer is considered as an end point and the reduction of its incidence with pigment level is discussed. It is concluded that whilst EMP provides protection, its extent depends on the end point chosen for evaluation. MED is a convenient photobiological end point but is rather insensitive, whereas skin cancer is sensitive but impractical for laboratory studies. Our current state of knowledge of melanin lacks information on its absorption and scattering coefficients and its refractive index. Methods for the quantitative measurement of EMP are also urgently required. C1 MEMPHIS STATE UNIV,DEPT PHYS,MEMPHIS,TN 38152. RAPID PRECIS LABS,CORDOVA,TN 38018. MEL-CO,VACAVILLE,CA 95687. RP KOLLIAS, N (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 107 TC 249 Z9 260 U1 10 U2 53 PU ELSEVIER SCIENCE SA LAUSANNE PI LAUSANNE 1 PA PO BOX 564, 1001 LAUSANNE 1, SWITZERLAND SN 1011-1344 J9 J PHOTOCH PHOTOBIO B JI J. Photochem. Photobiol. B-Biol. PD MAY PY 1991 VL 9 IS 2 BP 135 EP 160 DI 10.1016/1011-1344(91)80147-A PG 26 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA FN549 UT WOS:A1991FN54900001 PM 1907647 ER PT J AU BIEDERMAN, J AF BIEDERMAN, J TI SUDDEN-DEATH IN CHILDREN TREATED WITH A TRICYCLIC ANTIDEPRESSANT SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Editorial Material ID DEPRESSED-PATIENTS; ANTI-DEPRESSANTS; PLASMA-LEVELS; IMIPRAMINE; DESIPRAMINE; DISEASE; DISORDER; ADD C1 HARVARD UNIV,SCH MED,PSYCHIAT,BOSTON,MA 02115. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. NR 24 TC 63 Z9 63 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1991 VL 30 IS 3 BP 495 EP 498 DI 10.1097/00004583-199105000-00023 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA FM316 UT WOS:A1991FM31600023 PM 2055889 ER PT J AU OSHEA, JP SOUTHERN, JF DAMBRA, MN MAGRO, C GUERRERO, JL MARSHALL, JE VLAHAKES, GV LEVINE, RA WEYMAN, AE AF OSHEA, JP SOUTHERN, JF DAMBRA, MN MAGRO, C GUERRERO, JL MARSHALL, JE VLAHAKES, GV LEVINE, RA WEYMAN, AE TI EFFECTS OF PROLONGED TRANSESOPHAGEAL ECHOCARDIOGRAPHIC IMAGING AND PROBE MANIPULATION ON THE ESOPHAGUS - AN ECHOCARDIOGRAPHIC-PATHOLOGICAL STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article; Proceedings Paper CT 61ST ANNUAL SCIENTIFIC SESSION OF THE AMERICAN HEART ASSOC CY NOV 14-17, 1988 CL WASHINGTON, DC SP AMER HEART ASSOC ID TWO-DIMENSIONAL ECHOCARDIOGRAPHY AB Transesophageal echocardiography is being increasingly utilized in the operating room and intensive care and ambulatory settings. However, to date no data are available concerning possible trauma of the transesophageal echocardiographic technique to the esophagus due to probe insertion, manipulation or direct ultrasound energy transmission. To test the hypothesis that transesophageal manipulations caused no traumatic or thermal injury to the esophageal mucosa, 12 animals were studied with continuous transeophageal echocardiography for a period of variable duration (mean 4.6 h +/- 51 min). The study group consisted of four monkeys (mean weight 5.7 +/- 0.6 kg and eight mongrel dogs (mean weight 29.8 +/- 1.4 kg). The eight dogs were studied during the right heart bypass with full heparinization for 6.6 +/- 0.2 h, whereas the four monkeys were studied for 60 to 90 min in the absence of cardiopulmonary bypass and anticoagulation. Immediately after completion of transesophageal echocardiography in each case, the esophagus was entirely excised. Detailed macroscopic and microscopic examination of the esophagus revealed no significant mucosal or thermal injury. This preliminary animal study suggest that transesophageal echocardiography is safe for the esophageal mucosa in animals as small as 5 kg in weight, despite prolonged use and in the presence of systemic anticoagulation. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT SURG,DIV CARDIAC SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,CARDIAC ULTRASOUND LAB,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,CARDIAC ANESTHESIA GRP,BOSTON,MA 02114. NR 13 TC 36 Z9 37 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAY PY 1991 VL 17 IS 6 BP 1426 EP 1429 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA FJ444 UT WOS:A1991FJ44400029 PM 2016462 ER PT J AU WHALEN, RK WHITCOMB, RW CROWLEY, WF MCGOVERN, FJ AF WHALEN, RK WHITCOMB, RW CROWLEY, WF MCGOVERN, FJ TI PRIAPISM IN HYPOGONADAL MEN RECEIVING GONADOTROPIN-RELEASING-HORMONE SO JOURNAL OF UROLOGY LA English DT Article DE PRIAPISM; PITUITARY HORMONE RELEASING HORMONES ID TESTOSTERONE AB To our knowledge we report the first 2 cases of priapism occurring in hypogonadal men receiving gonadotropin releasing hormone therapy. Hypogonadal patients receiving hormonal therapy should be informed about the possibility of priapism and the importance of early urological consultation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT REPROD ENDOCRINOL,BOSTON,MA 02114. RP WHALEN, RK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,BOSTON,MA 02114, USA. NR 9 TC 7 Z9 7 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 MAY PY 1991 VL 145 IS 5 BP 1051 EP 1052 PG 2 WC Urology & Nephrology SC Urology & Nephrology GA FJ844 UT WOS:A1991FJ84400036 PM 2016792 ER PT J AU WONG, SW SCHAFFER, PA AF WONG, SW SCHAFFER, PA TI ELEMENTS IN THE TRANSCRIPTIONAL REGULATORY REGION FLANKING HERPES-SIMPLEX VIRUS TYPE-1 ORIS STIMULATE ORIGIN FUNCTION SO JOURNAL OF VIROLOGY LA English DT Article ID IMMEDIATE-EARLY GENE; HUMAN CYTOMEGALO-VIRUS; BOX-BINDING-PROTEINS; EPSTEIN-BARR VIRUS; DNA-REPLICATION; PROMOTER ELEMENTS; ADENOVIRUS ORIGIN; INTERGENIC REGION; ANIMAL VIRUS; CORE ORIGIN AB Like other DNA-containing viruses, the three origins of herpes simplex virus type 1 (HSV-1) DNA replication are flanked by sequences containing transcriptional regulatory elements. In a transient plasmid replication assay, deletion of sequences comprising the transcriptional regulatory elements of ICP4 and ICP22/47, which flank oriS, resulted in a greater than 80-fold decrease in origin function compared with a plasmid, pOS-822, which retains these sequences. In an effort to identify specific cis-acting elements responsible for this effect, we conducted systematic deletion analysis of the flanking region with plasmid pOS-822 and tested the resulting mutant plasmids for origin function. Stimulation by cis-acting elements was shown to be both distance and orientation dependent, as changes in either parameter resulted in a decrease in oriS function. Additional evidence for the stimulatory effect of flanking sequences on origin function was demonstrated by replacement of these sequences with the cytomegalovirus immediate-early promoter, resulting in nearly wild-type levels of oriS function. In competition experiments, cotransfection of cells with the test plasmid, pOS-822, and increasing molar concentrations of a competitor plasmid which contained the ICP4 and ICP22/47 transcriptional regulatory regions but lacked core origin sequences resulted in a significant reduction in the replication efficiency of pOS-822, demonstrating that factors which bind specifically to the oriS-flanking sequences are likely involved as auxiliary proteins in oriS function. Together, these studies demonstrate that trans-acting factors and the sites to which they bind play a critical role in the efficiency of HSV-1 DNA replication from oriS in transient-replication assays. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [5T32CA09031, R37CA20260]; NIAID NIH HHS [R01AI28537] NR 56 TC 56 Z9 56 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAY PY 1991 VL 65 IS 5 BP 2601 EP 2611 PG 11 WC Virology SC Virology GA FG777 UT WOS:A1991FG77700057 PM 1850034 ER PT J AU COLLINS, JF ANZUETO, AA PETERS, JI DELOSSANTOS, R GONZALEZ, DC JOHANSON, WG SEIDENFELD, JJ COALSON, JJ JENKINSON, SG AF COLLINS, JF ANZUETO, AA PETERS, JI DELOSSANTOS, R GONZALEZ, DC JOHANSON, WG SEIDENFELD, JJ COALSON, JJ JENKINSON, SG TI ELASTASE ACTIVITY IN BRONCHOALVEOLAR LAVAGE FLUID FROM OXYGEN-EXPOSED, PSEUDOMONAS-INFECTED BABOONS SO LUNG LA English DT Article DE ARDS; ELASTASE; ACUTE LUNG INJURY; BRONCHOALVEOLAR LAVAGE ID RESPIRATORY-DISTRESS SYNDROME; OXIDIZED ALPHA-1-PROTEINASE INHIBITOR; DIFFUSE ALVEOLAR DAMAGE; NOSOCOMIAL PNEUMONIA; ELASTOLYTIC ACTIVITY; NEUTROPHIL ELASTASE; HUMAN-LEUKOCYTE; LUNG INJURY; MYELOPEROXIDASE; PATHOGENESIS AB The adult respiratory distress syndrome is a major cause of morbidity and mortality in critical care patients. Lung injury in this syndrome is frequently associated with lung infection. The combined insults result in an influx of neutrophils and damage to the pulmonary epithelium. We investigated whether active neutrophil elastolytic activity was present in the bronchoalveolar fluid in baboons with mild or moderate hyperoxic lung injury and infection. Group A (N = 7) was exposed for 6 days to FIO2 = 0.8 and then inoculated by intratracheal bolus with Pseudomonas aeruginosa strain DGI-R130 (PA); the FIO2 was reduced to 0.5. Group B (N = 6) was exposed to similar concentrations of inspired oxygen but inoculated with buffered saline. Antibiotics included parenteral penicillin and topical gentamicin and polymyxin B. All 3 were given continuously in group B but stopped 24 h prior to PA inoculation in group A. Bronchoalveolar lavage fluid was collected 1 week before oxygen administration, when the FIO2 was reduced (day 6 or 7) and prior to necropsy (day 11). Hemodynamic, pulmonary function, microbiological, and biochemical variables were studied. Injured, infected animals (group A) had significant elevations of mean pulmonary artery pressure and decreases in total lung capacity and PaO2 compared both to baseline and to group B at day 11. At autopsy, group A had significant increases of bronchoalveolar lavage fluid (BALF) neutrophils and bacterial pathogens. Elastase levels in BALF (equal to 0 at baseline) rose to 136 +/- 98 ng/ml in group A vs. 6 +/- 14 ng/ml in group B. The elastase was inhibited by inhibitors of serine proteases including ones specific for neutrophil elastase. On Sephacryl S-300 chromatography the elastase activity eluted near human alpha-macroglobulin and separated from other proteolytic activity. These studies demonstrate a significant level of elastase in BALF from injured, infected baboons compared to injured, uninfected animals. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM DIS CRIT CARE,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. SW FDN BIOMED RES,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NHLBI NIH HHS [HL-23578] NR 38 TC 6 Z9 6 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0341-2040 J9 LUNG JI Lung PD MAY-JUN PY 1991 VL 169 IS 3 BP 165 EP 179 DI 10.1007/BF02714152 PG 15 WC Respiratory System SC Respiratory System GA FR159 UT WOS:A1991FR15900004 PM 1895779 ER PT J AU MOORE, GJ HROVAT, MI GONZALEZ, RG AF MOORE, GJ HROVAT, MI GONZALEZ, RG TI SIMULTANEOUS MULTINUCLEAR MAGNETIC-RESONANCE-IMAGING AND SPECTROSCOPY SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID P-31 NMR; METABOLITES C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MIT,RADIOL SCI PROGRAM,CAMBRIDGE,MA 02139. MIT,FRANCIS BITTER NATL MAGNET LAB,CAMBRIDGE,MA 02139. HARVARD UNIV,BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. RI Moore, Gregory/E-7184-2010 OI Moore, Gregory/0000-0001-8541-3194 NR 15 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD MAY PY 1991 VL 19 IS 1 BP 105 EP 112 DI 10.1002/mrm.1910190110 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA FJ084 UT WOS:A1991FJ08400009 PM 2046525 ER PT J AU PRAGER, JM MIKULIS, DJ AF PRAGER, JM MIKULIS, DJ TI THE RADIOLOGY OF HEADACHE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID TEMPOROMANDIBULAR-JOINT; ELDERLY SUBJECTS; MIGRAINE; MR; CT; LESIONS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIOL,NEURORADIOL SECT,BOSTON,MA 02114. RP PRAGER, JM (reprint author), UNIV CHICAGO,DEPT RADIOL,NEURORADIOL SECT,BOX 429,5841 S MARYLAND AVE,CHICAGO,IL 60637, USA. NR 16 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAY PY 1991 VL 75 IS 3 BP 525 EP 544 PG 20 WC Medicine, General & Internal SC General & Internal Medicine GA FJ960 UT WOS:A1991FJ96000003 PM 2020211 ER PT J AU KAWAMURA, J MEYER, JS AF KAWAMURA, J MEYER, JS TI HEADACHES DUE TO CEREBROVASCULAR-DISEASE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID FIBROMUSCULAR DYSPLASIA; CAROTID ENDARTERECTOMY; CEREBELLAR HEMORRHAGE; DISSECTION; STROKE C1 DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LABS,2002 HOLCOMBE BLVD,HOUSTON,TX 77211. BAYLOR UNIV,DEPT NEUROL,HOUSTON,TX 77030. NR 29 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAY PY 1991 VL 75 IS 3 BP 617 EP 630 PG 14 WC Medicine, General & Internal SC General & Internal Medicine GA FJ960 UT WOS:A1991FJ96000009 PM 2020217 ER PT J AU TISHKOFF, DX JOHNSON, AW KOLODNER, RD AF TISHKOFF, DX JOHNSON, AW KOLODNER, RD TI MOLECULAR AND GENETIC-ANALYSIS OF THE GENE ENCODING THE SACCHAROMYCES-CEREVISIAE STRAND EXCHANGE PROTEIN SEP1 SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID HUMAN-CELLS; PARTIAL-PURIFICATION; PACHYTENE ARREST; HETERODUPLEX DNA; BINDING PROTEIN; RECOMBINATION; YEAST; SEGREGATION; ATP; DIVISION AB Vegetatively grown Saccharomyces cerevisiae cells contain an activity that promotes a number of homologous pairing reactions. A major portion of this activity is due to strand exchange protein 1 (Sep1), which was originally purified as a 132,000-M(r) species (R. Kolodner, D. H. Evans, and P. T. Morrison, Proc. Natl. Acad. Sci. USA 84:5560-5564, 1987). The gene encoding Sep1 was cloned, and analysis of the cloned gene revealed a 4,587-bp open reading frame capable of encoding a 175,000-M(r) protein. The protein encoded by this open reading frame was overproduced and purified and had a relative molecular weight of approximately 160,000. The 160,000-M(r) protein was at least as active in promoting homologous pairing as the original 132,000-M(r) species, which has been shown to be a fragment of the intact 160,000-M(r) Sep1 protein. The SEP1 gene mapped to chromosome VII within 20 kbp of RAD54. Three Tn10LUK insertion mutations in the SEP1 gene were characterized. sep1 mutants grew more slowly than wild-type cells, showed a two- to fivefold decrease in the rate of spontaneous mitotic recombination between his4 heteroalleles, and were delayed in their ability to return to growth after UV or gamma-irradiation. Sporulation of sep1/sep1 diploids was defective, as indicated by both a 10- to 40-fold reduction in spore formation and reduced spore viability of approximately 50%. The majority of sep1/sep1 diploid cells arrested in meiosis after commitment to recombination but prior to the meiosis I cell division. Return-to-growth experiments showed that sep1/sep1 his4X/his4B diploids exhibited a five- to sixfold greater meiotic induction of His+ recombinants than did isogenic SEP1/SEP1 strains. sep1/sep1 mutants also showed an increased frequency of exchange between HIS4, LEU2, and MAT and a lack of positive interference between these markers compared with wild-type controls. The interaction between sep1, rad50 and spo13 mutations suggested that SEP1 acts in meiosis in a pathway that is parallel to the RAD50 pathway. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIGMS NIH HHS [GM13594, GM29383] NR 73 TC 92 Z9 93 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1991 VL 11 IS 5 BP 2593 EP 2608 PG 16 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ155 UT WOS:A1991FJ15500029 PM 1840632 ER PT J AU MERCHANT, JL DEMEDIUK, B BRAND, SJ AF MERCHANT, JL DEMEDIUK, B BRAND, SJ TI A GC-RICH ELEMENT CONFERS EPIDERMAL GROWTH-FACTOR RESPONSIVENESS TO TRANSCRIPTION FROM THE GASTRIN PROMOTER SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID C-FOS GENE; FACTOR-ALPHA; MAMMALIAN-CELLS; EGF RECEPTOR; TYROSINE PHOSPHORYLATION; MESSENGER-RNA; BINDING SITE; TRANSIN GENE; I GENE; PROTEIN AB Epidermal growth factor (EGF) and transforming growth factor-alpha are important determinants of mucosal integrity in the gastrointestinal tract, and they act both directly and indirectly to prevent ulceration in the stomach. Consistent with this physiological role, EGF stimulates transcription of gastrin, a peptide hormone which regulates gastric acid secretion and mucosal growth. EGF stimulation of gastrin transcription is mediated by a GC-rich gastrin EGF response element (gERE) (GGGGCGGGGTGGGGGG) which lies between -54 and -68 in the human gastrin promoter. The gERE sequence also confers weaker responsiveness to phorbol ester stimulation. The gERE sequence differs from previously described EGF response elements. The gERE DNA sequence specifically interacts with a GH4 DNA-binding protein distinct from previously described transcription factors (Egr-1 and AP2) which bind GC-rich sequences and mediate transcriptional activation by growth factors. Furthermore, the gERE element does not bind the Sp1 transcription factor even though the gERE sequence contains a high-affinity Sp1-binding site (GGCGGG). C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 65 TC 73 Z9 74 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 MAY PY 1991 VL 11 IS 5 BP 2686 EP 2696 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ155 UT WOS:A1991FJ15500038 PM 2017173 ER PT J AU ZMUIDZINAS, A MAMON, HJ ROBERTS, TM SMITH, KA AF ZMUIDZINAS, A MAMON, HJ ROBERTS, TM SMITH, KA TI INTERLEUKIN-2-TRIGGERED RAF-1 EXPRESSION, PHOSPHORYLATION, AND ASSOCIATED KINASE-ACTIVITY INCREASE THROUGH G1 AND S IN CD3-STIMULATED PRIMARY HUMAN T-CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTEIN-KINASE; TYROSINE PHOSPHORYLATION; BIOLOGICAL-ACTIVITY; MOLECULAR-CLONING; MESSENGER-RNA; LYMPHOCYTES-T; GROWTH-FACTOR; ACTIVATION; RECEPTOR; GENE AB To gain further insight into the role of Raf-1 in normal cell growth, c-raf-1 mRNA expression, Raf-1 protein production, and Raf-1-associated kinase activity in normal human T cells were analyzed. In contrast to the constitutive expression of Raf-1 in continuously proliferating cell lines, c-raf-1 mRNA and Raf-1 protein levels were barely detectable in freshly isolated G0 T lymphocytes. Previous work with fibroblasts has suggested that Raf-1 plays a signaling role in the G0-G1 phase transition. In T cells, triggering via the T-cell antigen receptor (TCR)-CD3 complex (TCR/CD3) resulted in an approximately fourfold increase in c-raf-1 mRNA. In addition, the promotion of G1 progression by interleukin 2 (IL-2) was associated with a 5- to 10-fold immediate/early induction of c-raf-1 mRNA, resulting in up to a 12-fold increase in Raf-1 protein expression. TCR/CD3 activation did not alter the phosphorylation state of Raf-1, whereas interleukin 2 receptor stimulation resulted in a rapid increase in the phosphorylation state of a subpopulation of Raf-1 molecules progressively increasing throughout G1. These findings were complemented by assays for Raf-1-associated kinase activity which revealed a gradual accumulation of serine and threonine autokinase activity in Raf-1 immunoprecipitates during G1, which remained elevated throughout DNA replication. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT MED,HANOVER,NH 03756. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,DEPT BIOCHEM,HANOVER,NH 03756. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,COMM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA 43803, CA 50661, CA 17643] NR 71 TC 86 Z9 86 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1991 VL 11 IS 5 BP 2794 EP 2803 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ155 UT WOS:A1991FJ15500050 PM 1708096 ER PT J AU RON, D BRASIER, AR HABENER, JF AF RON, D BRASIER, AR HABENER, JF TI ANGIOTENSINOGEN GENE-INDUCIBLE ENHANCER-BINDING PROTEIN-1, A MEMBER OF A NEW FAMILY OF LARGE NUCLEAR PROTEINS THAT RECOGNIZE NUCLEAR FACTOR KAPPA-B-BINDING SITES THROUGH A ZINC FINGER MOTIF SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Note ID SEQUENCE; DNA; EXPRESSION; ACTIVATOR; INTERACT; MEDIATOR AB Transcriptional activation of the rat angiotensinogen gene during the acute-phase response is dependent on a previously characterized acute-phase response element (APRE) that binds at least two types of nuclear proteins: a cytokine-inducible activity indistinguishable from nuclear factor kappa-B (NF-kappa-B) and a family of C/EBP-like proteins. We screened a rat liver cDNA expression library with a labeled APRE DNA probe and isolated a single clone that encodes a sequence-specific APRE-binding protein. This new protein, the angiotensinogen gene-inducible enhancer-binding protein 1 (AGIE-BP1), is encoded by a large continuous open reading frame and contains a zinc finger motif virtually identical to the DNA-binding domain of a recently described human protein, MBP-1/PRDII-BF1, and a homologous mouse protein, alpha-A-CRYBP1. Outside the binding domain, the sequences diverged considerably. Southern blot analysis indicated that AGIE-BP1 and alpha-A-CRYBP1 are encoded by separate genes, thus defining a new family of DNA-binding proteins. Electrophoretic mobility shift assays, methylation interference, and DNase I footprint protection assays with the bacterially expressed DNA-binding domain of AGIE-BP1 demonstrated a binding specificity indistinguishable from that of purified NF-kappa-B. Antiserum raised against the bacterially expressed DNA-binding domain of AGIE-BP1 detected on immunoblots of cellular proteins a large (> 250-kDa) nuclear protein. Northern (RNA) blot analysis of RNAs from different rat tissues and cell lines indicated different levels of expression of the large (> 10-kb) AGIE-BP1 transcript in different tissues. The potential role of AGIE-BP1 in the regulation of gene expression is discussed. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP RON, D (reprint author), MASSACHUSETTS GEN HOSP,MOLEC ENDOCRINOL LAB,50 BLOSSOM ST,BOSTON,MA 02114, USA. NR 30 TC 61 Z9 62 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1991 VL 11 IS 5 BP 2887 EP 2895 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA FJ155 UT WOS:A1991FJ15500061 PM 2017183 ER PT J AU ALBANESE, C KAY, TWH TROCCOLI, NM JAMESON, JL AF ALBANESE, C KAY, TWH TROCCOLI, NM JAMESON, JL TI NOVEL CYCLIC ADENOSINE-3',5'-MONOPHOSPHATE RESPONSE ELEMENT IN THE HUMAN CHORIONIC-GONADOTROPIN BETA-SUBUNIT GENE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID SIGNAL-TRANSDUCTION PATHWAYS; ACTING SEQUENCES DIFFERENT; DEPENDENT PROTEIN-KINASE; NUCLEAR FACTOR CREB; ALPHA-SUBUNIT; MESSENGER-RNA; DNA-BINDING; TRANSCRIPTIONAL REGULATION; SOMATOSTATIN GENE; CAMP STIMULATION AB CG is encoded by separate alpha- and beta-subunit genes. Expression of both genes is stimulated by cAMP, but the kinetics of activation are different, with cAMP stimulation of the alpha-gene preceding that of the beta-gene. The cAMP response element (CRE) in the alpha-gene contains a palindromic DNA sequence, TGACGTCA, that binds the transcription factor CREB, a nuclear phosphoprotein that is activated by protein kinase-A. Previously, detailed characterization of a CRE in the CG-beta-gene had been difficult due to low levels of expression in transfected cells. In this study the 5'-flanking sequence of the CG-beta-gene was fused to a sensitive luciferase (LUC) reporter gene, allowing delineation of a CG-beta-CRE in transient expression assays performed in JEG-3 choriocarcinoma cells. The full-length CG-beta-promoter, -3700 to 362 basepairs (bp), was stimulated 8- to 14-fold by treatment with 1 mM 8-bromo-cAMP. Analyses of a series of deletion mutants in the CG-beta-promoter demonstrated that -311 CG-beta-LUC retained nearly complete cAMP stimulation, but deletion to -187 bp eliminated cAMP responsiveness. Overlapping DNA fragments between -311 and -30 bp were fused to a heterologous promoter (-99-alpha-LUC) to further define the locations of basal elements and CREs. Basal expression required a combination of at least two distinct elements between -311 and -30 bp, whereas cAMP responsiveness was conferred by sequences between -311 and -202 bp. Shorter DNA sequences within this region were insufficient for cAMP stimulation, suggesting that more than one element may be required. DNase-I footprinting and gel mobility shift studies demonstrated at least three distinct protein-binding sites within the CG-beta-CRE sequence. Recombinant CREB (expressed in E. coli) did not bind to these sites, and they share no sequence homology with the alpha-gene CRE, indicating that a cAMP-responsive transcription factor other than CREB interacts with the CG-beta-promoter. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,THYROID UNIT,FRUIT ST,BOSTON,MA 02114. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-23519] NR 59 TC 50 Z9 50 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 MAY PY 1991 VL 5 IS 5 BP 693 EP 702 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA FM567 UT WOS:A1991FM56700011 PM 1649392 ER PT J AU FEINBAUM, RL STORZ, G AUSUBEL, FM AF FEINBAUM, RL STORZ, G AUSUBEL, FM TI HIGH-INTENSITY AND BLUE-LIGHT REGULATED EXPRESSION OF CHIMERIC CHALCONE SYNTHASE GENES IN TRANSGENIC ARABIDOPSIS-THALIANA PLANTS SO MOLECULAR & GENERAL GENETICS LA English DT Article DE ARABIDOPSIS; TRANSGENIC LINES; CHALCONE SYNTHASE; BLUE LIGHT; PROMOTER ID CELL-SUSPENSION CULTURES; FAR-RED LIGHT; ULTRAVIOLET-LIGHT; UV-LIGHT; AGROBACTERIUM-TUMEFACIENS; ANTHOCYANIN PRODUCTION; INDUCED ACCUMULATION; PARSLEY CELLS; PHYTOCHROME; TRANSFORMATION AB To establish a genetic system for dissection of light-mediated signal transduction in plants, we analyzed the light wavelengths and promoter sequences responsible for the light-induced expression of the Arabidopsis thaliana chalcone synthase (CHS) promoter fused to the beta-glucuronidase (GUS) marker gene. Transgenic A. thaliana lines carrying 1975, 523, 186, and 17 bp of the CHS promoter fused to the GUS gene were generated, and the expression of these chimeric genes was monitored in response to high intensity light in mature plants and to different wavelengths of light in seedlings. Fusion constructs containing 1975 and 523 bp of CHS promoter sequence behaved identically to the endogenous CHS gene under all conditions. Expression of these constructs was induced specifically in response to high intensity white light and blue light. The response to blue light was seen in the presence of the P(fr) form of phytochrome. Fusion constructs containing 186 bp of promoter sequence showed reduced basal levels of expression and only weak stimulation by blue light but were induced significantly by high intensity white light. These analyses showed that the expression of the A. thaliana CHS gene is responsive to a specific blue light receptor and that sequences between -523 and -186 bp are required for optimal basal and blue light-induced expression of this gene. The experiments lay the foundation for a simple genetic screen for light response mutants. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. OI Storz, Gisela/0000-0001-6698-1241 NR 34 TC 70 Z9 73 U1 0 U2 7 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD MAY PY 1991 VL 226 IS 3 BP 449 EP 456 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA FN094 UT WOS:A1991FN09400014 PM 2038307 ER PT J AU ROZENTAL, JM AF ROZENTAL, JM TI POSITRON EMISSION TOMOGRAPHY (PET) AND SINGLE-PHOTON EMISSION COMPUTED-TOMOGRAPHY (SPECT) OF BRAIN-TUMORS SO NEUROLOGIC CLINICS LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; CEREBRAL GLUCOSE-UTILIZATION; 8-DRUGS-IN-ONE-DAY CHEMOTHERAPY; LINEAR-ACCELERATOR; MALIGNANT GLIOMAS; METABOLIC CHANGES; CANCER-THERAPY; ADULT PATIENTS; BLOOD-FLOW; TC-99M-HMPAO C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,NEUROL SERV,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,RES SERV,MADISON,WI 53705. UNIV WISCONSIN HOSP,DEPT NEUROL,MADISON,WI 53792. UNIV WISCONSIN HOSP,DEPT NEUROSURG,MADISON,WI 53792. NR 75 TC 6 Z9 6 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD MAY PY 1991 VL 9 IS 2 BP 287 EP 305 PG 19 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA FM843 UT WOS:A1991FM84300004 PM 1944100 ER PT J AU MAZUREK, MF BEAL, MF AF MAZUREK, MF BEAL, MF TI CHOLECYSTOKININ AND SOMATOSTATIN IN ALZHEIMERS-DISEASE POSTMORTEM CEREBRAL-CORTEX SO NEUROLOGY LA English DT Article ID SENILE DEMENTIA; IMMUNOREACTIVE NEURONS; RAT; RELEASE; BRAIN; ACETYLCHOLINESTERASE; NEUROPEPTIDES; NEOCORTEX; GABA AB The neuropeptides cholecystokinin (CCK) and somatostatin are synthesized in separate, but morphologically similar, populations of locally projecting neurons in cerebral cortex. Concentrations of somatostatin are markedly diminished in Alzheimer's disease (AD), suggesting possible dysfunction of the intrinsic cortical neurons in which it is produced. We determined whether cortical levels of CCK might be similarly affected in AD by dissecting postmortem brain samples from 14 histologically confirmed cases of AD and 17 age-matched controls and measuring CCK and somatostatin by radioimmunoassay. CCK-like immunoreactivity was significantly reduced in the AD brains by 24 to 38% in five of the 11 cortical areas examined but was normal in the remaining regions. Somatostatin concentrations measured in the same tissue extracts were consistently decreased by 45 to 65%. These results indicate that (1) CCK-immunoreactive neurons in cortex are affected by the AD process, and (2) the changes in levels of CCK are less dramatic than the reductions of somatostatin immunoreactivity. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MCMASTER UNIV,MED CTR,DEPT BIOMED SCI NEUROSCI,HAMILTON L8N 3Z5,ONTARIO,CANADA. RP MAZUREK, MF (reprint author), MCMASTER UNIV,MED CTR,DEPT MED NEUROL,1200 MAIN ST W,HAMILTON L8N 3Z5,ONTARIO,CANADA. FU NIA NIH HHS [P50AG051134] NR 30 TC 32 Z9 32 U1 0 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAY PY 1991 VL 41 IS 5 BP 716 EP 719 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA FK928 UT WOS:A1991FK92800021 PM 1674117 ER PT J AU HEALEY, EA BARNES, PD KUPSKY, WJ SCOTT, RM SALLAN, SE BLACK, PM TARBELL, NJ AF HEALEY, EA BARNES, PD KUPSKY, WJ SCOTT, RM SALLAN, SE BLACK, PM TARBELL, NJ TI THE PROGNOSTIC-SIGNIFICANCE OF POSTOPERATIVE RESIDUAL TUMOR IN EPENDYMOMA SO NEUROSURGERY LA English DT Article DE EPENDYMOMA; NEUROIMAGING; RADIATION THERAPY ID INTRACRANIAL EPENDYMOMAS; RADIATION-THERAPY; SURVIVAL; CHILDHOOD; RADIOTHERAPY; BRAIN AB Between 1970 and 1989, 29 patients with intracranial ependymomas were evaluated and treated at the Children's Hospital in Boston. With a median follow-up of 82 months, the actuarial survival rates at 5 and 10 years were 61 +/- 10% and 46 +/- 12%, respectively. Anaplastic histological findings were uncommon (2 of 29). Initial postoperative radiotherapy was given to 25 patients, with a median tumor dose of 5360 cGy. With a median time to recurrence of 22 months, local failure (within 2 cm of original enhancing mass) was the predominant pattern of relapse (15 of 16 failures). The presence of radiographic residual disease seen on postoperative magnetic resonance imaging or computed tomographic scans was the most important prognostic variable for patients with intracranial ependymoma. Analysis of the 19 patients who underwent postoperative imaging revealed a 75 +/- 15% 5-year freedom from progressive disease for 9 patients with no residual disease, as compared with 0% freedom from progressive disease for the 10 patients with gross residual disease (P = 0.03). In contrast, the surgical assessment of residual disease was not significant (P = 0.4). Age at presentation was also a significant prognostic factor. The overall actuarial survival rate at 12 years for infants 24 months or younger at diagnosis was 0%, as compared with 62 +/- 13% for older patients (P = 0.03). For non-anaplastic ependymomas, complete surgical resection followed by local-field, high-dose (> 54 Gy) radiotherapy appears to offer the greatest chance for long-term survival. Because of the markedly reduced survival rate for patients with radiologically apparent postoperative disease, maximal surgical resection and novel therapeutic endeavors appear warranted for this high-risk group. Future protocols should use postoperative imaging, not operative reports, to stratify patients with ependymoma. C1 CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,300 LONGWOOD AVE,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,DEPT RADIOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,JOINT CTR RADIAT THERAPY,DEPT NEUROSURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. NR 35 TC 164 Z9 166 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD MAY PY 1991 VL 28 IS 5 BP 666 EP 672 PG 7 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA FJ828 UT WOS:A1991FJ82800005 PM 1876244 ER PT J AU ODRICH, MG JAKOBIEC, FA LANCASTER, WD KENYON, KR KELLY, LD KORNMEHL, EW STEINERT, RF GROVE, AS SHORE, JW GREGOIRE, L ALBERT, DM AF ODRICH, MG JAKOBIEC, FA LANCASTER, WD KENYON, KR KELLY, LD KORNMEHL, EW STEINERT, RF GROVE, AS SHORE, JW GREGOIRE, L ALBERT, DM TI A SPECTRUM OF BILATERAL SQUAMOUS CONJUNCTIVAL TUMORS ASSOCIATED WITH HUMAN PAPILLOMAVIRUS TYPE-16 SO OPHTHALMOLOGY LA English DT Article ID CERVICAL NEOPLASIA; DNA-SEQUENCES; AMPLIFICATION; CARCINOMAS; HYBRIDIZATION AB Three patients with bilateral tumors presenting as multiple keratinizing and verrucous lesions of the bulbar and tarsal conjunctiva were determined by DNA amplification and hybridization studies to harbor human papillomavirus type 16 (HPV-16). Results of biopsy in two patients showed inflitrating squamous cell carcinoma in one eye and dysplasia or carcinoma in situ in the fellow eye. In the third patient, focal, inflamed, hypertrophic, papillary lesions with pseudoglandular invaginations of the surface epithelium were found in the tarsal conjunctivae of both eyes. These are the first documented cases of bilateral conjunctival tumors associated with human papillomavirus. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. WAYNE STATE UNIV,SCH MED,DEPT MOLEC BIOL & GENET,DETROIT,MI 48201. WAYNE STATE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DETROIT,MI 48201. UNIV OTTAWA,DEPT MICROBIOL & IMMUNOL,OTTAWA K1N 6N5,ONTARIO,CANADA. OTTAWA CIVIC HOSP,MED LAB,OTTAWA K1Y 4E9,ONTARIO,CANADA. NR 29 TC 41 Z9 43 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 MAY PY 1991 VL 98 IS 5 BP 628 EP 635 PG 8 WC Ophthalmology SC Ophthalmology GA FL048 UT WOS:A1991FL04800020 PM 1648188 ER PT J AU BELLINGER, DC WERNOVSKY, G RAPPAPORT, LA MAYER, JE CASTANEDA, AR FARRELL, DM WESSEL, DL LANG, P HICKEY, PR JONAS, RA NEWBURGER, JW AF BELLINGER, DC WERNOVSKY, G RAPPAPORT, LA MAYER, JE CASTANEDA, AR FARRELL, DM WESSEL, DL LANG, P HICKEY, PR JONAS, RA NEWBURGER, JW TI COGNITIVE-DEVELOPMENT OF CHILDREN FOLLOWING EARLY REPAIR OF TRANSPOSITION OF THE GREAT-ARTERIES USING DEEP HYPOTHERMIC CIRCULATORY ARREST SO PEDIATRICS LA English DT Article DE DEEP HYPOTHERMIC CIRCULATORY ARREST; COGNITIVE FUNCTION; CARDIOPULMONARY BYPASS; TRANSPOSITION OF THE GREAT ARTERIES ID INTACT VENTRICULAR SEPTUM; CARDIAC-SURGERY; BLOOD-FLOW; OPERATION; IQ AB Twenty-eight children who underwent corrective cardiac surgery in early infancy had developmental evaluations to explore whether cardiopulmonary bypass perfusion variables are associated with later cognitive function. All had transposition of the great arteries repaired by the arterial switch operation using deep hypothermic circulatory arrest. The mean duration of deep hypothermic circulatory arrest was 64 +/- 10 minutes (mean +/- SD). Median age at repair was 4 days (range 1 to 125 days). Tests of development were administered at age 7 to 53 months: Bayley Scales for children younger than 30 months of age (n = 18) and McCarthy Scales for older children (n = 10). Overall cognitive development score was 101.2 +/- 11.1. Duration of deep hypothermic circulatory arrest was not associated with performance. However, for core cooling periods of less than 20 minutes' duration, shorter cooling periods were associated with lower scores (r = .85, n = 11, P < .001). These data suggest that patients undergoing relatively long periods of deep hypothermic circulatory arrest may require some minimum time of cardiopulmonary bypass cooling to avoid central nervous system injury. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT CARDIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT CARDIAC SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT CARDIOVASC SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT ANESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. RP BELLINGER, DC (reprint author), CHILDRENS HOSP MED CTR,DEPT NEUROL,NEUROEPIDEMIOL UNIT,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL41786]; NIEHS NIH HHS [ES00138] NR 30 TC 121 Z9 121 U1 2 U2 3 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1991 VL 87 IS 5 BP 701 EP 707 PG 7 WC Pediatrics SC Pediatrics GA FL115 UT WOS:A1991FL11500017 PM 2020517 ER PT J AU BAUMAN, ML AF BAUMAN, ML TI MICROSCOPIC NEUROANATOMICAL ABNORMALITIES IN AUTISM SO PEDIATRICS LA English DT Article ID EARLY INFANTILE-AUTISM; LEFT-RIGHT ASYMMETRIES; MEMORY DEFICITS; CELL COUNTS; HIPPOCAMPUS; AMYGDALA; BRAIN; CEREBELLUM; MONKEYS; INVOLVEMENT C1 MASSACHUSETTS GEN HOSP,CHILDRENS NEUROL SERV,BOSTON,MA 02114. RP BAUMAN, ML (reprint author), BOSTON CITY HOSP,DEPT NEUROL,818 HARRISON AVE,BOSTON,MA 02118, USA. NR 49 TC 176 Z9 179 U1 2 U2 6 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1991 VL 87 IS 5 SU S BP 791 EP 796 PG 6 WC Pediatrics SC Pediatrics GA FL809 UT WOS:A1991FL80900007 PM 2020538 ER PT J AU BAUMAN, ML COURCHESNE, E DENCKLA, MB FOLSTEIN, SE JAMES, LS MINSHEW, NJ NELSON, KB PIVEN, J RAPIN, I AF BAUMAN, ML COURCHESNE, E DENCKLA, MB FOLSTEIN, SE JAMES, LS MINSHEW, NJ NELSON, KB PIVEN, J RAPIN, I TI AN UPDATE ON AUTISM - A DEVELOPMENTAL DISORDER SO PEDIATRICS LA English DT Editorial Material C1 BOSTON CITY HOSP,DEPT NEUROL,BOSTON,MA 02118. JOHNS HOPKINS UNIV,SCH MED,DEPT PSYCHIAT,DIV PSYCHIAT GENET,BALTIMORE,MD 21205. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. UNIV CALIF SAN DIEGO,SCH MED,DEPT NEUROSCI,LA JOLLA,CA 92093. NINCDS,NEUROEPIDEMIOL BRANCH,BETHESDA,MD 20892. RP BAUMAN, ML (reprint author), MASSACHUSETTS GEN HOSP,CHILDRENS NEUROL SERV,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1991 VL 87 IS 5 SU S BP R5 EP R6 PG 2 WC Pediatrics SC Pediatrics GA FL809 UT WOS:A1991FL80900001 ER PT J AU BRAND, JG TEETER, JH KUMAZAWA, T HUQUE, T BAYLEY, DL AF BRAND, JG TEETER, JH KUMAZAWA, T HUQUE, T BAYLEY, DL TI TRANSDUCTION MECHANISMS FOR THE TASTE OF AMINO-ACIDS SO PHYSIOLOGY & BEHAVIOR LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL SYMP ON UMAMI CY OCT 07-10, 1990 CL SICILY, ITALY DE CHEMICAL SENSES; TASTE; GLUTAMATE; RECEPTORS; ION CHANNEL ID ICTALURUS-PUNCTATUS; RECEPTOR-SITES; CATFISH; BINDING; SENSATION; CELLS; SPECIFICITY; GLUTAMATE; MEMBRANES; TISSUE AB Amino acids are important taste stimuli for a variety of animals. One animal model, the channel catfish, I. punctatus, possesses sensitive taste receptor systems for several amino acids. Neurophysiological and biochemical receptor binding studies suggest the presence of at least three receptor pathways: one is a relatively nonspecific site(s) responsive to short-chain neutral amino acids such as L-alanine (L-ALA); another is responsive to the basic amino acid L-arginine (L-ARG); still another is a low affinity site for L-proline (L-PRO). Several possible transduction pathways are available in the taste system of this animal model for these amino acids. One of these, formation of inositol trisphosphate (IP3) and cyclic AMP (cAMP), is mediated by GTP-binding regulatory proteins, while another involves ion channels directly activated by stimuli. L-ALA is a potent stimulus to cAMP and IP3 accumulation, while L-ARG at low concentrations is without effect. On the other hand, L-ARG and L-PRO, but not L-ALA, are able to activate stimulus-specific and cation-selective channels in taste epithelial membranes reconstituted in phospholipid bilayers at the tips of patch pipettes. Preliminary studies using mouse taste tissue demonstrate that monosodium-L-glutamate (MSG) did not enhance production of IP3 or cAMP. However, in reconstitution experiments using taste epithelium of mouse, conductance changes due to MSG are observed. The specificity of this channel(s) and its uniqueness have yet to be determined. C1 UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP BRAND, JG (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. FU NIDCD NIH HHS [DC-00356, DC-00327] NR 26 TC 41 Z9 43 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD MAY PY 1991 VL 49 IS 5 BP 899 EP 904 DI 10.1016/0031-9384(91)90201-X PG 6 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA FP005 UT WOS:A1991FP00500011 PM 1679559 ER PT J AU JAIN, JN LONSDALE, DM AF JAIN, JN LONSDALE, DM TI NUCLEOTIDE-SEQUENCE OF REPEAT-2 OF THE MITOCHONDRIAL-DNA FROM THE MAIZE N-CYTOPLASM SO PLANT MOLECULAR BIOLOGY LA English DT Note DE MAIZE; MITOCHONDRIAL DNA; REPEATED SEQUENCE C1 CTR PLANT SCI RES,CAMBRIDGE LAB,DEPT MOLEC GENET,COLNEY LANE,NORWICH NR4 7UJ,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. NR 3 TC 1 Z9 1 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-4412 J9 PLANT MOL BIOL JI Plant Mol.Biol. PD MAY PY 1991 VL 16 IS 5 BP 935 EP 936 DI 10.1007/BF00015089 PG 2 WC Biochemistry & Molecular Biology; Plant Sciences SC Biochemistry & Molecular Biology; Plant Sciences GA FR645 UT WOS:A1991FR64500021 PM 1859874 ER PT J AU CHENG, CL ACEDO, GN DEWDNEY, J GOODMAN, HM CONKLING, MA AF CHENG, CL ACEDO, GN DEWDNEY, J GOODMAN, HM CONKLING, MA TI DIFFERENTIAL EXPRESSION OF THE 2 ARABIDOPSIS NITRATE REDUCTASE GENES SO PLANT PHYSIOLOGY LA English DT Article ID MESSENGER-RNA; SQUASH COTYLEDONS; LIGHT; ACCUMULATION; THALIANA; SEQUENCE; TOBACCO; NUCLEAR; DEHYDROGENASE; PROTEIN AB The differential regulation of the two nitrate reductase (NR, EC 1.6.61) genes of Arabidopsis thaliana L. Heynh was examined. cDNAs corresponding to each of the NR genes (NR1 and NR2) were used to measure changes in the steady-state levels of NR mRNA in response to nitrate, light, circadian rhythm, and tissue specificity. Although nitrate-induction kinetics of the two genes are very similar, NR1 is expressed in the absence of nitrate at a higher basal level than NR2. Nitrate induction is transient both in the roots and leaves, however the kinetics are different: the induction and decline in the roots precede that in the leaves. Light induces the expression of each of the genes with significantly different kinetics: NR2 reached saturation more rapidly than did NR1. Both genes showed similar diurnal patterns of circadian rhythm, with NR2 mRNA accumulating earlier in the morning. C1 UNIV IOWA,DEPT BIOL,IOWA CITY,IA 52242. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. N CAROLINA STATE UNIV,DEPT GENET,RALEIGH,NC 27695. RP CHENG, CL (reprint author), UNIV IOWA,DEPT BOT,IOWA CITY,IA 52242, USA. NR 29 TC 86 Z9 90 U1 0 U2 3 PU AMER SOC PLANT PHYSIOLOGISTS PI ROCKVILLE PA 15501 MONONA DRIVE, ROCKVILLE, MD 20855 SN 0032-0889 J9 PLANT PHYSIOL JI Plant Physiol. PD MAY PY 1991 VL 96 IS 1 BP 275 EP 279 DI 10.1104/pp.96.1.275 PG 5 WC Plant Sciences SC Plant Sciences GA FN157 UT WOS:A1991FN15700042 PM 16668164 ER PT J AU GREENBERG, BM MASEM, M WANG, YX RUBIN, P MAY, JW AF GREENBERG, BM MASEM, M WANG, YX RUBIN, P MAY, JW TI EFFICACY OF INTRAARTERIAL HEPARIN IN MAINTAINING MICROVASCULAR PATENCY - AN EXPERIMENTAL-MODEL SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID THROMBOSIS; AGGREGATION; DEXTRAN AB Human-grade sodium heparin was studied to determine thrombosis model patency rates between an intraarterial infusion versus an intravenous method of delivery in a rabbit model. Specific differences in patency and partial thromboplastin times were studied in each group and compared with a saline-perfused group. Three animal groups (New Zealand white rabbits) were established (total = 35 animals). Standardized femoral arterial 5-mm inversion grafts (AIG) were done in each animal in each group. The animals in the control group received intravenous saline infusion, while the two treatment groups received intravenous heparin (12 animals) or intraarterial heparin (12 animals minus 1 anesthesia death). The route of instillation of the infusate was selected at random after completing the inversion grafts. A proximal epigastric branch was utilized for access in those animals randomized to the intraarterial group. Intravenous delivery was accomplished by means of a femoral venous catheter in the vena cava. A 72-hour period of infusion was used in all animals. A dose of 45 units per hour of heparin following a 500-unit bolus was used in the intravenous group. After an identical bolus dose, 25 units per hour of heparin was adminstered in the intraarterial group. The control (saline group) was given 1 cc saline (in a volume equal to the heparin-dosed groups) daily for 3 days. Arterial inversion graft patency rates were assessed by direct inspection at day 5. Systemic and regional (i.e., distal to the inversion graft) partial thromboplastin times (PTT) were measured in representative control, IV, and intraarterial heparin-treated groups. Complications were recorded. One animal in the intraarterial group died under general anesthesia. Arterial inversion graft patency measured on day 5 in the intraarterial group was 82 percent (9 of 11) as compared with 50 percent (6 of 12) in the intravenous group. Only 8 percent (1 of 12) of anastomoses in the saline control group remained patent at 5 days. The Fisher exact test showed a significant difference (p < 0.001) between intraarterial heparin- and saline-perfused groups. A p value of less than 0.05 (not significant) was found in comparing intravenous heparin with the intraarterial heparin-perfused groups or in comparing IV heparin with the saline-perfused group. Representative electron microscopy of arterial inversion grafts from heparin-treated animals, either intraarterial or intravenous, showed reendothelialization of the arterial wall within 1 week in open grafts. Complication rates in the three groups did not differ significantly. Systemic PTT values averaged 55 seconds in the IV heparin group and 28 seconds in the saline group. At these selected doses, systemic PTT values were normal (< 35 seconds) in the intraarterial group, despite regionally elevated values (PTT regionally between 88 and 150 seconds, average = 110 seconds; N = 5 animals) in blood drawn distal to the arterial inversion graft. Intraarterial heparin administration resulted in significantly higher patency rates as compared with the saline-perfused group (p < 0.001). Although patency rates in both the intraarterial and intravenous groups were improved, pairwise comparison only approached significance at the p = 0.05 value. Complication rates in all groups were low. Clinical ramifications of using a local heparin delivery system for anticoagulation therapy are apparent. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST & RECONSTRUCT SURG,BOSTON,MA 02114. NR 19 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD MAY PY 1991 VL 87 IS 5 BP 933 EP 940 DI 10.1097/00006534-199105000-00020 PG 8 WC Surgery SC Surgery GA FJ404 UT WOS:A1991FJ40400020 PM 2017503 ER PT J AU SMILEY, ST REERS, M MOTTOLAHARTSHORN, C LIN, M CHEN, A SMITH, TW STEELE, GD CHEN, LB AF SMILEY, ST REERS, M MOTTOLAHARTSHORN, C LIN, M CHEN, A SMITH, TW STEELE, GD CHEN, LB TI INTRACELLULAR HETEROGENEITY IN MITOCHONDRIAL-MEMBRANE POTENTIALS REVEALED BY A J-AGGREGATE-FORMING LIPOPHILIC CATION JC-1 SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE FLUORESCENCE MICROSCOPY; VITAL DYE; RESPIRATION; 5,5',6,6'-TETRACHLORO-1,1',3,3'-TETRAETHYLBENZIMIDAZOLOCARBOCYANINE IODIDE ID BEHAVIOR; CELLS AB By using a potential-dependent J-aggregate-forming delocalized lipophilic cation, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide (JC-1), we find that membrane potentials across mitochondria in a living cell can be heterogeneous. Remarkably, even within a long contiguous mitochondrion, regional heterogeneity in membrane potentials appears to be possible. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SMILEY, ST (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIGMS NIH HHS [GM 38318] NR 15 TC 936 Z9 959 U1 6 U2 57 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 MAY PY 1991 VL 88 IS 9 BP 3671 EP 3675 DI 10.1073/pnas.88.9.3671 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FK184 UT WOS:A1991FK18400034 PM 2023917 ER PT J AU BAUER, A MCCONKEY, DJ HOWARD, FD CLAYTON, LK NOVICK, D KOYASU, S REINHERZ, EL AF BAUER, A MCCONKEY, DJ HOWARD, FD CLAYTON, LK NOVICK, D KOYASU, S REINHERZ, EL TI DIFFERENTIAL SIGNAL TRANSDUCTION VIA T-CELL RECEPTOR CD3-ZETA-2, CD3-ZETA-ETA, AND CD3-ETA-2 ISOFORMS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CA2+ MOBILIZATION; PHOSPHATIDYLINOSITOL TURNOVER; PROTEIN TYROSINE KINASE; INTERLEUKIN-2 PRODUCTION ID ANTIGEN RECEPTOR; ZETA-CHAIN; COMPLEX; GENE; PHOSPHATIDYLINOSITOL; PHOSPHORYLATION; IDENTIFICATION; CHROMOSOME-11; EXPRESSION; ACTIVATION AB The T-cell antigen receptor (TCR) consists of an antigen-binding heterodimer, termed Ti, which is noncovalently associated with the invariant CD3 subunits (gamma, delta, epsilon, zeta, and eta). The CD3-zeta and -eta subunits form either homodimeric or heterodimeric structures in turn associated with the other components of the TCR complex. This feature increases the structural complexity of TCRs by creating "isoforms." Both CD3-zeta and -eta are thought to play an important role in signal transduction triggered by antigen/major histocompatibility complex. To compare signaling functions of TCR isoforms, MA5.8, a CD3-zeta-eta- variant of the cytochrome c-specific, I-E(k)-restricted T-cell hybridoma 2B4.11, was stably transfected with cDNAs encoding CD3-zeta and/or CD3-eta, and resulting clones were characterized. The findings indicate that signals inducing Ca2+ mobilization, phosphatidylinositol turnover, and interleukin 2 production are each transmitted by the above TCR isoforms. In contrast, tyrosine phosphorylation of the CD3-zeta subunit but not the CD3-eta subunit follows TCR stimulation. Given the general importance of tyrosine phosphorylation for receptor signaling, it is likely that this difference between TCR isoforms plays a regulatory role in T-lineage function by qualitatively or quantitatively altering signaling events. C1 HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. RP HARVARD UNIV, SCH MED, DANA FARBER CANC INST, IMMUNOBIOL LAB, BOSTON, MA 02115 USA. RI Koyasu, Shigeo/J-5583-2015 OI Koyasu, Shigeo/0000-0001-9585-3038 NR 33 TC 56 Z9 56 U1 0 U2 3 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY PY 1991 VL 88 IS 9 BP 3842 EP 3846 DI 10.1073/pnas.88.9.3842 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FK184 UT WOS:A1991FK18400069 PM 1708889 ER PT J AU WOISETSCHLAEGER, M JIN, XW YANDAVA, CN FURMANSKI, LA STROMINGER, JL SPECK, SH AF WOISETSCHLAEGER, M JIN, XW YANDAVA, CN FURMANSKI, LA STROMINGER, JL SPECK, SH TI ROLE FOR THE EPSTEIN-BARR-VIRUS NUCLEAR ANTIGEN-2 IN VIRAL PROMOTER SWITCHING DURING INITIAL-STAGES OF INFECTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE INFECTION OF PRIMARY LYMPHOCYTES-B; EPSTEIN-BARR VIRUS NUCLEAR ANTIGEN-2-DEPENDENT ENHANCER; S1 NUCLEASE PROTECTION; INVITRO TRANSCRIPTION; DNASE-I FOOTPRINTING ID B-CELLS; TRANSCRIPTION; DNA; RNA; LYMPHOCYTES; EXPRESSION; SEQUENCES; LYMPHOMA; GENOMES; STRAIN AB During latent Epstein-Barr virus (EBV) infection of human B lymphocytes, six viral nuclear antigens (EBNAs) are expressed from long primary transcripts by means of alternative splicing and alternative polyadenylylation sites. These transcripts initiate from one of two promoters, Cp or Wp, that function in a mutually exclusive fashion. Wp is exclusively utilized during the initial stages of infection of primary B lymphocytes, followed by a switch to Cp usage. These studies have been extended to show that (i) a mutant EBV strain lacking the gene encoding EBNA 2 fails to switch from Wp to Cp usage in primary B lymphocytes, although the virus contains a functional Cp; (ii) a region from -429 to -245 base pairs upstream of Cp is essential for Cp activity in B lymphocytes, but only in the context of upstream and downstream sequences; (iii) this region contains an EBNA 2-dependent enhancer; and (iv) DNase I protection employing nuclear extracts from B and T lymphocytes revealed a B-cell-specific footprint in the region of the EBNA 2-dependent enhancer. These results support a model for viral promoter switching during the initial stages of infection in which Wp activity leads to the expression of EBNA 2, followed by activation of Cp through the EBNA 2-dependent enhancer. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP WOISETSCHLAEGER, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 7554, CA 43143] NR 24 TC 112 Z9 114 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 MAY PY 1991 VL 88 IS 9 BP 3942 EP 3946 DI 10.1073/pnas.88.9.3942 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FK184 UT WOS:A1991FK18400089 PM 1850841 ER PT J AU HENDRICKSON, EA QIN, XQ BUMP, EA SCHATZ, DG OETTINGER, M WEAVER, DT AF HENDRICKSON, EA QIN, XQ BUMP, EA SCHATZ, DG OETTINGER, M WEAVER, DT TI A LINK BETWEEN DOUBLE-STRAND BREAK-RELATED REPAIR AND V(D)J RECOMBINATION - THE SCID MUTATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE DNA REPAIR; X-IRRADIATION ID RAY-SENSITIVE MUTANTS; COMBINED IMMUNE-DEFICIENCY; NEUTRAL FILTER ELUTION; HAMSTER OVARY CELL; PRE-B CELLS; MAMMALIAN-CELLS; CROSS-SENSITIVITY; MICE; DEFECT; GENES AB We show here that mammalian site-specific recombination and DNA-repair pathways share a common factor. The effects of DNA-damaging agents on cell lines derived from mice homozygous for the scid (severe combined immune deficiency) mutation were studied. Surprisingly, all scid cell lines exhibited a profound hypersensitivity to DNA-damaging agents that caused double-strand breaks (x-irradiation and bleomycin) but not to other chemicals that caused single-strand breaks or cross-links. Neutral filter elution assays demonstrated that the x-irradiation hypersensitivity could be correlated with a deficiency in repairing double-strand breaks. These data suggest that the scid gene product is involved in two pathways: DNA repair of random double-strand breaks and the site-specific and lymphoid-restricted variable-(diversity)-joining [V(D)J] DNA rearrangement process. We propose that the scid gene product performs a similar function in both pathways and may be a ubiquitous protein. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. MIT,WHITEHEAD INST,CAMBRIDGE,MA 02139. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. RI Schatz, David/A-6748-2013 OI Schatz, David/0000-0002-5669-1176 FU NICHD NIH HHS [5F32HD07034]; NIGMS NIH HHS [GM39312] NR 30 TC 302 Z9 302 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 MAY PY 1991 VL 88 IS 10 BP 4061 EP 4065 DI 10.1073/pnas.88.10.4061 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FM042 UT WOS:A1991FM04200001 PM 1709732 ER PT J AU ROCK, KL GRAMM, C BENACERRAF, B AF ROCK, KL GRAMM, C BENACERRAF, B TI LOW-TEMPERATURE AND PEPTIDES FAVOR THE FORMATION OF CLASS-I HETERODIMERS ON RMA-S CELLS AT THE CELL-SURFACE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MAJOR HISTOCOMPATIBILITY COMPLEX; H-2; BETA-2-MICROGLOBULIN; CYTOTOXIC LYMPHOCYTE-T ID HEAVY-CHAINS; LYMPHOCYTES-T; BETA-2-MICROGLOBULIN; MOLECULES; ASSOCIATION; ANTIGEN; BINDING; INVITRO; HLA; BIOSYNTHESIS AB RMA-S murine cells have a mutation that interferes with the assembly of class I major histocompatibility complex (MHC) heterodimers and are deficient in the expression of class I molecules on the cell surface. The mutant phenotype has been reported to be normalized upon incubation of RMA-S cells at 25-degrees-C. We find that much of the increased expression of class I heterodimers is dependent on culturing RMA-S cells in bovine serum or with purified bovine beta-2-microglobulin. Furthermore, epitopes that are associated with class I MHC molecules that have bound xenogeneic beta-2-microglobulin are preferentially formed on RMA-S cells cultured at 25-degrees-C. These heterologous class I molecules are thermolabile. Increased expression of class I molecules has also been observed on RMA-S cells incubated at 37-degrees-C in the presence of class I-restricted peptides. We find that the increased expression of D(b) molecules induced by influenza virus nucleoprotein residues 365-380 is similarly dependent on culturing RMA-S cells in bovine serum or with purified bovine beta-2-microglobulin. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROCK, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI20248] NR 29 TC 67 Z9 67 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 MAY PY 1991 VL 88 IS 10 BP 4200 EP 4204 DI 10.1073/pnas.88.10.4200 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA FM042 UT WOS:A1991FM04200030 PM 1709736 ER EF