FN Thomson Reuters Web of Science™ VR 1.0 PT J AU SWINFORD, RD TANG, SS DIAMANT, D INGELFINGER, JR AF SWINFORD, RD TANG, SS DIAMANT, D INGELFINGER, JR TI HIGH-SALT EXPOSURE UP-REGULATES TRANSFORMING GROWTH-FACTOR-BETA-1 (TGF-BETA-1) EXPRESSION IN IMMORTALIZED PROXIMAL TUBULE CELLS (IRPTC) SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP, CHILDRENS 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 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 1995 VL 37 IS 4 BP A372 EP A372 PN 2 PG 1 WC Pediatrics SC Pediatrics GA QP082 UT WOS:A1995QP08202215 ER PT J AU TAKAHASHI, LK KIM, H AF TAKAHASHI, LK KIM, H TI RELATIVE CONTRIBUTIONS OF PITUITARY-ADRENAL HORMONES TO THE ONTOGENY OF BEHAVIORAL-INHIBITION IN THE RAT SO PHYSIOLOGY & BEHAVIOR LA English DT Article DE PREWEANLING RATS; BEHAVIORAL INHIBITION; FREEZING; ULTRASONIC VOCALIZATIONS; HYPOPHYSECTOMY; ADRENALECTOMY; ACTH; CORTICOSTERONE ID PREWEANLING RATS; BRAIN-DEVELOPMENT; BETA-ENDORPHIN; CORTICOTROPIN; CORTICOSTERONE; SECRETION; RESPONSES AB Recent investigations revealed that adrenalectomized (ADX) rat pups exhibit deficits in behavioral inhibition. Furthermore, administration of exogenous corticosterone (CORT) restores behavioral inhibition in ADX pups. Although these studies suggest that CORT has an important role in the development of behavioral inhibition, the relative behavioral effects of elevated pituitary hormone secretion induced by ADX are not known. Therefore, experiments were conducted to assess the potential behavioral effects of elevated adrenocorticotropin (ACTH) secretion induced by ADX and to further evaluate the contribution of endogenous CORT to the development of behavioral inhibition. In Experiment 1., we verified that 10-day-old ADX rats exhibit high levels of plasma ACTH throughout the preweaning period associated with the development of behavioral inhibition. In Experiment 2, 10-day-old pups were hypophysectomized (HYPOX) and ADX acid were compared behaviorally to sham-operated controls on day 14. When tested in the presence of an anesthetized unfamiliar adult male rat, HYPOX + ADX pups exhibited low levels of freezing accompanied by ultrasonic vocalizations. These pups also had reduced concentrations of plasma ACTH and CORT. In Experiment 3, 10-day-old pups were HYPOX and tested for behavioral inhibition on day 14. In comparison to sham-operated controls, HYPOX rats exhibited significantly lower levels of freezing and had reduced plasma concentrations of ACTH and CORT. Results demonstrate clearly that deficits in freezing occur even in the presence of low plasma ACTH concentrations. Therefore, elevated secretion of pituitary hormones is not a major factor that contributes to the ADX-induced deficits in behavioral inhibition. In addition, results considerably strengthen the contention that endogenous adrenal steroids have a prominent role in the development of neural pathways regulating the expression of behavioral inhibition. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53792. RP TAKAHASHI, LK (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [MH-43986] NR 36 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 0031-9384 J9 PHYSIOL BEHAV JI Physiol. Behav. PD APR PY 1995 VL 57 IS 4 BP 711 EP 716 DI 10.1016/0031-9384(94)00324-6 PG 6 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA QL348 UT WOS:A1995QL34800015 PM 7777608 ER PT J AU AMARANTE, MTJ CONSTANTINESCU, MA OCONNOR, D YAREMCHUK, MJ AF AMARANTE, MTJ CONSTANTINESCU, MA OCONNOR, D YAREMCHUK, MJ TI CYANOACRYLATE FIXATION OF THE CRANIOFACIAL SKELETON - AN EXPERIMENTAL-STUDY SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID STAINLESS-STEEL; BONE; PLATES AB This study examined the feasibility of achieving bone fixation of the upper facial skeleton using n-butyl-2-cyanoacrylate. We compared the fixation obtained with this adhesive to that obtained with plates and screws in an animal model. The stability of fixation of both osteotomies and onlay grafts was studied in six minipigs. Three osteotomies were performed on each side of the skull. Additionally, a parietal split-thickness autograft was fixated to the nasal bone as an onlay. Plates and screws were used on the right and adhesive on the left. The animals were killed at 6 weeks, and both sides were compared biomechanically and histologically. Clinical assessment showed stability of all fragments. No statistical difference was found in the comparison of the maximum torque to failure between analogous plated and glued sides. Radiographic cephalometry revealed no significant displacement of the fragments. Histologic analysis demonstrated bony union. In this study, n-butyl-2-cyanoacrylate was as effective as plates and screws in the fixation of surgically created osteotomies of the upper facial skeleton. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV PLAST & RECONSTRUCT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ORTHOPED BIOMECH LAB,BOSTON,MA 02114. NR 29 TC 41 Z9 43 U1 0 U2 1 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 APR PY 1995 VL 95 IS 4 BP 639 EP 646 PG 8 WC Surgery SC Surgery GA QM073 UT WOS:A1995QM07300004 PM 7892307 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI ARTHRITIS OF RECENT-ONSET - A GUIDE TO EVALUATION AND INITIAL THERAPY FOR PRIMARY-CARE PHYSICIANS SO POSTGRADUATE MEDICINE LA English DT Article AB Correct early diagnosis of acute and recent-onset arthritis is important to prognosis. The erosive damage done by rheumatoid arthritis occurs earlier in the disease course than previously realized, and more specific therapies to minimize damage are becoming available, Also, arthritis may be the initial clue to a serious systemic disease. Determining whether one, several, or many joints are affected can narrow the diagnostic possibilities, Arthrocentesis and synovial fluid testing provide much information and should be done at initial evaluation if possible. The presence or absence of fever, rash, family history of joint disease, and exposure to infective organisms can further direct diagnostic studies and treatment, In general, to avoid masking clues, drug therapy should be delayed for mild symptoms until diagnosis is complete. C1 UNIV PENN,SCH MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. RP SCHUMACHER, HR (reprint author), VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,ARTHRITIS IMMUNOL UNIT,39TH & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. NR 8 TC 2 Z9 2 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 0032-5481 J9 POSTGRAD MED JI Postgrad. Med. PD APR PY 1995 VL 97 IS 4 BP 52 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA QR457 UT WOS:A1995QR45700009 PM 7716092 ER PT J AU WILSON, CC HIRSCH, MS AF WILSON, CC HIRSCH, MS TI COMBINATION ANTIRETROVIRAL THERAPY FOR THE TREATMENT OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Article ID RECOMBINANT INTERFERON-ALPHA; HIV-1 REPLICATION INVITRO; AIDS-RELATED COMPLEX; REVERSE-TRANSCRIPTASE INHIBITORS; 3-DRUG SYNERGISTIC INHIBITION; IMMUNE-DEFICIENCY SYNDROME; KAPOSIS SARCOMA; SOLUBLE CD4; A-INTERFERON; PHASE-I C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 85 TC 5 Z9 5 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 1081-650X J9 P ASSOC AM PHYSICIAN JI Proc. Assoc. Am. Phys. PD APR PY 1995 VL 107 IS 1 BP 19 EP 27 PG 9 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA TF497 UT WOS:A1995TF49700003 PM 8630741 ER PT J AU BIERER, BE AF BIERER, BE TI MECHANISMS OF ACTION OF IMMUNOSUPPRESSIVE AGENTS - CYCLOSPORINE-A, FK506, AND RAPAMYCIN SO PROCEEDINGS OF THE ASSOCIATION OF AMERICAN PHYSICIANS LA English DT Review ID CIS-TRANS-ISOMERASE; CALCINEURIN PHOSPHATASE-ACTIVITY; T-CELL ACTIVATION; P70 S6 KINASE; PEPTIDYL-PROLYL ISOMERASE; CYCLOPHILIN-RELATED PROTEIN; HUMAN FK506-BINDING PROTEIN; A-TREATED MICE; BINDING-PROTEIN; SIGNAL-TRANSDUCTION C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. RP BIERER, BE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,DANA 1710A,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI32514] NR 134 TC 10 Z9 10 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 1081-650X J9 P ASSOC AM PHYSICIAN JI Proc. Assoc. Am. Phys. PD APR PY 1995 VL 107 IS 1 BP 28 EP 40 PG 13 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA TF497 UT WOS:A1995TF49700004 PM 8630742 ER PT J AU SCHERER, RF CANTY, AL PETERSON, FL COOPER, RF AF SCHERER, RF CANTY, AL PETERSON, FL COOPER, RF TI IDENTIFICATION OF MANAGERIAL BEHAVIOR DIMENSIONS IN A FEDERAL HEALTH-CARE AGENCY SO PSYCHOLOGICAL REPORTS LA English DT Article AB Understanding the behavior of managers provides an opportunity to assess congruencies between organizational needs and managerial skills. This assessment is critical in federal health-care wherein the environment is rapidly changing. In the current investigation, dimensions of managerial behavior for 267 managers in a federal health-care agency were identified. Recommendations are provided with respect to the relevance of using these dimensions for organizational training and development activities. C1 UNIV MISSISSIPPI,UNIVERSITY,MS 38677. US DEPT VET AFFAIRS,DAYTON,OH. RP SCHERER, RF (reprint author), WRIGHT STATE UNIV,COLL BUSINESS & ADM,DAYTON,OH 45435, USA. NR 9 TC 2 Z9 2 U1 1 U2 2 PU PSYCHOLOGICAL REPORTS PI MISSOULA PA P O BOX 9229, MISSOULA, MT 59807 SN 0033-2941 J9 PSYCHOL REP JI Psychol. Rep. PD APR PY 1995 VL 76 IS 2 BP 675 EP 679 PG 5 WC Psychology, Multidisciplinary SC Psychology GA RB714 UT WOS:A1995RB71400061 PM 7667482 ER PT J AU SCHWARTZ, CE COLE, BF VICKREY, BG GELBER, RD AF SCHWARTZ, CE COLE, BF VICKREY, BG GELBER, RD TI THE Q-TWIST APPROACH TO ASSESSING HEALTH-RELATED QUALITY-OF-LIFE IN EPILEPSY SO QUALITY OF LIFE RESEARCH LA English DT Article DE OUTCOMES; QUALITY OF LIFE; NEUROLOGICAL DISEASE; EPILEPSY; PATIENT PERSPECTIVE; Q-TWIST ID ANTERIOR TEMPORAL LOBECTOMY; ADJUSTED SURVIVAL ANALYSIS; ADJUVANT THERAPY; BREAST-CANCER; FOLLOW-UP; DETERMINANTS AB We propose to develop a methodology for evaluating clinical interventions for epilepsy in terms of their effects on disease-related outcomes, social cost and quality of life, while incorporating patient preference. The technique represents an extension of the 'quality-adjusted time without symptoms and toxicities' (Q-TWiST) method, which has been previously used to evaluate treatments for cancer and AIDS with respect to their costs in terms of toxicities, and benefits in terms of improved progression-free and overall survival. The extensions we propose to develop allow additional dimensions of quality of life relevant to epilepsy to be included in the analysis. We demonstrate a possible application of the proposed Q-TWiST method with a hypothetical example comparing surgery vs antiepileptic medication management alone for seizure control. The trade-offs between these alternative treatments are highlighted, along with patient importance weightings regarding various dimensions of quality of life. We describe further research needed to develop the methodology fully and comment on its potential usefulness. C1 HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT NEUROL, LOS ANGELES, CA USA. ROCKY MT MULTIPLE SCLEROSIS CTR, ENGLEWOOD, CO USA. BROWN UNIV, DEPT COMMUNITY HLTH, PROVIDENCE, RI 02912 USA. BROWN UNIV, DIV APPL MATH, PROVIDENCE, RI 02912 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV BIOSTAT, BOSTON, MA 02115 USA. RP SCHWARTZ, CE (reprint author), FRONTIER SCI & TECHNOL RES FDN INC, 303 BOYLSTON ST, BROOKLINE, MA 02146 USA. RI Cole, Bernard/I-3775-2012 FU NINDS NIH HHS [K08 NS01669] NR 29 TC 17 Z9 17 U1 0 U2 1 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0962-9343 J9 QUAL LIFE RES JI Qual. Life Res. PD APR PY 1995 VL 4 IS 2 BP 135 EP 141 DI 10.1007/BF01833607 PG 7 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA QY268 UT WOS:A1995QY26800005 PM 7780380 ER PT J AU AMES, D CARTER, J WIRSHING, WC MARDER, SR GOLDSTEIN, MJ AF AMES, D CARTER, J WIRSHING, WC MARDER, SR GOLDSTEIN, MJ TI CLOZAPINE ASSOCIATED EOSINOPHILIA AND NEUTROPENIA SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 2 Z9 2 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD APR PY 1995 VL 15 IS 1-2 BP 141 EP 142 DI 10.1016/0920-9964(95)95439-G PG 2 WC Psychiatry SC Psychiatry GA QN952 UT WOS:A1995QN95200415 ER PT J AU MARDER, SR AF MARDER, SR TI INTEGRATING PSYCHOSOCIAL AND PHARMACOLOGICAL STRATEGIES FOR MAINTENANCE THERAPY SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD APR PY 1995 VL 15 IS 1-2 BP 159 EP 159 DI 10.1016/0920-9964(95)95494-T PG 1 WC Psychiatry SC Psychiatry GA QN952 UT WOS:A1995QN95200468 ER PT J AU AMES, D BARTZOKIS, G PIERRE, J SUN, A BERISFORD, MA MARDER, SR WIRSHING, WC AF AMES, D BARTZOKIS, G PIERRE, J SUN, A BERISFORD, MA MARDER, SR WIRSHING, WC TI THE RELATIONSHIP OF SERUM IRON INDEXES TO AKATHISIA, TARDIVE-DYSKINESIA, AND PLASMA PROLIXIN LEVELS SO SCHIZOPHRENIA RESEARCH LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RI Bartzokis, George/K-2409-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD APR PY 1995 VL 15 IS 1-2 BP 212 EP 212 DI 10.1016/0920-9964(95)95650-X PG 1 WC Psychiatry SC Psychiatry GA QN952 UT WOS:A1995QN95200626 ER PT J AU ADAMS, PD KAELIN, WG AF ADAMS, PD KAELIN, WG TI TRANSCRIPTIONAL CONTROL BY E2F SO SEMINARS IN CANCER BIOLOGY LA English DT Article DE CELL-CYCLE; DP; E2F; RB; TRANSCRIPTION ID RETINOBLASTOMA GENE-PRODUCT; CELL-CYCLE; BINDING PROTEIN; ADENOVIRUS-E1A PREVENTS; SUSCEPTIBILITY GENE; MOLECULAR-CLONING; COMPLEX-FORMATION; TUMOR SUPPRESSOR; RB PROTEIN; C-MYC AB Considerable evidence suggests that the E2F/DRTF1 family Of transcription factors (hereafter referred to as 'E2F') plays a critical role in cell growth control. For example, the ability of several small DNA tumour viruses, such as SV40, adenovirus and human papillomavirus to transform certain. cells is tightly linked to their ability to deregulate E2F. Furthermore, E2F appears to directly regulate the transcription of a diverse set of genes implicated in DNA replication and cell growth control. Finally, a number of known cell cycle regulators, some of which are commonly mutated in human tumours, appear to exert their effects, at least in part, by altering E2F activity. Among these are pRb, p53, cdk-2, cdk-4 and certain cyclins. RP ADAMS, PD (reprint author), DANA FARBER CANC INST,ROOM 634,MAYER BLDG,44 BINNEY ST,BOSTON,MA 02115, USA. NR 75 TC 125 Z9 127 U1 0 U2 2 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 1044-579X J9 SEMIN CANCER BIOL JI Semin. Cancer Biol. PD APR PY 1995 VL 6 IS 2 BP 99 EP 108 DI 10.1006/scbi.1995.0013 PG 10 WC Oncology SC Oncology GA QY289 UT WOS:A1995QY28900006 PM 7647312 ER PT J AU HAYES, DF HENDERSON, IC SHAPIRO, CL AF HAYES, DF HENDERSON, IC SHAPIRO, CL TI TREATMENT OF METASTATIC BREAST-CANCER - PRESENT AND FUTURE-PROSPECTS SO SEMINARS IN ONCOLOGY LA English DT Article; Proceedings Paper CT Symposium on the Current Status of Vinorelbine (Navelbine) in Breast Cancer CY APR 28-MAY 01, 1994 CL MCLEAN, VA SP BURROUGHS WELLCOME CO ID PRIMARY ENDOCRINE TREATMENT; PREVIOUSLY TREATED PATIENTS; HIGH-DOSE CHEMOTHERAPY; PHASE-II TRIAL; RANDOMIZED TRIAL; COMBINATION CHEMOTHERAPY; MULTIDRUG RESISTANCE; PROGNOSTIC FACTORS; CHEMOHORMONAL THERAPY; POSTMENOPAUSAL WOMEN C1 UNIV CALIF SAN FRANCISCO,MOFFITT LONG HOSP,MED CTR,DIV MED ONCOL,SAN FRANCISCO,CA 94110. RP HAYES, DF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BREAST EDUC CTR,44 BINNEY ST,BOSTON,MA 02115, USA. NR 136 TC 62 Z9 62 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD APR PY 1995 VL 22 IS 2 SU 5 BP 5 EP 21 PG 17 WC Oncology SC Oncology GA RA784 UT WOS:A1995RA78400002 PM 7537913 ER PT J AU STAFFORD, RS AF STAFFORD, RS TI MORALITY, MORTALITY, VOL-1 - KAMM,FM SO SOCIAL SCIENCE & MEDICINE LA English DT Book Review RP STAFFORD, RS (reprint author), MASSACHUSETTS GEN HOSP,GEN INTERNAL MED UNIT,BOSTON,MA 02114, USA. OI Stafford, Randall/0000-0003-1805-1271 NR 1 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 0277-9536 J9 SOC SCI MED JI Soc. Sci. Med. PD APR PY 1995 VL 40 IS 8 BP 1163 EP 1164 DI 10.1016/0277-9536(95)90227-9 PG 2 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA QN941 UT WOS:A1995QN94100019 ER PT J AU YOKOZAWA, T MIYAUCHI, A KUMA, K SUGAWARA, M AF YOKOZAWA, T MIYAUCHI, A KUMA, K SUGAWARA, M TI ACCURATE AND SIMPLE METHOD OF DIAGNOSING THYROID-NODULES BY THE MODIFIED TECHNIQUE OF ULTRASOUND-GUIDED FINE-NEEDLE ASPIRATION BIOPSY SO THYROID LA English DT Article ID MANAGEMENT; GUIDANCE AB We describe an accurate and simple method of diagnosing thyroid nodules by the modified technique of ultrasound-guided fine needle aspiration biopsy (UG-FNAB). An Aloka SSD 2000 focus type scanner (Aloka Co., Tokyo, Japan) equipped with a 10-MHz mechanical sector probe and a 7.5-MHz convex probe was used. First, a clear picture of the thyroid gland was taken with the use of the 10-MHz probe to determine the abnormalities. Then, a 7.5-MHz probe (1.5 x 0.8 cm of surface area) was used to guide the needle perpendicularly to the neck. This method enabled us to obtain samples from nodules greater than 5 mm. We applied this technique to 1000 patients who had uncertain diagnosis by the conventional method of FNAB. The advantages of this method are as follows: (i) The use of a small probe (7.5 MHz) is most important, since a needle can be inserted by watching the monitor without an assistant. (ii) The biopsy site can be chosen precisely. (iii) Small thyroid cancers, i.e., 5 mm cancer, can be biopsied without any difficulty. (iv) A life-threatening anaplastic carcinoma can be diagnosed at an early stage. (v) An intraglandular metastasis to the opposite lobe can be detected. (vi) Cystic carcinoma, difficult to diagnose by FNAB, can be diagnosed accurately. This method is highly recommended for all clinicians who are currently doing FNAB. C1 KAGAWA MED SCH,DEPT SURG 2,TAKAMATSU,KAGAWA,JAPAN. W LOS ANGELES VET AFFAIRS MED CTR,DIV ENDOCRINOL & METAB,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90073. NR 9 TC 111 Z9 112 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD APR PY 1995 VL 5 IS 2 BP 141 EP 145 DI 10.1089/thy.1995.5.141 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QZ364 UT WOS:A1995QZ36400012 PM 7647575 ER PT J AU ROTEM, A MATTHEW, HWT HSIAO, PH TONER, M TOMPKINS, RG YARMUSH, ML AF ROTEM, A MATTHEW, HWT HSIAO, PH TONER, M TOMPKINS, RG YARMUSH, ML TI THE ACTIVITY OF CYTOCHROME P450IA1 IN STABLE CULTURED RAT HEPATOCYTES SO TOXICOLOGY IN VITRO LA English DT Article ID ARYL-HYDROCARBON HYDROXYLASE; ETHOXYRESORUFIN-O-DEETHYLASE; SANDWICH CONFIGURATION; COLLAGEN SANDWICH; INTACT HUMAN; INDUCTION; LIVER; METABOLISM; EXPRESSION; 3-METHYLCHOLANTHRENE AB In this study, a stable, differentiated culture format (primary hepatocytes cultured between two layers of collagen gel) was used to study the effect of the inducer 3,3',4,4'-tetrachlorobiphenyl (TCB) on the activity of cytochrome P450IA1. P450IA1 (ethoxyresorufin O-deethylase) enzymatic activity was measured using the rate of conversion of ethoxyresorufin (ER) to resorufin (R). After 14 days of induction with 10(-6) M TCB, hepatocytes in the double collagen gel configuration exhibited a maximum activity of 180.3 +/- 46.8 pmol R/mu g DNA/hr (3.6 +/- 0.9 nmol R/10(6) cells/hr) compared with 34.9 +/- 3.8 pmol R/mu g DNA/hr for cells cultured on a single layer of gel. At a TCB level of 10(-5) M, the P450IA1 activity in the double-gel configuration peaked at 220.8 +/- 37.0 pmol R/mu g DNA/hr. Cessation of 10(-6) M TCB induction produced a decrease in activity to 25.8 +/- 4.1 pmol R/mu g DNA/hr within 4 hr. Subsequent re-application of the inducer caused an increase in activity to 76.5 +/- 11.1 pmol R/mu g DNA/hr within 6 hr, reaching a maximal value of 131.0 +/- 38.6 pmol R/mu g DNA/hr within 12 hr. Since TCB is rapidly metabolized by hepatocytes, a continuous perfusion culture system was developed to examine the effect of exposure to a constant level of TCB. Continuous perfusion of the cells with 10(-8) or 10(-7) M TCB, resulted in activities significantly higher than those of cultures induced by daily application of induction medium. A mechanistic model of TCB-dependent induction of P450IA1 was developed using kinetic parameters estimated from static culture data. The model accurately predicted cyclic variations in P450IA1 activity in static culture, and the steady-state activity level of perfusion cultures. This work describes procedures for exposing stable hepatocyte cultures to either continuous or declining levels of consumable inducers and for measuring the activity of cytochrome P450IA1 in cultured hepatocytes by a non-invasive method. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SHRINERS BURNS INST,DEPT SURG,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. NR 27 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 0887-2333 J9 TOXICOL IN VITRO JI Toxicol. Vitro PD APR PY 1995 VL 9 IS 2 BP 139 EP 149 DI 10.1016/0887-2333(94)00207-B PG 11 WC Toxicology SC Toxicology GA QU195 UT WOS:A1995QU19500007 PM 20650073 ER PT J AU PILEPICH, MV KRALL, JM ALSARRAF, M JOHN, MJ DOGGETT, RLS SAUSE, WT LAWTON, CA ABRAMS, RA ROTMAN, M RUBIN, P SHIPLEY, WU GRIGNON, D CAPLAN, R COX, JD AF PILEPICH, MV KRALL, JM ALSARRAF, M JOHN, MJ DOGGETT, RLS SAUSE, WT LAWTON, CA ABRAMS, RA ROTMAN, M RUBIN, P SHIPLEY, WU GRIGNON, D CAPLAN, R COX, JD TI ANDROGEN DEPRIVATION WITH RADIATION-THERAPY COMPARED WITH RADIATION-THERAPY ALONE FOR LOCALLY ADVANCED PROSTATIC-CARCINOMA - A RANDOMIZED COMPARATIVE TRIAL OF THE RADIATION-THERAPY ONCOLOGY GROUP SO UROLOGY LA English DT Note ID DEFINITIVE RADIOTHERAPY; HORMONAL CYTOREDUCTION; ANTIGEN; CANCER; ADENOCARCINOMA; BIOPSY; IRRADIATION; SERUM; FLUTAMIDE; PATTERNS AB Objectives. Androgen deprivation therapy before and during radiation therapy could, by reducing tumor volume, increase local tumor control, disease-free survival, and overall survival in patients with locally advanced adenocarcinomas of the prostate. Methods. In a randomized controlled clinical trial, patients with large T2, T3, and T4 prostate tumors, but no evidence of osseous metastasis, were randomized to receive goserelin 3.6 mg subcutaneously every 4 weeks and flutamide 250 mg orally three times daily 2 months before and during the radiation therapy course (Arm I) compared with radiation therapy alone (Arm II). Pelvic irradiation was administered with 1.8 to 2.0 Gy per day to a total dose of 45 +/- 1 Gy followed by a boost to the prostate target Volume to a total dose of 65 to 70 Gy. Results. Of 471 randomized patients, 456 were evaluable, 226 on Arm I and 230 on Arm II. With a median potential follow-up of 4.5 years, the cumulative incidence of local progression at 5 years was 46% in Arm I and 71% in Arm II (P < 0.001). The 5-year incidence of distant metastasis on Arms I and II was 34% and 41%, respectively (P = 0.09). Progression-free survival rates including normal prostate-specific antigen (PSA) levels for 396 patients with at least one PSA recorded were 36% in Arm I and 15% in Arm II at 5 years (P < 0.001). At this time, no significant difference in overall survival could be detected (P = 0.7). Conclusions. Short-term androgen deprivation with radiation therapy results in a marked increase in local control and disease-free survival compared with pelvic irradiation alone in patients with locally advanced;carcinoma of the prostate. Long-term surveillance is required to assess effects on overall survival. C1 RADIAT THERAPY ONCOL GRP,STAT UNIT,PHILADELPHIA,PA. WAYNE STATE UNIV,DETROIT,MI. KAWEAH DELTA CANC CARE CTR,VISALIA,CA. RADIAT ONCOL CTR,SACRAMENTO,CA. LATTER DAY ST HOSP,SALT LAKE CITY,UT. MED COLL WISCONSIN,MILWAUKEE,WI. JOHNS HOPKINS ONCOL CTR,BALTIMORE,MD. SUNY HLTH SCI CTR,BROOKLYN,NY. UNIV ROCHESTER,MED CTR,ROCHESTER,NY. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. RP PILEPICH, MV (reprint author), C MCAULEY HLTH SYST,POB 995,ANN ARBOR,MI 48106, USA. FU NCI NIH HHS [CA-32115, CA-21661] NR 30 TC 410 Z9 417 U1 1 U2 2 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD APR PY 1995 VL 45 IS 4 BP 616 EP 623 DI 10.1016/S0090-4295(99)80053-3 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA QQ902 UT WOS:A1995QQ90200014 PM 7716842 ER PT J AU FRANK, H WEISSLEDER, R PAPISOV, M AF FRANK, H WEISSLEDER, R PAPISOV, M TI ANTIBODY LABELED MR-IMAGING AND QUANTIFICATION OF MYOCARDIAL-INFARCTION SO ZEITSCHRIFT FUR KARDIOLOGIE LA German DT Article DE MYOCARDIAL INFARCTION, INFARCTION SITE; MR IMAGING ID SUPERPARAMAGNETIC IRON-OXIDE; CONTRAST AGENT; CELLS; SEPARATION; TOMOGRAPHY; MYOSIN AB A magnetically labeled antimyosin (MION-AM) has previously been developed for immunospecific MR imaging in vivo. The current study was designed to extend previous feasibility studies and to correlate MR infarct size to that determined by histopathology. The left anterior coronary artery (LAD) was temporarily occluded in rabbits (n = 10) and subsequently reperfused for 1 h prior to the administration of 100 mu mol Fe/kg of MION-AM (corresponding to 0.5 mg AM). One hour after IV administration, the infarcted myocardium appeared hypointense by MRI as a result of target-specific attachment of the magnetic T2 label to damaged but not normal myocardium. There was a close correlation between infarct size determined by MR and pathology (SE 2500/30: r = 0.92, p less than or equal to 0.0001; SE 2500/60: r = 0.85, p less than or equal to 0.0001). Our results are evidence that a) immunospecific magnetic probes can be utilized for cardiac MR imaging, and b) that these or similar agents may aid in the quantitation of myocardial infarct size. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CTR NMR,BOSTON,MA 02114. RP FRANK, H (reprint author), UNIV VIENNA,INNERE MED KARDIOL KLIN 2,WAHRINGER GUERTEL 18-20,A-1090 VIENNA,AUSTRIA. NR 22 TC 1 Z9 2 U1 0 U2 1 PU DR DIETRICH STEINKOPFF VERLAG PI BERLIN 33 PA C/O SPRINGER-VERLAG, HEIDELBERGER PLATZ 3, 1000 BERLIN 33, GERMANY SN 0300-5860 J9 Z KARDIOL JI Z. Kardiol. PD APR PY 1995 VL 84 IS 4 BP 311 EP 315 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QW879 UT WOS:A1995QW87900009 PM 7785304 ER PT J AU UDDIN, S KATZAV, S WHITE, MF PLATANIAS, LC AF UDDIN, S KATZAV, S WHITE, MF PLATANIAS, LC TI INSULIN-DEPENDENT TYROSINE PHOSPHORYLATION OF THE VAV PROTOONCOGENE PRODUCT IN CELLS OF HEMATOPOIETIC ORIGIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SRC HOMOLOGY-2 DOMAINS; PHOSPHATIDYLINOSITOL 3'-KINASE; SIGNALING PATHWAYS; SH2 DOMAIN; IRS-1; RECEPTOR; PROTEINS; MITOGENESIS; ASSOCIATION; ACTIVATION AB Insulin activates the ras signaling pathway and promotes hematopoietic cell proliferation. One possible mediator in such signaling is the vav proto oncogene product (p95(vav)), which is specifically expressed in cells of hematopoietic origin and contains domains typical of guanine nucleotide exchange factors as well as Src homology 2 and Src homology 3 domains, We studied the tyrosine phosphorylation of p95(vav) in hematopoietic cells expressing insulin receptors. Immunoblotting experiments with an antiphosphotyrosine monoclonal antibody disclosed that insulin induces rapid and transient tyrosine phosphorylation of p95(vav) in the human U-266 myeloma cell line. These findings were confirmed by immunoprecipitation experiments performed with P-32-labeled cells and phosphoamino acid analysis of the bands corresponding to p95(vav). Similarly, insulin dependent tyrosine phosphorylation of p95(vav) was observed in the human IM-9 and mouse J558L hematopoietic cell lines. Furthermore, insulin treatment of cells led to the association of the Src homology 2 domain of p95(vav) with the activated P-subunit of the insulin receptor in vitro. Altogether, these data suggest that p95(vav) is a substrate for the insulin receptor tyrosine kinase and may be involved in an insulin signaling pathway linking receptor-generated signals to Pas or other GTP-binding proteins in cells of hematopoietic origin. C1 EDWARD HINES VET ADM MED CTR,HINES,IL 60141. SIR MORTIMER B DAVIS JEWISH HOSP,LADY DAVIS INST MED RES,TERRY FOX MOLEC ONCOL GRP,MONTREAL,PQ H3T 1E2,CANADA. MCGILL UNIV,DEPT MED,MONTREAL,PQ H3G 1Y6,CANADA. MCGILL UNIV,DEPT ONCOL,MONTREAL,PQ H3G 1Y6,CANADA. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. RP UDDIN, S (reprint author), LOYOLA UNIV,DIV HEMATOL ONCOL,BLDG 112,2160 S 1ST AVE,MAYWOOD,IL 60153, USA. FU NIDDK NIH HHS [DK-38712, DK-43808] NR 38 TC 31 Z9 31 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 31 PY 1995 VL 270 IS 13 BP 7712 EP 7716 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QQ431 UT WOS:A1995QQ43100098 PM 7535775 ER PT J AU YAO, RJ COOPER, GM AF YAO, RJ COOPER, GM TI REQUIREMENT FOR PHOSPHATIDYLINOSITOL-3 KINASE IN THE PREVENTION OF APOPTOSIS BY NERVE GROWTH-FACTOR SO SCIENCE LA English DT Article ID PROGRAMMED CELL-DEATH; TRK PROTOONCOGENE PRODUCT; PC12 CELLS; NEURONAL DIFFERENTIATION; TYROSINE KINASE; FACTOR RECEPTOR; PHEOCHROMOCYTOMA CELLS; PDGF RECEPTOR; BINDING-SITE; MAP KINASE AB Nerve growth factor (NGF) induces both differentiation and survival of neurons by binding to the Trk receptor protein tyrosine kinase. Although Pas is required for differentiation, it was not required for NGF-mediated survival of rat pheochromocytoma PC-12 cells in serum-free medium. However, the ability of NGF to prevent apoptosis (programmed cell death) was inhibited by wortmannin or LY294002, two specific inhibitors of phosphatidylinositol (PI)-3 kinase. Moreover, platelet-derived growth factor (PDGF) prevented apoptosis of PC-12 cells expressing the wild-type PDGF receptor, but not of cells expressing a mutant receptor that failed to activate PI-3 kinase. Cell survival thus appears to be mediated by a PI-3 kinase signaling pathway distinct from the pathway that mediates differentiation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [R01 CA 18689] NR 52 TC 1158 Z9 1184 U1 2 U2 18 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 31 PY 1995 VL 267 IS 5206 BP 2003 EP 2006 DI 10.1126/science.7701324 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QQ068 UT WOS:A1995QQ06800047 PM 7701324 ER PT J AU ZHANG, R ALT, FW DAVIDSON, L ORKIN, SH SWAT, W AF ZHANG, R ALT, FW DAVIDSON, L ORKIN, SH SWAT, W TI DEFECTIVE SIGNALING THROUGH THE T-CELL AND B-CELL ANTIGEN RECEPTORS IN LYMPHOLD CELLS LACKING THE VAV PROTOONCOGENE SO NATURE LA English DT Article ID TYROSINE PHOSPHORYLATION; PROTOONCOGENE PRODUCT; HEMATOPOIETIC-CELLS; CROSS-LINKING; EXPRESSION; KINASE; CD40; REARRANGEMENT; STIMULATION; REQUIREMENT AB THE product of the vav proto-oncogene(1), p95(vav) or Vav, is tyrosine phosphorylated upon stimulation of T and B cells by antigen(2-4) and other(5-8) receptors, and contains motifs associated,vith signal transduction(1,9-11). To determine its role in vivo, we used vav-gene-targeted embryonic stem(12) cells and RAG-2(-/-) blastocyst complementation(13). The vav(-/-)-RAG-2(-/-) chimaeras displayed thymic atrophy with reduced numbers of peripheral T cells. Whereas the total number of B cells was normal, the subset of peritoneal B-1 (CD5(+))(14) cells was missing. The vav(-/-) T and B cells were hyporeactive when stimulated through antigen receptors, but vav(-/-) T cells proliferated on exposure to phorbol ester and calcium ionophore(15), whereas B cells responded normally to bacterial mitogen, lipopolysaccharide or the CD40 ligand(16-18). Thus, we have established here a functional role for vav in the control of T- and B-cell development and activation. C1 CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. NR 26 TC 365 Z9 367 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 30 PY 1995 VL 374 IS 6521 BP 470 EP 473 DI 10.1038/374470a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP899 UT WOS:A1995QP89900063 PM 7700359 ER PT J AU ROELKE, M ONUNAIN, SS AF ROELKE, M ONUNAIN, SS TI SHOCK DELIVERED BY AN IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR IN RESPONSE TO SPONTANEOUS VENTRICULAR FIBRILLATION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ROELKE, M (reprint author), NEWARK BETH ISRAEL MED CTR,NEWARK,NJ 07112, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 30 PY 1995 VL 332 IS 13 BP 860 EP 860 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA QP228 UT WOS:A1995QP22800005 PM 7870141 ER PT J AU SHAEFFER, JR KANIA, MA AF SHAEFFER, JR KANIA, MA TI DEGRADATION OF MONOUBIQUITINATED ALPHA-GLOBIN BY 26S PROTEASOMES SO BIOCHEMISTRY LA English DT Article ID MOLECULAR-WEIGHT PROTEASES; DODECYL-SULFATE; UBIQUITIN; PROTEIN; PURIFICATION; COMPLEX; ATP; SYSTEM; CHAINS; CELLS AB Ubiquitin-I-125-alpha-globin conjugate fractions containing either one (Ub(1)-alpha), two (Ub(2)-alpha), or a mixture of three and four (Ub(3,4)-alpha) molecules of ubiquitin (Ub), covalently linked to one I-125-alpha-globin molecule were isolated after incubation of a proteolysis reaction mixture containing ATP, ubiquitin aldehyde-treated reticulocyte lysate, and human I-125-alpha-globin. Each of the purified conjugate fractions or an identically-purified control sample of unconjugated I-125-alpha-globin was incubated as a substrate in companion proteolysis reaction mixtures containing either purified 26S or 20S rabbit reticulocyte proteasomes. The initial rate of ATP-dependent degradation of the Ub(1)-alpha conjugate by the 26S proteasomes was similar to 0.44% (1.1 fmol)/min while that of the free I-125-alpha-globin was undetectable. The initial rates of ATP-dependent degradation by the 26S proteasomes of the Ub(2)-alpha and Ub(3,4)-alpha conjugates conjugates were 2- to 3-fold that of the Ub(1)-alpha species. Conversely, the degradation of free I-125-alpha-globin and its ubiquitinated conjugates by the 20S proteasomes was not dependent on ATP, nor did it increase with the size of the Ub adduct. Analysis of the products of a reaction mixture with 26S proteasomes by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed no conversion of the Ub(1)-alpha conjugate substrate to higher-molecular-mass conjugates. These results suggest that monoubiquitinated alpha-globin can be degraded significantly and specifically by interaction directly with the 26S proteasomes. This finding is consistent with the hypothesis that a substantial fraction of the Ub(1)-alpha conjugate intermediate in the ATP-dependent proteolysis of I-125-alpha-globin in whole reticulocyte lysate [Shaeffer, J. R. (1994) J. Biol. Chem. 269, 22205-22210] is degraded by this interaction. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. RP SHAEFFER, JR (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL 29379]; NIDDK NIH HHS [DK 07737] NR 43 TC 32 Z9 32 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 28 PY 1995 VL 34 IS 12 BP 4015 EP 4021 DI 10.1021/bi00012a020 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QP971 UT WOS:A1995QP97100020 PM 7696267 ER PT J AU WHORISKEY, SK USMAN, N SZOSTAK, JW AF WHORISKEY, SK USMAN, N SZOSTAK, JW TI TOTAL CHEMICAL SYNTHESIS OF A RIBOZYME DERIVED FROM A GROUP-I INTRON SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HAMMERHEAD RIBOZYME; 2'-HYDROXYL GROUPS; RNA; BINDING; OLIGORIBONUCLEOTIDES; TETRAHYMENA; CLEAVAGE; TEMPLATE; DOMAIN; SITE AB We describe the complete chemical synthesis of a ribozyme that catalyzes template-directed oligonucleotide ligation, The specific activity of the synthetic ribozyme is nearly identical to that of the same enzyme generated by in vitro transcription with T7 RNA polymerase. The ribozyme is derived from a group I intron and consists of three RNA fragments of 36, 43, and 59 nt that self-assemble to form a catalytically active complex, We have site-specifically substituted ribonucleotide analogs into this enzyme and have identified two 2'-hydroxyl groups that are required for full catalytic activity, In contrast, neither the 2'-hydroxyl nor the exocyclic amino group of the conserved guanosine in the guanosine binding site is necessary for catalysis, By allowing the ribozyme to be modified as easily as its substrates, this synthetic ribozyme system should be useful for testing specific hypotheses concerning ribozyme-substrate interactions and tertiary interactions within the ribozyme. C1 MASSACHUSETTS GEN HOSP,DEPT BIOL MOLEC,BOSTON,MA 02114. MIT,DEPT BIOL,CAMBRIDGE,MA 02138. FU NIGMS NIH HHS [GM45315] NR 24 TC 11 Z9 11 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 MAR 28 PY 1995 VL 92 IS 7 BP 2465 EP 2469 DI 10.1073/pnas.92.7.2465 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP889 UT WOS:A1995QP88900012 PM 7708666 ER PT J AU BLANCHO, G GIANELLO, P GERMANA, S BAETSCHER, M SACHS, DH LEGUERN, C AF BLANCHO, G GIANELLO, P GERMANA, S BAETSCHER, M SACHS, DH LEGUERN, C TI MOLECULAR-IDENTIFICATION OF PORCINE INTERLEUKIN-10 - REGULATION OF EXPRESSION IN A KIDNEY ALLOGRAFT MODEL SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; POLYMERASE CHAIN-REACTION; INHIBITORY FACTOR IL-10; MESSENGER-RNA LEVELS; CYTOKINE SYNTHESIS; PERIPHERAL TOLERANCE; MINIATURE SWINE; RENAL-ALLOGRAFTS; CELL; CYCLOSPORINE AB Clones encoding porcine interleukin 10 (IL-10) were isolated from a cDNA library produced from phytohemagglutinin-activated pig peripheral blood mononuclear cells, The porcine IL-10 nucleotide sequence was found to be highly homologous to the rat, mouse, and human IL-10 counterparts and to one of the open reading frames from the Epstein-Barr virus, In addition, pig IL-10 caused inhibition of gamma-interferon gene transcription as determined by a bioassay, To investigate the possible immunomodulatory role of IL-10, its expression during the induction of tolerance to kidney allografts by cyclosporin A in miniature swine was also investigated. Delayed expression and higher levels of IL-10 were observed in tolerant animals compared with animals rejecting their allografts. Since tolerance is achieved by a short course of cyclosporin A, we have also studied the in vitro effect of this drug on IL-10 gene transcription in blood mononuclear cells and have found that cyclosporin A inhibits IL-10 gene activation in T cells but does not interfere with IL-10 transcription in lipopolysaccharide-activated cells. These results suggest that the overexpression of IL-10, observed in cell populations infiltrating grafts from tolerant animals, may be a function of monocytes and/or B cells. C1 BIOTRANSPLANT INC,BOSTON,MA 02129. RP BLANCHO, G (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129, USA. FU NIAID NIH HHS [3 RO1 AI31046, 1 RO1 AI33053] NR 29 TC 42 Z9 47 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 MAR 28 PY 1995 VL 92 IS 7 BP 2800 EP 2804 DI 10.1073/pnas.92.7.2800 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP889 UT WOS:A1995QP88900080 PM 7708727 ER PT J AU CARROLL, M ZHU, Y DANDREA, AD AF CARROLL, M ZHU, Y DANDREA, AD TI ERYTHROPOIETIN-INDUCED CELLULAR-DIFFERENTIATION REQUIRES PROLONGATION OF THE G(1) PHASE OF THE CELL-CYCLE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CYTOKINE; ERYTHROPOIETIN RECEPTOR; ERYTHROPOIESIS; INTERLEUKIN 3 ID COLONY-STIMULATING FACTOR; ERYTHROID-DIFFERENTIATION; FRIEND-VIRUS; CYTOPLASMIC DOMAIN; FACTOR-RECEPTOR; MESSENGER-RNA; GROWTH; INDUCTION; GENE; PROLIFERATION AB Erythropoietin (EPO), like many other hematopoietic growth factors, can induce either growth or differentiation of hematopoietic cells. Little is known about the molecular basis of this cellular decision, in part because of a paucity of cell lines in which these two phenomena can be dissociated. Ectopic expression of the EPO receptor (EPO-R) in Ba/F3, a murine interleukin 3 (IL-3)-dependent progenitor cell line, confers EPO-dependent cell growth. In these cells (Ba/F3-EPO-R), EPO also induces beta-globin mRNA, a specific marker of erythroid differentiation. Here we show that the induction of erythroid differentiation by EPO requires a delay in cell growth and a prolongation of the (G(1)) phase of the cell cycle. Interestingly, this effect on G(1) prolongation was concentration dependent. At low EPO concentrations (0.05-0.1 unit of EPO per ml; 1 pM EPO = 0.01 unit of EPO per ml), EPO prolonged G(1) and induced differentiation; at high concentrations (0.5-10.0 units per ml), EPO shortened G(1) and preferentially stimulated growth, IL-3 stimulated Ba/F3 growth but not differentiation at all growth factor concentrations ranging from 0.1 to 500 pM. Moreover, IL-3 suppressed EPO-induced beta-globin induction in a dose-dependent manner. This suppression correlated with the shortening of G(1) by IL-3. Taken together, these data demonstrate distinct effects of EPO and IL-3 and a balance between erythroid growth and differentiation that is cell cycle dependent. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV HEMATOL & ONCOL,BOSTON,MA 02115. FU NIDDK NIH HHS [R01 DK43889-03] NR 29 TC 60 Z9 60 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 MAR 28 PY 1995 VL 92 IS 7 BP 2869 EP 2873 DI 10.1073/pnas.92.7.2869 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP889 UT WOS:A1995QP88900094 PM 7708739 ER PT J AU NARULA, N STOW, JL AF NARULA, N STOW, JL TI DISTINCT COATED VESICLES LABELED FOR P200 BUD FROM TRANS-GOLGI NETWORK MEMBRANES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE VESICLE TRAFFICKING; GOLGI; VESICLE COAT ID ADP-RIBOSYLATION FACTOR; GTP-BINDING PROTEIN; BETA-COP; BREFELDIN-A; ENDOPLASMIC-RETICULUM; COMPLEX; COATOMER; CELLS; STACK; IDENTIFICATION AB Golgi-associated cytoplasmic proteins, such as the coatomer protein complex, are required for vesicle budding and trafficking. We have previously described a cytoplasmic phosphoprotein, p200, which binds dynamically and specifically to Golgi membranes. The p200 protein is dissociated from Golgi membranes in the presence of brefeldin A and it is induced to bind to Golgi membranes by activation of guanine nucleotide binding proteins (G proteins) with guanosine 5'-[gamma-thio] triphosphate or aluminum fluoride. To establish the role of p200 in vesicle budding, we localized membrane-bound p200 in intact cells and on isolated Golgi membranes. We show that p200 is preferentially associated with vesicles in the trans-Golgi network (TGN). Activation of G proteins induced budding and accumulation of small, coated vesicles from Golgi membranes and p200 was localized on the cytoplasmic surface of some of these resides. Using immunogold labeling we further demonstrate that p200 and beta-COP are localized on different populations of Golgi-derived vesicles. These data establish that p200 is involved in the budding and coating of a class of Golgi vesicles that are likely to be derived from the TGN. The data also show that there are distinct populations of non-clathrin-coated vesicles budded from Golgi membranes, and vesicles labeled for either beta-COP or p200 may represent transport vesicles for separate steps of protein transport. C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. OI Stow, Jennifer/0000-0002-5409-9101 NR 36 TC 57 Z9 58 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 MAR 28 PY 1995 VL 92 IS 7 BP 2874 EP 2878 DI 10.1073/pnas.92.7.2874 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP889 UT WOS:A1995QP88900095 PM 7708740 ER PT J AU HOHMANN, EL OLETTA, CA LOOMIS, WP MILLER, SI AF HOHMANN, EL OLETTA, CA LOOMIS, WP MILLER, SI TI MACROPHAGE-INDUCIBLE EXPRESSION OF A MODEL ANTIGEN IN SALMONELLA-TYPHIMURIUM ENHANCES IMMUNOGENICITY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID ESCHERICHIA-COLI; VIRULENCE DETERMINANTS; ORAL IMMUNIZATION; VIBRIO-CHOLERAE; SUICIDE VECTOR; B-SUBUNIT; CONSTRUCTION; PROTEINS; VACCINE; STRAINS AB Attenuated Salmonella are useful oral vaccine vectors capable of carrying multiple heterologous antigen genes, but optimal expression of foreign antigens has not yet been achieved. We hypothesized that Salmonella phoP-activated genes, which are transcriptionally activated within antigen-processing macrophages, could prove useful for delivery of heterologous antigens to the immune system. We have created a suicide vector that allows the stable chromosomal insertion of heterologous antigen genes within the phoP-activated gene C (pagC) of Salmonella and permits the expression of heterologous antigens as fusion proteins between the first 84 amino acids of PagC and the chosen antigen. The Escherichia coli phoA gene encoding alkaline phosphatase was cloned into this vector; the resultant plasmid was used to construct Salmonella typhimurium strains that express PagC-alkaline phosphatase fusion proteins from a single chromosomal gene copy. Such strains were administered orally and i.p. as vaccines to BALB/c mice and compared with control strains expressing alkaline phosphatase constitutively. After 3 weeks, mouse sera were analyzed for IgG responses to S. typhimurium lipopolysaccharide and alkaline phosphatase. Remarkably, though all mice had comparable antibody responses to lipopolysaccharide, only mice immunized with strains bearing phoP-activated fusion genes had antibody responses to the heterologous antigen. We conclude that expression of a heterologous antigen from an S. typhimurium in vivo-induced promotor that is activated within macrophages markedly enhances the immunogenicity of a model antigen expressed from a single chromosomal gene copy. RP HOHMANN, EL (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI30479]; NIDDK NIH HHS [K12DK01410] NR 36 TC 57 Z9 61 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 MAR 28 PY 1995 VL 92 IS 7 BP 2904 EP 2908 DI 10.1073/pnas.92.7.2904 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QP889 UT WOS:A1995QP88900101 PM 7708746 ER PT J AU DAVALLI, AM OGAWA, Y RICORDI, C SCHARP, DW BONNERWEIR, S WEIR, GC AF DAVALLI, AM OGAWA, Y RICORDI, C SCHARP, DW BONNERWEIR, S WEIR, GC TI A SELECTIVE DECREASE IN THE BETA-CELL MASS OF HUMAN ISLETS TRANSPLANTED INTO DIABETIC NUDE-MICE SO TRANSPLANTATION LA English DT Article ID PANCREATIC-ISLETS; INSULIN-SECRETION; IMPLANTATION; NORMOGLYCEMIA; AUTOGRAFTS AB Streptozocin-induced diabetic nude mice (blood glucose 493+/-14 mg/dl) received aliquots of 2000 human islet equivalents (IE) under the kidney capsule and were then followed for up to 30 days with measurement of blood glucose concentrations and body weight. Characterization of islet aliquots before the implantation included the assessment of the endocrine beta cell and nonbeta cell mass, estimated by point counting morphometry of immunostained sections. Islet transplantation was followed by a rapid decrease in blood glucose levels and by a progressive increase in body weight; 15 days after transplantation mean glycemic levels were 102+/-11 mg/dl and further decreased to 70+/-3 mg/dl at 30 days. Despite the progressive improvement in the glucose levels, the beta cell mass of the islet grafts significantly decreased over time from 2.63+/-0.2 mg, at the time of transplantation, to 1.16+/-0.1 and 0.86+/-0.1 mg 15 and 30 days, respectively, after transplantation. In contrast, the endocrine nonbeta cell mass remained stable from before the implantation to 30 days after. Therefore, the endocrine nonbeta cell/beta cell ratio increased from 14% at the time of transplantation, to 35% and 37%, 15 and 30 days, respectively, after transplantation. The rate of replication of the transplanted beta cells was similar in the grafts harvested at 15 and 30 days, with the percentage of beta cells positive for bromo-2'deoxyuridine (BrdU) incorporation being in the range of similar to 0.1% 6 hr after the BrdU injection. These data demonstrate that an important decrease in beta cell mass takes place immediately after islet transplantation-the most dramatic decrease occurring in the first 15 days and persisting even after revascularization has occurred. However, endocrine nonbeta cell mass remained stable indicating that engrafted nonbeta cells are less likely to die than beta cells. The finding that the nonbeta/beta cell ratio of a human islet graft can increase over time, raises questions about whether such a change in islet structure could have an influence upon function. C1 SCI INST SAN RAFFAELE,I-20132 MILAN 1,ITALY. UNIV MIAMI,DIABET RES INST,MIAMI,FL. WASHINGTON UNIV,ST LOUIS,MO. RP DAVALLI, AM (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. OI Ricordi, Camillo/0000-0001-8092-7153 FU NIDDK NIH HHS [DK-35449, DK-36836] NR 23 TC 129 Z9 133 U1 0 U2 5 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1995 VL 59 IS 6 BP 817 EP 820 DI 10.1097/00007890-199503270-00003 PG 4 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA QQ425 UT WOS:A1995QQ42500003 PM 7701574 ER PT J AU GIANELLO, PR LORF, T YAMADA, K FISHBEIN, JM NICKELEIT, V VITIELLO, DM SACHS, DH AF GIANELLO, PR LORF, T YAMADA, K FISHBEIN, JM NICKELEIT, V VITIELLO, DM SACHS, DH TI INDUCTION OF TOLERANCE TO RENAL-ALLOGRAFTS ACROSS SINGLE-HAPLOTYPE MHC DISPARITIES IN MINIATURE SWINE SO TRANSPLANTATION LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; LIVER-TRANSPLANTATION; CYCLOSPORIN-A; CLASS-I; ANTIGENS; LOCALIZATION; RESPONSES; CELLS; SUPPRESSION; SURVIVAL AB We have previously demonstrated that a 12-day course of cyclosporine A (CsA) leads to the induction of tolerance to renal allografts in 100% of recipients selectively mismatched at class I for both haplotypes, and in 71% of recipients selectively mismatched at class II for both haplotypes, but in 0% of recipients mismatched for two haplotypes at both class I and class II. We have postulated that the mechanism by which tolerance is induced may therefore require matching for either class I or class II antigens. One might predict from this hypothesis that tolerance would also be induced in donor-recipient combinations sharing one full haplotype (e.g., AC-->AD), which mimics the clinically relevant transplant combination of parent to offspring. We have therefore investigated the effects of the CsA regimen on renal transplants in this combination. Without immunosuppression, such kidney allografts were uniformly rejected (n=12; 10.6+/-2.4 days). In contrast, a course of CsA (10-13 mg/kg/day) during the first 12 postoperative days induced long-term acceptance of the allograft in 67% (4/6) of recipients. Some acceptor animals also showed specific unresponsiveness to donor antigens as measured by in vitro assays and by failure to develop anti-donor antibodies, Tolerance was confirmed in four of these animals by failure to reject a second transplant SLA-matched to the first kidney donor without additional immunosuppression. These results suggest the feasibility of inducing specific tolerance across a single-haplotype mismatch in the majority of the cases, which could have clinical implications for living-related transplants. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. FU NHLBI NIH HHS [HL18646]; NIAID NIH HHS [AI31046] NR 35 TC 28 Z9 28 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 27 PY 1995 VL 59 IS 6 BP 884 EP 890 DI 10.1097/00007890-199503270-00015 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA QQ425 UT WOS:A1995QQ42500015 PM 7701585 ER PT J AU LEE, JS SEE, RH GALVIN, KM WANG, J SHI, Y AF LEE, JS SEE, RH GALVIN, KM WANG, J SHI, Y TI FUNCTIONAL INTERACTIONS BETWEEN YY1 AND ADENOVIRUS E1A SO NUCLEIC ACIDS RESEARCH LA English DT Article ID SERUM RESPONSE FACTOR; TRANSCRIPTION FACTOR; POLYMERASE-II; NF-E1 YY-1; C-MYC; PROTEIN; PROMOTER; BINDS; ACTIVATION; DELTA AB YY1 is a C2H2-type zinc finger transcription factor that is a member of the human GLI-Kruppel family of proteins. YY1 represses transcription when bound upstream of transcription initiation sites. The repression can be relieved by adenovirus E1A and activation of target genes occurs. We have mapped the repression domain of YY1 to the C-terminal region, overlapping its DNA binding domain. We have also identified an activation domain within the first 69 amino acids of YY1. The YY1 C-terminal region is involved in physical interactions with E1A and is functionally necessary for YY1 to respond to E1A. This suggests that relief of YY1 repression by E1A involves YY1-E1A physical interactions. Although not involved in interactions with E1A, the N-terminal activation domain is also necessary for YY1 to respond to E1A. Presumably, under repressing conditions, the activation domain is masked by the conformation of YY1, but is released upon binding of E1A and is required to subsequently activate transcription. Consistent with this hypothesis, an ATF-2-YY1 chimeric protein containing the activation domain of ATF-P and the C-terminal two-thirds of YY1 is still a potent repressor. Unlike the mutant YY1 lacking its own N-terminal activation domain, the chimeric protein is fully responsive to E1A. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,COMM VIROL,BOSTON,MA 02115. DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA58997] NR 35 TC 65 Z9 66 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1995 VL 23 IS 6 BP 925 EP 931 DI 10.1093/nar/23.6.925 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QU682 UT WOS:A1995QU68200007 PM 7731805 ER PT J AU BOUBNOV, NV WILLS, ZP WEAVER, DT AF BOUBNOV, NV WILLS, ZP WEAVER, DT TI CODING SEQUENCE COMPOSITION FLANKING EITHER SIGNAL ELEMENT ALTERS V(D)J RECOMBINATION EFFICIENCY SO NUCLEIC ACIDS RESEARCH LA English DT Article ID JOINING SIGNALS; DNA; TDT AB Lymphoid V(D)J rearrangement is targeted by recombination signal sequences (RSS) bordering V, D or J exons, We demonstrate that the DNA composition of flanking coding positions, particularly poly(A) or poly(T) stretches at one or both RSS, diminishes V(D)J recombination up to 100-fold, Positionally correct cleavages occur in the inhibited reactions, since the junctions formed show the same frequency of precision as uninhibited reactions, Open/shut cleavage/rejoining is not increased at a normal RSS in substrates containing inhibitory A/T homopolymers versus random sequence at a second RSS, Thus recombinase action at both cleavage sites is severely disrupted by modified coding sequences. C1 DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [CA54326, CA52694]; NIGMS NIH HHS [GM39312] NR 25 TC 24 Z9 24 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0305-1048 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD MAR 25 PY 1995 VL 23 IS 6 BP 1060 EP 1067 DI 10.1093/nar/23.6.1060 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QU682 UT WOS:A1995QU68200025 PM 7731794 ER PT J AU GARDELLA, TJ LUCK, MD WILSON, AK KEUTMANN, HT NUSSBAUM, SR POTTS, JT KRONENBERG, HM AF GARDELLA, TJ LUCK, MD WILSON, AK KEUTMANN, HT NUSSBAUM, SR POTTS, JT KRONENBERG, HM TI PARATHYROID-HORMONE (PTH)-PTH-RELATED PEPTIDE HYBRID PEPTIDES REVEAL FUNCTIONAL INTERACTIONS BETWEEN THE 1-14 AND 15-34 DOMAINS OF THE LIGAND SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR-BINDING DOMAINS; NMR SOLUTION STRUCTURE; HUMORAL HYPERCALCEMIA; MALIGNANCY; FRAGMENT; PROTEIN; KIDNEY; SPECTROSCOPY; MEMBRANES; SEQUENCES AB Parathyroid hormone (PTH) and parathyroid hormone-related peptide (PTHrP) bind to a common PTH/ PTHrP receptor. To explore structure-function relations in these ligands, we synthesized and functionally evaluated PTH-PTHrP hybrid peptides in which the homologous 1-14 portions were exchanged. Hybrid-2, PTH(1-14)-PTHrP-(15-34)NH2, bound to LLC-PK1 cells expressing the cloned rat PTH/PTHrP receptor with high affinity (IC50 congruent to 7 nM). In contrast, hybrid-1, PTHrP(1-14)-PTH-(15-34)NH2, bound with much weaker affinity (IC50 congruent to 8,700 nM). Thus, the 1-14 region of PTHrP is incompatible with the 15-34 region of PTH. The carboxyl-terminal incompatibility site was identified as residues 19-21 (Glu-Arg-Val in PTH and Arg-Arg-Arg in PTHrP); extending the amino-terminal PTHrP sequence to residue 21 but not to 18 cured the hybrid's binding defect. The amino-terminal incompatibility site was identified as position 5 (Ile in PTH and His in PTHrP), because Ile(5)-hybrid-1 bound with high affinity (IC50 congruent to 20 nM). The importance of these identified residues in the native ligands was established by evaluating the effects of substitutions at these sites in a series of PTH and PTHrP analog peptides. Overall, the results are consistent with the hypothesis that, in both PTH and PTHrP, the 1-14 and 15-34 domains interact when binding to the receptor and that residues 5, 19, and 21 contribute either directly or indirectly to this interaction. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP GARDELLA, TJ (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 29 TC 47 Z9 47 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 MAR 24 PY 1995 VL 270 IS 12 BP 6584 EP 6588 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QQ855 UT WOS:A1995QQ85500026 PM 7896796 ER PT J AU PULIDO, R KRUEGER, NX SERRAPAGES, C SAITO, H STREULI, M AF PULIDO, R KRUEGER, NX SERRAPAGES, C SAITO, H STREULI, M TI MOLECULAR CHARACTERIZATION OF THE HUMAN TRANSMEMBRANE PROTEIN-TYROSINE-PHOSPHATASE-DELTA - EVIDENCE FOR TISSUE-SPECIFIC EXPRESSION OF ALTERNATIVE HUMAN TRANSMEMBRANE PROTEIN-TYROSINE-PHOSPHATASE-DELTA ISOFORMS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LEUKOCYTE COMMON ANTIGEN; CELL-ADHESION MOLECULES; IMMUNOGLOBULIN SUPERFAMILY; NERVOUS-SYSTEM; EXTRACELLULAR REGION; SURFACE RECOGNITION; POINT MUTATION; CLEAVAGE SITE; VASE EXON; NG-CAM AB Protein-tyrosine phosphatases (PTPases) play an essential role in the regulation of cell activation, proliferation, and differentiation. A major subfamily of these enzymes is the transmembrane-type PTPases that contain extracellular regions comprised of Ig-like and fibronectin type III (FN-III)-like domains, Characterization of the human transmembrane PTPase delta (HPTP delta) revealed the existence of multiple HPTP delta isoforms that vary in their extracellular regions. The full-length HPTP delta isoform has an extracellular region containing three Ig-like and eight FN-III-like domains connected via a transmembrane peptide to an intracellular region with two PTPase domains, whereas another isoform lacks four of the eight FN-III like domains. Furthermore, other HPTP delta isoforms exist that lack 9 amino acids within the second Ig-like domain and 4 amino acids at the junction of the second and third Ig-like domains or 9 amino acids within the fifth FN-III-like domain, Reverse transcription polymerase chain reaction analysis demonstrated that HPTP delta isoforms lacking these short peptides are expressed in kidney, whereas isoforms containing these peptides are expressed in the brain, Analysis of HPTP delta biosynthesis demonstrated that HPTP delta is expressed as a complex of two noncovalently associated subunits derived from a proprotein and that the HPTP delta ectodomain is shed from the cell surface. Mutational analysis of the HPTP delta proprotein cleavage site revealed the existence of two or three functional and overlapping furin-like endoprotease cleavage sites. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP PULIDO, R (reprint author), CHILDRENS HOSP,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA55547] NR 54 TC 55 Z9 56 U1 7 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 24 PY 1995 VL 270 IS 12 BP 6722 EP 6728 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QQ855 UT WOS:A1995QQ85500047 PM 7896816 ER PT J AU CONSTANTZ, BR ISON, IC FULMER, MT POSER, RD SMITH, ST VANWAGONER, M ROSS, J GOLDSTEIN, SA JUPITER, JB ROSENTHAL, DI AF CONSTANTZ, BR ISON, IC FULMER, MT POSER, RD SMITH, ST VANWAGONER, M ROSS, J GOLDSTEIN, SA JUPITER, JB ROSENTHAL, DI TI SKELETAL REPAIR BY IN-SITU FORMATION OF THE MINERAL PHASE OF BONE SO SCIENCE LA English DT Article AB A process has been developed for the in situ formation of the mineral phase of bone. inorganic calcium and phosphate sources are combined to form a paste that is surgically implanted by injection. Under physiological conditions, the material hardens in minutes concurrent with the formation of dahllite. After 12 hours, dahllite formation was nearly complete, and an ultimate compressive strength of 55 megapascals was achieved. The composition and crystal morphology of the dahllite formed are similar to those of bone. Animal studies provide evidence that the material is remodeled in vivo. A novel approach to skeletal repair is being tested in human trials for various applications; in one of the trials the new biomaterial is being percutaneously placed into acute fractures. After hardening, it serves as internal fixation to maintain proper alignment while healing occurs. C1 STANFORD UNIV,DEPT CHEM,STANFORD,CA 94305. UNIV MICHIGAN,ORTHORPAED SURG SECT,ANN ARBOR,MI 48109. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP CONSTANTZ, BR (reprint author), NORIAN CORP,CUPERTINO,CA 95014, USA. NR 20 TC 535 Z9 565 U1 4 U2 58 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 24 PY 1995 VL 267 IS 5205 BP 1796 EP 1799 DI 10.1126/science.7892603 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QN702 UT WOS:A1995QN70200031 PM 7892603 ER PT J AU BABA, TW JEONG, YS PENNINCK, D BRONSON, R GREENE, MF RUPRECHT, RM AF BABA, TW JEONG, YS PENNINCK, D BRONSON, R GREENE, MF RUPRECHT, RM TI PATHOGENICITY OF LIVE, ATTENUATED SIV AFTER MUCOSAL INFECTION OF NEONATAL MACAQUES SO SCIENCE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; LONG TERMINAL REPEAT; INDEPENDENT DOWN-REGULATION; VIRION-ASSOCIATED PROTEIN; CELL-SURFACE CD4; MUTATIONAL ANALYSIS; NEF-PROTEIN; THROMBOCYTOPENIC PURPURA; RHESUS MACAQUES; HOMOSEXUAL MEN AB Adult macaques do not develop disease after infection with a nef deletion mutant of the simian immunodeficiency virus (SIV) and are protected against challenge with pathogenic virus. This finding led to the proposal to use nef-deleted viruses as live, attenuated vaccines to prevent human acquired immunodeficiency syndrome (AIDS). In contrast, neonatal macaques developed persistently high levels of viremia after oral exposure to an SIV nef, vpr, and negative regulatory element (NRE) deletion mutant. Severe hemolytic anemia, thrombocytopenia, and CD4(+) T cell depletion were observed, indicating that neither nef nor vpr determine pathogenicity in neonates. Because such constructs have retained their pathogenic potential, they should not be used as candidate live, attenuated virus vaccines against human AIDS. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT PEDIAT,DIV NEWBORN MED,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. TUFTS UNIV,SCH VET MED,DEPT RADIOL,GRAFTON,MA 01536. TUFTS UNIV,SCH VET MED,DEPT VET PATHOL,BOSTON,MA 02111. FU PHS HHS [R01-A132330, R01-A135533] NR 72 TC 437 Z9 440 U1 0 U2 1 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 24 PY 1995 VL 267 IS 5205 BP 1820 EP 1825 DI 10.1126/science.7892606 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QN702 UT WOS:A1995QN70200039 PM 7892606 ER PT J AU MAY, JW AF MAY, JW TI TRANSFER OF A TOE TO THE HAND SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 23 PY 1995 VL 332 IS 12 BP 785 EP 785 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA QN442 UT WOS:A1995QN44200005 PM 7862182 ER PT J AU MONCURE, AC RASHID, A SLATER, GJ KELSEY, PB AF MONCURE, AC RASHID, A SLATER, GJ KELSEY, PB TI A 60-YEAR-OLD MAN WITH HYPERTROPHIC CARDIOMYOPATHY AND ISCHEMIC COLITIS - FIBROMUSCULAR DYSPLASIA OF THE SUPERIOR MESENTERIC-ARTERY, ISCHEMIC COLITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID MANAGEMENT; DISEASE; COLON C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP MONCURE, AC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 30 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 MAR 23 PY 1995 VL 332 IS 12 BP 804 EP 810 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA QN442 UT WOS:A1995QN44200008 ER PT J AU SMALL, GW MAZZIOTTA, JC COLLINS, MT BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A LARUE, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM HAINES, JL PERICAKVANCE, MA ROSES, AD AF SMALL, GW MAZZIOTTA, JC COLLINS, MT BAXTER, LR PHELPS, ME MANDELKERN, MA KAPLAN, A LARUE, A ADAMSON, CF CHANG, L GUZE, BH CORDER, EH SAUNDERS, AM HAINES, JL PERICAKVANCE, MA ROSES, AD TI APOLIPOPROTEIN-E TYPE-4 ALLELE AND CEREBRAL GLUCOSE-METABOLISM IN RELATIVES AT RISK FOR FAMILIAL ALZHEIMER-DISEASE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; SENILE DEMENTIA; ONSET; GENE; CHROMOSOME-14; RELIABILITY; PREVALENCE; EPSILON-4; PATTERNS; REGIONS AB Objective.-Cerebral parietal hypometabolism and left-right asymmetry occur early in the course of Alzheimer disease (AD), and the apolipoprotein E type 4 allele (APOE epsilon 4) is a risk factor for familial AD. To determine if APOE epsilon 4 is associated with lowered brain function in nondemented relatives at risk for familiar AD, we studied 12 relatives with APOE epsilon 4 and 19 relatives without APOE epsilon 4. We also compared them with seven patients with probable AD. Design.-After grouping subjects according to diagnosis and genotype, brain function measures were compared among groups. Setting.-University medical center. Patients.-At-risk subjects had mild memory complaints, normal cognitive performance, and at least two relatives with AD. Subjects with APOE epsilon 4 did not differ from those without APOE epsilon 4 in mean age at examination (56.4 vs 55.5 years) or in neuropsychological performance (mean Mini-Mental State Examination score, 28.8 vs 29.3). Main Outcome Measures.-Cerebral glucose metabolism was measured using positron emission tomography and fludeoxyglucose F 18. Results.-Parietal metabolism was significantly lower and left-right parietal asymmetry was significantly higher in at-risk subjects with APOE epsilon 4 compared with those without APOE epsilon 4, Patients with dementia had significantly lower parietal metabolism than did at-risk subjects with APOE epsilon 4. Conclusions.-These results suggest that the inheritance of APOE epsilon 4 is associated with reduced cerebral parietal metabolism and increased asymmetry in nondemented relatives at risk for probable AD, Longitudinal study will determine if glucose metabolic measures provide a means to monitor experimental treatment responses during the early phases of the disorder. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PHARMACOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT RADIOL SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DIV BRAIN MAPPING,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,CTR ALZHEIMERS DIS,LOS ANGELES,CA 90024. VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF IRVINE,DEPT PHYS,IRVINE,CA. UNIV NEW MEXICO,DEPT PSYCHIAT,ALBUQUERQUE,NM. DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,DURHAM,NC. DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC. DUKE UNIV,MED CTR,DIV NEUROBIOL,DURHAM,NC. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RP SMALL, GW (reprint author), UNIV CALIF LOS ANGELES,SCH MED,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024, USA. RI Haines, Jonathan/C-3374-2012 FU NIA NIH HHS [AG05128, AG10123, U24 AG021886]; NIMH NIH HHS [1R29 MH46424] NR 59 TC 433 Z9 442 U1 3 U2 10 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 22 PY 1995 VL 273 IS 12 BP 942 EP 947 DI 10.1001/jama.273.12.942 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA QM173 UT WOS:A1995QM17300029 PM 7884953 ER PT J AU PEELMAN, LJ CHARDON, P NUNES, M RENARD, C GEFFROTIN, C VAIMAN, M VANZEVEREN, A COPPIETERS, W VANDEWEGHE, A BOUQUET, Y CHOY, WW STROMINGER, JL SPIES, T AF PEELMAN, LJ CHARDON, P NUNES, M RENARD, C GEFFROTIN, C VAIMAN, M VANZEVEREN, A COPPIETERS, W VANDEWEGHE, A BOUQUET, Y CHOY, WW STROMINGER, JL SPIES, T TI THE BAT1 GENE IN THE MHC ENCODES AN EVOLUTIONARILY CONSERVED PUTATIVE NUCLEAR-RNA HELICASE OF THE DEAD FAMILY SO GENOMICS LA English DT Article ID TRANSLATION INITIATION FACTOR-EIF-4A; MAJOR HISTOCOMPATIBILITY COMPLEX; SWINE LEUKOCYTE ANTIGEN; BINDING-PROTEINS; SEQUENCE; CLONING; DNA; IDENTIFICATION; REPLICATION; FACTOR-4A AB The BAT1 gene has previously been identified about 30 kb upstream from the tumor necrosis factor (TNF) locus and close to a NF kappa b-related gene of the nuclear factor family in the major histocompatibility complex (MHC) of human, mouse, and pig. We now show that the BAT1 translation product is the homolog of the rat p47 nuclear protein, the WM6 Drosophila gene product, and probably also Ce08102 of Caenorhabditis elegans, all members of the DEAD protein family of ATP-dependent RNA helicases. This family has more than 40 members, including the eukaryotic translation initiation factor-4A (eIF-4A), the human nuclear protein p68, and the Drosophila oocyte polar granule component vasa. BAT1 spans about 10 kb, is split into 10 exons of varying length, and encodes a protein of 428 amino acids (similar to 48 kDa). Human and pig BAT1 cDNAs display 95.6% identity in the coding region and 80% identity in the 5' and 3' noncoding regions. Several repeat sequences of different types were identified in introns of the porcine BAT1 gene. Three different mRNAs, 4.1, 1.7, and 0.9 kb, respectively, were detected in all tissues analyzed upon hybridization with porcine BAT1 cDNA Transfection and expression of human BAT1 cDNA after tagging with a heterologous antibody recognition epitope revealed a nuclear localization of the hybrid protein. An MspI RFLP was detected in an SLA class I typed family, confirming the localization of the BAT1 gene in the porcine MHC. BAT1 thus encodes a putative nuclear ATP-dependent RNA helicase and is likely to have an indispensable function. (C) 1995 Academic Press, Inc. C1 INRA,CEA,DSV,DPTE,RADIOL APPL LAB,F-78352 JOUY EN JOSAS,FRANCE. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. FRED HUTCHINSON CANC RES CTR,DIV CLIN RES,SEATTLE,WA 98104. RP PEELMAN, LJ (reprint author), STATE UNIV GHENT,FAC VET MED,DEPT ANIM BREEDING & GENET,HEIDESTR 19,B-9820 MERELBEKE,BELGIUM. NR 35 TC 47 Z9 50 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR 20 PY 1995 VL 26 IS 2 BP 210 EP 218 DI 10.1016/0888-7543(95)80203-X PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA QR156 UT WOS:A1995QR15600006 PM 7601445 ER PT J AU LOCKE, JL AF LOCKE, JL TI MORE THAN WORDS CAN SAY SO NEW SCIENTIST LA English DT Article C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP LOCKE, JL (reprint author), MASSACHUSETTS GEN HOSP,NEUROLINGUIST LAB,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NEW SCIENTIST PUBL EXPEDITING INC PI ELMONT PA 200 MEACHAM AVE, ELMONT, NY 11003 SN 0262-4079 J9 NEW SCI JI New Sci. PD MAR 18 PY 1995 VL 145 IS 1969 BP 30 EP 33 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QN335 UT WOS:A1995QN33500034 ER PT J AU HEITH, AM MORSE, CR TSUJITA, T VOLPACELLI, SA FLOOD, JG LAPOSATA, M AF HEITH, AM MORSE, CR TSUJITA, T VOLPACELLI, SA FLOOD, JG LAPOSATA, M TI FATTY-ACID ETHYL-ESTER SYNTHASE CATALYZES THE ESTERIFICATION OF ETHANOL TO COCAINE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID COCAETHYLENE; METABOLISM; RAT AB Fatty acid ethyl esters (FAEE), esterification products of ethanol and fatty acids, have been implicated as mediators of ethanol induced organ damage. It has been shown that FAEE synthase, the enzyme responsible for the formation of FAEE, is present selectively in the organs damaged by ethanol abuse. Cocaethylene is a cocaine metabolite generated in the presence of ethanol which has been established as enhancing cocaine toxicity. In the present study we show that purified FAEE synthase also catalyzes the formation of cocaethylene. A linear relationship (r=0.998) was demonstrated between the amount of purified FAEE synthase (mu g) and cocaethylene synthesis (mmol/hr). We further showed a correlation (r=0.804) between the two enzyme activities in selected tissues. These findings provide evidence that purified FAEE synthase has cocaethylene synthetic ability and FAEE synthase may be responsible for a portion of cocaethylene synthesis in vivo. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. EHIME UNIV,SCH MED,DEPT MED BIOCHEM,SHIGENOBU,EHIME 79102,JAPAN. RP HEITH, AM (reprint author), MASSACHUSETTS GEN HOSP,DIV CLIN LABS,ROOM 235,GRAY BLDG,32 FRUIT ST,GRB 235,BOSTON,MA 02114, USA. NR 19 TC 14 Z9 14 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 17 PY 1995 VL 208 IS 2 BP 549 EP 554 DI 10.1006/bbrc.1995.1373 PG 6 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QM952 UT WOS:A1995QM95200014 PM 7695606 ER PT J AU KANG, JX LEAF, A AF KANG, JX LEAF, A TI PREVENTION AND TERMINATION OF BETA-ADRENERGIC AGONIST-INDUCED ARRHYTHMIAS BY FREE POLYUNSATURATED FATTY-ACIDS IN NEONATAL RAT CARDIAC MYOCYTES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CYCLIC ADENOSINE-MONOPHOSPHATE; DIETARY-LIPID MODULATION; VENTRICULAR-FIBRILLATION; MYOCARDIAL-ISCHEMIA; ION CHANNELS; HEART-CELLS; FISH OIL; VULNERABILITY; REPERFUSION; STIMULATION AB Polyunsaturated omega-3 fatty acids, which have been shown to prevent ischemia-induced ventricular fibrillation in prepared dogs, were tested in cultured neonatal rat cardiac myocytes for their ability to prevent the tachyarrhythmias induced by isoproterenol, a beta-adrenergic agonist. We found that polyunsaturated fatty acids (5-10 mu M), especially the fish oil omega-3 fatty acids, but not monouunsaturated and saturated fatty acids were able to effectively prevent and terminate the arrhythmias induced by isoproterenol (as well as by cAMP and cholera toxin) without affecting the cell contractility, and that their action was independent of their metabolites and incorporation into membrane phospholipid. These protective effects of the free fatty acids may contribute, at least in part, to their reported preventive effects on ischemia-induced ventricular fibrillation and sudden cardiac death. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BROCKTON W ROXBURY VET AFFAIRS MED CTR,BOSTON,MA 02132. RP KANG, JX (reprint author), HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [R01-DK 38165] NR 34 TC 91 Z9 92 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 17 PY 1995 VL 208 IS 2 BP 629 EP 636 DI 10.1006/bbrc.1995.1385 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QM952 UT WOS:A1995QM95200026 PM 7695617 ER PT J AU HIRSHMAN, MF FAGNANT, PM HORTON, ED KING, PA HORTON, ES AF HIRSHMAN, MF FAGNANT, PM HORTON, ED KING, PA HORTON, ES TI PIOGLITAZONE TREATMENT FOR 7 DAYS FAILED TO CORRECT THE DEFECT IN GLUCOSE-TRANSPORT AND GLUCOSE-TRANSPORTER TRANSLOCATION IN OBESE ZUCKER RAT (FA/FA) SKELETAL-MUSCLE PLASMA-MEMBRANES SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID PERIPHERAL INSULIN-RESISTANCE; EXERCISE; VESICLES; NUMBER; KINASE AB Insulin resistance in the obese (fa/fa) Zucker rat is associated with decreased insulin stimulated glucose transport in skeletal muscle, due primarily to a failure of insulin to stimulate GLUT4 translocation to the plasma membrane from an intracellular pool (1). The thiazolidinedione analog Pioglitazone (PIO) has been shown to improve glucose tolerance in this and other animal models of insulin resistance. The current study was designed to determine whether 7 days of Pioglitazone treatment (20 mg/kg/day by gavage) would improve glucose transport and/or glucose transporter translocation and intrinsic activity in plasma membranes prepared from hindlimb skeletal muscle of obese Zucker (fa/fa) rats. Basal plasma glucose and insulin concentrations in these animals were unchanged by Pioglitazone, while basal plasma triglyceride and nonesterified fatty acid concentrations (NEFA) were reduced by Pioglitazone treatment (501+/-88 vs 161+/-1 3 mg/dl, P<0.0001) and (678+/-95 vs 467+/-75 mu M, P<0.05) respectively. Pioglitazone had no effect on basal or insulin stimulated glucose influx (V-max or K-m) into plasma membrane vesicles determined under equilibrium exchange conditions compared to controls. Plasma membrane glucose transporter number (R(o)) (measured by cytochalasin B binding) under basal or insulin stimulated conditions was unchange by Pioglitazone and R(o) failed to increase following insulin stimulation in either group. Glucose transporter turnover number (V-max/R(o)) increased 2-fold with insulin stimulation compared to basal in both control and Pioglitazone groups, similar to turnover numbers observed in normal rats. These data confirm that impaired glucose transporter translocation in muscle of the Zucker rat is a major factor contributing to its insulin resistance. We conclude that the improved glucose tolerance observed in fa/fa rats following Pioglitazone treatment is not due to an improvement in basal or insulin stimulated skeletal muscle plasma membrane glucose transport or glucose transporter translocation and that Pioglitazone treatment does not affect transporter intrinsic activity. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. RP HIRSHMAN, MF (reprint author), UNIV VERMONT,COLL MED,DEPT MED,DIV METAB ENDOCRINOL & NUTR,BURLINGTON,VT 05404, USA. FU NIDDK NIH HHS [R01 DK26317] NR 23 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD MAR 17 PY 1995 VL 208 IS 2 BP 835 EP 845 DI 10.1006/bbrc.1995.1412 PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QM952 UT WOS:A1995QM95200053 PM 7695642 ER PT J AU MENDEZ, AJ AF MENDEZ, AJ TI MONENSIN AND BREFELDIN-A INHIBIT HIGH-DENSITY LIPOPROTEIN-MEDIATED CHOLESTEROL EFFLUX FROM CHOLESTEROL-ENRICHED CELLS - IMPLICATIONS FOR INTRACELLULAR CHOLESTEROL TRANSPORT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PLASMA-MEMBRANE SPHINGOMYELIN; PROTEIN-KINASE-C; CULTURED FIBROBLASTS; GOLGI-APPARATUS; ENDOPLASMIC-RETICULUM; ADIPOSE-CELLS; SMOOTH-MUSCLE; APOLIPOPROTEINS; MACROPHAGES; ESTERIFICATION AB Mechanisms and pathways of excess cholesterol removal from intracellular sites of accumulation to extracellular cholesterol accepters remain poorly defined. To gain further insights, compounds known to affect cellular protein transport pathways were tested for their effects on high density lipoprotein (HDL) mediated cholesterol efflux from cultured cells enriched with cholesterol. Monensin, nigericin, and brefeldin A inhibited the ability of HDL to decrease cellular cholesterol esterification, stimulate sterol biosynthesis, and promote the efflux of labeled cholesterol and cholesterol mass from fibroblasts and smooth muscle cells. HDL-mediated decrease in cell cholesterol esterification was inhibited up to 80% by these compounds compared with control incubations over an HDL concentration of 5-100 mu g/ml and up to 18 h of incubation, Up-regulation of sterol biosynthesis after depletion of cell cholesterol by HDL increased over 10- fold; however, inclusion of monensin or brefeldin A during the incubation completely prevented the increase of sterol biosynthesis by HDL. Efflux of [H-3]cholesterol to HDL from prelabeled cells was inhibited up to 40% by these compounds, and this effect persisted when cholesterol esterification was blocked. Similarly, monensin and brefeldin A inhibited up to 50% of HDL-mediated cholesterol mass efflux relative to controls, Treatment of cells with cholesterol oxidase demonstrated an increase of intracellular cholesterol after exposure to monensin or nigericin and to a lesser extent with brefeldin A. These data show that monensin, nigericin, and brefeldin A sequester cholesterol from sites normally available for efflux by HDL. Since these compounds act by disruption of Golgi complex structure and function, a rob for this intracellular organelle in transport of cholesterol between intracellular sites and the plasma membrane for eventual removal by extracellular accepters such as HDL is suggested. RP MENDEZ, AJ (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,JACKSON 1422,32 FRUIT ST,BOSTON,MA 02114, USA. NR 49 TC 67 Z9 68 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 17 PY 1995 VL 270 IS 11 BP 5891 EP 5900 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QM945 UT WOS:A1995QM94500032 PM 7890720 ER PT J AU SEGALAT, L ELKES, DA KAPLAN, JM AF SEGALAT, L ELKES, DA KAPLAN, JM TI MODULATION OF SEROTONIN-CONTROLLED BEHAVIORS BY G(O) IN CAENORHABDITIS-ELEGANS SO SCIENCE LA English DT Article ID BETA-GAMMA-SUBUNITS; G-PROTEIN; NERVOUS-SYSTEM; ALPHA-SUBUNIT; NEMATODE; MYRISTOYLATION; STIMULATION; GENES AB Seven transmembrane receptors and their associated heterotrimeric guanine nucleotide-binding proteins (G proteins) have been proposed to play a key role in modulating the activities of neurons and muscles. The physiological function of the Caenorhabditis elegans G protein G(o) has been genetically characterized. Mutations in the goa-l gene, which encodes an a subunit of G(o) (G alpha(o)), cause behavioral defects similar to those observed in mutants that lack the neurotransmitter serotonin (5-HT), and goa-1 mutants are partially resistant to exogenous 5-HT. Mutant animals that lack G alpha(o) and transgenic animals that overexpress G alpha(o) [goa-l(xs) animals] have reciprocal defects in locomotion, feeding, and egg laying behaviors. In normal animals, all of these behaviors are regulated by 5-HT. These results demonstrate that the level of G(o) activity is a critical determinant of several C. elegans behaviors and suggest that G(o) mediates many of the behavioral effects of 5-HT. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NINDS NIH HHS [NS32196] NR 37 TC 224 Z9 227 U1 2 U2 12 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 17 PY 1995 VL 267 IS 5204 BP 1648 EP 1651 DI 10.1126/science.7886454 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QM397 UT WOS:A1995QM39700038 PM 7886454 ER PT J AU SHIEKHATTAR, R MERMELSTEIN, F FISHER, RP DRAPKIN, R DYNLACHT, B WESSLING, HC MORGAN, DO REINBERG, D AF SHIEKHATTAR, R MERMELSTEIN, F FISHER, RP DRAPKIN, R DYNLACHT, B WESSLING, HC MORGAN, DO REINBERG, D TI CDK-ACTIVATING KINASE COMPLEX IS A COMPONENT OF HUMAN TRANSCRIPTION FACTOR TFIIH SO NATURE LA English DT Article ID RNA POLYMERASE-II; CARBOXYL-TERMINAL-DOMAIN; INITIATION AB TRANSCRIPTION factor IIH (TFIIH) contains a kinase capable of phosphorylating the carboxy-terminal domain (CTD) of the largest subunit of RNA polymerase II (RNAPII)1-3. Here we report the identification of the Cdk-activating kinase (Cak) complex (Cdk7 and cyclin H) as a component of TFIIH after extensive purification of TFIIH by chromatography. We find that affinity-purified antibodies directed against cyclin H inhibit TFIIH-dependent transcription and that both cyclin H and Cdk7 antibodies inhibit phosphorylation of the CTD of the largest subunit of the RNAPII in the preinitiation complex. Cak is present in at least two distinct complexes, TFIIH and a smaller complex that is unable to phosphorylate RNAPII in the preinitiation complex. Both Cak complexes, as well as recombinant Cak, phosphorylate a CTD peptide. Finally, TFIIH was shown to phosphorylate both Cdc2 and Cdk2, suggesting that there could be a link between transcription and the cell cycle machinery. C1 UNIV MED & DENT NEW JERSEY, ROBERT WOOD JOHNSON MED SCH, DEPT BIOCHEM, HOWARD HUGHES MED INST, PISCATAWAY, NJ 08854 USA. UNIV CALIF SAN FRANCISCO, DEPT PHYSIOL, SAN FRANCISCO, CA 94143 USA. MASSACHUSETTS GEN HOSP, CTR CANC, MOLEC ONCOL LAB, BOSTON, MA 02129 USA. RI Drapkin, Ronny/E-9944-2016 OI Drapkin, Ronny/0000-0002-6912-6977 NR 17 TC 315 Z9 321 U1 0 U2 4 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 EI 1476-4687 J9 NATURE JI Nature PD MAR 16 PY 1995 VL 374 IS 6519 BP 283 EP 287 DI 10.1038/374283a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QM387 UT WOS:A1995QM38700056 PM 7533895 ER PT J AU ETCHASON, J PETZ, L KEELER, E CALHOUN, L KLEINMAN, S SNIDER, C FINK, A BROOK, R AF ETCHASON, J PETZ, L KEELER, E CALHOUN, L KLEINMAN, S SNIDER, C FINK, A BROOK, R TI THE COST-EFFECTIVENESS OF PREOPERATIVE AUTOLOGOUS BLOOD DONATIONS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; TRANSFUSION-INDUCED IMMUNOMODULATION; QUALITY-OF-LIFE; NON-A-HEPATITIS; NON-B-HEPATITIS; INFECTION; HEALTH; REPLACEMENT; COLLECTION; COMPONENTS AB Background. Since the recognition that human immunodeficiency virus is transmissible by blood transfusion there has been increasing public and professional support for autologous blood donations before elective surgery. Autologous blood donation is, however, a more expensive process than the donation of allogeneic blood by community volunteers, Furthermore, there have been recent improvements in the safety of the volunteer blood supply, Methods. We used a decision-analysis model to assess the cost effectiveness of donating autologous blood for four surgical procedures, Cost data were collected from the observation of transfusion practice at the University of California, Los Angeles, in 1992, Estimates of the risks of transfusion-associated diseases and the costs of treating them came from the medical literature. Cost effectiveness was expressed in dollars per quality-adjusted year of life saved. We performed sensitivity analyses of the variables in our model and examined the effect of strategies suggested to reduce costs. Results. Substituting autologous for allogeneic blood resulted in little expected health benefit (0.0002 to 0.00044 quality-adjusted year of life saved) at considerable additional cost ($68 to $4,783 per unit of blood). The additional cost of autologous blood was primarily a function of the discarding of units that were donated but not transfused and of a more labor-intensive donation process, The cost-effectiveness values ranged from $235,000 to over $23 million per quality-adjusted year of life saved. Conclusions. Given the improved safety of allogeneic transfusions today, the increased protection afforded by donating autologous blood is limited and may not justify the increased cost. C1 UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT PATHOL & LAB MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,CTR HLTH SCI,DEPT HLTH SERV,LOS ANGELES,CA 90024. RAND CORP,SANTA MONICA,CA. RP ETCHASON, J (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,DIV GEN INTERNAL MED,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. RI Brugnara, Carlo/A-8041-2010 OI Brugnara, Carlo/0000-0001-8192-8713 FU NHLBI NIH HHS [K07 HL02151] NR 46 TC 356 Z9 360 U1 1 U2 4 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 16 PY 1995 VL 332 IS 11 BP 719 EP 724 DI 10.1056/NEJM199503163321106 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA QL788 UT WOS:A1995QL78800006 PM 7854380 ER PT J AU JANG, IK BLOCK, PC NEWELL, JB TUZCU, EM PALACIOS, IF AF JANG, IK BLOCK, PC NEWELL, JB TUZCU, EM PALACIOS, IF TI PERCUTANEOUS MITRAL BALLOON VALVOTOMY FOR RECURRENT MITRAL-STENOSIS AFTER SURGICAL COMMISSUROTOMY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID VALVULOPLASTY; CATHETER AB Immediate outcome and Lt-year follow-vp results of percutaneous mitral balloon valvotomy (PMV) in patients with previous surgical mitral commissurotomy are studied. Repeat surgical mitral commissurotomy in patients with previous surgical commissurotomy is associated with higher mortality and morbidity. PMV has been proven to be safe and could be an ideal alternative in this patient group. The results of 68 patients with previous surgical commissurotomy were compared with those of 261 patients without prior surgical intervention. A good outcome, defined as the final mitral valve area >1.5 cm(2), was obtained in 51% of the patients with prior surgical commissurotomy compared with 71% in the control group (p = 0.002). During the 4-year follow-up period, there were more patients who required mitral valve replacement (19% vs 7%; p = 0.004) and who were in New York Heart Association functional class iii and IV (85% vs 71%; p = 0.02) among those with prior surgical commissurotomy. However, when these patients were divided according to echocardiographic score, chose with a score less than or equal to 8 had immediate outcome and long-Arm results similar to those without prior commissurotomy. PMV can be performed safely in patients with prior surgical commissurotomy. Although results of long-term follow-up in these patients is not as good as those in patients without prior surgical commissurotomy, those with a low echocardiographic score had similar excellent longterm results. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,CARDIAC CATHETERIZAT LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. ST VINCENT HEART INST,PORTLAND,OR. NR 20 TC 35 Z9 37 U1 0 U2 2 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 15 PY 1995 VL 75 IS 8 BP 601 EP 605 DI 10.1016/S0002-9149(99)80625-0 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QL378 UT WOS:A1995QL37800011 PM 7887386 ER PT J AU BOND, CA RAEHL, CL PITTERLE, ME AF BOND, CA RAEHL, CL PITTERLE, ME TI COST OF PHARMACEUTICAL SERVICES IN US HOSPITALS IN 1992 SO AMERICAN JOURNAL OF HEALTH-SYSTEM PHARMACY LA English DT Article DE ADMINISTRATION; CLINICAL PHARMACY; COSTS; DATA COLLECTION; DRUG DISTRIBUTION SYSTEMS; ECONOMICS; EDUCATION, PHARMACEUTICAL; GEOGRAPHY; PERSONNEL, PHARMACY; PHARMACEUTICAL SERVICES; PHARMACISTS, HOSPITAL; PHARMACY, INSTITUTIONAL, HOSPITAL; SALARIES; UNITED STATES ID CLINICAL PHARMACY; CASE-MIX; CARE; OUTCOMES; SEVERITY; ILLNESS AB The results of a 1992 national survey of hospital-based pharmaceutical services are reported and compared with data collected during a similar survey in 1989. A questionnaire was mailed to pharmacy directors at all 3756 medical-surgical hospi tals in the United States that had 50 or more licensed beds. Cost results were evaluated both as unadjusted data and as data adjusted for severity of illness with the case mix index. The response rate was 43% (1597 usable responses). Mean +/- S.D. unadjusted medication costs per occupied bed were $9850 +/- 4744 (a 46% increase over 1989 costs); significant differences were observed for geographic region, hospital ownership, drug delivery system, and pharmacy director's education. Mean +/- S.D. unadjusted total pharmacy costs per occupied bed were $16,550 +/- 6,249 (a 40% increase over 1989 costs); significant differences were observed for geographic region, hospital ownership, drug delivery system, and pharmacy director's education. Other mean +/- S.D. unadjusted pharmacy cost components were as follows: injectable solution costs, $2627 +/- 2191 (a 38% increase over 1989 costs); inventory costs, $2029 +/- 2593 (70% increase); pharmacist salary costs per occupied bed, $2997 +/- 1267 (33% increase); pharmacy technician costs per occupied bed, $995 +/- 876 (24% increase); pharmacist salary costs per full-time equivalent (FTE), $43,798 +/- 12,206 (14% increase); pharmacy technician salary costs per FTE, $18,953 +/- 6,154 (15% increase); and pharmacy staff development costs per occupied bed, $45 +/- 41 (29% increase). Pharmacist salary costs associated with centrally based clinical pharmacy services ranged from a high of $361 per occupied bed per year for drug-use evaluation to a low of $15 per occupied bed per year for inservice education. Pharmacist salary costs for patient-specific pharmaceutical services ranged from $3 per patient for medical rounds to $8 per patient for cardiopulmonary resuscitation team participation and drug protocol management. A 1992 survey provided comprehensive data on the cost structure of hospital-based pharmaceutical services and a basis for comparison with 1989 cost data. C1 UNIV WISCONSIN,SCH MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,ARRHYTHMIA CLIN,MADISON,WI 53706. RP BOND, CA (reprint author), UNIV WISCONSIN,SCH PHARM,425 N CHARTER ST,MADISON,WI 53706, USA. NR 51 TC 9 Z9 9 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 1079-2082 J9 AM J HEALTH-SYST PH JI Am. J. Health-Syst. Pharm. PD MAR 15 PY 1995 VL 52 IS 6 BP 603 EP 613 PG 11 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QM521 UT WOS:A1995QM52100005 PM 7606574 ER PT J AU DAQUILA, RT JOHNSON, VA WELLES, SL JAPOUR, AJ KURITZKES, DR DEGRUTTOLA, V REICHELDERFER, PS COOMBS, RW CRUMPACKER, CS KAHN, JO RICHMAN, DD AF DAQUILA, RT JOHNSON, VA WELLES, SL JAPOUR, AJ KURITZKES, DR DEGRUTTOLA, V REICHELDERFER, PS COOMBS, RW CRUMPACKER, CS KAHN, JO RICHMAN, DD TI ZIDOVUDINE RESISTANCE AND HIV-1 DISEASE PROGRESSION DURING ANTIRETROVIRAL THERAPY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE ZIDOVUDINE; DRUG RESISTANCE; HUMAN IMMUNODEFICIENCY VIRUS-1; ANTIVIRAL AGENTS; DIDANOSINE ID HUMAN-IMMUNODEFICIENCY-VIRUS; SYNCYTIUM-INDUCING PHENOTYPE; REVERSE-TRANSCRIPTASE; SENSITIVITY; CAPACITY; CHILDREN; MUTATION; INVITRO; AIDS AB Objective: To evaluate the association between resistance of human immunodeficiency virus type 1 (HIV-1) to zidovudine and clinical progression. Design: Retrospective analysis of specimens from patients in the AIDS Clinical Trials Group (ACTG) protocol 116B/117, a randomized comparison of didanosine with continued zidovudine therapy in patients with advanced HIV-1 disease who had received 16 weeks or more of previous zidovudine therapy. Setting: Participating ACTG virology laboratories. Patients: 187 patients with baseline HIV-1 isolates. Measurements: Zidovudine susceptibility testing and assays for syncytium-inducing phenotype were done on baseline HIV-1 isolates. Relative hazards for clinical progression or death associated with baseline clinical, virologic, and immunologic factors were determined from Cox proportional hazards regression models. Results: Compared with other patients, 15% (26 of 170) with isolates showing high-level zidovudine resistance (50% inhibitory zidovudine concentration greater than or equal to 1.0 mu M) had 1.74 times the risk for progressing to a new AIDS-defining event or death (95% CI, 1.00 to 3.03) and 2.78 times the risk for death (CI, 1.21 to 6.39) in analyses that controlled for baseline CD4(+) T-lymphocyte count, syncytium-inducing HIV-1 phenotype, disease stage, and randomized treatment assignment. The clinical benefit of didanosine was not limited to patients with highly zidovudine-resistant baseline HIV-1 isolates. Conclusions: High-level resistance of HIV-1 to zidovudine predicted more rapid clinical progression and death when adjusted for other factors. However, patients with advanced HIV-1 disease may benefit from a change in monotherapy from zidovudine to didanosine whether high-level HIV-1 resistance to zidovudine is present or absent, and laboratory assessment of zidovudine resistance is not necessary for deciding when to switch monotherapy from zidovudine to didanosine. C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. UNIV ALABAMA,SCH MED,BIRMINGHAM,AL. VET AFFAIRS MED CTR,BIRMINGHAM,AL. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. VET AFFAIRS MED CTR,DENVER,CO. NIAID,BETHESDA,MD 20892. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. SAN FRANCISCO GEN HOSP,AIDS PROGRAM,SAN FRANCISCO,CA. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. VET AFFAIRS MED CTR,LA JOLLA,CA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA. FU NIAID NIH HHS [AI 27659, AI 32775, AI 29193] NR 38 TC 231 Z9 232 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 15 PY 1995 VL 122 IS 6 BP 401 EP 408 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA QM266 UT WOS:A1995QM26600001 PM 7856987 ER PT J AU ABREU, MM BOCHOW, TW AF ABREU, MM BOCHOW, TW TI CALCIUM-CHANNEL BLOCKERS AND CHOROIDAL NEOVASCULAR MEMBRANE FORMATION - A CASE-CONTROL STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1001 EP S1001 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504629 ER PT J AU AIELLO, LP PIERCE, EA FOLEY, ED SULLIVAN, R CHEN, H FERRARA, N KING, GL SMITH, LEH AF AIELLO, LP PIERCE, EA FOLEY, ED SULLIVAN, R CHEN, H FERRARA, N KING, GL SMITH, LEH TI INHIBITION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) REDUCES RETINAL NEOVASCULARIZATION IN THE MOUSE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. GENENTECH INC,DEPT OPHTHALMOL,S SANF FRANCISCO,CA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S401 EP S401 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501862 ER PT J AU AMBERSON, DA BAEHR, W SUBBARAYA, I BERSON, EL DRYJA, TP AF AMBERSON, DA BAEHR, W SUBBARAYA, I BERSON, EL DRYJA, TP TI SCREEN FOR MUTATIONS IN THE GENE ENCODING GUANYLATE-CYCLASE ACTIVATING PROTEIN IN PATIENTS WITH RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB & BERMAN GUND LAB,BOSTON,MA 02114. BAYLOR COLL MED,DEPT OPHTHALMOL,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S826 EP S826 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503808 ER PT J AU AN, BB DREYER, EB AF AN, BB DREYER, EB TI THE EFFECT OF PRIMARY OPEN-ANGLE GLAUCOMA AND ITS TREATMENT ON VISUAL-ACUITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S77 EP S77 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500368 ER PT J AU AYYALA, RS BELLOWS, AR AF AYYALA, RS BELLOWS, AR TI BLEB INFECTION VS INFLAMMATION BLEBITIS FOLLOWING FILTERING SURGERY WITH MITOMYCIN-C SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S345 EP S345 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501616 ER PT J AU BELLOWS, AR KAYE, LD JOHNSON, S HUTCHINSON, BT SHINGLETON, BJ AF BELLOWS, AR KAYE, LD JOHNSON, S HUTCHINSON, BT SHINGLETON, BJ TI MITOMYCIN-C TRABECULECTOMY FOR NEOVASCULAR GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S89 EP S89 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500433 ER PT J AU BERGER, JW TALAMO, JH KIM, SH LAMARCHE, KJ DAMICO, DJD SNYDER, RW MARDELLINO, G AF BERGER, JW TALAMO, JH KIM, SH LAMARCHE, KJ DAMICO, DJD SNYDER, RW MARDELLINO, G TI TEMPERATURE-MEASUREMENTS DURING PHACOEMULSIFICATION AND ER-YAG LASER PHACOABLATION IN HUMAN CADAVER EYES AND MODEL SYSTEMS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,LASER RES LAB,BOSTON,MA 02114. UNIV ARIZONA,SCH MED,DEPT OPHTHALMOL,TUCSON,AZ 85721. COHERENT INC,PALO ALTO,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S798 EP S798 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503684 ER PT J AU BERNSTEIN, PS TSONG, ED RANDO, RR AF BERNSTEIN, PS TSONG, ED RANDO, RR TI ISOLATION OF A CAROTENOID BINDING-PROTEIN FROM BOVINE RETINA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S5 EP S5 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500020 ER PT J AU BHISTIKUL, RB MOSCARITOLO, K DREYER, EB AF BHISTIKUL, RB MOSCARITOLO, K DREYER, EB TI NEURITE BEARING RETINAL GANGLION-CELLS ARE MORE SENSITIVE TO NMDA-MEDIATED TOXICITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S934 EP S934 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504293 ER PT J AU BOCHOW, TW KIM, R BERGER, JW DAMICO, DJ AF BOCHOW, TW KIM, R BERGER, JW DAMICO, DJ TI PHOTOVITRECTOMY - A NOVEL-APPROACH FOR VITREOUS REMOVAL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT MORPHOL,LASER RES LAB,RETINA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S834 EP S834 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503838 ER PT J AU BONFOCO, E NICOTERA, P SMITH, JA DREYER, EB LIPTON, SA AF BONFOCO, E NICOTERA, P SMITH, JA DREYER, EB LIPTON, SA TI RETINAL GANGLION-CELLS DIE BY AN APOPTOTIC-LIKE MECHANISM IN HUMAN GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. PROGRAM NEUROSCI,BOSTON,MA. KAROLINSKA INST,DEPT ENVIRONM MED,S-10401 STOCKHOLM 60,SWEDEN. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S964 EP S964 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504435 ER PT J AU BROCKERHOFF, SE HURLEY, JB NEUHAUSS, S DRIEVER, W DOWLING, JE AF BROCKERHOFF, SE HURLEY, JB NEUHAUSS, S DRIEVER, W DOWLING, JE TI OPTOKINETIC RESPONSES IN WILD-TYPE AND MUTANT LARVAL ZEBRAFISH SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CVRC,BOSTON,MA 02129. HARVARD UNIV,CAMBRIDGE,MA 02138. UNIV WASHINGTON,HHMI,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 1 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S918 EP S918 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504212 ER PT J AU BURSELL, SE CLERMONT, AC LIN, YW GOLDBERG, MF RHO, DS KOPPLE, A AIELLO, LM KING, GL AF BURSELL, SE CLERMONT, AC LIN, YW GOLDBERG, MF RHO, DS KOPPLE, A AIELLO, LM KING, GL TI RETINAL BLOOD-FLOW IS REDUCED IN TYPE-II DIABETIC-PATIENTS WITH NO DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S480 EP S480 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502213 ER PT J AU CASTELBUONO, A RIZZO, JF AF CASTELBUONO, A RIZZO, JF TI DISTRIBUTIONS OF HUMAN PHOTORECEPTORS, RETINAL GANGLION-CELLS AND AREA OF THE STRIATE CORTEX APPLIED TO GOLDMANN FIELD CHARTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S455 EP S455 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502089 ER PT J AU CEISLER, E DREYER, EB AF CEISLER, E DREYER, EB TI ACRYLAMIDE IS TOXIC TO RETINAL GANGLION-CELLS INDEPENDENT OF SIZE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S933 EP S933 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504285 ER PT J AU CHAUM, E KINI, MM ASHRAFZADEH, MT PRUSTY, S HOLLANDER, W WALSH, D SANDELL, JH AF CHAUM, E KINI, MM ASHRAFZADEH, MT PRUSTY, S HOLLANDER, W WALSH, D SANDELL, JH TI OPHTHALMIC MANIFESTATIONS OF CHRONIC HYPERTENSIVE RETINOPATHY, WITH AND WITHOUT HYPERLIPIDEMIA, IN A COHORT OF CYNOMOLGUS MONKEYS - A PROSPECTIVE CONTROLLED-STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV MASSACHUSETTS,MED CTR,DEPT OPHTHALMOL,WORCESTER,MA 01605. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. BOSTON UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,DEPT ANAT & NEUROBIOL,BOSTON,MA 02118. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S757 EP S757 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503491 ER PT J AU CHENG, HM XIONG, J XIONG, H NAKAMURA, J LASHKARI, K AF CHENG, HM XIONG, J XIONG, H NAKAMURA, J LASHKARI, K TI WATER-MOVEMENT IN THE AQUEOUS CHAMBER IN RESPONSE TO ANTIGLAUCOMA DRUGS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RETINA ASSOCIATES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S731 EP S731 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503371 ER PT J AU CHYNN, EW PATALANO, VJ AF CHYNN, EW PATALANO, VJ TI THE DIAGNOSTIC YIELD AND THERAPEUTIC IMPLICATIONS OF THE ROUTINE EYE EXAM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S429 EP S429 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501962 ER PT J AU CIULLA, TA HAIMOVICI, R RILEY, EJ DAMICO, DJ AF CIULLA, TA HAIMOVICI, R RILEY, EJ DAMICO, DJ TI INTRAVITREAL TOXICITY OF DENTAL ADHESIVES IN THE RABBIT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. BOSTON UNIV,SCH MED,BOSTON,MA 02118. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S617 EP S617 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502837 ER PT J AU CLERMONT, AC TAKAGI, C JIROUSEK, MR BURSELL, SE KING, GL AF CLERMONT, AC TAKAGI, C JIROUSEK, MR BURSELL, SE KING, GL TI A PKC-BETA ISOFORM SELECTIVE ANTAGONIST NORMALIZED RETINAL BLOOD-FLOW IN STZ DIABETIC RATS - 1ST REPORT OF AN ORAL-AGENT SELECTIVE FOR THE PKC-BETA ISOENZYME SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S173 EP S173 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500830 ER PT J AU COLBY, KA KUROKI, M TOLENTINO, MJ KIM, RY ADAMIS, AP AF COLBY, KA KUROKI, M TOLENTINO, MJ KIM, RY ADAMIS, AP TI ISCHEMIA/REPERFUSION INCREASES RETINAL VEGF GENE-EXPRESSION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S895 EP S895 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504102 ER PT J AU CONNOLLY, EJ SIEGNER, SW HART, LJ NETLAND, PA MILLER, JW AF CONNOLLY, EJ SIEGNER, SW HART, LJ NETLAND, PA MILLER, JW TI COLOR DOPPLER STUDY OF OCULAR BLOOD-FLOW IN THE PRIMATE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S103 EP S103 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500495 ER PT J AU COOK, JR PARKS, WC RAIZMAN, MB KRUEGER, RR ASSIL, KK FINI, ME AF COOK, JR PARKS, WC RAIZMAN, MB KRUEGER, RR ASSIL, KK FINI, ME TI CELLULAR SOURCE OF TISSUE-DEGRADING ENZYMES IN HEALING AND NONHEALING CORNEAL WOUNDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NEW ENGLAND EYE CTR,BOSTON,MA. WASHINGTON UNIV,SCH MED,MED CTR,ST LOUIS,MO 63110. ANHEUSER BUSCH EYE INST,ST LOUIS,MO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S28 EP S28 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500127 ER PT J AU DAMICO, DJ AF DAMICO, DJ TI CLINICAL-EXPERIENCE WITH AN ERBIUM-YAG LASER FOR VITREORETINAL SURGICAL MANEUVERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,LASER RES LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S834 EP S834 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503836 ER PT J AU DANA, MR SCHAUMBERG, DA MOYES, AL GOMES, JAP HOLLAND, EJ LAIBSON, PR SUGAR, A SUGAR, J AF DANA, MR SCHAUMBERG, DA MOYES, AL GOMES, JAP HOLLAND, EJ LAIBSON, PR SUGAR, A SUGAR, J TI OUTCOME OF PENETRATING KERATOPLASTY FOR OCULAR TRAUMA IN CHILDREN - A MULTICENTER EXPERIENCE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WILLS EYE HOSP & RES INST,PHILADELPHIA,PA 19107. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CTR OPHTHALM RES,BOSTON,MA 02115. UNIV MINNESOTA,DEPT OPHTHALMOL,MINNEAPOLIS,MN 55455. UNIV MICHIGAN,KELLOGG EYE CTR,ANN ARBOR,MI 48109. UNIV ILLINOIS,EYE & EAR INFIRM,CHICAGO,IL 60612. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S652 EP S652 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502976 ER PT J AU DRYJA, TP AF DRYJA, TP TI MOLECULAR-GENETICS OF RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S220 EP S220 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501003 ER PT J AU DUH, EJ TAKAGI, H NISHIO, Y AIELLO, LP KING, GL AF DUH, EJ TAKAGI, H NISHIO, Y AIELLO, LP KING, GL TI CHARACTERIZATION AND PARTIAL SEQUENCE-ANALYSIS OF A GENE DOWN-REGULATED IN RETINAL PERICYTES BY HYPERGLYCEMIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN RES LABS,BOSTON,MA. JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S486 EP S486 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502241 ER PT J AU DUTT, JE RIBLET, R FOSTER, CS AF DUTT, JE RIBLET, R FOSTER, CS TI MAPPING OF THE SUSCEPTIBILITY LOCUS IN A MURINE MODEL OF HERPES-SIMPLEX KERATITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. MED BIOL INST,LA JOLLA,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S147 EP S147 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500709 ER PT J AU EGAN, KM WANG, XI GRAGOUDAS, ES KELSEY, KT AF EGAN, KM WANG, XI GRAGOUDAS, ES KELSEY, KT TI CONSTITUTIONAL ALTERATIONS ON CHROMOSOME-9 IN PATIENTS WITH UVEAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. RI Kelsey, Karl/I-1252-2014 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S770 EP S770 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503546 ER PT J AU EPPSTEIN, JA KRANTZ, BS CALLAHAN, KM WASINGER, F WANG, Q BURSELL, SE AF EPPSTEIN, JA KRANTZ, BS CALLAHAN, KM WASINGER, F WANG, Q BURSELL, SE TI SCREENING FOR DIABETES-MELLITUS USING LENS SCATTERING AND FLUORESCENCE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SPECTRX INC,ATLANTA,GA. JOSLIN DIABET CTR,EYE UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 2 U2 3 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S819 EP S819 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503785 ER PT J AU FEKE, GT NETLAND, PA KONNO, S GOGER, DG FUJIO, N AF FEKE, GT NETLAND, PA KONNO, S GOGER, DG FUJIO, N TI TOPICAL VERAPAMIL LOWERS INTRAOCULAR-PRESSURE AND INCREASES OPTIC-NERVE HEAD CAPILLARY BLOOD SPEED IN NORMAL SUBJECTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,SCHEPENS EYE RES INST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S823 EP S823 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503797 ER PT J AU FILATOV, V KIM, SH KENYON, KR TALAMO, JH AF FILATOV, V KIM, SH KENYON, KR TALAMO, JH TI THE EFFECT OF TISSUE HYDRATION ON THE CORNEAL SURFACE SMOOTHNESS FOLLOWING EXCIMER PHOTOREFRACTIVE KERATECTOMY IN RABBITS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,CORNEA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CORNEA CONSULTANTS,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S707 EP S707 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503244 ER PT J AU FOLEY, ED AIELLO, LP PIERCE, EA SULLIVAN, R CHEN, WY KNAPP, JR KOPCHICK, JJ SMITH, LEH AF FOLEY, ED AIELLO, LP PIERCE, EA SULLIVAN, R CHEN, WY KNAPP, JR KOPCHICK, JJ SMITH, LEH TI THE EFFECT OF GROWTH-HORMONE ON A MOUSE MODEL OF PROLIFERATIVE RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. OHIO UNIV,EDISON BIOTECHNOL INST,ATHENS,OH 45701. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1047 EP S1047 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504828 ER PT J AU FOSTER, BS HU, LK KIM, R GRAGOUDAS, ES YOUNG, LHY AF FOSTER, BS HU, LK KIM, R GRAGOUDAS, ES YOUNG, LHY TI PHOTODYNAMIC THERAPY (PDT) OF PIGMENTED CHOROIDAL MELANOMA USING LOW-DOSE BENZOPORPHYRIN DERIVATIVE (BPD) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S488 EP S488 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502249 ER PT J AU GAUDIO, AR SANDBERG, MA AF GAUDIO, AR SANDBERG, MA TI THE CLINICAL-SIGNIFICANCE OF SLOW DAZZLE RECOVERY IN AGE-RELATED MACULAR DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUD RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S233 EP S233 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501056 ER PT J AU GIOVANONI, A SIEGNER, SW SCHROEDER, A RICHARDSON, D ERICKSON, KA NETLAND, PA AF GIOVANONI, A SIEGNER, SW SCHROEDER, A RICHARDSON, D ERICKSON, KA NETLAND, PA TI IDENTIFICATION OF L-TYPE AND N-TYPE CALCIUM CHANNELS IN HUMAN EYES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S587 EP S587 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502714 ER PT J AU GIRARD, B PARK, SS FONT, RL HAUW, JJ YOUNG, LHY AF GIRARD, B PARK, SS FONT, RL HAUW, JJ YOUNG, LHY TI IMMUNOHISTOCHEMICAL LOCALIZATION OF GANCICLOVIR IN HUMAN EYES TREATED WITH INTRAVENOUS OR INTRAVITREAL GANCICLOVIR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HOP AULNAY BOIS,DEPT OPHTHALMOL,AULNAY SOUS BOIS,FRANCE. UNIV TEXAS,SW MED CTR,DEPT OPHTHALMOL,DALLAS,TX 75230. MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. BAYLOR COLL MED,CULLEN EYE INST,DEPT OPHTHALMOL,HOUSTON,TX 77030. HOP LA PITIE SALPETRIERE,F-75651 PARIS 13,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S322 EP S322 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501502 ER PT J AU GOLDBERG, MF SHARUK, GS CLERMONT, AC KOPPLE, A AIELLO, LM BURSELL, SE AF GOLDBERG, MF SHARUK, GS CLERMONT, AC KOPPLE, A AIELLO, LM BURSELL, SE TI THE ROLE OF ANTIHISTAMINE IN THE MODULATION OF RETINAL BLOOD-FLOW IN NONDIABETIC PATIENTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S104 EP S104 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500500 ER PT J AU GOSS, L PADILLA, T BHOL, K FOSTER, CS AHMED, AR AF GOSS, L PADILLA, T BHOL, K FOSTER, CS AHMED, AR TI ORAL PEMPHIGOID SERA RECOGNIZE DIFFERENT ANTIGENS THAN OCULAR CICATRICIAL PEMPHIGOID SERA IN AN IMMUNOBLOT ASSAY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1025 EP S1025 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504741 ER PT J AU GREGORY, J ELOVIC, A TALAMO, JH AF GREGORY, J ELOVIC, A TALAMO, JH TI EXPRESSION OF TGF-BETA-1 MESSENGER-RNA IN RABBIT CORNEAL EPITHELIUM AND STROMA AFTER EXCIMER PHOTOREFRACTIVE KERATECTOMY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH DENT,ORAL PATHOL LAB,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S178 EP S178 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500847 ER PT J AU HAIMOVICI, R CIULLA, TA MILLER, JW GEORGE, A HASAN, T SCHOMACKER, KT GRAGOUDAS, ES AF HAIMOVICI, R CIULLA, TA MILLER, JW GEORGE, A HASAN, T SCHOMACKER, KT GRAGOUDAS, ES TI ROSE-BENGAL, CAPSC, AND CHLORIN E6 FUNDUS ANGIOGRAPHY IN THE RABBIT EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S236 EP S236 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501072 ER PT J AU HAVRILIKOVA, K MELLOTT, M KAUFMAN, AH FOSTER, SC COLVIN, RB AF HAVRILIKOVA, K MELLOTT, M KAUFMAN, AH FOSTER, SC COLVIN, RB TI DIFFERENCE IN APPEARANCE OF FIBRONECTIN ISOFORMS AFTER ALKALI BURN AND KERATECTOMY IN RAT CORNEA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. UNIV CINCINNATI,CINCINNATI,OH 45221. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S567 EP S567 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502628 ER PT J AU HELENA, MC FILATOV, V JOHNSTON, WT LAMARCHE, K TALAMO, JH AF HELENA, MC FILATOV, V JOHNSTON, WT LAMARCHE, K TALAMO, JH TI EFFECTS OF 50-PERCENT ETHANOL VS MECHANICAL EPITHELIAL DEBRIDEMENT ON KERATOCYTE LOSS AND INFLAMMATORY RESPONSE AFTER EXCIMER PHOTOREFRACTIVE KERATECTOMY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S24 EP S24 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500104 ER PT J AU HU, LK KIM, RY GRAGOUDAS, ES YOUNG, LHY AF HU, LK KIM, RY GRAGOUDAS, ES YOUNG, LHY TI PERITUMOR TREATMENT APPROACH IN PHOTODYNAMIC THERAPY (PDT) FOR PIGMENTED CHOROIDAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S488 EP S488 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502251 ER PT J AU HUANG, SH HUANG, X PITTLER, SJ OLIVEIRA, L BERSON, EL DRYJA, TP AF HUANG, SH HUANG, X PITTLER, SJ OLIVEIRA, L BERSON, EL DRYJA, TP TI A MUTATION IN THE GENE ENCODING THE ALPHA-SUBUNIT OF ROD CGMP-PHOSPHODIESTERASE (PDEA) IN RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE & GBERMAN GUND LABS,BOSTON,MA 02114. UNIV SO ALABAMA,COLL MED,DEPT BIOCHEM,MOBILE,AL 36688. UNIV SO ALABAMA,COLL MED,DEPT OPHTHALMOL,MOBILE,AL 36688. UNIV SO ALABAMA,COLL MED,DEPT MOLEC BIOL,MOBILE,AL 36688. NR 0 TC 10 Z9 10 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S825 EP S825 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503805 ER PT J AU HUSAIN, D KRAMER, M MICHAUD, N MOULTON, R FLOTTE, T GRAGOUDAS, ES MILLER, JW AF HUSAIN, D KRAMER, M MICHAUD, N MOULTON, R FLOTTE, T GRAGOUDAS, ES MILLER, JW TI PHOTODYNAMIC THERAPY (PDT) OF EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION (CNV) USING BENZOPORPHYRIN DERIVATIVE (BPD-MA) - DYE DELIVERY AND TREATMENT PARAMETERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S225 EP S225 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501023 ER PT J AU IGARASHI, H XIONG, J XIONG, H LEE, TY NAKAMURA, J CHENG, HM AF IGARASHI, H XIONG, J XIONG, H LEE, TY NAKAMURA, J CHENG, HM TI METABOLIC CHANGES IN LENSES EXPOSED TO BASIC FIBROBLAST GROWTH-FACTOR (BFGF) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S258 EP S258 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501167 ER PT J AU JIN, J HETH, CA ROOF, DJ AF JIN, J HETH, CA ROOF, DJ TI P23H MUTANT HUMAN OPSIN IN TRANSGENIC MURINE RETINA TRUNCATION OF N-TERMINUS AND LACK OF GLYCOSYLATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S424 EP S424 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501940 ER PT J AU JOHNSON, SM CHENG, HM NETLAND, PA AF JOHNSON, SM CHENG, HM NETLAND, PA TI MAGNETIC-RESONANCE-IMAGING OF CYCLODIALYSIS CLEFTS IN RABBITS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S340 EP S340 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501588 ER PT J AU JOSEPH, RM LI, T AF JOSEPH, RM LI, T TI PHOTORECEPTOR CELL-DEATH IN THE RD MICE MAY BE MEDIATED THROUGH A BCL-2 INDEPENDENT PATHWAY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S424 EP S424 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501941 ER PT J AU KAISER, PK HENG, JE VORWERK, C DREYER, EB AF KAISER, PK HENG, JE VORWERK, C DREYER, EB TI ETHAMBUTOL MEDIATED OPTIC NEUROPATHY - A ROLE FOR ENDOGENOUS ZINC IN CONTROLLING NMDA TOXICITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S164 EP S164 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500797 ER PT J AU KARATZA, EC STINSON, WG MILLER, JW GRAGOUDAS, ES DELORI, FC AF KARATZA, EC STINSON, WG MILLER, JW GRAGOUDAS, ES DELORI, FC TI FLUORESCENCE CHARACTERISTICS OF DYES FOR EXPERIMENTAL ANGIOGRAPHIC STUDIES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S247 EP S247 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501122 ER PT J AU KAUFMAN, AH FOSTER, CS KAO, CWC KAO, WWY AF KAUFMAN, AH FOSTER, CS KAO, CWC KAO, WWY TI CONJUNCTIVAL OVERGROWTH IN A PATIENT WITH STEVENS-JOHNSON SYNDROME DOES NOT EXPRESS CORNEA-SPECIFIC KERATIN-12 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV CINCINNATI,DEPT OPHTHALMOL,CINCINNATI,OH 45221. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S399 EP S399 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501855 ER PT J AU KAYE, LD WALTON, DS WAND, M AF KAYE, LD WALTON, DS WAND, M TI MITOMYCIN-C TRABECULECTOMY FOR REFRACTORY PEDIATRIC GLAUCOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. UNIV CONNECTICUT,DEPT OPHTHALMOL,HARTFORD,CT 06112. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S87 EP S87 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500419 ER PT J AU KIM, RY HU, LK GRAGOUDAS, ES YOUNG, LHY AF KIM, RY HU, LK GRAGOUDAS, ES YOUNG, LHY TI PHOTODYNAMIC THERAPY OF PIGMENTED CHOROIDAL MELANOMAS OF TAU-3-MM THICKNESS WITH A LIPOSOMAL PREPARATION OF BENZOPORPHYRIN DERIVATIVE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S488 EP S488 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502250 ER PT J AU KING, GL NORTHRUP, JM AIELLO, LP TAKAGI, H AF KING, GL NORTHRUP, JM AIELLO, LP TAKAGI, H TI ISOLATION - PARTIAL SEQUENCE-ANALYSIS OF VASCULAR ENDOTHELIAL GROWTH-FACTOR REGULATED GENES IN RETINAL ENDOTHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BEETHAM EYE INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S870 EP S870 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503977 ER PT J AU KORNSTEIN, HS FILATOV, VV TALAMO, JH AF KORNSTEIN, HS FILATOV, VV TALAMO, JH TI THE INFLUENCE OF AGE ON ONE-YEAR RESULTS OF EXCIMER-LASER PHOTOREFRACTIVE KERATECTOMY FOR MODERATE MYOPIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S983 EP S983 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504539 ER PT J AU KRAMER, M KENNEY, AG DELORI, F CONNOLLY, EJ HUSAIN, D GRAGOUDAS, ES MILLER, JW AF KRAMER, M KENNEY, AG DELORI, F CONNOLLY, EJ HUSAIN, D GRAGOUDAS, ES MILLER, JW TI IMAGING OF EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION (CNV) USING LIPOSOMAL BENZOPORPHYRIN DERIVATIVE MONO-ACID (BPD-MA) ANGIOGRAPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. SCHEPENS EYE RES INST,BOSTON,MA. NR 0 TC 6 Z9 6 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S236 EP S236 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501075 ER PT J AU KRZYSTOLIK, MG SAMY, CN DAMICO, DJ MUKAI, S AF KRZYSTOLIK, MG SAMY, CN DAMICO, DJ MUKAI, S TI THE CLINICAL SPECTRUM OF DIFFUSE INFILTRATING RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S489 EP S489 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502253 ER PT J AU KUROKI, M BEEREPOOT, LV VOEST, EE ADAMIS, AP AF KUROKI, M BEEREPOOT, LV VOEST, EE ADAMIS, AP TI REGULATION OF VEGF MESSENGER-RNA EXPRESSION BY REACTIVE OXYGEN INTERMEDIATES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S895 EP S895 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504104 ER PT J AU KWON, YH PAWLYK, B SANDBERG, MA AF KWON, YH PAWLYK, B SANDBERG, MA TI INTRAVITREAL KYNURENIC ACID REVERSIBLY SUPPRESSES THE ERG SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S448 EP S448 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502054 ER PT J AU LANE, AM EGAN, KM GRAGOUDAS, ES AF LANE, AM EGAN, KM GRAGOUDAS, ES TI SURVIVAL RATES AFTER IRRADIATION OF EYES WITH MALIGNANT-MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S487 EP S487 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502244 ER PT J AU LEGMANN, AS CHOI, JC MASSRY, GG HOLDS, JB RUBIN, PA SHORE, JW AF LEGMANN, AS CHOI, JC MASSRY, GG HOLDS, JB RUBIN, PA SHORE, JW TI CORRECTION OF BLEPHAROPTOSIS WITHOUT ALTERATION OF THE INTERPALPEBRAL HEIGHT IN PATIENTS WITH POOR CORNEAL PROTECTIVE MECHANISMS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. ST LOUIS UNIV,ST LOUIS,MO 63103. OPHTHALM CONSULTANTS BOSTON,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S504 EP S504 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502332 ER PT J AU LIMSTROM, SA KRAMER, TR SNYDER, RW TALAMO, J JONES, H YARBOROUGH, JM MARCELLINO, G NOECKER, RJ AF LIMSTROM, SA KRAMER, TR SNYDER, RW TALAMO, J JONES, H YARBOROUGH, JM MARCELLINO, G NOECKER, RJ TI HISTOPATHOLOGY OF ERBIUM-YAG LASER-ABLATION OF THE CORNEA AND THE EFFECT OF VARIABLE HYDRATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV ARIZONA,DEPT OPHTHALMOL,TUCSON,AZ 85721. UNIV ARIZONA,DEPT PATHOL,TUCSON,AZ 85721. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. COHERENT LASERS INC,TUCSON,AZ. COHERENT INC,PALO ALTO,CA. NEW ENGLAND EYE CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S987 EP S987 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504552 ER PT J AU LJUBINOV, AV BURGESON, RE BUTKOWSKI, RJ HUANG, Z MAGUEN, E NESBURN, AB KENNEY, MC AF LJUBINOV, AV BURGESON, RE BUTKOWSKI, RJ HUANG, Z MAGUEN, E NESBURN, AB KENNEY, MC TI EXTRACELLULAR-MATRIX ALTERATIONS IN BULLOUS KERATOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASS GEN HOSP,BOSTON,MA. INCSTAR CORP,MINNEAPOLIS,MN. CEDARS SINAI MED CTR,OPHTHALMOL RES LABS,LOS ANGELES,CA 90048. RI Ljubimov, Alexander/E-5883-2013 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S828 EP S828 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503815 ER PT J AU LUCARELLI, MJ VITALE, AT RODRIGUEZ, A FOSTER, CS AF LUCARELLI, MJ VITALE, AT RODRIGUEZ, A FOSTER, CS TI NEOPLASTIC MASQUERADE SYNDROMES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,IMMUNOL SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S785 EP S785 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503622 ER PT J AU MAAS, R GLASER, T EPSTEIN, J CAI, J JEPEAL, L WALTON, D AF MAAS, R GLASER, T EPSTEIN, J CAI, J JEPEAL, L WALTON, D TI FUNCTION OF PAX6 IN HUMAN OCULAR DISORDERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S213 EP S213 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500973 ER PT J AU MERAYOLLOVES, J ZHAO, T DUTT, JE FOSTER, CS AF MERAYOLLOVES, J ZHAO, T DUTT, JE FOSTER, CS TI IN-VIVO DEPLETION OF V-BETA-8+ AND V-BETA-3+ T-CELLS PROTECTS MICE AGAINST NECROTIZING HERPES-SIMPLEX KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S427 EP S427 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501955 ER PT J AU MICHAUD, NA MILLER, JW HUSAIN, D KRAMER, M FLOTTE, TJ AF MICHAUD, NA MILLER, JW HUSAIN, D KRAMER, M FLOTTE, TJ TI EPITHELIAL ACINAR STRUCTURES IN EXPERIMENTAL CHOROIDAL NEOVASCULAR MEMBRANES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S552 EP S552 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502560 ER PT J AU MILLER, JW SHIMA, DT TOLENTINO, M GRAGOUDAS, ES FERRERA, N CONNOLLY, EJ FOLKMAN, J DAMORE, PA ADAMS, AP AF MILLER, JW SHIMA, DT TOLENTINO, M GRAGOUDAS, ES FERRERA, N CONNOLLY, EJ FOLKMAN, J DAMORE, PA ADAMS, AP TI INHIBITION OF VEGF PREVENTS OCULAR NEOVASCULARIZATION IN A MONKEY MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GENENTECH INC,S SAN FRANCISCO,CA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S401 EP S401 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501861 ER PT J AU MILLER, S RIZZO, JF WYATT, JL AF MILLER, S RIZZO, JF WYATT, JL TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - LONG-TERM BIOCOMPATIBILITY OF MATERIALS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S746 EP S746 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503441 ER PT J AU MONTENEGRO, MH MURCIA, A KASAHARA, N SIBAYAN, SB SIMMONS, RB SMITH, TJ SIMMONS, RJ AF MONTENEGRO, MH MURCIA, A KASAHARA, N SIBAYAN, SB SIMMONS, RB SMITH, TJ SIMMONS, RJ TI HIGH-DOSE INTRAOPERATIVE MITOMYCIN-C TRABECULECTOMY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,NEW ENGLAND EYE RES FDN,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S86 EP S86 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500418 ER PT J AU MUKAI, S MUNZENRIDER, JE HUG, EB GRAGOUJDAS, ES AF MUKAI, S MUNZENRIDER, JE HUG, EB GRAGOUJDAS, ES TI PROTON-BEAM THERAPY OF BILATERAL RETINOBLASTOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S488 EP S488 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502252 ER PT J AU NATHANSON, JA SCANLON, C SCAVONE, C AF NATHANSON, JA SCANLON, C SCAVONE, C TI A NEW MECHANISM OF ACTION FOR NITRIC-OXIDE AND ATRIAL-NATRIURETIC-FACTOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROPHARAMCOL RES LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S823 EP S823 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503801 ER PT J AU NETLAND, PA VIDAL, I RASKY, A HERNANDEZ, MR AF NETLAND, PA VIDAL, I RASKY, A HERNANDEZ, MR TI ELASTOSIS OF THE LAMINA-CRIBROSA IN GLAUCOMATOUS OPTIC NEUROPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SCHEPENS EYE INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S607 EP S607 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502803 ER PT J AU NGUYEN, QD KAISER, PK DREYER, EB AF NGUYEN, QD KAISER, PK DREYER, EB TI THE BUPHTHALMIC GLAUCOMATOUS RABBIT EYE - AMINO-ACID ANALYSES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S968 EP S968 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504458 ER PT J AU NICAEUS, TE TOLENTINO, M ADAMIS, AP RUBIN, AD AF NICAEUS, TE TOLENTINO, M ADAMIS, AP RUBIN, AD TI SUCRALFATE AND BASIC FIBROBLAST GROWTH-FACTOR PROMOTE ENDOTHELIAL-CELL PROLIFERATION AROUND POROUS ORBITAL IMPLANTS IN-VITRO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S500 EP S500 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502311 ER PT J AU NOECKER, RJ KRAMER, TR SNYDER, RW YARBOROUGH, JM MARCELLINO, G TALAMO, J JONES, H AF NOECKER, RJ KRAMER, TR SNYDER, RW YARBOROUGH, JM MARCELLINO, G TALAMO, J JONES, H TI LONG-TERM HEALING OF THE CENTRAL CORNEA AFTER PHOTOREFRACTIVE KERATECTOMY USING AN ERBIUM-YAG LASER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. UNIV ARIZONA,DEPT OPHTHALMOL,TUCSON,AZ 85721. COHERENT LASERS INC,TUCSON,AZ. COHERENT INC,PALO ALTO,CA. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S986 EP S986 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504551 ER PT J AU PARMINDER, AH MURAKAMI, A INANA, G BERSON, EL DRYJA, TP AF PARMINDER, AH MURAKAMI, A INANA, G BERSON, EL DRYJA, TP TI SCREEN FOR MUTATIONS IN THE HUMAN RECOVERIN GENE IN PATIENTS WITH RETINITIS-PIGMENTOSA AND ALLIED DISEASES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB & BERMAN GUND,BOSTON,MA 02114. UNIV MIAMI,SCH MED,BASCOM PALMER EYE INST,MIAMI,FL 33152. NR 2 TC 0 Z9 0 U1 1 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S893 EP S893 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504091 ER PT J AU PAWLYK, BS SANDBERG, MA BERSON, EL AF PAWLYK, BS SANDBERG, MA BERSON, EL TI ISOLATION OF FOCAL ROD ELECTRORETINOGRAMS FROM THE DARK-ADAPTED HUMAN EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S446 EP S446 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502043 ER PT J AU PENG, YW FINN, JT LI, J DRYJA, TP MCGEE, TL HAHN, LB BERSON, EL YAU, KW AF PENG, YW FINN, JT LI, J DRYJA, TP MCGEE, TL HAHN, LB BERSON, EL YAU, KW TI PUTATIVE FUNCTIONAL DEFECTS IN ROD CGMP-GATED CHANNEL MUTANTS IMPLICATED IN RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB & HOWE LAB,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,SCH MED,DEPT OPHTHALMOL,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,SCH MED,HHMI,BALTIMORE,MD 21205. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S919 EP S919 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504220 ER PT J AU PRALEA, AM PRALEA, C STAWSKI, S PAGLINAUAN, C HAINES, JL WIGGS, JL AF PRALEA, AM PRALEA, C STAWSKI, S PAGLINAUAN, C HAINES, JL WIGGS, JL TI GENETIC-LINKAGE ANALYSIS OF THE PIGMENT DISPERSION SYNDROME SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S554 EP S554 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502565 ER PT J AU RAPUANO, CJ DANA, MR GOMES, JAP LAIBSON, PR AF RAPUANO, CJ DANA, MR GOMES, JAP LAIBSON, PR TI ASTIGMATIC EFFECT OF GRAFT ALIGNMENT IN PENETRATING KERATOPLASTY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 WILLS EYE HOSP & RES INST,PHILADELPHIA,PA 19107. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S653 EP S653 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502977 ER PT J AU REMULLA, JFC SANDBERG, MA AF REMULLA, JFC SANDBERG, MA TI SENSITIVITY OF FULL-FIELD CONE ERG IMPLICIT TIME TO REDUCTIONS IN RETINAL ILLUMINATION - DEPENDENCE ON FLICKER FREQUENCY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S447 EP S447 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502044 ER PT J AU RHO, DS CLRMONT, AC TAKAGI, C BURSELL, SE AF RHO, DS CLRMONT, AC TAKAGI, C BURSELL, SE TI INDOMETHACIN INHIBITION OF VASODILATORY PROSTAGLANDINS ENHANCES RETINAL CIRCULATORY RESPONSE TO ANGIOTENSIN-II IN ONE WEEK DIABETIC RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1041 EP S1041 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504809 ER PT J AU RIZZO, JF MILLER, S WYATT, JL EDELL, D AF RIZZO, JF MILLER, S WYATT, JL EDELL, D TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - REPRODUCIBILITY OF ELECTRICALLY-EVOKED VISUAL CORTICAL RESPONSES IN RABBITS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MIT,LINCOLN LAB,LEXINGTON,MA 02173. MIT,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 2 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S927 EP S927 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504255 ER PT J AU ROSENFELD, PJ SPECHT, A JOHNS, DR SMITH, LEH AF ROSENFELD, PJ SPECHT, A JOHNS, DR SMITH, LEH TI PROGRESSIVE EXTERNAL OPHTHALMOPLEGIA IN A 5-YEAR-OLD BOY WITH A BALANCED CHROMOSOMAL TRANSLOCATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S954 EP S954 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504386 ER PT J AU ROWE, SG CHATURVEDI, N DREYER, EB AF ROWE, SG CHATURVEDI, N DREYER, EB TI INCREASED PRESSURE IMPAIRS THE ABILITY OF MULLER CELLS TO DETOXIFY GLUTAMATE IN-VITRO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 2 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S965 EP S965 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504439 ER PT J AU SADOW, PM WESTMAYS, JA GUPTAL, R ZIESKE, J WILLIAMS, T FINI, ME AF SADOW, PM WESTMAYS, JA GUPTAL, R ZIESKE, J WILLIAMS, T FINI, ME TI REGULATION OF GELATINASE IN CORNEAL KERATINOCYTES BY AP-2 TRANSCRIPTION FACTOR SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. SCHEPENS EYE RES INST,CAMBRIDGE,MA. YALE UNIV,DEPT BIOL,NEW HAVEN,CT 06520. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S28 EP S28 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500129 ER PT J AU SAMY, CN GONZALEZ, VH MUKAI, S AF SAMY, CN GONZALEZ, VH MUKAI, S TI BENZOPORPHYRIN DERIVATIVE (BPD) ANGIOGRAPHY OF INTRAOCULAR RETINOBLASTOMA IN THE RABBIT MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S489 EP S489 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502254 ER PT J AU SANDBERG, MA WEIGELDIFRANCO, C ROSNER, B BERSON, EL AF SANDBERG, MA WEIGELDIFRANCO, C ROSNER, B BERSON, EL TI THE RELATIONSHIP BETWEEN VISUAL-FIELD SIZE AND ELECTRORETINOGRAM AMPLITUDE IN RETINITIS-PIGMENTOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S875 EP S875 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503996 ER PT J AU SIBAYAN, SAB SMITH, TJ KASAHARA, N MONTENEGRO, MH AF SIBAYAN, SAB SMITH, TJ KASAHARA, N MONTENEGRO, MH TI CLINICAL-EVALUATION OF THE TOMEY PROTON TONOMETER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SCHEPENS EYE RES INST,NEW ENGLAND GLAUCOMA RES FDN,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S82 EP S82 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500396 ER PT J AU SIEGEL, M YOUNG, JA TALAMO, JH AF SIEGEL, M YOUNG, JA TALAMO, JH TI CONTOUR RESOLUTION OF THE EYESYS CORNEAL ANALYSIS SYSTEM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 NYU,DEPT OPHTHALMOL,NEW YORK,NY 10003. MASSACHUSETTS EYE & EAR INFIRM,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S304 EP S304 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501406 ER PT J AU SIEGNER, SW NETLAND, PA KARDITSAS, SD ERICKSON, KA AF SIEGNER, SW NETLAND, PA KARDITSAS, SD ERICKSON, KA TI THE EFFECT OF CALCIUM-CHANNEL BLOCKERS ALONE AND IN COMBINATION WITH OTHER ANTIGLAUCOMA MEDICATIONS ON INTRAOCULAR-PRESSURE IN THE PRIMATE EYE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S733 EP S733 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503375 ER PT J AU SMITH, JA LATTMAN, J PINEDA, R LUCARELLI, MJ RUBIN, PAD AF SMITH, JA LATTMAN, J PINEDA, R LUCARELLI, MJ RUBIN, PAD TI RETROSPECTIVE EVALUATION OF OCULAR AND ORBITAL TRAUMA VIA ORBITAL COMPUTED-TOMOGRAPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S507 EP S507 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502344 ER PT J AU SMITH, LEH PIERCE, EA AIELLO, LP FOLEY, ED SULLIVAN, R ROOK, SL ROBINSON, GS AF SMITH, LEH PIERCE, EA AIELLO, LP FOLEY, ED SULLIVAN, R ROOK, SL ROBINSON, GS TI INHIBITION OF PROLIFERATIVE RETINOPATHY USING ANTISENSE PHOSPHOROTHIOATE OLIGONUCLEOTIDES AGAINST VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF/VPF) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HYBRIDON INC,WORCESTER,MA. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S871 EP S871 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503982 ER PT J AU SOHEILIAN, M KARIMIAN, F JAVADI, MA SAJJADI, H AHMADIEH, H AZARMINA, M VALAEE, N AF SOHEILIAN, M KARIMIAN, F JAVADI, MA SAJJADI, H AHMADIEH, H AZARMINA, M VALAEE, N TI CATARACT-EXTRACTION AND POSTERIOR CHAMBER INTRAOCULAR-LENS IMPLANTATION IN FUCHS HETEROCHROMIC IRIDOCYCLITIS (FHIC) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 SHAHID BEHESTI UNIV MED SCI,DEPT OPHTHALMOL,TEHRAN,IRAN. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S781 EP S781 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503600 ER PT J AU STINSON, WG KARATZA, EC GRAGOUDAS, ES KENNEY, AG TOLENTINO, MJ MILLER, JW AF STINSON, WG KARATZA, EC GRAGOUDAS, ES KENNEY, AG TOLENTINO, MJ MILLER, JW TI DIGITAL QUANTIFICATION OF EXPERIMENTAL OCULAR NEOVASCULARIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S31 EP S31 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500142 ER PT J AU STRISSEL, KJ FRANKS, KL FINI, ME AF STRISSEL, KJ FRANKS, KL FINI, ME TI MECHANISMS DETERMINING THE BALANCE OF STIMULATORY AND INHIBITORY CYTOKINES CONTROLLING STROMAL REMODELING SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S866 EP S866 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503958 ER PT J AU TAKAGI, C KING, GL CLERMONT, AC TAKAGI, H BURSELL, SE AF TAKAGI, C KING, GL CLERMONT, AC TAKAGI, H BURSELL, SE TI ENDOTHELIN-A (ETA) RECEPTOR MEDIATION IS INVOLVED IN THE REGULATION OF NORMAL RETINAL CIRCULATION AND IN HYPEROXIC RETINAL AUTOREGULATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S134 EP S134 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500649 ER PT J AU TAKAGI, H KING, GL FERRARA, N AIELLO, LP AF TAKAGI, H KING, GL FERRARA, N AIELLO, LP TI ADENOSINE IS A POTENTIAL MEDIATOR OF THE HYPOXIA-INDUCED GENE-REGULATION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) AND ITS RECEPTOR (KDR) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 GENENTECH INC,S SAN FRANCISCO,CA. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S870 EP S870 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503975 ER PT J AU TOLENTINO, MJ MILLER, JW GRAGOUDAS, ES MOULTON, R CHATZISTEFANOU, K FLYNN, E FERRARA, N ADAMIS, AP AF TOLENTINO, MJ MILLER, JW GRAGOUDAS, ES MOULTON, R CHATZISTEFANOU, K FLYNN, E FERRARA, N ADAMIS, AP TI VASCULAR ENDOTHELIAL GROWTH-FACTOR IS SUFFICIENT TO PRODUCED OCULAR NEOVASCULARIZATION IN A NONHUMAN PRIMATE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. GENENTECH INC,SAN FRANCISCO,CA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S402 EP S402 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501866 ER PT J AU TOU, TT CHOI, JC PARTINGTON, MT YUHAN, KR WHITAKER, LA SHORE, JW AF TOU, TT CHOI, JC PARTINGTON, MT YUHAN, KR WHITAKER, LA SHORE, JW TI OPHTHALMIC FINDINGS ASSOCIATED WITH UNILATERAL NON-COMPENSATIONAL PLAGIOCEPHALY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. OPHTHALM CONSULTANTS BOSTON,BOSTON,MA. UNIV PENN,CHILDRENS HOSP,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S72 EP S72 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500347 ER PT J AU TUGALTUTKUN, I URGANCIOGLU, M FOSTER, CS AF TUGALTUTKUN, I URGANCIOGLU, M FOSTER, CS TI IMMUNOPATHOLOGIC STUDY OF THE CONJUNCTIVA IN PATIENTS WITH BEHCETS-DISEASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 ISTANBUL FAC MED,DEPT OPHTHALMOL,ISTANBUL,TURKEY. MASSACHUSETTS EYE & EAR INFIRM,HKILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1025 EP S1025 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504740 ER PT J AU VIDAURRILEAL, J CANTUCHARLES, C TALAMO, JH AF VIDAURRILEAL, J CANTUCHARLES, C TALAMO, JH TI EXCIMER PRK FOR MYOPIA AND ASTIGMATISM WITH THE COHERENT-SCHWIND KERATOM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HOSP SAN JOSE,MONTERREY,NUEVO LEON,MEXICO. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,CORNEA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S190 EP S190 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500889 ER PT J AU VOLPE, NJ RIZZO, JF LESSELL, S AF VOLPE, NJ RIZZO, JF LESSELL, S TI CLINICAL FINDINGS OF 20 PATIENTS WITH ACUTE IDIOPATHIC BLINDSPOT ENLARGEMENT SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV PENN,SCHEIE EYE INST,PHILADELPHIA,PA 19104. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S676 EP S676 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503089 ER PT J AU VORWERK, CK MOSCARITOLA, K DREYER, EB AF VORWERK, CK MOSCARITOLA, K DREYER, EB TI NMDA MEDIATED RETINAL GANGLION-CELL TOXICITY AS A FUNCTION OF CALCIUM AND MAGNESIUM CONCENTRATIONS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S935 EP S935 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504295 ER PT J AU WARNER, MA JAHRLING, KV RUBIN, PAD AF WARNER, MA JAHRLING, KV RUBIN, PAD TI ACQUIRED ANOPHTHALMIA - AN OUTCOMES ANALYSIS OF ENUCLEATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S76 EP S76 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500362 ER PT J AU WESTMAYS, JA SADOW, PM STRISSEL, KJ CINTRON, C FINI, ME AF WESTMAYS, JA SADOW, PM STRISSEL, KJ CINTRON, C FINI, ME TI INTERLEUKIN-1-ALPHA MEDIATES COLLAGENASE SYNTHESIS IN PASSAGED CORNEAL FIBROBLASTS AND FIBROBLASTS ISOLATED FROM PENETRATING KERATECTOMY WOUNDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. SCHEPENS EYE RES INST,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S866 EP S866 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91503957 ER PT J AU WIGGS, JL HAINES, JL PAGLINAUAN, C STAWSKI, S PRALEA, AM PRALEA, C AF WIGGS, JL HAINES, JL PAGLINAUAN, C STAWSKI, S PRALEA, AM PRALEA, C TI GENETIC-ANALYSIS OF AUTOSOMAL-DOMINANT JUVENILE GLAUCOMA - EVIDENCE FOR GENETIC-LOCUS HETEROGENEITY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1034 EP S1034 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504782 ER PT J AU WOLF, TC ASSIL, KK VERITY, S TALAMO, JH RAPOZA, PA CHAYET, A LANE, S KENYON, KR AF WOLF, TC ASSIL, KK VERITY, S TALAMO, JH RAPOZA, PA CHAYET, A LANE, S KENYON, KR TI COMBINED TECHNIQUE (GENESIS) RADIAL KERATOTOMY (RK) - A PROSPECTIVE, MULTICENTER STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MCGEE EYE INST,OKLAHOMA CITY,OK. ANHEUSER BUSCH INC,ST LOUIS,MO 63118. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. BAJA CALIF EYE INST,TIJUANA,MEXICO. UNIV MINNESOTA,STILLWATER,OK. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S434 EP S434 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501984 ER PT J AU WYATT, J MANN, J EDELL, D RAFFEL, J RIZZO, JF AF WYATT, J MANN, J EDELL, D RAFFEL, J RIZZO, JF TI DEVELOPMENT OF A SILICON RETINAL IMPLANT - DEMONSTRATION OF MICROELECTRONIC SYSTEM FOR OPTICAL-TRANSMISSION OF SIGNAL AND POWER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MIT,LINCOLN LAB,LEXINGTON,MA 02173. MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S249 EP S249 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501129 ER PT J AU XIA, P IWAMOTO, MA KING, GL AF XIA, P IWAMOTO, MA KING, GL TI HIGH-GLUCOSE REGULATES NA,K-ATPASE THROUGH THE ACTIVATION OF PKC-DEPENDENT PHOSPHOLIPASE-A2 IN RETINAL ENDOTHELIAL-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. RI Xia, Pu/G-3090-2010 OI Xia, Pu/0000-0003-4705-8878 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1066 EP S1066 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504896 ER PT J AU YOO, SH DREYER, EB AF YOO, SH DREYER, EB TI GLIAL FIBRILLARY ACIDIC PROTEIN REACTIVITY IN GLAUCOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S330 EP S330 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501541 ER PT J AU YOUNG, JA TALAMO, JH CHUNG, W AF YOUNG, JA TALAMO, JH CHUNG, W TI A NEW PARAMETER FOR CALCULATION OF EFFECTIVE KERATOMETRY AFTER KERATOREFRACTIVE SURGERY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S307 EP S307 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91501427 ER PT J AU YOUNG, LHY KIM, RY KENNEY, AG HU, LK GRAGOUDAS, ES AF YOUNG, LHY KIM, RY KENNEY, AG HU, LK GRAGOUDAS, ES TI BIODISTRIBUTION OF PHOTOSENSITIZER BENZOPORPHYRIN DERIVATIVE (BPD) WITHIN EXPERIMENTAL CHOROIDAL MELANOMAS USING ANGIOGRAPHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S488 EP S488 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91502248 ER PT J AU ZHAO, TZ MERAYOLLOVES, J ELOVIC, A DUTT, JE WONG, DTW FOSTER, CS AF ZHAO, TZ MERAYOLLOVES, J ELOVIC, A DUTT, JE WONG, DTW FOSTER, CS TI EXPRESSION OF TRANSFORMING GROWTH FACTORS-ALPHA (TGF-ALPHA) AND BETA-1 (TGF-BETA-1) BY EOSINOPHILS IN MURINE ALLERGIC CONJUNCTIVA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH ORAL PATHOL,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S1024 EP S1024 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91504737 ER PT J AU ZURAKOWSKI, D CHATURVEDI, N NICHOLS, DP LIPTON, SA DREYER, EB AF ZURAKOWSKI, D CHATURVEDI, N NICHOLS, DP LIPTON, SA DREYER, EB TI NITRATES SLOW PROGRESSION OF GLAUCOMATOUS OPTIC NEUROPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1995 VL 36 IS 4 BP S219 EP S219 PG 1 WC Ophthalmology SC Ophthalmology GA QM915 UT WOS:A1995QM91500998 ER PT J AU ZHANG, W FRANKEL, WL ADAMSON, WT ROTH, JA MANTELL, MP BAIN, A ZIEGLER, TR SMITH, RJ ROMBEAU, JL AF ZHANG, W FRANKEL, WL ADAMSON, WT ROTH, JA MANTELL, MP BAIN, A ZIEGLER, TR SMITH, RJ ROMBEAU, JL TI INSULIN-LIKE GROWTH-FACTOR-I IMPROVES MUCOSAL STRUCTURE AND FUNCTION IN TRANSPLANTED RAT SMALL-INTESTINE SO TRANSPLANTATION LA English DT Article ID SMALL-BOWEL TRANSPLANTATION; PROMOTES BACTERIAL TRANSLOCATION; AMINO-ACID-METABOLISM; IGF-I; GASTROINTESTINAL-TRACT; RECEPTORS; GLUCOSE; INJURY; GUT; LOCALIZATION AB The transplanted small intestine develops significant mucosal atrophy, impaired nutrient and water absorption, and increased bacterial translocation to mesenteric lymph nodes in rats maintained on elemental diets or total parenteral nutrition, This study determined the effects of administration of an peptide growth factor (insulin-like growth factor-I[IGF-I]) on the mucosal structure and barrier function of rat small bowel isografts, Thirty-six adult Lewis rats underwent either resection of the distal 60% of the small bowel and proximal colon followed by a 40-cm orthotopic jejunal isograft or proximal small bowel transection and distal small bowel resection to leave an analogous length of small intestine in control animals, Ah rats received an isocaloric, isonitrogenous, polymeric diet (200 kcal/kg/day, 2 gN/kg/day) by gastrostomy and were infused with either IGF-I (2.4 mg/kg/day) or vehicle by osmotic pumps subcutaneously. After 10 days of treatment, jejunal crypt cell production, mucosal morphometric indices, glucose and water absorption, body weight, and bacterial translocation to mesenteric lymph nodes (MLN) were measured. Jejunal mRNA content for IGF-I, IGF-I receptor, and IGF-binding proteins 3 and 4 (IGFBP-3,4) were determined by Northern blotting. Crypt cell production, villus height, crypt depth, and villus surface area were significantly increased in control and transplanted jejunum of rats infused with IGF-I when compared to animals given vehicle alone. Additionally, jejunal glucose absorption and water absorption were significantly improved in both IGF-I groups when compared with their respective vehicle controls. IGF-I infusion increased body weight in transplanted and control animals and markedly reduced bacterial translocation to MLN after small bowel transplantation. Jejunal levels of IGF-I mRNA were significantly increased in transplanted animals when compared to transected controls, IGF-I treatment significantly increased IGFBP-3 tissue mRNA levels in both transected and transplanted animals. These results demonstrate that IGF-I administration, after small bowel transplantation, improves mucosal structure and absorptive function and reduces bacterial translocation to MLN. IGF-I may have important effects in transplanted small bowel both as an endogenous and administered growth factor. C1 HOSP UNIV PENN,DEPT SURG,PHILADELPHIA,PA 19104. BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. NR 50 TC 52 Z9 56 U1 0 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 15 PY 1995 VL 59 IS 5 BP 755 EP 761 DI 10.1097/00007890-199503150-00020 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA QM656 UT WOS:A1995QM65600020 PM 7533956 ER PT J AU GIANELLO, PR FISHBEIN, JM ROSENGARD, BR LORF, T VITIELLO, DM ARN, JS SACHS, DH AF GIANELLO, PR FISHBEIN, JM ROSENGARD, BR LORF, T VITIELLO, DM ARN, JS SACHS, DH TI TOLERANCE TO CLASS I-DISPARATE RENAL-ALLOGRAFTS IN MINIATURE SWINE - MAINTENANCE OF TOLERANCE DESPITE INDUCTION OF SPECIFIC ANTIDONOR CTL RESPONSES SO TRANSPLANTATION LA English DT Article ID LYMPHOCYTES-T; TRANSPLANTATION; CYCLOSPORINE; REJECTION; INVIVO; SURVIVAL; ANTIGEN; RAT AB Miniature swine that become tolerant to renal allografts across an MHC class I barrier following a short course of cyclosporine are unresponsive to donor class I antigens in cell-mediated lymphocytotoxicity. However, skin grafts bearing donor class I plus third-party class II antigens are promptly rejected, and the animals then develop marked cell-mediated lymphocytotoxic reactivity to donor class I antigens in vitro, but do not reject the kidney transplants. We show here that CTL generation is directed toward the same donor class I antigens as are expressed by the kidney donor, and is not the result of recognition in vitro of the tolerated class I antigen plus peptides of minor antigens shared between the skin graft donor and the stimulator/target cells. We also show that detection by CTLs of peptides expressed by skin but not by kidney is also not a sufficient explanation of the results, since the survival of skin grafts from the kidney donor is also prolonged, even after precursor CTL can be detected in vitro. The data are most consistent with suppression in vivo in tolerant animals of the helper pathways necessary for activation of precursor CTLs. Differences in patterns of cytokine expression by graft infiltrating cells may provide a mechanism for local suppression of help in this model. Finally, we have examined antibody production after sensitizing by skin grafts in long-term tolerant animals and have found that anti-donor class I antibodies are not produced, even though the same animals produce both anti-class II and anti-third-party class I antibodies. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NHLBI NIH HHS [HL18646]; NIAID NIH HHS [AI31046] NR 26 TC 29 Z9 29 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD MAR 15 PY 1995 VL 59 IS 5 BP 772 EP 777 DI 10.1097/00007890-199503150-00023 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA QM656 UT WOS:A1995QM65600023 PM 7886806 ER PT J AU MUNROE, DJ LOEBBERT, R BRIC, E WHITTON, T PRAWITT, D VU, D BUCKLER, A WINTERPACHT, A ZABEL, B HOUSMAN, DE AF MUNROE, DJ LOEBBERT, R BRIC, E WHITTON, T PRAWITT, D VU, D BUCKLER, A WINTERPACHT, A ZABEL, B HOUSMAN, DE TI SYSTEMATIC SCREENING OF AN ARRAYED CDNA LIBRARY BY PCR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID EXPRESSED SEQUENCE TAGS; EXON AMPLIFICATION; GENE; CANDIDATE; DNA; HYBRIDIZATION; SELECTION; GENOME; MAP AB We have developed a PCR-based method for rapid and effective screening of arrayed cDNA libraries. This strategy directly addresses the limitations of conventional hybridization-based schemes and provides a more rapid, cost-effective, and sensitive method compatible with large-scale and routine cDNA clone recovery. To prepare arrayed libraries, 1-2 x 10(6) cDNA clones were propagated as individual plaques on solid medium in 24-well culture dishes at approximate to 250 plaque-forming units per well. Phage suspensions were prepared from each well and transferred to a 96-well format. To screen the library, pools were generated that correspond to each individual 96-well plate and to each row acid column within ''blocks'' of sis plates each. Library screening for specific cDNA clones was conducted in a systematic and hierarchical fashion beginning with the plate pools. Next, the row/column pools corresponding to each positive plate pool were screened. Finally, isolated clones from within each positive well were identified by hybridization. We have applied this approach to the screening of an arrayed human brain cDNA library resulting in the recovery of cDNAs corresponding to >25 genes and expressed sequence tags. C1 UNIV MAINZ,CHILDRENS HOSP,D-55101 MAINZ,GERMANY. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02114. RP MUNROE, DJ (reprint author), MIT,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139, USA. FU NHGRI NIH HHS [5-R01-HG00299-15]; NHLBI NIH HHS [5-PO1-HL41484-06] NR 32 TC 45 Z9 51 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 MAR 14 PY 1995 VL 92 IS 6 BP 2209 EP 2213 DI 10.1073/pnas.92.6.2209 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QM408 UT WOS:A1995QM40800087 PM 7892249 ER PT J AU VIDARD, L COLARUSSO, LJ BENACERRAF, B AF VIDARD, L COLARUSSO, LJ BENACERRAF, B TI SPECIFIC T-CELL TOLERANCE MAY REFLECT SELECTIVE ACTIVATION OF LYMPHOKINE SYNTHESIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID STIMULATORY FACTOR-I; INTERFERON-GAMMA; PROTECTIVE IMMUNITY; CYTOKINE PRODUCTION; DOWN-REGULATION; LYMPHOCYTES-T; ANTIGEN; SUBSETS; TH1; INTERLEUKIN-4 AB Selective T-cell unresponsiveness, as measured by interleukin 2, (IL-2) synthesis upon challenge with antigen, was induced in SJL mice by ovalbumin (OVA) in incomplete or complete Freund's adjuvant administered i.p. or s.c. Ten days later, the mice were given booster injections of 100 mu g of OVA/complete Freund's adjuvant. On day 20, lymph node and spleen cells were challenged in vitro with serial dilutions of OVA. There was an antigen-specific dose-dependent down, regulation of IL-2 production and T-cell proliferation in lymph node T cells. Concomitantly, 100 mu g of OVA up regulated IL-4 and, to a lesser extent, interferon gamma (IFN-gamma) production, particularly by spleen T cells. Altogether, these data indicate that the drop of IL-2 production and T cell proliferation, as well as the up regulation of IL-4 and IFN-gamma production, are complex manifestations of an evolving T-cell response. The maturation of the T-cell response leads to the production of different patterns of lymphokines, which may be significantly affected, as desired, by dosage, timing, and route of immunization, as well as by the choice of adjuvants. RP VIDARD, L (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 46967] NR 30 TC 29 Z9 29 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 MAR 14 PY 1995 VL 92 IS 6 BP 2259 EP 2262 DI 10.1073/pnas.92.6.2259 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QM408 UT WOS:A1995QM40800097 PM 7892258 ER PT J AU BROWN, RH AF BROWN, RH TI AMYOTROPHIC-LATERAL-SCLEROSIS - RECENT INSIGHTS FROM GENETICS AND TRANSGENIC MICE SO CELL LA English DT Review ID MITOCHONDRIAL ENERGY-METABOLISM; CU/ZN SUPEROXIDE-DISMUTASE; MOTOR-NEURON DISEASE; NITRIC-OXIDE; BRAIN; CHROMOSOME-21; PATHOLOGY; GLUTAMATE; MUTATIONS; DEFECTS RP BROWN, RH (reprint author), MASSACHUSETTS GEN HOSP,NEUROMUSC RES NEUROL SERV,CECIL B DAY LAB,BOSTON,MA 02114, USA. NR 44 TC 316 Z9 316 U1 1 U2 8 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 10 PY 1995 VL 80 IS 5 BP 687 EP 692 DI 10.1016/0092-8674(95)90346-1 PG 6 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM399 UT WOS:A1995QM39900004 PM 7889564 ER PT J AU BLUNT, T FINNIE, NJ TACCIOLI, GE SMITH, GCM DEMENGEOT, J GOTTLIEB, TM MIZUTA, R VARGHESE, AJ ALT, FW JEGGO, PA JACKSON, SP AF BLUNT, T FINNIE, NJ TACCIOLI, GE SMITH, GCM DEMENGEOT, J GOTTLIEB, TM MIZUTA, R VARGHESE, AJ ALT, FW JEGGO, PA JACKSON, SP TI DEFECTIVE DNA-DEPENDENT PROTEIN-KINASE ACTIVITY IS LINKED TO V(D)J RECOMBINATION AND DNA-REPAIR DEFECTS ASSOCIATED WITH THE MURINE SCID MUTATION SO CELL LA English DT Article ID STRAND BREAK REPAIR; COMBINED IMMUNE-DEFICIENCY; RAY SENSITIVE MUTANTS; HAMSTER OVARY CELLS; RNA POLYMERASE-II; TRANSCRIPTION FACTORS; JUNCTIONAL SEQUENCES; IONIZING-RADIATION; HUMAN CHROMOSOME-8; RECEPTOR GAMMA AB Murine cells homozygous for the severe combined immune deficiency mutation (scid) and V3 mutant hamster cells fall into the same complementation group and show similar defects in V(D)J recombination and DNA double-stranded break repair. Here we show that both cell types lack DNA-dependent protein kinase (DNA-PK) activity owing to defects in DNA-PKcs, the catalytic subunit of this enzyme. Furthermore, we demonstrate that yeast artificial chromosomes containing the DNA-PKcs, gene complement both the DNA repair and recombination deficiencies of V3 cells, and we conclude that DNA-PKcs, is encoded by the XRCC7 gene. As DNA-PK binds to DNA ends and is activated by these structures, our findings provide novel insights into V(D)J recombination and DNA repair processes. C1 UNIV CAMBRIDGE,DEPT ZOOL,CAMBRIDGE CB2 1QR,ENGLAND. UNIV SUSSEX,MRC,CELL MUTAT UNIT,BRIGHTON BN1 9RR,E SUSSEX,ENGLAND. HARVARD UNIV,CHILDRENS HOSP,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT GENET,BOSTON,MA 02115. ONTARIO CANC INST,TORONTO,ON M4X 1K9,CANADA. RP BLUNT, T (reprint author), UNIV CAMBRIDGE,WELLCOME CANC RES CAMPAIGN INST,TENNIS COURT RD,CAMBRIDGE CB2 1QR,ENGLAND. RI demengeot, jocelyne/K-8072-2014; Dry, Kate/I-2328-2014; OI Demengeot, Jocelyne/0000-0002-4761-614X FU NIAID NIH HHS [AI-20047, AI-35714-01]; Wellcome Trust NR 54 TC 704 Z9 707 U1 0 U2 7 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 10 PY 1995 VL 80 IS 5 BP 813 EP 823 DI 10.1016/0092-8674(95)90360-7 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QM399 UT WOS:A1995QM39900018 PM 7889575 ER PT J AU ADRIE, C MORENO, P BLOCH, KD HURFORD, WE GUERRERO, L ZAPOL, WM GOLD, HK SEMIGRAN, MJ AF ADRIE, C MORENO, P BLOCH, KD HURFORD, WE GUERRERO, L ZAPOL, WM GOLD, HK SEMIGRAN, MJ TI INHALED NITRIC-OXIDE DECREASES REOCCLUSION IN A CANINE MODEL OF CORONARY THROMBOLYSIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT CARDIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 0 TC 2 Z9 2 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A876 EP A876 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40601462 ER PT J AU BURTON, MD KINANE, B KAZEMI, H AF BURTON, MD KINANE, B KAZEMI, H TI SPONTANEOUS VENTILATION AND CHEMOSENSITIVE RESPONSES IN NEONATAL MICE BORNED TO HETEROZYGOUS RET-KINASE MINUS PARENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A666 EP A666 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600241 ER PT J AU CASTILLO, L BEAUMIER, L SANCHEZ, M YOUNG, VR AF CASTILLO, L BEAUMIER, L SANCHEZ, M YOUNG, VR TI WHOLE-BODY NITRIC-OXIDE SYNTHESIS IN HUMANS BY LABELING N-14 UREIDO CITRULLINE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MIT,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A865 EP A865 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40601396 ER PT J AU CHAKRABARTI, R SARANTOS, P ABOUHAMZE, A SOUBA, WW AF CHAKRABARTI, R SARANTOS, P ABOUHAMZE, A SOUBA, WW TI REGULATION OF GLUTAMINE-SYNTHETASE EXPRESSION IN A RAT INTESTINAL EPITHELIAL-CELL LINE DURING INFECTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV FLORIDA,GAINESVILLE,FL. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A953 EP A953 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40601914 ER PT J AU CLARK, RA FUHLBRIGGE, RC LOWE, JB SPRINGER, TA AF CLARK, RA FUHLBRIGGE, RC LOWE, JB SPRINGER, TA TI TISSUE DISTRIBUTION OF HUMAN FUCOSYL-TRANSFERASES BY IMMUNOHISTOCHEMISTRY SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A794 EP A794 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600979 ER PT J AU DIACOVO, TG ROTH, SJ BAINTON, DF SPRINGER, TA AF DIACOVO, TG ROTH, SJ BAINTON, DF SPRINGER, TA TI MAC-1 (CD11B/CD18) MEDIATES NEUTROPHIL ADHESION TO AND TRANSMIGRATION ACROSS SURFACE ADHERENT PLATELETS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT PATHOL,SAN FRANCISCO,CA 94143. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A796 EP A796 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600988 ER PT J AU FRENDI, G REENSTRA, W XANTHOPOULOS, L KENDIG, L ROLLINS, B AF FRENDI, G REENSTRA, W XANTHOPOULOS, L KENDIG, L ROLLINS, B TI MACROPHAGES ARE KEY ELEMENTS OF TISSUE DESTRUCTION IN A NOVEL MODEL OF EXPERIMENTAL COLITIS SO FASEB JOURNAL LA English DT Meeting Abstract C1 BOSTON UNIV,MED CTR,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A1035 EP A1035 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40602380 ER PT J AU FUHLBRIGGE, RC ALON, R SPRINGER, TA AF FUHLBRIGGE, RC ALON, R SPRINGER, TA TI REGULATION OF LYMPHOCYTE E-SELECTIN (ES) LIGAND EXPRESSION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A773 EP A773 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600860 ER PT J AU GONG, JL SUDA, T SCHNEEBERGER, EE AF GONG, JL SUDA, T SCHNEEBERGER, EE TI DENDRITIC CELLS (DC) ARE ENRICHED IN THE PULMONARY VASCULAR COMPARTMENT SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A1035 EP A1035 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40602377 ER PT J AU GOODYEAR, LJ AF GOODYEAR, LJ TI EXERCISE AND INSULIN-MEDIATED SIGNALING IN SKELETAL-MUSCLE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN RES LAB,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A977 EP A977 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40602053 ER PT J AU HERBERT, V SHAW, S JAYATILLEKE, E AF HERBERT, V SHAW, S JAYATILLEKE, E TI SERUM FERRITIN-IRON (HOLOFERRITIN) - A NEW TEST FOR IRON-DEFICIENCY OR EXCESS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MT SINAI MED CTR,NEW YORK,NY. QUIXOTE ASSOCIATES INC,NEW YORK,NY. BRONX VET ADM MED CTR,NEW YORK,NY. NR 1 TC 2 Z9 2 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A974 EP A974 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40602033 ER PT J AU ISSEKUTZ, AC SPRINGER, TA AF ISSEKUTZ, AC SPRINGER, TA TI CONTRIBUTION OF ICAM-1,ICAM-2, AND E-SELECTIN TO NEUTROPHIL TRANSENDOTHELIAL MIGRATION SO FASEB JOURNAL LA English DT Meeting Abstract C1 DALHOUSIE UNIV,HALIFAX,NS B3J 3G9,CANADA. CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A773 EP A773 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600861 ER PT J AU KRADIN, RL ZHAO, LH PINTO, C AF KRADIN, RL ZHAO, LH PINTO, C TI CAPSAICIN INHIBITS THE LOCALIZATION OF IA+ DC AND T-CELLS AROUND LUNG VENULES DURING A PULMONARY DTH RESPONSE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,IMMUNOL PULM LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A919 EP A919 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40601715 ER PT J AU LIU, K ROMAN, JS KAMALI, V NAUGHTON, BA KELLER, J RUSCETTI, FW ROODMAN, D BONEWALD, L MEAGHER, RM PURCHIO, AF TWARDZIK, DR AF LIU, K ROMAN, JS KAMALI, V NAUGHTON, BA KELLER, J RUSCETTI, FW ROODMAN, D BONEWALD, L MEAGHER, RM PURCHIO, AF TWARDZIK, DR TI STEM-CELL PROLIFERATION FACTOR (SCPF) INDUCES THE EXPANSION OF PRIMITIVE CD34 CELLS IN CULTURE SO FASEB JOURNAL LA English DT Meeting Abstract C1 ADV TISSUE SCI INC,LA JOLLA,CA 92037. NCI,FREDERICK,MD 21702. HOXWORTH BLOOD CTR,CINCINNATI,OH 45267. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A940 EP A940 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40601840 ER PT J AU MELDER, RJ MUNN, LL YAMADA, S OHKUBO, C JAIN, RK AF MELDER, RJ MUNN, LL YAMADA, S OHKUBO, C JAIN, RK TI T-LYMPHOCYTE ROLLING AND ARREST ON TNF-ALPHA-ACTIVATED ENDOTHELIUM - ENHANCEMENT BY RBCS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB TUMOR BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Munn, Lance/L-3950-2016 OI Munn, Lance/0000-0003-0698-7232 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A797 EP A797 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600997 ER PT J AU MIRZA, NM PACHAS, WN YUNIS, EJ DUBEY, DP AF MIRZA, NM PACHAS, WN YUNIS, EJ DUBEY, DP TI NATURAL-KILLER CYTOTOXICITY AS A PREDICTOR OF REHABILITATION RESPONSE OF GERIATRIC-PATIENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SPAULDING REHAB HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A791 EP A791 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600963 ER PT J AU NICKELEIT, V ZAGACHIN, L PETERS, J COLVIN, RB AF NICKELEIT, V ZAGACHIN, L PETERS, J COLVIN, RB TI FIBRONECTIN DEPOSITION AND GENE-EXPRESSION IN BENIGN AND MALIGNANT HUMAN BREAST-TUMORS SO FASEB JOURNAL LA English DT Meeting Abstract C1 CEDARS SINAI MED CTR,LOS ANGELES,CA 90048. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A661 EP A661 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600211 ER PT J AU RODNEY, G ANDRADE, F MAXWELL, L NAPIER, B JERVIS, W WOLYNEIC, W WEGNER, C LEVINE, S ANZUETO, A JENKINSON, S AF RODNEY, G ANDRADE, F MAXWELL, L NAPIER, B JERVIS, W WOLYNEIC, W WEGNER, C LEVINE, S ANZUETO, A JENKINSON, S TI SUPEROXIDE-DISMUTASE (SOD) PROTECTS DIAPHRAGM (DPH) AGAINST IMPAIRMENT BY INSPIRATORY RESISTIVE LOADING (IRL) SO FASEB JOURNAL LA English DT Meeting Abstract C1 BOEHRINGER INGELHEIM KG,INGELHEIM,CT. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Andrade, Francisco/F-1258-2011 OI Andrade, Francisco/0000-0002-2460-5798 NR 2 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A652 EP A652 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600162 ER PT J AU ROTH, SJ DIACOVO, TG BAINTON, DF SPRINGER, TA AF ROTH, SJ DIACOVO, TG BAINTON, DF SPRINGER, TA TI NEUTROPHILS TRANSMIGRATE THROUGH PLATELETS IN A NOVEL IN-VITRO CHEMOTAXIS ASSAY SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. UNIV CALIF SAN FRANCISCO,SCH MED,DEPT PATHOL,SAN FRANCISCO,CA 94143. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A796 EP A796 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600991 ER PT J AU VONANDRIAN, UH HASSLEN, SR ERLANDSEN, SL BUTCHER, EC AF VONANDRIAN, UH HASSLEN, SR ERLANDSEN, SL BUTCHER, EC TI THE SURFACE-TOPOGRAPHY OF ADHESION MOLECULES - A CRITICAL ROLE IN LEUKOCYTE TRAFFICKING SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 10 PY 1995 VL 9 IS 4 BP A773 EP A773 PN 2 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QM406 UT WOS:A1995QM40600858 ER PT J AU ORKIN, SH AF ORKIN, SH TI TRANSCRIPTION FACTORS AND HEMATOPOIETIC DEVELOPMENT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Review ID GATA-BINDING PROTEINS; BETA-GLOBIN LOCUS; TRANSGENIC MICE; DNA-BINDING; NF-M; EXPRESSION; GENE; CONTAINS; CLONING; CELLS C1 HOWARD HUGHES MED INST,BOSTON,MA 02115. RP ORKIN, SH (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 53 TC 198 Z9 199 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 MAR 10 PY 1995 VL 270 IS 10 BP 4955 EP 4958 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QL580 UT WOS:A1995QL58000001 PM 7890597 ER PT J AU DRACHMAN, JG GRIFFIN, JD KAUSHANSKY, K AF DRACHMAN, JG GRIFFIN, JD KAUSHANSKY, K TI THE C-MPL LIGAND (THROMBOPOIETIN) STIMULATES TYROSINE PHOSPHORYLATION OF JAK2, SHC, AND C-MPL SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID FACTOR RECEPTOR SUPERFAMILY; SIGNAL TRANSDUCTION; ERYTHROPOIETIN RECEPTOR; CYTOPLASMIC REGION; MOLECULAR-CLONING; BETA-SUBUNIT; SRC-FAMILY; GROWTH; INTERLEUKIN-3; PROTEIN AB alpha-Mpl is a member of the cytokine receptor superfamily, expressed primarily on hematopoietic cells. Recently, the c-Mpl Ligand was cloned and found to have thrombopoietic activity. In this paper we report that ligand binding induced tyrosine phosphorylation in BaF3 cells engineered to express the murine Mpl receptor (BaF3/mMpl). Phosphorylation occurred within 1 min at cytokine concentrations sufficient for proliferation of receptor-bearing cells. Using specific antibodies for immunoprecipitation and Western blotting, several of these phosphorylated proteins were identified. Shc and Jak2, known cytokine signaling molecules, and the c-Mpl receptor were shown to be major substrates for tyrosine phosphorylation. In contrast, phospholipase C-gamma and phosphatidylinositol 3-kinase displayed little and no tyrosine phosphorylation, respectively, after thrombopoietin stimulation. Co-immunoprecipitation studies demonstrated that Jak2 became physically associated with c-Mpl relatively late in the observed time course (20-60 min), significantly later than tyrosine phosphorylation of Jak2 (15 min). These results suggest that c-Mpl induces signal transduction pathways similar to those of other known cytokines. Additionally, in light of its late physical association with c-Mpl following Ligand binding, Jak2 may not be the initiating tyrosine kinase in the thrombopoietin-induced signaling cascade. C1 UNIV WASHINGTON,SCH MED,DEPT MED,SEATTLE,WA 98195. HARVARD UNIV,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02155. FU NCI NIH HHS [CA31615]; NIDDK NIH HHS [R01DK43719] NR 45 TC 180 Z9 182 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 MAR 10 PY 1995 VL 270 IS 10 BP 4979 EP 4982 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QL580 UT WOS:A1995QL58000007 PM 7534285 ER PT J AU SALGIA, R LI, JL LO, SH BRUNKHORST, B KANSAS, GS SOBHANY, ES SUN, YP PISICK, E HALLEK, M ERNST, T TANTRAVAHI, R CHEN, LB GRIFFIN, JD AF SALGIA, R LI, JL LO, SH BRUNKHORST, B KANSAS, GS SOBHANY, ES SUN, YP PISICK, E HALLEK, M ERNST, T TANTRAVAHI, R CHEN, LB GRIFFIN, JD TI MOLECULAR-CLONING OF HUMAN PAXILLIN, A FOCAL ADHESION PROTEIN PHOSPHORYLATED BY P210(BCR/ABL) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID COLONY-STIMULATING FACTOR; CHRONIC MYELOGENOUS LEUKEMIA; CYSTEINE-RICH PROTEIN; LIM-DOMAIN PROTEINS; SWISS 3T3 CELLS; TYROSINE PHOSPHORYLATION; EXTRACELLULAR-MATRIX; SIGNAL TRANSDUCTION; KINASE PP125FAK; SH3 DOMAINS AB Paxillin is a 68-kDa focal adhesion protein that is phosphorylated on tyrosine residues in fibroblasts in response to transformation by v-src, treatment with platelet-derived growth factor, or cross-linking of integrins. Paxillin has been shown to have binding sites for the SH3 domain of Src and the SH2 domain of Crk in vitro and to coprecipitate with two other focal adhesion proteins, vinculin and focal adhesion kinase (p125(fak)). After preliminary studies showed that paxillin was a substrate for the hematopoietic oncogene p210(BCR/ABL), we investigated the role of this protein in hematopoietic cell transformation and signal transduction. A full-length cDNA encoding human paxillin was cloned, revealing multiple protein domains, including four tandem LIM domains, a proline-rich domain containing a consensus SH3 binding site, and three potential Crk-SH2 binding sites. The paxillin gene was localized to chromosome 12q24 by fluorescence in situ hybridization analysis. A chicken paxillin cDNA was also cloned and is predicted to encode a protein approximately 90% identical to human paxil-lin. Paxillin coprecipitated with p210(BCR/ABL) and mul-tiple other cellular proteins in myeloid cell lines, suggesting the formation of multimeric complexes. In normal hematopoietic cells and myeloid cell lines, tyrosine phosphorylation of paxillin and co-precipitation with other cellular proteins was rapidly and transiently induced by interleukin-3 and several other hematopoietic growth factors. The predicted structure of paxillin implicates this molecule in protein protein interactions involved in signal transduction from growth factor receptors and the BCR/ABL oncogene fusion protein to the cytoskeleton. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CYTOGENET,BOSTON,MA 02115. OI Li, Jian-Liang/0000-0002-6487-081X FU NCI NIH HHS [CA36167, CA 60821]; NIGMS NIH HHS [GM 3818] NR 63 TC 250 Z9 254 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 MAR 10 PY 1995 VL 270 IS 10 BP 5039 EP 5047 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QL580 UT WOS:A1995QL58000017 PM 7534286 ER PT J AU BHANDARI, B WENZEL, UO MARRA, F ABBOUD, HE AF BHANDARI, B WENZEL, UO MARRA, F ABBOUD, HE TI A NUCLEAR-PROTEIN IN MESANGIAL CELLS THAT BINDS TO THE PROMOTER REGION OF THE PLATELET-DERIVED GROWTH FACTOR-A CHAIN GENE - INDUCTION BY PHORBOL ESTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MICROVASCULAR ENDOTHELIAL-CELLS; NF-KAPPA-B; MAJOR HISTOCOMPATIBILITY COMPLEX; GLUTAMINE-SYNTHETASE GENE; VIRUS TYPE-1 ENHANCER; SMOOTH-MUSCLE CELLS; TRANSCRIPTION FACTOR; MESSENGER-RNAS; EXPRESSION; SEQUENCE AB Mesangial cells predominantly express platelet-derived growth factor (PDGF)-A chain mRNA and release PDGF. Mesangial cell PDGF-A chain mRNA abundance is regulated by several agents including phorbol esters. We have recently demonstrated that induction of PDGF-A chain mRNA abundance in response to phorbol 12-myristate 13-acetate is primarily due to gene transcription. We have now analyzed the 5'-flanking region of the PDGF-A chain promoter to identify DNA binding protein(s) which have the potential to regulate PDGF-A chain gene transcription in human mesangial cells. DNase I footprint analysis of the 5'-flanking region of the PDGF-A chain promoter identifies a DNase I protected region at the location -82 to -102 corresponding to the sequence 5'-GGCCCGGAATCCGGGGGAGGC-3'. Therefore, nuclear extracts from human mesangial cells contain a protein, PDGF-A-BP-1, that binds to a DNA sequence (-82 to -102) in the promoter region of the PDGF-A chain gene. Gel mobility shift analysis using labeled oligomer corresponding to the binding site for PDGF-A-BP-1 indicates that PDGF-A-BP-1 is induced by phorbol ester in mesangial cells as well as fat-storing cells (>20 fold). Egr-1. protein does not bind to labeled PDGF-A-BP-1 oligomer and does not compete with the binding of PDGF-A-BP-1. In addition, SP-1 binding sequence does not compete with the binding sequence of the mesangial cell protein. PDGF-A-BP-1 appears to represent a novel protein which is induced by phorbol ester and thus has the potential for an important role in the transcriptional regulation of the PDGF-A chain gene in mesangial cells and other vascular pericytes. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP BHANDARI, B (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. RI Marra, Fabio/K-7263-2016 OI Marra, Fabio/0000-0001-8629-0878 FU NIDDK NIH HHS [DK 43988] NR 44 TC 19 Z9 19 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 MAR 10 PY 1995 VL 270 IS 10 BP 5541 EP 5548 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QL580 UT WOS:A1995QL58000089 PM 7890673 ER PT J AU COSO, OA CHIARIELLO, R KALINEC, G KYRIAKIS, JM WOODGETT, J GUTKIND, JS AF COSO, OA CHIARIELLO, R KALINEC, G KYRIAKIS, JM WOODGETT, J GUTKIND, JS TI TRANSFORMING G-PROTEIN-COUPLED RECEPTORS POTENTLY ACTIVATE JNK (SAPK) - EVIDENCE FOR A DIVERGENCE FROM THE TYROSINE KINASE SIGNALING PATHWAY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GENES; JUN; PHOSPHORYLATION; TRANSDUCTION; RAS AB The expression of human muscarinic acetylcholine receptors (mAChRs) in NIH 3T3 cells has been used as a model for studying proliferative signaling through G protein-coupled receptors. In this biological system, the mi class of mAChRs can effectively transduce mitogenic signals (Stephens, E. V., Kalinec, G., Brann, M. R., and Gutkind, J. S. (1993) Oncogene 8, 19-26) and induce malignant transformation if persistently activated (Gutkind, J. S., Novotny, E. A., Brann, M. R., and Robbins, K. C. (1991) Proc. Natl. Acad. Sci. U. S. A. 88, 4703-4708). Moreover, available evidence suggests that the mi-signaling pathway converges at the level of p21(ras) with that emerging from tyrosine kinase receptors (Crespo, P., Xu, N., Simonds, W. F., and Gutkind, J. S. (1994) Nature 369, 418-420). To explore nuclear events involved in growth regulation by G protein-coupled receptors in this setting, we compared the effect of platelet-derived growth factor (PDGF) and the cholinerse agonist, carbachol, on the expression of mRNA for members of the jun and fos family of nuclear proto-oncogenes. We found that activation of m1 receptors by carbachol induces the expression of a distinct set of nuclear transcription factors. In particular, carbachol caused a much greater induction of c-jun mRNA and AP-1 activity. These responses did not correlate with protein kinase C stimulation nor with the activation of mitogen-activated protein (MAP) kinases. Recently, it has been shown that a novel family of kinases structurally related to MAP kinases, stress-activated protein kinases, or Jun kinases (JNKs), phospho rylate in vivo the amino-terminal transactivating domain of the c-Jun protein, thereby increasing its transcriptional activity. In view of our results, this observation prompted us to ask whether m1 and PDGF can differentially activate JNKs. Here, we show that m1 mAChRs can induce a remarkable increase in JNK activity, which was temporally distinct from that of MAP kinase and was entirely protein kinase C independent. In contrast, PDGF failed to activate JNK in these cells, although it stimulated MAP kinase to an extent even greater than that for carbachol. These findings demonstrate that G protein-coupled receptors can signal through pathways leading to the activation of JNK, thus diverging at this level with those signaling routes utilized by tyrosine kinase receptors. C1 NIDR,CELLULAR DEV & ONCOL LAB,MOLEC SIGNALING UNIT,BETHESDA,MD 20892. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIABET UNIT,BOSTON,MA 02129. PRINCESS MARGARET HOSP,ONTARIO CANC INST,TORONTO,ON M4X 1K9,CANADA. RI Gutkind, J. Silvio/A-1053-2009; Woodgett, Jim/F-1087-2010; Chiariello, Mario/O-3642-2014 OI Woodgett, Jim/0000-0003-3731-5797; Chiariello, Mario/0000-0001-8434-5177 NR 28 TC 211 Z9 212 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 MAR 10 PY 1995 VL 270 IS 10 BP 5620 EP 5624 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QL580 UT WOS:A1995QL58000100 PM 7890682 ER PT J AU BORRIELLO, F OLIVEROS, J CHEN, A FREEMAN, GJ NADLER, LM SHARPE, AH AF BORRIELLO, F OLIVEROS, J CHEN, A FREEMAN, GJ NADLER, LM SHARPE, AH TI DIFFERENTIAL EXPRESSION OF ALTERNATE MB7-2 TRANSCRIPTS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 65 EP 65 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86400207 ER PT J AU SHARPE, AH BORRIELLO, F TIVOL, EA FREEMAN, GJ AF SHARPE, AH BORRIELLO, F TIVOL, EA FREEMAN, GJ TI MICE DEFICIENT IN THE COSTIMULATORY MOLECULES, B7-1 AND B7-2 SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 84 EP 84 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86400283 ER PT J AU BIGBY, M SHARPE, A WANG, JH MOLNAR, A WU, P WINANDY, S GEORGOPOULOS, K AF BIGBY, M SHARPE, A WANG, JH MOLNAR, A WU, P WINANDY, S GEORGOPOULOS, K TI THE IKAROS GENE IS REQUIRED FOR THE DEVELOPMENT OF ALL LYMPHOID LINEAGES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 3 U2 3 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 112 EP 112 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86400397 ER PT J AU BIANCONE, L ANDRES, G AHN, H DAI, C STAMENKOVIC, I AF BIANCONE, L ANDRES, G AHN, H DAI, C STAMENKOVIC, I TI IN-VIVO ROLE OF THE CD40-CD40L, CTLA4/CD28-B7 AND CD2-CD48 INTERACTIONS IN MERCURIC CHLORIDE-INDUCED AUTOIMMUNE-DISEASE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 CHARLESTOWN NAVY YARD,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 136 EP 136 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86400489 ER PT J AU NAGY, ZA FALCIONI, F VIDOVIC, D BELUNIS, C BOLIN, D MORIMOTO, C AF NAGY, ZA FALCIONI, F VIDOVIC, D BELUNIS, C BOLIN, D MORIMOTO, C TI INFLUENCE OF COSTIMULATORY AND CELL-ADHESION MOLECULES ON THE AVIDITY OF T-CELLS FOR ANTIGEN SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HOFFMANN LA ROCHE INC,DEPT INFLAMMAT & AUTOIMMUNE DIS,NUTLEY,NJ 07110. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 174 EP 174 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86400642 ER PT J AU POWELL, SN LUO, CM TANG, W MCKEEL, KL DEFRANK, JD ANNE, PR AF POWELL, SN LUO, CM TANG, W MCKEEL, KL DEFRANK, JD ANNE, PR TI HIGH-FREQUENCY ERROR-PRONE DNA RECOMBINATION IN ATAXIA-TELANGIECTASIA (A-T) CELL-LINES SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 318 EP 318 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401147 ER PT J AU KUPFER, GM DANDREA, AD AF KUPFER, GM DANDREA, AD TI COMPLEMENTATION OF FANCONI-ANEMIA GROUP-C (FACC) CELLS WITH FACC CDNA CORRECTS SPECIFIC DRUG-INDUCED CYTOTOXICITY AND CELL-CYCLE ARREST SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CHILDRENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 325 EP 325 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401177 ER PT J AU CUOMO, CA KIRCH, SA OETTINGER, MA AF CUOMO, CA KIRCH, SA OETTINGER, MA TI REGIONS OF RAG-1 AND RAG-2 NECESSARY FOR INITIAL CLEAVAGE AND COMPLETION OF V(D)J RECOMBINATION SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 347 EP 347 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401262 ER PT J AU BREAKEFIELD, XO SENAESTEVES, M KRAMM, C PECHAN, P CHASE, M LIVERMORE, J NILAVER, G MULDOON, LL CHIOCCA, AE KAYE, E NEUWELT, E AF BREAKEFIELD, XO SENAESTEVES, M KRAMM, C PECHAN, P CHASE, M LIVERMORE, J NILAVER, G MULDOON, LL CHIOCCA, AE KAYE, E NEUWELT, E TI EXTENDING GENE DELIVERY IN THE BRAIN USING VIRUS VECTORS SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 356 EP 356 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401285 ER PT J AU CHEN, L DONG, YH FINE, H KUFE, DW AF CHEN, L DONG, YH FINE, H KUFE, DW TI TARGETED PRODRUG ACTIVATION IN BREAST-CANCER CELLS MEDIATED BY A RECOMBINANT ADENOVIRUS CONTAINING THE DF3 TUMOR-ASSOCIATED ANTIGEN PROMOTER WITH HERPES-SIMPLEX VIRUS THYMIDINE KINASE GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 419 EP 419 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401523 ER PT J AU DONG, YH WEN, P MANOME, Y HERSHOWITZ, A CHEN, L KUFE, DW FINE, HA AF DONG, YH WEN, P MANOME, Y HERSHOWITZ, A CHEN, L KUFE, DW FINE, HA TI GENE-THERAPY OF RAT GLIOMAS USING ADENOVIRUS VECTOR-MEDIATED TRANSDUCTION OF THE CYTOSINE DEAMINASE GENE FOLLOWED BY TREATMENT WITH 5-FLUOROCYTOSINE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PHARMACOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 420 EP 420 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401527 ER PT J AU WEI, MX CHASE, M ONO, Y LI, FQ WAXMAN, DJ HOCHBERG, FH BREAKEFIELD, XO CHIOCCA, EA AF WEI, MX CHASE, M ONO, Y LI, FQ WAXMAN, DJ HOCHBERG, FH BREAKEFIELD, XO CHIOCCA, EA TI A NOVEL DRUG-SENSITIVITY GENE, CYTOCHROME-P450-2B1, ACTIVATES CYCLOPHOSPHAMIDE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. BOSTON UNIV,DEPT BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 428 EP 428 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401561 ER PT J AU AUSUBEL, FM KATAGIRI, F MINDRINOS, M REUBER, L YU, GL AF AUSUBEL, FM KATAGIRI, F MINDRINOS, M REUBER, L YU, GL TI CLONING AND CHARACTERIZATION OF THE ARABIDOPSIS-RPS2-DISEASE RESISTANCE GENE SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 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 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 473 EP 473 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401709 ER PT J AU SUN, L GOODMAN, HM AF SUN, L GOODMAN, HM TI ISOLATION OF GENES IN THE LIGHT SIGNALING PATHWAY BY MESSENGER-RNA DIFFERENTIAL DISPLAY SO JOURNAL OF CELLULAR BIOCHEMISTRY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0730-2312 J9 J CELL BIOCHEM JI J. Cell. Biochem. PD MAR 10 PY 1995 SU 21A BP 498 EP 498 PG 1 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QT864 UT WOS:A1995QT86401803 ER PT J AU TYLER, RC STELZNER, TJ RODMAN, DM BLOCH, KD MCMURTRY, IF AF TYLER, RC STELZNER, TJ RODMAN, DM BLOCH, KD MCMURTRY, IF TI HYPOXIC AND MONOCROTALINE BUT NOT FAWN-HOODED HYPERTENSIVE RAT LUNGS EXPRESS INCREASED MESSENGER-RNA FOR ENDOTHELIAL NITRIC-OXIDE SYNTHASE SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV COLORADO,HLTH SCI CTR,CARDIOVASC PULM RES LAB,DENVER,CO 80262. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP 131 EP 131 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98700791 ER PT J AU AFFENITO, SG VOGEL, S LAMMIKEEFE, CJ BACKSTRAND, JR WELCH, GW ADAMS, CH AF AFFENITO, SG VOGEL, S LAMMIKEEFE, CJ BACKSTRAND, JR WELCH, GW ADAMS, CH TI IDDM AND EATING DISORDERS - ALTERED GLYCEMIC CONTROL AND LIPID-METABOLISM SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV CONNECTICUT,SCH ALLIED HLTH,DEPT NUTR SCI,STORRS,CT 06269. JOSLIN DIABET CTR,BOSTON,MA 02215. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP 151 EP 151 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98700906 ER PT J AU ALAGAR, R TABAK, L GARG, HG KRADIN, RL KUPPEVELT, TV HALES, CA AF ALAGAR, R TABAK, L GARG, HG KRADIN, RL KUPPEVELT, TV HALES, CA TI RATS EXPOSED TO CIGARETTE-SMOKE HAVE ALTERATIONS IN LUNG PROTEOGLYCAN COMPOSITION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,IMMUNOPATHOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A433 EP A433 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702533 ER PT J AU AUCHINCLOSS, H SABATINE, M TERHORST, C LAUFER, T GLIMCHER, LH AF AUCHINCLOSS, H SABATINE, M TERHORST, C LAUFER, T GLIMCHER, LH TI CELL-MEDIATED XENOGRAFT REJECTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH PUBL HLTH,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A496 EP A496 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702897 ER PT J AU BEAGLE, JL SOTOARAPE, I BURTON, MD HOOP, B KAZEMI, H AF BEAGLE, JL SOTOARAPE, I BURTON, MD HOOP, B KAZEMI, H TI BIPHASIC HYPOXIC RESPONSE OF BRAIN-STEM GLUTAMATE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MASSACHUSETT COLL PHARM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A567 EP A567 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703308 ER PT J AU BRETON, S ALPER, SL GLUCK, SL SLY, WS BARKER, JE BROWN, D AF BRETON, S ALPER, SL GLUCK, SL SLY, WS BARKER, JE BROWN, D TI DEPLETION OF INTERCALATED CELLS (IC) IN COLLECTING DUCTS OF CARBONIC-ANHYDRASE-II (CAII) DEFICIENT (CAR2) MICE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. BETH ISRAEL HOSP,MOLEC MED & RENAL UNIT,BOSTON,MA 02215. WASHINGTON UNIV,DIV RENAL,ST LOUIS,MO. JEWISH HOSP ST LOUIS,DIV RENAL,ST LOUIS,MO 63110. WASHINGTON UNIV,DEPT BIOCHEM,ST LOUIS,MO. JACKSON LABS,BAR HARBOR,ME. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A564 EP A564 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703293 ER PT J AU CARLBERG, KA GWOSDOW, AR ALVIN, BL AF CARLBERG, KA GWOSDOW, AR ALVIN, BL TI EXERCISE DURING PREGNANCY AND STRESS RESPONSES IN OFFSPRING OF RATS SO FASEB JOURNAL LA English DT Meeting Abstract C1 EASTERN WASHINGTON UNIV,DEPT BIOL,CHENEY,WA 99004. EASTERN WASHINGTON UNIV,DEPT MATH,CHENEY,WA 99004. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A363 EP A363 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702126 ER PT J AU CHRISTODOULIDES, N DURANTE, W SCHAFER, AI AF CHRISTODOULIDES, N DURANTE, W SCHAFER, AI TI REGULATION OF GUANYLYL CYCLASE ACTIVITY BY VASCULAR SMOOTH-MUSCLE CELL-DERIVED CARBON-MONOXIDE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HOUSTON VAMC,HOUSTON,TX 77030. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A328 EP A328 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98701929 ER PT J AU CLINTON, SK EMENHISER, C GIOVANNUCCI, EL BOSTWICK, DG SCHWARTZ, SJ AF CLINTON, SK EMENHISER, C GIOVANNUCCI, EL BOSTWICK, DG SCHWARTZ, SJ TI CIS-TRANS ISOMERS OF LYCOPENE IN THE HUMAN PROSTATE - A ROLE IN CANCER PREVENTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. MAYO CLIN & MAYO FDN,DEPT PATHOL,ROCHESTER,MN 55905. N CAROLINA STATE UNIV,DEPT FOOD SCI,RALEIGH,NC 27695. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A442 EP A442 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702587 ER PT J AU DURANTE, W LIAO, L IFTIKHAR, I SCHAFER, AI AF DURANTE, W LIAO, L IFTIKHAR, I SCHAFER, AI TI DIFFERENTIAL REGULATION OF L-ARGININE TRANSPORT AND NITRIC-OXIDE PRODUCTION BY CULTURED VASCULAR CELLS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HOUSTON VAMC,HOUSTON,TX 77030. BAYLOR COLL MED,HOUSTON,TX 77030. NR 0 TC 0 Z9 0 U1 0 U2 1 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A556 EP A556 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703246 ER PT J AU EVANS, AB ALHIMYARY, AJ HROVAT, MI PAPPAGIANOPOULOS, P WAIN, JC GINNS, LC SYSTROM, DM AF EVANS, AB ALHIMYARY, AJ HROVAT, MI PAPPAGIANOPOULOS, P WAIN, JC GINNS, LC SYSTROM, DM TI EXERCISING SKELETAL-MUSCLE ENERGY-METABOLISM AND PH HOMEOSTASIS FOLLOWING LUNG TRANSPLANTATION - A 31P-MRS STUDY SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,FRANCIS BITTER NATL MAGNET LAB,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A350 EP A350 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702053 ER PT J AU GUO, ZM WU, WT HALEYZITLIN, V RICHARDSON, A AF GUO, ZM WU, WT HALEYZITLIN, V RICHARDSON, A TI THE USE OF CULTURED RAT HEPATOCYTES TO STUDY THE REPAIR OF SPECIFIC GENES SO FASEB JOURNAL LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A540 EP A540 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703148 ER PT J AU HARDY, SC YOUNG, VR CASTILLO, L NURKO, S GARCIAARANDA, JA WORONA, DL ATKINSON, A KLEINMAN, RE AF HARDY, SC YOUNG, VR CASTILLO, L NURKO, S GARCIAARANDA, JA WORONA, DL ATKINSON, A KLEINMAN, RE TI MEASUREMENT OF ALBUMIN SYNTHESIS RATES EMPLOYING THE FLOODING TECHNIQUE OF STABLE-ISOTOPE INFUSION IN HEALTHY-YOUNG CHILDREN AND ADULTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MIT,COMBINED PROGRAM PEDIAT GI & NUTR,CAMBRIDGE,MA 02138. HOSP INFANTIL MEXICO DR FEDERICO GOMEZ,MEXICO CITY,DF,MEXICO. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A584 EP A584 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703408 ER PT J AU HERLIHY, JP RYAN, LK ENTRICAN, G JOSEPH, PM VERMEULEN, MW HALES, CA AF HERLIHY, JP RYAN, LK ENTRICAN, G JOSEPH, PM VERMEULEN, MW HALES, CA TI EFFECT OF SMOKE EXPOSURE ON ALVEOLAR MACROPHAGE PRODUCTION OF PMN APOPTOSIS RETARDING FACTORS SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MOREDUN RES INST,EDINBURGH EH17 7JH,MIDLOTHIAN,SCOTLAND. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A570 EP A570 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703328 ER PT J AU HURFORD, WE HOCHACHKA, PW SCHNEIDER, RC GUYTON, GP STANEK, K ZAPOL, DG LIGGINS, GC ZAPOL, WM AF HURFORD, WE HOCHACHKA, PW SCHNEIDER, RC GUYTON, GP STANEK, K ZAPOL, DG LIGGINS, GC ZAPOL, WM TI SPLENIC CONTRACTION, CATECHOLAMINE RELEASE AND BLOOD-VOLUME REDISTRIBUTION DURING VOLUNTARY DIVING OF THE WEDDELL SEAL SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. UBC,DEPT ZOOL,VANCOUVER,BC,CANADA. NAT WOMENS HOSP,POSTGRAD SCH OBSTET & GYNAECOL,AUCKLAND,NEW ZEALAND. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 0 TC 0 Z9 0 U1 0 U2 2 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A353 EP A353 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702073 ER PT J AU KAUFMAN, DS SCHOON, RA ROBERTSON, MJ LEIBSON, PJ AF KAUFMAN, DS SCHOON, RA ROBERTSON, MJ LEIBSON, PJ TI INHIBITION OF SELECTIVE SIGNALING EVENTS IN NK CELLS RECOGNIZING MHC CLASS-I SO FASEB JOURNAL LA English DT Meeting Abstract C1 MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A493 EP A493 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702879 ER PT J AU KHAN, A TOMITA, Y SYKES, M AF KHAN, A TOMITA, Y SYKES, M TI ASSOCIATION OF THYMOCYTE T-CELL RECEPTOR (TCR) AND CD4 DOWN-MODULATION WITH DONOR-SPECIFIC TOLERANCE SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A236 EP A236 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98701395 ER PT J AU MARKOWITZ, DH IMANAKA, H KACMAREK, RM PAPPAGIANOPOULOS, PP BOUCHER, CA COCKRILL, BA KANAREK, DJ SYSTROM, DM AF MARKOWITZ, DH IMANAKA, H KACMAREK, RM PAPPAGIANOPOULOS, PP BOUCHER, CA COCKRILL, BA KANAREK, DJ SYSTROM, DM TI INHALED NITRIC-OXIDE AND INCREMENTAL EXERCISE PERFORMANCE SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,RESP CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A359 EP A359 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702105 ER PT J AU PAHLAVANI, MA HARRIS, MD RICHARDSON, A AF PAHLAVANI, MA HARRIS, MD RICHARDSON, A TI AGE-RELATED-CHANGES IN TRANSCRIPTION FACTOR NFAT IN RAT LYMPHOCYTES SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A534 EP A534 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703116 ER PT J AU RIMM, IJ KRENGER, W YUI, K KATSUMATA, M FERRARA, JLM AF RIMM, IJ KRENGER, W YUI, K KATSUMATA, M FERRARA, JLM TI TCR-BETA TRANSGENIC MICE FAIL TO MEDIATE A GVHR DUE TO DEFECTS OF THE IL-2 PATHWAYS INVOLVED IN ALLORECOGNITION SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. UNIV PENN,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A497 EP A497 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702901 ER PT J AU SANTAMBROGIO, L SOBEL, RA SALSBURY, H LEES, MB AF SANTAMBROGIO, L SOBEL, RA SALSBURY, H LEES, MB TI MYELIN PROTEOLIPID PROTEIN (PLP) ANALOGS - IN-SITU MECHANISMS OF EAE PREVENTION SO FASEB JOURNAL LA English DT Meeting Abstract C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. STANFORD UNIV,SCH MED,VA MED CTR,DEPT PATHOL,PALO ALTO,CA 94304. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A485 EP A485 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702832 ER PT J AU SCREMIN, OU LI, MG AF SCREMIN, OU LI, MG TI SEVERE CORTICAL CONTUSION INDUCES HYPEREMIA IN THE SYMMETRICAL CONTRALATERAL CORTEX SO FASEB JOURNAL LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90073. NR 0 TC 1 Z9 1 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A381 EP A381 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702232 ER PT J AU SILVERMAN, ES THOMPSON, BT QUINN, DA KINANE, TB BONVENTRE, JV HALES, CA AF SILVERMAN, ES THOMPSON, BT QUINN, DA KINANE, TB BONVENTRE, JV HALES, CA TI ACTIVATION OF NA+/H+ EXCHANGE IN PULMONARY-ARTERY SMOOTH-MUSCLE SEGMENTS DURING HYPOXIC-INDUCED PULMONARY VASCULAR REMODELING SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,PULM UNIT,BOSTON,MA 02114. SHRINERS HOSP CRIPPLED CHILDREN,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A432 EP A432 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702529 ER PT J AU THOMPSON, BT GARG, HG HALES, CA AF THOMPSON, BT GARG, HG HALES, CA TI VARIABLE DEGREES OF N- AND O- SULFATION IN HEPARINS MAY EXPLAIN VARIABLE ANTIPROLIFERATIVE ACTIVITIES SO FASEB JOURNAL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PULM CRIT CARE UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A432 EP A432 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702527 ER PT J AU WILLIAMS, AW ERDMAN, JW GUGGER, ET BOSTWICK, DG CLINTON, SK AF WILLIAMS, AW ERDMAN, JW GUGGER, ET BOSTWICK, DG CLINTON, SK TI BETA-CAROTENE IS FOUND IN THE HUMAN PROSTATE AND CAN BE CONVERTED TO RETINOL BY PROSTATE CELLS IN-VITRO SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV ILLINOIS,DEPT FOOD SCI,DIV NUTR SCI,URBANA,IL 61801. MAYO CLIN & MAYO FDN,DEPT PATHOL,ROCHESTER,MN 55905. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A459 EP A459 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702681 ER PT J AU WILLIAMS, MD VANREMMEN, H RICHARDSON, A AF WILLIAMS, MD VANREMMEN, H RICHARDSON, A TI CHARACTERIZATION OF THE CATALASE PROMOTER SO FASEB JOURNAL LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHYSIOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A396 EP A396 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98702317 ER PT J AU YU, YM RYAN, C BURKE, JF TOMPKINS, RG YOUNG, VR AF YU, YM RYAN, C BURKE, JF TOMPKINS, RG YOUNG, VR TI ARGININE, CITRULLINE AND LEUCINE KINETICS IN SEVERELY BURNED, ADULT PATIENTS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02142. NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A573 EP A573 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703346 ER PT J AU YUAN, F LEUNIG, M BERK, DA TORCHILIN, VP JAIN, RK AF YUAN, F LEUNIG, M BERK, DA TORCHILIN, VP JAIN, RK TI TUMOR MICROVASCULAR PERMEABILITY - IMPLICATION FOR TRANSPORT PATHWAYS SO FASEB JOURNAL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Berk, David/A-4863-2012 OI Berk, David/0000-0002-3855-6886 NR 0 TC 0 Z9 0 U1 0 U2 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 9 PY 1995 VL 9 IS 3 BP A616 EP A616 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA QL987 UT WOS:A1995QL98703592 ER PT J AU SINGH, AK GULATI, S AF SINGH, AK GULATI, S TI EFFECT OF ISCHEMIA-REPERFUSION INJURY ON THE MORPHOLOGY OF PEROXISOMES SO MOLECULAR AND CELLULAR BIOCHEMISTRY LA English DT Article DE PEROXISOMES; BIOGENESIS; KIDNEY; ISCHEMIA; REPERFUSION ID RAT-LIVER PEROXISOMES; SUPEROXIDE-DISMUTASE; MYOCARDIAL REPERFUSION; RENAL CIRCULATION; XANTHINE-OXIDASE; FREE-RADICALS; CELL INJURY; KIDNEY; BIOGENESIS; CATALASE AB We have previously demonstrated that ischemic injury changed the density of peroxisomes into two distinct peaks, one with a normal density (1.21 g/cm(3); Peak I) and a second peak with a lighter density (1.14 g/cm(3); Peak II). We studied the peroxisomes from both peaks under the Electron microscope. Examination of peak I following ischemia showed loss of matrix proteins and damaged limiting membranes with leakage of DAB positive material in direct proportion to the duration of ischemia. Upon reperfusion of the ischemic liver Peak I showed more severe damage to the organelle. These observations clearly demonstrated that ischemia reperfusion injury causes structural damage to peroxisomes. Interestingly ultrastructural examination of Peak II following ischemia showed evidence of perisomal proliferation with budding of existing peroxisomes and the presence of micro peroxisomes (changes similar to those noted under conditions leading to perisomal proliferation). However, peak II following reperfusion showed only damaged organelle. These observations underline the importance of peroxisomes in the response of the cell to ischemia-reperfusion injury. C1 MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. RP SINGH, AK (reprint author), RALPH H JOHNSON VA MED CTR,DEPT PATHOL & LAB MED,109 BEE ST,CHARLESTON,SC 29401, USA. NR 39 TC 6 Z9 6 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0300-8177 J9 MOL CELL BIOCHEM JI Mol. Cell. Biochem. PD MAR 9 PY 1995 VL 144 IS 1 BP 19 EP 26 DI 10.1007/BF00926736 PG 8 WC Cell Biology SC Cell Biology GA QT315 UT WOS:A1995QT31500004 PM 7791741 ER PT J AU DYNLACHT, BD AF DYNLACHT, BD TI RETINOBLASTOMA PROTEIN - POL-I GETS REPRESSED SO NATURE LA English DT Editorial Material ID RNA POLYMERASE-I; TRANSCRIPTION FACTOR; BINDING RP DYNLACHT, BD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC ONCOL LAB,149 13TH ST,BOSTON,MA 02129, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 9 PY 1995 VL 374 IS 6518 BP 114 EP 114 DI 10.1038/374114a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QL397 UT WOS:A1995QL39700030 PM 7877677 ER PT J AU WONG, JT GIRARDET, C SLATER, GJ HARRIS, NL MOSCICKI, RA AF WONG, JT GIRARDET, C SLATER, GJ HARRIS, NL MOSCICKI, RA TI A 58-YEAR-OLD MAN WITH COMMON VARIABLE IMMUNODEFICIENCY, SPLENOMEGALY, AND HEMOLYTIC-ANEMIA - MALIGNANT-LYMPHOMA, LARGE-CELL IMMUNOBLASTIC, B-CELL TYPE, ASSOCIATED WITH EPSTEIN-BARR VIRAL-INFECTION INVOLVING THE SPLEEN AND LYMPH-NODES - SPLENIC INFARCTS AND EXTRAMEDULLARY HEMATOPOIESIS - CYTOMEGALOVIRUS LYMPHADENITIS - (COMMON VARIABLE IMMUNODEFICIENCY) - (AUTOIMMUNE HEMOLYTIC-ANEMIA) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID GENE-EXPRESSION; HYPOGAMMAGLOBULINEMIA; DEFICIENCY; DISEASES; REGISTRY; CANCER; IGG C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP WONG, JT (reprint author), MASSACHUSETTS GEN HOSP,IMMUNOL & ALLERGY UNIT,BOSTON,MA 02114, USA. NR 37 TC 7 Z9 7 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAR 9 PY 1995 VL 332 IS 10 BP 663 EP 671 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA QK066 UT WOS:A1995QK06600008 ER PT J AU FEIGIN, AM ARONOV, EV TEETER, JH BRAND, JG AF FEIGIN, AM ARONOV, EV TEETER, JH BRAND, JG TI THE PROPERTIES OF ION CHANNELS FORMED BY THE COUMARIN ANTIBIOTIC, NOVOBIOCIN, IN LIPID BILAYERS SO BIOCHIMICA ET BIOPHYSICA ACTA-BIOMEMBRANES LA English DT Article DE NOVOBIOCIN; ION CHANNEL; HPLC PURIFICATION ID PHOSPHOLIPID SURFACE-CHARGE; AMPHOTERICIN-B CHANNELS; GRAMICIDIN-A; K+ CHANNEL; FROG-SKIN; CONDUCTANCE; MEMBRANES; SELECTIVITY; NYSTATIN; STATES AB The coumarin antibiotic novobiocin forms ion channels of varying conductances in lipid bilayers. The conductances (about 20, 22, 14, 7 and 2 pS for 100 mM NH4Cl, CsCl, KCl, NaCl and LiCl, respectively) and selectivities (cation transference numbers in the range of 0.97-0.98) of one type of novobiocin-induced channel are similar to those found for channels formed by gramicidin A, an antibiotic of very different structure. The conductance of novobiocin channels of this type was independent of the species of the membrane lipid. This observation suggests that novobiocin molecules directly form these channels, and that channels are not formed through defects in lipid structure. The similarity in conductance and ion selectivity between channels induced by novobiocin and those formed by gramicidin A suggests that these structurally different molecules form channels with comparable internal diameter and internal surface charge distribution. Using HPLC purification we argue that the channel-forming activity of novobiocin is related to the activity of the novobiocin molecule itself, and not to a contaminant of the commercially available novobiocin sodium salt preparation. C1 UNIV PENN,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RP FEIGIN, AM (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. 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 0005-2736 J9 BBA-BIOMEMBRANES JI Biochim. Biophys. Acta-Biomembr. PD MAR 8 PY 1995 VL 1234 IS 1 BP 43 EP 51 DI 10.1016/0005-2736(94)00257-P PG 9 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA QL423 UT WOS:A1995QL42300007 PM 7533542 ER PT J AU SINGER, PA COOPER, DS LEVY, EG LADENSON, PW BRAVERMAN, LE DANIELS, G GREENSPAN, FS MCDOUGALL, IR NIKOLAI, TF AF SINGER, PA COOPER, DS LEVY, EG LADENSON, PW BRAVERMAN, LE DANIELS, G GREENSPAN, FS MCDOUGALL, IR NIKOLAI, TF TI TREATMENT GUIDELINES FOR PATIENTS WITH HYPERTHYROIDISM AND HYPOTHYROIDISM SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID THYROXINE AB Objective.-To develop a set of minimum clinical guidelines for use by primary care physicians in the evaluation and management of patients with hyperthyroidism and hypothyroidism. Participants.-Guidelines were developed by a nine-member ad hoc Standards of Care Committee of the American Thyroid Association (the authors of this article). The participants were selected by the committee chair and the president of the American Thyroid Association on the basis of their clinical experience. The committee members represented different geographic areas within the United States, in order to take. into account different practice styles. Evidence.-Guideline were developed on the basis of expert opinion of the participants, as well as on available published information. Consensus Process.-Input was obtained from all of the participants, each of whom wrote an initial section of the document. A complete draft document was then written by three participants (P.A.S., D.S.C., and E.G.L.) and resubmitted to the entire committee for revision. The revised document was then submitted to the entire membership of the American Thyroid Association for written comments, which were then reviewed (mainly by P.A.S., D.S.C., and E.G.L.). Many of the suggestions of the American Thyroid Association members were incorporated into the final draft, which was then approved by the Executive Council of the American Thyroid Association. The entire process, from initial drafts to final approval, took approximately 18 months. Conclusions.-A set of minimum clinical guidelines for the diagnosis and treatment of hyperthyroidism and hypothyroidism were developed by consensus of a group of experienced thyroidologists. The guidelines are intended to be used by physicians in their care of patients with thyroid disorders, with the expectation that more effective care can be provided, and at a cost savings. C1 JOHNS HOPKINS UNIV,SCH MED,DIV ENDOCRINOL,BALTIMORE,MD. MT SINAI HOSP,DIV ENDOCRINOL,BALTIMORE,MD. UNIV MIAMI,SCH MED,DIV ENDOCRINOL,MIAMI,FL. UNIV MASSACHUSETTS,SCH MED,DIV ENDOCRINOL,WORCESTER,MA. MASSACHUSETTS GEN HOSP,THYROID UNIT,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,SCH MED,DIV ENDOCRINOL,SAN FRANCISCO,CA. STANFORD UNIV,SCH MED,DIV NUCL MED,STANFORD,CA. MARSHFIELD CLIN FDN MED RES & EDUC,MARSHFIELD,WI. RP SINGER, PA (reprint author), UNIV SO CALIF,SCH MED,DIV ENDOCRINOL DIABET & HYPERTENS,1355 S SAN PABLO ST,ROOM 120,LOS ANGELES,CA 90033, USA. NR 13 TC 254 Z9 271 U1 2 U2 10 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 8 PY 1995 VL 273 IS 10 BP 808 EP 812 DI 10.1001/jama.273.10.808 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA QJ750 UT WOS:A1995QJ75000034 PM 7532241 ER PT J AU PECHAN, PA YOSHIDA, T PANAHIAN, N MOSKOWITZ, MA BREAKEFIELD, XO AF PECHAN, PA YOSHIDA, T PANAHIAN, N MOSKOWITZ, MA BREAKEFIELD, XO TI GENETICALLY-MODIFIED FIBROBLASTS PRODUCING NGF PROTECT HIPPOCAMPAL-NEURONS AFTER ISCHEMIA IN THE RAT SO NEUROREPORT LA English DT Article DE NERVE GROWTH FACTOR; NGF; GLOBAL ISCHEMIA; HIPPOCAMPUS; NEUROPROTECTION; GENE THERAPY; FIBROBLASTS; TRANSPLANTATION; NEURON-SPECIFIC ENOLASE ID NERVE GROWTH-FACTOR; TRANSIENT FOREBRAIN ISCHEMIA; INJURY; DEATH; MODEL; CELLS; AMELIORATION; EXPRESSION; RECEPTOR; ATROPHY AB THE neuroprotective effect of nerve growth factor (NGF) on the pyramidal cells in the vulnerable CA1-CA2 sectors of the hippocampus was investigated in a rat model of transient forebrain ischemia. A genetically modified fibroblast line that secretes high levels of NGF was implanted 7 days before induction of ischemia between the hippocampal CA1-CA2 subfields in the right hemisphere. Rats were then subjected to 10 min of cerebral ischemia in a four vessel occlusion model. Morphological changes in the CA1 and CA2 subfields were evaluated 7 days after ischemia. Animals in the NGF-protected group had significantly higher numbers of normal appearing neurons in the right CA1 and CA2 regions, compared with their nonimplanted left hemispheres, to non-implanted animals or to animals implanted with non-modified cells. The data confirmed that NGF can protect CA1-CA2 hippocampal neurons from ischemic damage by implantation of genetically engineered cells producing NGF. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT NEUROSURG,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT NEUROL,STRIKE RES LAB,BOSTON,MA 02129. HARVRAD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,DEPT NEUROSURG,STROKE RES LAB,BOSTON,MA 02129. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS10828, NS24279] NR 22 TC 68 Z9 69 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAR 7 PY 1995 VL 6 IS 4 BP 669 EP 672 DI 10.1097/00001756-199503000-00021 PG 4 WC Neurosciences SC Neurosciences & Neurology GA QN868 UT WOS:A1995QN86800021 PM 7605924 ER PT J AU ZHU, JH REYNET, C CALDWELL, JS KAHN, CR AF ZHU, JH REYNET, C CALDWELL, JS KAHN, CR TI CHARACTERIZATION OF RAD, A NEW MEMBER OF RAS/GTPASE SUPERFAMILY, AND ITS REGULATION BY A UNIQUE GTPASE-ACTIVATING PROTEIN (GAP)-LIKE ACTIVITY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INSULIN-RECEPTOR; MUTATIONAL ANALYSIS; CATALYTIC DOMAIN; BINDING PROTEIN; XENOPUS-OOCYTES; PHOSPHORYLATION; P21; LOCALIZATION; PROTEOLYSIS; ADIPOCYTES AB We have recently identified a new member of the Ras/GTPase superfamily termed Rad which has unique sequence features and is overexpressed in the skeletal muscle of humans with type II diabetes (Reynet, C., and Kahn, C. R. (1993) Science, 262, 1441-1444), When expressed in bacteria as a glutathione S-transferase fusion protein, Rad bound [alpha(32)P]GTP quickly and saturably, Binding was specific for guanine nucleotides and displayed unique magnesium dependence such that both GTP and GDP binding were optimal at relatively high Mg2+ concentrations (1-10 mM), Rad had low intrinsic GTPase activity which was greatly enhanced by a GTPase-activating protein (GAP) activity present in various tissues and cell lines. Several known GAPs had no stimulatory effect toward Rad, Conversion of Ser to Asn at position 66 in Rad (equivalent to position 12 in Ras) resulted in a total loss of GTP binding. Mutation of pro(61) (equivalent to Gly(12) in Ras) or Gln(109) (equivalent to Gln(61) in Ras) had no effect on Rad GTPase activity, whereas creation of a double mutation at these positions resulted in exceptionally high intrinsic GTPase activity, lit vitro, Rad was phosphorylated by the catalytic subunit of cAMP-dependent protein kinase (PK). Phosphopeptide mapping indicated two PKA phosphorylation sites near the C-OOH terminus. Rad also coprecipitated a serine/threonine kinase activity from extracts of various tissues and cell lines which catalyzed phosphorylation on Rad but was not inhibited by PKA inhibitor. Thus, Rad is a GTP-binding protein and a GTPase which has some structure/function similarities to Ras, but displays unique features. Rad may also be phosphorylated on serine/threonine residues by PHA and other kinases, as well as regulated by its own GAP which is present in many tissues and cell types. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. FU NIDDK NIH HHS [DK 36836, DK 45935] NR 37 TC 50 Z9 51 U1 1 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 MAR 3 PY 1995 VL 270 IS 9 BP 4805 EP 4812 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QK084 UT WOS:A1995QK08400090 PM 7876254 ER PT J AU ROSOWSKY, A MOTA, CE QUEENER, SF WALTHAM, M ERCIKANABALI, E BERTINO, JR AF ROSOWSKY, A MOTA, CE QUEENER, SF WALTHAM, M ERCIKANABALI, E BERTINO, JR TI 2,4-DIAMINO-5-SUBSTITUTED-QUINAZOLINES AS INHIBITORS OF A HUMAN DIHYDROFOLATE-REDUCTASE WITH A SITE-DIRECTED MUTATION AT POSITION-22 AND OF THE DIHYDROFOLATE REDUCTASES FROM PNEUMOCYSTIS-CARINII AND TOXOPLASMA-GONDII SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TRIMETREXATE; POTENT; IDENTIFICATION; QUINAZOLINES; ANTIFOLATE; EXPRESSION; AGENTS; AIDS AB 2,4-Diaminoquinazoline antifolates with a lipophilic side chain at the 5-position, and in one case with a das sic al (p-aminobenzoyl)-L-glutam ate side chain, were synthesized as potentially selective inhibitors of a site-directed mutant of human dihydrofolate reductase (DHFR) containing phenylalanine instead of leucine at position 22. This mutant enzyme is approximately 100-fold more resistant than native enzyme to the classical antifolate methotrexate (MTX), yet shows minimal cross resistance to the nonclassical antifolates piritrexim (PTX) and trimetrexate (TMQ). Although they were much less potent than trimetrexate and piritrexim, the lipophilic 5-substituted analogues were all found to bind approximately 10 times better to the mutant DHFR than to the wild-type enzyme. The potency of the analogue with a classical (p-aminobenzoyl)-L-glutamate side chain was similarly diminished in comparison with MTX, but the difference in its binding affinity to the two DHFR species was only 5-fold. Thus, by making subtle structural changes in the antifolate molecule, it may be possible to attack resistance due to mutational alterations in the active site of the target enzyme. Also, to test the hypothesis that DHFR from Pneumocystis carinii and Toxoplasma gondii may have a less sterically restrictive active site than the enzyme from mammalian cells, inhibition assays using several of the lipophilic analogues in the series were carried out against the P. carinii and T. gondii reductases in comparison with the enzyme from rat liver. In contrast to their preferential binding to mutant versus wild-type human DHFR, binding of these analogues to the P. carinii and T. gondii enzymes was weaker than binding to rat enzyme. It thus appears that, if the active site of the DHFR from these parasites is less sterically restrictive than the active site of the mammalian enzyme, this difference cannot be successfully exploited by moving the side chain from the 6-position to the 5-position. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. INDIANA UNIV,SCH MED,DEPT PHARMACOL & TOXICOL,INDIANAPOLIS,IN 46202. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY 10021. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. RI Waltham, Mark/A-1728-2009 FU NCI NIH HHS [R01-CA25394]; NIAID NIH HHS [R01-AI29904, N01-AI35171] NR 25 TC 17 Z9 17 U1 0 U2 1 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD MAR 3 PY 1995 VL 38 IS 5 BP 745 EP 752 DI 10.1021/jm00005a002 PG 8 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA QL254 UT WOS:A1995QL25400002 PM 7877140 ER PT J AU ARANY, Z NEWSOME, D OLDREAD, E LIVINGSTON, DM ECKNER, R AF ARANY, Z NEWSOME, D OLDREAD, E LIVINGSTON, DM ECKNER, R TI A FAMILY OF TRANSCRIPTIONAL ADAPTER PROTEINS TARGETED BY THE E1A ONCOPROTEIN SO NATURE LA English DT Article ID TISSUE-SPECIFIC EXTINGUISHER; REGULATORY SUBUNIT; TSE1 ENCODES; CYCLIC-AMP; ACTIVATION; KINASE; GENE AB THE cellular protein p300 is a target of the adenoviral E1A oncoprotein and is thought to participate in preventing the G0/G1 transition in the cell cycle, activating certain enhancers and stimulating differentiation pathways(1). CBP is a protein that is associated with and coactivates the transcription factor CREB, mediating the induction by cyclic AMP of certain responsive promoters(2-4). The sequences of p300 and CBP are highly related(4,5). We show here that p300, like CBP2, can stimulate transcription, This activity is directly aml specifically inhibited by E1A. We also find that CBP exists in a DNA-bound complex containing a member of the CREB family and that E1A and CBP interact with one another in vivo. In keeping with the idea that E1A functionally targets CBP, cAMP-dependent transcription is repressed by E1A. Thus, p300 and CBP define a family of transcriptional adaptor proteins that are specifically targeted by the E1A oncoprotein. RP ARANY, Z (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 16 TC 480 Z9 483 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 2 PY 1995 VL 374 IS 6517 BP 81 EP 84 DI 10.1038/374081a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK079 UT WOS:A1995QK07900058 PM 7870178 ER PT J AU LEE, JW RYAN, F SWAFFIELD, JC JOHNSTON, SA MOORE, DD AF LEE, JW RYAN, F SWAFFIELD, JC JOHNSTON, SA MOORE, DD TI INTERACTION OF THYROID-HORMONE RECEPTOR WITH A CONSERVED TRANSCRIPTIONAL MEDIATOR SO NATURE LA English DT Article ID 26-S PROTEASE; TRANSACTIVATION; ACTIVATION; MODULATOR; DOMAIN; YEAST AB THE thyroid-hormone receptors are hormone-dependent transcription factors that control expression of many target genes(1,2). This regulation is presumably a consequence of hormone-dependent contacts between the receptors and the basal transcription machinery(3). We used the yeast two-hybrid system(4,5) to identify a candidate human transcriptional mediator that interacts with both the thyroid-hormone receptor and the retinoid-X receptor in a ligand-dependent fashion. This protein, Trip1 (for thyroid-hormone-receptor Interacting protein), shares striking sequence conservation with the yeast transcriptional mediator Sug1 (refs 6, 7). Here we show that Trip1 can functionally substitute for Sug1 in yeast, and that both proteins interact in vitro with the thyroid-hormone receptor, acid with the transcriptional activation domains of yeast GAL4 and of herpes virus VP16. C1 UNIV TEXAS,SW MED CTR,DEPT MED,DALLAS,TX 75235. UNIV TEXAS,SW MED CTR,DEPT BIOCHEM,DALLAS,TX 75235. RP LEE, JW (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,WELLMAN 9,BOSTON,MA 02114, USA. NR 20 TC 384 Z9 386 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD MAR 2 PY 1995 VL 374 IS 6517 BP 91 EP 94 DI 10.1038/374091a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK079 UT WOS:A1995QK07900061 PM 7870181 ER PT J AU ISHIOKA, C BALLESTER, R ENGELSTEIN, M VIDAL, M KASSEL, J THE, I BERNARDS, A GUSELLA, JF FRIEND, SH AF ISHIOKA, C BALLESTER, R ENGELSTEIN, M VIDAL, M KASSEL, J THE, I BERNARDS, A GUSELLA, JF FRIEND, SH TI A FUNCTIONAL ASSAY FOR HETEROZYGOUS MUTATIONS IN THE GTPASE-ACTIVATING PROTEIN RELATED DOMAIN OF THE NEUROFIBROMATOSIS TYPE-1 GENE SO ONCOGENE LA English DT Article DE NF1; FUNCTIONAL ASSAY IN YEAST FASAY ID GAP-RELATED DOMAIN; SACCHAROMYCES-CEREVISIAE; RAS GTPASE; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; GEL-ELECTROPHORESIS; ADENYLATE-CYCLASE; MAMMALIAN GAP; CDC25 GENE; YEAST; PRODUCT AB The GTPase-activating protein related domain of the human neurofibromatosis type 1 protein (NF1GRD) can down-regulate RAS in Saccharomyces cerevisiae, Using a technique termed the FASAY method, for Functional Analysis of Separated Alleles in Yeast, we designed a rapid method for detection of heterozygous NF1GRD loss-of-function mutations, In our method, PCR amplified NF1GRD cDNA is directly cloned into a centromeric vector by homologous recombination in a cdc25 temperature-sensitive mutant strain expressing human Ha-ras. This strain is dependent on the Ha-uas for growth, allowing a simple growth assay for NF1GRD loss-of-function mutations, In a test of our method, two alternatively spliced NF1GRD cDNAs (type I and II) inhibited yeast growth whereas four mutants with amino acid substitutions at highly conserved residues did not, This simple method thus permits the rapid screening for heterozygous germline or somatic NF1GRD mutations, In an initial application of this method, no mutations disrupting NF1GRD function were detected in lymphoblasts from 11 previously untested neurofibromatosis type 1 patients. C1 MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET UNIT, BOSTON, MA 02129 USA. TOHOKU UNIV, INST DEV AGING & CANC, SENDAI, MIYAGI 980, JAPAN. UNIV CALIF SANTA BARBARA, DEPT BIOL SCI, SANTA BARBARA, CA 93106 USA. HARVARD UNIV, CHILDRENS HOSP,SCH MED,DANA FARBER INST, DEP PEDIAT,DIV HEMATOL ONCOL, BOSTON, MA 02114 USA. RP MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02129 USA. RI The, Inge/B-8884-2011 FU PHS HHS [WS 22224] NR 48 TC 10 Z9 10 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 EI 1476-5594 J9 ONCOGENE JI Oncogene PD MAR 2 PY 1995 VL 10 IS 5 BP 841 EP 847 PG 7 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QL038 UT WOS:A1995QL03800005 PM 7898926 ER PT J AU BURT, VK YAGER, J LUNDGREN, J AF BURT, VK YAGER, J LUNDGREN, J TI PROVIDING RESIDENTS WITH A COMPREHENSIVE EDUCATIONAL-PROGRAM IN OUTPATIENT PSYCHIATRY - INTEGRATING AN OUTPATIENT CURRICULUM INTO OUTPATIENT MANAGEMENT TEAMS SO ACADEMIC PSYCHIATRY LA English DT Article ID PROJECTIVE IDENTIFICATION; PSYCHOTHERAPY AB As part of their efforts to prepare psychiatry residents for comprehensive, practical out-patient psychiatric practice, the authors have established an organized training program in ambulatory psychiatry. The program consists of outpatientf management teams that run from mid-PGY-2 to PGY-4, a specified minimum number of mandatory outpatient hours for continuity patient care, and suggested guidelines for residents' outpatient experiences. An outpatient management team curriculum has been designed for team leaders and trainees that consists of specific topics in outpatient care, associated learning objectives, and readings for each topic. This curriculum, which supplements our previous program of conferences, individual supervision, and a yearlong psychotherapy seminar series, has been refined over the past 5 years. The authors describe the program and the topics included in the curriculum. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT PSYCHIAT,LOS ANGELES,CA. RP BURT, VK (reprint author), UNIV CALIF LOS ANGELES,SCH MED,INST NEUROPSYCHIAT,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. NR 52 TC 0 Z9 0 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 1042-9670 J9 ACAD PSYCHIATR JI Acad. Psych. PD SPR PY 1995 VL 19 IS 1 BP 22 EP 33 PG 12 WC Education & Educational Research; Psychiatry SC Education & Educational Research; Psychiatry GA QK312 UT WOS:A1995QK31200004 PM 24435570 ER PT J AU BUCKLEY, KM DELUCA, SA AF BUCKLEY, KM DELUCA, SA TI PULMONARY LYMPHANGIOMYOMATOSIS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Lymphangiomyomatosis is a rare disease of unknown etiology characterized by hamartomatous proliferation of smooth muscle in the pulmonary lymphatics, blood vessels and airways. The disease occurs exclusively in women of reproductive age. Although the clinical course and radiographic findings may strongly suggest lymphangiomyomatosis, definitive diagnosis is made by obtaining open-lung biopsy. The clinical course of lymphangiomyomatosis is progressive, leading to pulmonary insufficiency and death within 10 years. Treatment with hormonal manipulation and/or oophorectomy has resulted in temporary improvement or stabilization of the disease process. RP BUCKLEY, KM (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 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 MAR PY 1995 VL 51 IS 4 BP 831 EP 833 PG 3 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA QM003 UT WOS:A1995QM00300018 PM 7887359 ER PT J AU AMMAR, A WONG, M SINGH, BN AF AMMAR, A WONG, M SINGH, BN TI DIVERGENT EFFECTS OF CHRONIC AMIODARONE ADMINISTRATION ON SYSTOLIC AND DIASTOLIC FUNCTION IN PATIENTS WITH HEART-DISEASE SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID VENTRICULAR-FUNCTION; ARRHYTHMIAS; FAILURE AB The purpose of this study was to determine the effects of chronic amiodarone treatment on systolic and diastolic function in patients with cardiac disease undergoing treatment for resistant ventricular arrhythmias. Previous studies have shown that chronic amiodarone treatment either has no effect or increases left ventricular ejection fraction, but the effects on diastolic properties of the ventricle have not been defined. Twelve male patients were given loading doses of amiodarone followed by a maintenance regimen. Serial measurements of heart rate, blood pressure and indexes of systolic and diastolic function were measured by Doppler echocardiographic techniques at baseline conditions and at 2, 8, and 12 weeks of drug therapy. Changes in altered thyroid state were excluded by serial determinations of thyroid function, Amiodarone increased left ventricular ejection fraction (+16%, p <0.01 by 8 weeks), decreased presystolic ejection period/left ventricular ejection time (-12%, p <0.01 by 8 weeks), and increased velocity of circumferential fiber shortening (+22%, p <0.05 by 8 weeks). Amiodarone decreased mitral inflow velocity peak E/peak A (-7%, p <0.01 by 12 weeks), and increased deceleration and isovolumic relaxation times incrementally (+36% [p <0.001] and +23% [p <0.001], respectively, at 12 weeks). Chronically administered amiodarone can improve systolic function and exert a negative lusitropic action in patients with heart disease. C1 W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,CARDIOL SECT W111E,LOS ANGELES,CA 90073. ZAGAZIG UNIV,ZAGAZIG,EGYPT. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. NR 27 TC 17 Z9 18 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAR 1 PY 1995 VL 75 IS 7 BP 465 EP 469 DI 10.1016/S0002-9149(99)80582-7 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QH855 UT WOS:A1995QH85500008 PM 7863990 ER PT J AU THOMAS, SH STONE, CK AUSTIN, PE MARCH, JA BRINKLEY, S AF THOMAS, SH STONE, CK AUSTIN, PE MARCH, JA BRINKLEY, S TI UTILIZATION OF A PRESSURE-SENSING MONITOR TO IMPROVE IN-FLIGHT CHEST COMPRESSIONS SO AMERICAN JOURNAL OF EMERGENCY MEDICINE LA English DT Note DE CPR; HELICOPTERS; IN-FLIGHT; CHEST COMPRESSIONS AB University School of Medicine has demonstrated impairment of chest compression efficacy in the setting of an airborne 80-105 helicopter. This study was undertaken to determine whether in-flight compression efficacy could be improved with utilization of a pressure-sensing monitor providing real-time feedback during cardiopulmonary resuscitation (CPR). Ten flight nurses each performed two minutes of in-flight chest compressions on a mannequin that electronically assessed compression depth and hand placement. The session was then repeated using the pressure-sensing device., The mean proportion of correct compressions (95.7 +/- 3.2%) achieved with utilization of the pressure-sensing monitor was significantly higher (P <.01) than the corresponding proportion for the control group (33.4 +/- 12.1%). This study demonstrated that the difficulties of performing effective in-flight chest compressions are largely overcome with utilization of a pressure-sensing device providing real-time feedback on compression efficacy. ((C) 1995 by W.B. Saunders Company) RP THOMAS, SH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT EMERGENCY MED,DIV EMERGENCY MED,MGH CLIN 117,BOSTON,MA 02114, USA. OI March, Juan/0000-0002-8780-4882 NR 0 TC 19 Z9 19 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0735-6757 J9 AM J EMERG MED JI Am. J. Emerg. Med. PD MAR PY 1995 VL 13 IS 2 BP 155 EP 157 DI 10.1016/0735-6757(95)90083-7 PG 3 WC Emergency Medicine SC Emergency Medicine GA QQ147 UT WOS:A1995QQ14700008 PM 7893298 ER PT J AU FREBOURG, T BARBIER, N YAN, YX GARBER, JE DREYFUS, M FRAUMENI, J LI, FP FRIEND, SH AF FREBOURG, T BARBIER, N YAN, YX GARBER, JE DREYFUS, M FRAUMENI, J LI, FP FRIEND, SH TI GERM-LINE P53 MUTATIONS IN 15 FAMILIES WITH LI-FRAUMENI SYNDROME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID CANCER-PRONE FAMILY; BREAST-CANCER; SPLICING MUTATION; GENE; PROTEIN; PATIENT; PEDIGREE; TUMORS; SITE AB Germ-line mutations of the tumor-suppressor gene p53 have been observed in some families with the Li-Fraumeni syndrome (LFS), a familial cancer syndrome in which affected relatives develop a diverse set of early-onset malignancies including breast carcinoma, sarcomas, and brain tumors. The analysis of the p53 gene in LFS families has been limited, in most studies to date, to the region between exon 5 and exon 9. In order to determine the frequency and distribution of germ-line p53 mutations in LFS, we sequenced the 10 coding exons of the p53 gene in lymphocytes and fibroblast cell lines derived from 15 families with the syndrome. Germ-line mutations were observed in eight families. Six mutations were missense mutations located between exons 5 and 8. One mutation was a nonsense mutation in exon 6, and one mutation was a splicing mutation in intron 4, generating aberrant shorter p53 RNA(s). In three families, a mutation of the p53 gene was observed in the fibroblast cell line derived from the proband. However, the mutation was not found in affected relatives in two families and in the blood from the one individual, indicating that the mutation probably occurred during cell culture in vitro. In four families, no mutation was observed. This study indicates that germ-line p53 mutations in LFS are mostly located between exons 5 and 8 and that similar to 50% of patients with LFS have no germ-line mutations in the coding region of the p53 gene. The observation of p53 mutations occurring during primary cultures of human fibroblasts shows that analysis for germ-line p53 mutations must be performed on cells that have not been grown in vitro. C1 MASSACHUSETTS GEN HOSP E,DIV MOLEC GENET,BOSTON,MA. CHILDRENS HOSP,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CANC CONTROL,BOSTON,MA 02115. NCI,DIV CANC ETIOL,EPIDEMIOL & BIOSTAT PROGRAM,BETHESDA,MD 20892. NR 49 TC 138 Z9 142 U1 2 U2 2 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 MAR PY 1995 VL 56 IS 3 BP 608 EP 615 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA QK918 UT WOS:A1995QK91800008 PM 7887414 ER PT J AU ROMANGOLDSTEIN, S MITCHELL, P CROSSEN, JR WILLIAMS, PC TINDALL, A NEUWELT, EA AF ROMANGOLDSTEIN, S MITCHELL, P CROSSEN, JR WILLIAMS, PC TINDALL, A NEUWELT, EA TI MR AND COGNITIVE TESTING OF PATIENTS UNDERGOING OSMOTIC BLOOD-BRAIN-BARRIER DISRUPTION WITH INTRAARTERIAL CHEMOTHERAPY SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE BLOOD-BRAIN BARRIER; CHEMOTHERAPY; IATROGENIC DISEASE OR DISORDER; BRAIN, MAGNETIC RESONANCE ID CELL LUNG-CANCER; PRIMARY CNS LYMPHOMA; WHITE MATTER LESIONS; CEREBRAL-ANGIOGRAPHY; RADIATION-THERAPY; SURVIVORS; TUMORS; ABNORMALITIES; CT; NEUROTOXICITY AB PURPOSE: To determine whether osmotic blood-brain barrier disruption is associated with MR abnormalities or cognitive deterioration and, if so, whether the MR findings correlate with cognitive test results, METHODS: Fifteen brain tumor patients who had a complete tumor response (nine central nervous system lymphoma, three germ cell and two astrocytoma, and one primitive neuroectodermal tumor) treated with blood-brain barrier disruption procedures (318 total procedures) with intraarterial chemotherapy were included. MR images were evaluated for the development of white matter hyperintensity, vascular lesions, or atrophy. Cognitive testing was performed to assess deterioration caused by this therapy, RESULTS: In two patients white matter hyperintensity developed, in two small vascular lesions developed, and in one mild atrophy developed. One infarct was asymptomatic and the second one resulted in mild dysesthesia in one upper extremity. No patient showed diminished cognitive function on the posttherapy evaluation. CONCLUSION: In patients undergoing blood-brain barrier disruption with intraarterial chemotherapy, new abnormalities on MR imaging may develop. These patients maintain the same level of cognitive and neurologic function and MR findings do not correlate with the results of cognitive testing. C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT DIAGNOST RADIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT MED PSYCHOL,PORTLAND,OR 97201. PORTLAND VA MED CTR,PORTLAND,OR. ROYAL MELBOURNE HOSP,DEPT RADIOL,PARKVILLE,VIC 3050,AUSTRALIA. ST PETERS COMMUNITY HOSP,DEPT NEUROSCI,HELENA,MT. FU PHS HHS [31770] NR 50 TC 27 Z9 27 U1 0 U2 2 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 MAR PY 1995 VL 16 IS 3 BP 543 EP 553 PG 11 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA QM240 UT WOS:A1995QM24000022 PM 7793380 ER PT J AU KRUEGER, RR TALAMO, JH MCDONALD, MB VARNELL, RJ WAGONER, MD MCDONNELL, PJ AF KRUEGER, RR TALAMO, JH MCDONALD, MB VARNELL, RJ WAGONER, MD MCDONNELL, PJ TI CLINICAL ANALYSIS OF EXCIMER-LASER PHOTOREFRACTIVE KERATECTOMY USING A MULTIPLE ZONE TECHNIQUE FOR SEVERE MYOPIA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID FOLLOW-UP; SURGERY AB PURPOSE: In an investigational procedure, excimer laser photorefractive keratectomy for severe myopia was performed at three clinical trial centers to determine the effectiveness of the multiple zone technique. METHODS: A VisX Model Twenty/Twenty excimer laser (VisX, Santa Clara, California) was used to perform photorefractive keratectomy on 14 severely myopic eyes (-10.37 to -24.5 diopters) of 12 patients by using a multiple zone technique. Postoperative follow-up ranged from six months to two years; retreatments were performed on four patients, with a follow up of at least nine months. RESULTS: At six months postoperatively, before retreatment, three of the 14 eyes were within 2 diopters and seven of the 14 eyes were within 4 diopters of attempted correction. Regression of effect. to more severe myopia was worse in five eyes treated with nitrogen gas blowing. Retreatments also demonstrated considerable myopic regression. Three patients had loss of two or more lines of best corrected visual acuity, and these patients also had moderate or severe levels of haze. CONCLUSION: Excimer laser photorefractive keratectomy for severe myopia using a multiple zone technique is associated with considerable regression, haze, and loss of best corrected visual acuity, especially when performed in association with nitrogen gas blowing. C1 UNIV SO CALIF,SCH MED,DOHENY EYE INST,LOS ANGELES,CA 90033. UNIV SO CALIF,SCH MED,DEPT OPHTHALMOL,LOS ANGELES,CA 90033. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. LOUISIANA STATE UNIV,SCH MED,CTR EYE,NEW ORLEANS,LA. LOUISIANA STATE UNIV,SCH MED,DEPT OPHTHALMOL,NEW ORLEANS,LA. NR 20 TC 42 Z9 43 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 MAR PY 1995 VL 119 IS 3 BP 263 EP 274 PG 12 WC Ophthalmology SC Ophthalmology GA QK317 UT WOS:A1995QK31700001 PM 7872385 ER PT J AU AYLIFFE, W FOSTER, CS MARCOUX, P UPTON, M FINKELSTEIN, M KUPERWASER, M LEGMANN, A AF AYLIFFE, W FOSTER, CS MARCOUX, P UPTON, M FINKELSTEIN, M KUPERWASER, M LEGMANN, A TI RELAPSING ACUTE MYELOID-LEUKEMIA MANIFESTING AS HYPOPYON UVEITIS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CHEMOTHERAPY AB PURPOSE: Although acute lymphoblastic leukemia may masquerade as hypopyon uveitis, acute myeloid leukemia has only rarely been reported to cause this complication, and ocular relapse generally has been associated with evidence of malignant cells at other sites. We studied a patient with acute myeloid leukemia whose only sign of relapse was bilateral anterior uveitis with pseudo hypopyon that was refractory to topical and systemic corticosteroids. METHODS: A 26-year-old woman with acute myeloid leukemia in remission, who had bilateral anterior uveitis and increased intraocular pressure at initial examination, was studied clinically. Blood films, bone marrow smears, and, preparations were examined by using immunoperoxidase staining. RESULTS: Although there was no evidence of leukemia in the blood or bone marrow samples, the cells obtained from the anterior chamber showed myeloblastic leukemic cells with morphologic characteristics similar to those present in the original bone marrow biopsy obtained 14 months previously. Irradiation and chemotherapy were used to kill the malignant cells in the eve and central nervous system. The persisting glaucoma resolved after anterior chamber washout of necrotic tumor cells. CONCLUSIONS: Unusual features of uveitis in this patient indicated that she had a masquerade syndrome, despite normal results of bone marrow and blood film tests. Aspiration of intraocular cellular infiltrate for cytopathologic examination was required to obtain the correct diagnosis and enable treatment to commence without delay. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,SERV IMMUNOL,BOSTON,MA 02114. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,ONCOL SERV,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,OPHTHALMOL SERV,BOSTON,MA. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CYTOPATHOL SERV,BOSTON,MA. NR 13 TC 24 Z9 24 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 MAR PY 1995 VL 119 IS 3 BP 361 EP 364 PG 4 WC Ophthalmology SC Ophthalmology GA QK317 UT WOS:A1995QK31700016 PM 7872398 ER PT J AU PEKARY, AE BERG, L WANG, JY LEE, P DUBINETT, SM HERSHMAN, JM AF PEKARY, AE BERG, L WANG, JY LEE, P DUBINETT, SM HERSHMAN, JM TI TNF-ALPHA, TSH, AND AGING REGULATE TGF-BETA SYNTHESIS AND SECRETION IN FRTL-5 RAT-THYROID CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Article DE CELL CULTURE; NORTHERN ANALYSIS; ENZYME-LINKED IMMUNOSORBENT ASSAY; BIOASSAY; APOPTOSIS ID TRANSFORMING GROWTH-FACTOR; TUMOR-NECROSIS-FACTOR; MESSENGER-RNA; EXPRESSION; DNA; FACTOR-BETA-1; APOPTOSIS; IODINE; LINE AB Tumor necrosis factor-alpha (TNF-alpha), a cytokine produced by macrophages in response to a variety of pathological conditions, can inhibit thyroid cell function in vitro and in vivo. TNF-alpha induction of transforming growth factor-beta 1 (TGF-beta 1) in rat endothelial cells suggested that TGF-beta, a known mediator of inflammatory effects of TNF-alpha may be involved in the sensitivity of aged thyroid cells to TNF-alpha (G. Chen, A. E. Pekary, and J. M. Hershman. Endocrinology 131: 863-870, 1992). To determine whether TNF-alpha induces TGF-beta production in FRTL-5 cells, young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were grown to near confluency in medium containing 2 U/l of bovine thyroid-stimulating hormone [TSH; B-hormone (6H) medium] or no TSH [5-hormone (5H) medium]. TNF-alpha (0-100 ng/ml) was added 0-48 h before total RNA was extracted. Northern blots were hybridized with P-32-TGF-beta 1, -beta 2, and -beta 3 cDNAs. In aged cells TNF-alpha increased their TGF-beta 1 (and -beta 2 and -beta 3) mRNA levels 5.4-fold (and > 10-fold), respectively, while in young cells all TGF-beta mRNAs remained almost undetectable during incubation with TNF-alpha. In contrast, TNF-alpha and TSH had a highly significant stimulatory effect on the secretion rate of TGF-beta precursors in both young and old cells as measured in the mink lung cell bioassay. In summary, TNF-alpha and TSH enhance TGF-beta transcription and/or mRNA stability in aged, but not young, FRTL-5 cells, while TNF-alpha and TSH increase translation and secretion of TGF-beta in young and aged cells. C1 W LOS ANGELES VET AFFAIRS MED CTR, IMMUNOL PULM LAB, LOS ANGELES, CA 90073 USA. UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90073 USA. RP PEKARY, AE (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, ENDOCRINE RES LAB, BLDG 114, RM 200, 11301 WILSHIRE BLVD, LOS ANGELES, CA 90073 USA. NR 46 TC 21 Z9 22 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regulat. Integr. Compar. Physiol. PD MAR PY 1995 VL 268 IS 3 BP R808 EP R815 PG 8 WC Physiology SC Physiology GA QL386 UT WOS:A1995QL38600029 PM 7900924 ER PT J AU STAPLES, JF ZAPOL, WM BLOCH, KD KAWAI, N VAL, VMF HOCHACHKA, PW AF STAPLES, JF ZAPOL, WM BLOCH, KD KAWAI, N VAL, VMF HOCHACHKA, PW TI NITRIC-OXIDE RESPONSES OF AIR-BREATHING AND WATER-BREATHING FISH SO AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY LA English DT Note DE NITRIC OXIDE SYNTHASE; GAS BLADDER; HOPLERYTHRINUS UNITAENIATUS; TELEOST; LUNGFISH ID RELAXATION; VESSELS; CGMP AB Nitric oxide (NO), exogenously administered or endogenously produced by NO synthase (NOS), is an important regulator of lung ventilation and perfusion in mammals. This study attempts to investigate the evolutionary history of this system in fish and its possible relationship to air breathing. The gas bladder of Hoplerythrinus unitaeniatus (air-breathing teleost) and Oncorhynchus mykiss (non-air-breathing teleost) and the lung of Lepidosiren paradoxa (air-breathing dipnoan) all exhibited elevated guanosine 3',5'-cyclic monophosphate (cGMP) levels in response to 1 mu M sodium nitroprusside. Only the H. unitaeniatus gas bladder responded to 10 mu M acetylcholine chloride (ACh) with increased cGMP levels. The ACh response was inhibited by N-omega-nitro-L-arginine methyl ester, which inhibits NOS. These data suggest that although tissues from each species may respond to exogenous NO, only the gas bladder of H. unitaeniatus appears to synthesize NO through NOS, This is the first report of constitutive NOS outside of the central nervous system in a teleost. These results also imply that NOS did not necessarily coevolve with air breathing in fish. C1 MASSACHUSETTS GEN HOSP, DEPT ANESTHESIA, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP E, CARDIOVASC RES CTR, BOSTON, MA 02129 USA. INST NACL PESQUISAS, BR-69083 MANAUS, AMAZONAS, BRAZIL. RP STAPLES, JF (reprint author), UNIV BRITISH COLUMBIA, DEPT ZOOL, VANCOUVER, BC V6T 1Z4, CANADA. FU NHLBI NIH HHS [HL-45895, HL-42397] NR 26 TC 1 Z9 1 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6119 J9 AM J PHYSIOL-REG I JI Am. J. Physiol.-Regulat. Integr. Compar. Physiol. PD MAR PY 1995 VL 268 IS 3 BP R816 EP R819 PG 4 WC Physiology SC Physiology GA QL386 UT WOS:A1995QL38600030 PM 7535013 ER PT J AU TANG, SS JUNG, F DIAMANT, D BROWN, D BACHINSKY, D HELLMAN, P INGELFINGER, JR AF TANG, SS JUNG, F DIAMANT, D BROWN, D BACHINSKY, D HELLMAN, P INGELFINGER, JR TI TEMPERATURE-SENSITIVE SV40 IMMORTALIZED RAT PROXIMAL TUBULE CELL-LINE HAS FUNCTIONAL RENIN-ANGIOTENSIN SYSTEM SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; WISTAR RAT; LOSARTAN; ANGIOTENSIN II RECEPTOR; AQUAPORIN CHIP28; HEYMANN ANTIGEN GP330 ID CONVERTING ENZYME; HEYMANN NEPHRITIS; MOLECULAR-CLONING; EPITHELIAL-CELLS; KIDNEY CORTEX; MESSENGER-RNA; LOCALIZATION; RECEPTOR; ESTABLISHMENT; IDENTIFICATION AB Immortalized rat proximal tubule cell (IRPTC) lines should be useful for investigation of proximal tubule (PT) regulation and function but previously have been unavailable. We now report the establishment and characterization of an immortalized transformed, temperature-sensitive IRPTC cell line containing renin-angiotensin system (RAS) components. Primary PT cells prepared from male Wistar rats (4-5 wk old) after collagenase digestion, sieving, and Percoll gradient were cultured on collagen-coated T-75 flasks in Dulbecco's modified Eagle's medium containing 5% fetal calf serum. Subconfluent PT cells were transfected with the temperature-sensitive SV40 mutant viruses (tsA SV40) by direct exposure. After 7-8 wk, several clones were obtained, from which one has been characterized and designated as line 3-2. This cell line appears stable up to 45 passages. Clonal cells transformed with this virus exhibit a transformed phenotype at a permissive temperature of 34 degrees C and grow in multiple layers. When the cells are subsequently placed at a nonpermissive temperature of 41 degrees C, they return to morphology similar to that of untransformed cells of the same lineage. At either 34 degrees C or 41 degrees C, this cell line expresses a variety of PT markers including alkaline phosphatase, cytokeratin, carbonic anhydrase, and glucose transporter isoform 2 (GLUT2), while not expressing factor VIII. Uniquely, these cells also appear to express PT proteins gp330 and CHIP28, markers which are usually lost in cultured cells. Furthermore, the cell line expresses protein and mRNA components of RAS, including angiotensinogen, angiotensin converting enzyme, and renin. The IRPTC cell line expresses few angiotensin II (ANG II) receptors at 34 degrees C, the permissive temperature. However, at the nonpermissive temperature, 41 degrees C, IRPTC expresses ANG II receptor (dissociation constant of 0.7 nM; maximum binding capacity of 265 fmol/mg protein). ANG II (10(-8) M) induced a transient rise in cytoplasmic Ca2+ concentration, which was nearly abolished with losartan but not PD-123319, suggesting this finding is AT(1) receptor mediated. This cell line should provide an excellent model of PT and should make it possible to study the cell and molecular biology of the RAS, as well as other regulatory systems of the PT. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,RES PATHOL LAB, NEPHROL LAB,PEDIAT NEPHROL LAB, BOSTON, MA 02114 USA. UNIV UPPSALA HOSP, DEPT SURG, S-75185 UPPSALA, SWEDEN. FU NHLBI NIH HHS [HL-40210, HL-48455, HL-43131] NR 60 TC 77 Z9 77 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD MAR PY 1995 VL 268 IS 3 BP F435 EP F446 PG 12 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA QL359 UT WOS:A1995QL35900011 PM 7900843 ER PT J AU TSAI, GC GASTFRIEND, DR COYLE, JT AF TSAI, GC GASTFRIEND, DR COYLE, JT TI THE GLUTAMATERGIC BASIS OF HUMAN ALCOHOLISM SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID METHYL-D-ASPARTATE; ETHANOL WITHDRAWAL SEIZURES; LONG-TERM POTENTIATION; EXCITATORY AMINO-ACIDS; EVOKED ELECTROPHYSIOLOGICAL ACTIVITY; RECEPTOR IONOPHORE COMPLEX; CEREBELLAR GRANULE CELLS; ACTIVATED ION CURRENT; RAT STRIATAL SLICES; NMDA RECEPTOR AB Objective: Although alcoholism is one of the most common psychiatric diagnoses, understanding of its pathophysiology remains goer. Accumulating evidence suggests that neurophysiological and pathological effects of ethanol are mediated to a considerable extent through the glutamatergic system. This article reviews the evidence for ethanol's effects on glutamatergic transmission and proposes a glutamatergic basis for alcoholism. Method: The information was derived from original research. The authors located more than 100 articles from psychiatry and neuroscience journals that related ethanol to glutamatergic transmission. They critically reviewed the neurobiology of the glutamatergic system in alcoholism and synthesized a unifying glutamatergic theory. Results: Acute effects of ethanol disrupt glutamatergic neurotransmission by inhibiting the response of the N-methyl-D-aspartate (NMDA) receptor. Prolonged inhibition of the NMDA receptor by ethanol results in development of supersensitivity; acute removal of ethanol causes marked augmentation of activity of postsynaptic neurons, such as those in the noradrenergic system, and, in the extreme, glutamate-induced excitotoxicity. Neurobiological effects of alcoholism, such as intoxication, withdrawal seizures, delirium tremens, Wernicke-Korsakoff syndrome, and fetal alcohol syndrome, cart be understood as a spectrum of consequences of ethanol's effect on the glutamatergic system. Conclusions: A host of findings support the hypothesis that the unifying mechanism of action of ethanol is interference with glutamatergic neurotransmission, especially through the NMDA receptor. Alcoholism may be considered another member of the expanding family of glutamate-related neuropsychiatric disorders. These insights should increase understanding of the biologic vulnerabilities leading to ethanol abuse and dependence and aid development of more effective pharmacologic interventions. C1 HARVARD UNIV,MCLEAN HOSP,SCH MED,DEPT PSYCHIAT,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,ADDICT SERV,BOSTON,MA. MASSACHUSETTS GEN HOSP,MOLEC & DEV NEUROSCI LAB,BOSTON,MA. FU NIMH NIH HHS [MH-512901]; NINDS NIH HHS [NS-13584] NR 78 TC 262 Z9 268 U1 2 U2 17 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 MAR PY 1995 VL 152 IS 3 BP 332 EP 340 PG 9 WC Psychiatry SC Psychiatry GA QJ604 UT WOS:A1995QJ60400003 PM 7864257 ER PT J AU BIEDERMAN, J FARAONE, SV MICK, E SPENCER, T WILENS, T KIELY, K GUITE, J ABLON, JS REED, E WARBURTON, R AF BIEDERMAN, J FARAONE, SV MICK, E SPENCER, T WILENS, T KIELY, K GUITE, J ABLON, JS REED, E WARBURTON, R TI HIGH-RISK FOR ATTENTION-DEFICIT HYPERACTIVITY DISORDER AMONG CHILDREN OF PARENTS WITH CHILDHOOD-ONSET OF THE DISORDER - A PILOT-STUDY SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PSYCHIATRIC STATUS; GENERAL-POPULATION; FOLLOW-UP; ADULTS; BOYS; METHYLPHENIDATE; COMORBIDITY; PREVALENCE; GENETICS; PATTERNS AB Objective: Although well-documented in clinical and epidemiological studies of attention deficit hyperactivity disorder (ADHD) in children, the familial nature of the adult syndrome has not been well investigated. One approach to evaluate the familial nature of adult ADHD is through a high-risk design aimed at estimating the risk for the disorder in children of parents with childhood-onset ADHD. Method: Children at risk for ADHD were ascertained from the study group of 84 referred adults with clinical diagnoses of childhood onset of the disorder, confirmed by structured interviews. Diagnostic information on the disorder was derived from the ADHD module of the Schedule for Affective Disorders and Schizophrenia for School Age Children-Epidemiologic Version, supplemented with information regarding treatment for ADHD for the affected child and school history including repeated grades, placement in special classes, and tutoring. Results: Of the 84 children at risk, 48 (57%) met criteria for ADHD. The rate of the disorder in children of adults with the disorder was significantly higher than the previously reported rate of ADHD among siblings of children with the disorder. Of the 48 ADHD children of parents with the disorder, 36 (75%) were treated for it. The rates of school failure were almost identical to those previously reported in a group of referred children and adolescents with ADHD. Conclusions: These results support the validity of the adult diagnosis of ADHD and suggest that the adult form of this disorder may have stronger familial etiological risk factors than its pediatric form. If these results are confirmed, families selected through adult probands with ADHD might be especially useful for testing genetic hypotheses about the disorder. C1 HARVARD UNIV,SCH MED,BOSTON,MA. VET ADM MED CTR,PSYCHIAT SERV,BROCKTON,MA. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT WACC725,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Mick, Eric/0000-0001-8505-8145; Faraone, Stephen/0000-0002-9217-3982 NR 44 TC 135 Z9 136 U1 1 U2 9 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 MAR PY 1995 VL 152 IS 3 BP 431 EP 435 PG 5 WC Psychiatry SC Psychiatry GA QJ604 UT WOS:A1995QJ60400017 PM 7864271 ER PT J AU CHRISTAKIS, NA ASCH, DA AF CHRISTAKIS, NA ASCH, DA TI PHYSICIAN CHARACTERISTICS ASSOCIATED WITH DECISIONS TO WITHDRAW LIFE-SUPPORT SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID SUSTAINING TREATMENT; CRITICALLY ILL; INTENSIVE-CARE; ATTITUDES; PREFERENCES; EUTHANASIA AB Objective. This study was undertaken to identify attributes of physicians associated with physicians' decisions to withdraw life support. Methods. Of the 862 Pennsylvania internists surveyed and asked to make decisions in response to hypothetical vignettes and to report their actual experience with the withdrawal of life support, 485 (56%) responded. The data were analyzed with regression models. Results With other factors controlled physicians were more willing to withdraw life support if they were young, practiced in a tertiary care setting or spent more time in clinical practice; they were less willing if they were Catholic or Jewish. Physicians reported a higher frequency of actually withdrawing life support if they were-young, had more contact with ICU patients, spent more time in clinical practice, or were specialists. Physicians with a greater willingness to withdraw were more likely to report having done so. Conclusions. Physicians' personal characteristics are associated with both their preferences and their practice in the withdrawal of life support, and a greater willingness to withdraw is associated with a higher frequency, of withdrawal. The influence of physician characteristics demonstrates that patient preferences and clinical circumstances do not exclusively-govern such ethical decisions. C1 UNIV PENN,SCH MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA 19104. UNIV PENN,DEPT SOCIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP CHRISTAKIS, NA (reprint author), UNIV CHICAGO,MED CTR,ROOM W-700,5841 S MARYLAND AVE,CHICAGO,IL 60637, USA. RI Christakis, Nicholas/B-6690-2008; Christakis, Nicholas/C-3205-2009 NR 30 TC 112 Z9 113 U1 1 U2 2 PU AMER PUBLIC HEALTH ASSN INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD MAR PY 1995 VL 85 IS 3 BP 367 EP 372 DI 10.2105/AJPH.85.3.367 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA QM393 UT WOS:A1995QM39300017 PM 7892921 ER PT J AU MANG, H KACMAREK, RM RITZ, R WILSON, RS KIMBALL, WP AF MANG, H KACMAREK, RM RITZ, R WILSON, RS KIMBALL, WP TI CARDIORESPIRATORY EFFECTS OF VOLUME-CONTROLLED AND PRESSURE-CONTROLLED VENTILATION AT VARIOUS I/E RATIOS IN AN ACUTE LUNG INJURY MODEL SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID MEAN AIRWAY PRESSURE; RESPIRATORY-DISTRESS-SYNDROME; END-EXPIRATORY PRESSURE; DECELERATING INSPIRATORY FLOW; HYALINE-MEMBRANE DISEASE; ACUTE PULMONARY FAILURE; MECHANICAL VENTILATION; INVERSE RATIO; GAS-EXCHANGE; PEEP AB Numerous approaches to the provision of mechanical ventilation during acute lung injury are currently available. Of these, pressure control inverse ratio ventilation has been considered superior to volume control ventilation with PEEP with respect to improving gas exchange and minimizing cardiovascular compromise. However, no study systematically compares volume-controlled (VC) and pressure-controlled (PC) ventilation while maintaining mean airway pressure (MAP) constant at varying I/E ratios. We studied the effect of VC and PC with PEEP at normal (1:2) and inverse I/E ratios (2:1 and 4:1) on gas exchange, lung mechanics, and hemodynamics in a sheep lung injury model. Severe lung injury was induced in 12 sheep with bilateral lung ravages using normal saline; prelavage PO2 230 +/- 50 mm Hg, PEEP 5 cm H2O and postlavage, pretreatment PO2 70 +/- 20 mm Hg, PEEP 10 cm H2O both at Fl(O2) 0.50. MAP was kept constant throughout the study at 25 +/- 2 cm H2O while ventilating all animals with a VT of 10 ml/kg and a rate of 20/min by randomized application of VC and PC with I/E ratios of 1:2, 2:1, and 4:1. Despite liberal fluid administration, all ventilatory modes depressed cardiac output compared with preinjury values. However, gas exchange and hemodynamics did not differ among ventilation modes or I/E ratios. Of all the parameters investigated, the most striking changes occurred in peak inspiratory pressure (PIP) and PEEP: PC (I/E 2:1 and 4:1) resulted in significantly (p < 0.05) lower values for PIP and applied PEEP compared with control data (VC I/E ratio 1:1), and VC (I/E 4:1) resulted in significantly (p < 0.05) lower values for applied PEEP than VC I/E ratio 1:1. Auto PEEP levels during PC (I/E ratio 2:1 and 4:1) and VC (I/E 2:1 and 4:1) were significantly higher (p < 0.05) than VC I/E ratio 1:1. When MAP remained constant, alterations in the ventilation mode (PC or VC) or I/E ratio (1:2 to 4:1) produced no significant change in hemodynamic, oxygenation, or ventilation parameters in this sheep model. C1 MASSACHUSETTS GEN HOSP,DEPT RESP CARE,RESP CARE SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 36 TC 31 Z9 33 U1 0 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD MAR PY 1995 VL 151 IS 3 BP 731 EP 736 PG 6 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA QL391 UT WOS:A1995QL39100026 PM 7881663 ER PT J AU LUSTRIN, ES STALLMEYER, MJB BROWN, JH CHEW, FS AF LUSTRIN, ES STALLMEYER, MJB BROWN, JH CHEW, FS TI MULTIPLE-SCLEROSIS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note ID MR C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP LUSTRIN, ES (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 0 Z9 0 U1 0 U2 3 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1995 VL 164 IS 3 BP 672 EP 672 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QH860 UT WOS:A1995QH86000024 PM 7863891 ER PT J AU BROWN, EW MEGERIAN, CA MCKENNA, MJ WEBER, A AF BROWN, EW MEGERIAN, CA MCKENNA, MJ WEBER, A TI FIBROUS DYSPLASIA OF THE TEMPORAL BONE - IMAGING FINDINGS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article AB Lichtenstein [1] in 1938 coined the term fibrous dysplasia to describe a disorder characterized by the progressive replacement of normal bone elements by fibrous tissue. Histopathologically, these lesions consist of an abnormal proliferation of fibrous elements intermixed with haphazardly arranged trabeculae of woven bone. The disease can involve any bone in the body. In the head and neck, the skull and facial bones are involved in 10-25% of cases of monostotic fibrous dysplasia and in 50% of the polyostotic variety. Involvement of the temporal hone, however, is relatively rare, and only 53 cases have been reported. The three major radiographic classifications of fibrous dysplasia are pagetoid, sclerotic, and cystic. Any of these types may involve the temporal bone and related structures, including the external canal, middle ear, jugular foramen, or, rarely, the otic capsule. In this essay, we illustrate the radiographic features of the disease based on our experience with seven cases, seen at our institution since 1977, of fibrous dysplasia involving the temporal bone C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02114. RP BROWN, EW (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT RADIOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 6 TC 41 Z9 43 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 MAR PY 1995 VL 164 IS 3 BP 679 EP 682 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QH860 UT WOS:A1995QH86000026 PM 7863893 ER PT J AU CASTELLI, I STEINER, LA KAUFMANN, MA ALFILLE, PH SCHOUTEN, R WELCH, CA DROP, LJ AF CASTELLI, I STEINER, LA KAUFMANN, MA ALFILLE, PH SCHOUTEN, R WELCH, CA DROP, LJ TI COMPARATIVE EFFECTS OF ESMOLOL AND LABETALOL TO ATTENUATE HYPERDYNAMIC STATES AFTER ELECTROCONVULSIVE-THERAPY SO ANESTHESIA AND ANALGESIA LA English DT Article ID SEIZURE DURATION; ECT; HYPERTENSION; RESPONSES; PATIENT AB We studied 18 patients (age range, 53-90 yr) with at least one cardiovascular risk factor who were treated with electroconvulsive therapy (ECT) and compared effects of five pretreatments: no drug; esmolol, 1.3 or 4.4 mg/kg; or labetalol, 0.13 or 0.44 mg/kg. Each patient received all five treatments, during a series of five ECT sessions. Pretreatment was administered as a bolus within 10 s of induction or anesthesia. Doses of methohexital and succinylcholine were constant for the series of treatments and the assignment to no drug or to drug and dose was determined by randomized block design. Measurements of systolic and diastolic blood pressure SBP, DBP) and heart rate (HR) were recorded during the awake state and 1, 3, 5, and 10 min after the seizure. The deviation of ST segments from baseline was measured by an electrocardiogram (ECG) monitor equipped with ST-segment analysis software. The results (mean +/- SBM) show that without pretreatment, there were significant (P < 0.05) peak increases in SEP and HR (55 +/- 5 mm Hg and 37 +/- 6 bpm, respectively), recorded 1 min after the seizure. Comparable reductions (by approximately 50%) in these peak values were achieved after esmolol (1.3 mg/kg) or labetalol (0.13 mg/kg), and cardiovascular responses were nearly eliminated after the same drugs in doses of 4.4 and 0.44 mg/kg respectively. The deviation of ST-segment values from baseline in any lead was not measurably influenced by either antihypertensive drug. SEP values were lower after labetalol 10 min after the seizure, but not after esmolol. Asystolic time after the seizure was not significantly longer with either drug. No adverse reactions were observed. Because SEP effects were still present 10 min after the seizure, esmolol may be preferred if administration of a large dose of a beta-adrenergic blocker is contemplated. C1 MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,ANESTHESIA & PSYCHIAT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RI Steiner, Luzius/C-9836-2011 NR 18 TC 63 Z9 64 U1 1 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD MAR PY 1995 VL 80 IS 3 BP 557 EP 561 DI 10.1097/00000539-199503000-00022 PG 5 WC Anesthesiology SC Anesthesiology GA QJ611 UT WOS:A1995QJ61100022 PM 7864425 ER PT J AU ECKHARDT, WF FORMAN, S DENMAN, W GRILLO, HC MUEHRCKE, D AF ECKHARDT, WF FORMAN, S DENMAN, W GRILLO, HC MUEHRCKE, D TI ANOTHER USE FOR THE LARYNGEAL MASK AIRWAY - AS A BLOCKER DURING TRACHEOPLASTY SO ANESTHESIA AND ANALGESIA LA English DT Note ID TRACHEOPATHIA OSTEOPLASTICA; COMPUTED-TOMOGRAPHY C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,BOSTON,MA 02114. NR 19 TC 4 Z9 4 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD MAR PY 1995 VL 80 IS 3 BP 622 EP 624 PG 3 WC Anesthesiology SC Anesthesiology GA QJ611 UT WOS:A1995QJ61100036 PM 7864439 ER PT J AU HALL, PD LESHER, BA HALL, RK AF HALL, PD LESHER, BA HALL, RK TI ADJUVANT THERAPY OF NODE-NEGATIVE BREAST-CANCER SO ANNALS OF PHARMACOTHERAPY LA English DT Review ID COST-EFFECTIVENESS; TAMOXIFEN THERAPY; POSTMENOPAUSAL WOMEN; ESTROGEN-RECEPTORS; PROGNOSTIC FACTORS; DECISION-ANALYSIS; DOSE INTENSITY; BOWEL PROJECT; CATHEPSIN-D; FOLLOW-UP AB OBJECTIVE: To present the controversies regarding adjuvant cytotoxic chemotherapy or hormonal therapy in patients with node-negative breast cancer, and to evaluate the use of prognostic factors in identifying patients with node-negative breast cancer who will benefit from adjuvant therapy. DATA SOURCE: A MEDLINE search was performed to identify pertinent primary literature and review articles. Articles also were identified through Current Contents, textbooks, and bibliographies of selected articles. DATA EXTRACTION: The most recent clinical trials that evaluated cytotoxic chemotherapy or hormonal therapy in patients with node-negative breast cancer were chosen. Recent review articles and clinical trials that analyzed prognostic factors also were evaluated. DATA SYNTHESIS: The treatment of patients with node-negative breast cancer remains controversial. Approximately 60-80% of patients with this diagnosis will be alive 10 years after initial treatment without adjuvant therapy. The use of chemotherapy or hormonal therapy in node-negative disease increased after the 1988 National Cancer Institute Clinical Alert. Since that time, the research in node-negative breast cancer has focused on identifying prognostic factors and evaluating new treatment regimens. It is hoped that prognostic factors will help direct treatment decisions by identifying subgroups of patients who may benefit from adjuvant therapy. Prognostic factors currently being evaluated include tumor size, hormonal receptors, ploidy status, S-phase fraction, and cathepsin D. CONCLUSIONS: Many patients with node-negative breast cancer will be cured by local therapy alone. Even so, up to 58% of node-negative patients may develop recurrent disease. Reduction of breast cancer recurrence in patients with node-negative breast cancer has been documented as a result of adjuvant chemotherapy or tamoxifen. Of utmost priority is the identification of patients with node-negative breast cancer at highest risk for recurrence so that they may receive appropriate adjuvant therapy with curative intent, while sparing patients at lower risk for recurrence the toxic effects and financial burden incurred by unnecessary adjuvant treatment. C1 MED UNIV HOSP S CAROLINA,CHARLESTON,SC. HOLLINGS CANC CTR,CHARLESTON,IL. RALPH H JOHNSON VET AFFAIRS HOSP,CHARLESTON,IL. RP HALL, PD (reprint author), MED UNIV S CAROLINA,COLL PHARM,171 ASHLEY AVE,CHARLESTON,SC 29425, USA. NR 65 TC 2 Z9 2 U1 0 U2 0 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD MAR PY 1995 VL 29 IS 3 BP 289 EP 298 PG 10 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QN754 UT WOS:A1995QN75400011 PM 7606076 ER PT J AU SCHMIDT, J HOTZ, HG FOITZIK, T RYSCHICH, E BUHR, HJ WARSHAW, AL HERFARTH, C KLAR, E AF SCHMIDT, J HOTZ, HG FOITZIK, T RYSCHICH, E BUHR, HJ WARSHAW, AL HERFARTH, C KLAR, E TI INTRAVENOUS CONTRAST-MEDIUM AGGRAVATES THE IMPAIRMENT OF PANCREATIC MICROCIRCULATION IN NECROTIZING PANCREATITIS IN THE RAT SO ANNALS OF SURGERY LA English DT Article ID TRYPSINOGEN-ACTIVATION PEPTIDES; ENHANCED COMPUTED-TOMOGRAPHY; EARLY DIAGNOSIS; PREDICTION; NECROSIS; MODEL; ERYTHROCYTES; HEMATOCRIT; MORPHOLOGY; ISCHEMIA AB Background Previous reports demonstrated that radiographic contrast medium, as used in contrast-enhanced computed tomography, increases acinar necrosis and mortality in experimental pancreatitis. The authors studied the possibility that these changes may be related to an additional impairment of pancreatic microcirculation. Methods Fifty Wistar rats had acute pancreatitis induced by intraductal glycodeoxycholic acid (10 mmol/L for 10 min) and intravenous cerulein (5 mu g/kg/hr for 6 hrs). After rehydration (16 mL/kg), pancreatic capillary perfusion was quantified by means of intravital microscopy at baseline before intravenous infusion of contrast medium (n = 25) or saline (n = 25), and 30 and 60 minutes thereafter. In addition to total capillary flow, capillaries were categorized as high- or low-flow (> or < 1.6 nl/min). Results Pancreatic capillary flow did not change in either high- or low-flow capillaries after saline infusion. However, contrast medium infusion induced a significant decrease of total capillary flow (p < 0.001). Analysis according to the relative flow rate revealed that this was primarily because of a significant additional reduction of perfusion in low-flow capillaries (p < 0.0001). Furthermore, complete capillary stasis was observed in 15.9 +/- 3.4% after contrast medium as compared with 3.2 +/- 1.2% after saline infusion (p < 0.006). Conclusion Radiographic contrast medium aggravates the impairment of pancreatic microcirculation in experimental necrotizing pancreatitis. C1 MASSACHUSETTS GEN HOSP, DEPT SURG, BOSTON, MA 02114 USA. RP SCHMIDT, J (reprint author), UNIV HEIDELBERG, DEPT SURG, NEUENHEIMER FELD 110, D-69120 HEIDELBERG, GERMANY. NR 48 TC 58 Z9 60 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD MAR PY 1995 VL 221 IS 3 BP 257 EP 264 DI 10.1097/00000658-199503000-00007 PG 8 WC Surgery SC Surgery GA QL977 UT WOS:A1995QL97700007 PM 7717779 ER PT J AU BROTHERS, TE ROBISON, JG ELLIOTT, BM ARENS, C AF BROTHERS, TE ROBISON, JG ELLIOTT, BM ARENS, C TI IS INFRAPOPLITEAL BYPASS COMPROMISED BY DISTAL ORIGIN OF THE PROXIMAL ANASTOMOSIS SO ANNALS OF VASCULAR SURGERY LA English DT Article AB Distal origination of the proximal anastomosis (DOPA) of an infrapopliteal bypass beyond the adductor hiatus minimizes the length of graft required and optimizes use of scarce autogenous conduit. Sixty-two DOPA infrapopliteal revascularizations using autogenous vein performed for limb salvage over a 7-year period were reviewed and compared with 203 concurrent infrapopliteal bypasses originating more proximally (POPA). Life-table analysis revealed no difference at 54 months between DOPA and POPA bypass with regard to primary patency (57% vs. 50%, respectively) or secondary patency (67% vs. 65%, respectively). Differences in limb salvage at 54 months between DOPA and POPA bypasses did not reach statistical significance (53% vs. 66%, p = 0.12), although DOPA fared worse. Inferior limb salvage results in all infrapopliteal bypasses were correlated with the presence of tissue necrosis (52% vs. 70%, p < 0.001), which was more prevalent in patients undergoing DOPA bypass (71% vs. 49%, p < 0.01). The long-term patency of infrapopliteal bypass appears only marginally affected by DOPA. However, the prognosis for limb salvage in this setting is compromised as a result of the virulent behavior of the atherosclerotic disease that spares the superficial femoral artery while predominantly involving the popliteal and tibial vessels. C1 RALPH HENRY JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC. MED UNIV S CAROLINA,CHARLESTON,SC 29425. RI Arens, Christoph/G-1796-2013 OI Arens, Christoph/0000-0001-8072-1438 NR 4 TC 11 Z9 11 U1 0 U2 0 PU QUALITY MEDICAL PUBLISHING INC PI ST LOUIS PA 11970 BORMAN DR, STE 222, ST LOUIS, MO 63146 SN 0890-5096 J9 ANN VASC SURG JI Ann. Vasc. Surg. PD MAR PY 1995 VL 9 IS 2 BP 172 EP 178 DI 10.1007/BF02139660 PG 7 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA QR281 UT WOS:A1995QR28100007 PM 7786703 ER PT J AU SHOULSON, I FAHN, S OAKES, D ODOROFF, C LANG, A LANGSTON, JW LEWITT, P OLANOW, CW PENNEY, JB TANNER, C KIEBURTZ, K RUDOLPH, A PELUSIO, RM KOLLER, W OLANOW, W RODNITZKY, R FINK, JS GROWDON, JH PAULSON, G KURLAN, R FRIEDMAN, JH GANCHER, S NUTT, J RAJPUT, AH BENNETT, JB WOOTEN, GF GOETZ, C SHANNON, K BRIN, MF BRESSMAN, SB WEINER, MJ SANCHEZRAMOS, J JANKOVIC, J HOEHN, M TETRUD, J GRIMES, JD PFEIFFER, R SHULTS, C THAL, L GAUTHIER, S GOLBE, LI PERLMUTTER, JS MOSES, H REICH, SG HURTIG, HI STERN, M BARTER, R VETEREOVERFIELD, B GAUGER, L MALAPIRA, T DOBSON, J ATAMIAN, S TENNIS, M COHEN, JB DESCLOS, G HOFFMAN, E DENIO, L HUBER, S WOIKE, T ZOOG, K MENDELL, R DUDTE, K BEHR, J GARDINER, IF LANNON, M CARTER, J NORTHRUP, S KANIGAN, B TURK, M LANDOW, E SCHLICK, P MISTURA, K CARROLL, VS THELEN, JA DEMONG, C WINFIELD, L MOSKOWITZ, C INGENITO, A SHELDON, C CORNELIUS, L HEIBERG, D DUNNE, C BRADY, J KIERANS, C BELLESCANTLEBURY, L DUFF, J WEBER, H SAVOINI, D LEWIS, P KUTNER, SJ GRAY, P GLAESKE, C HOFMAN, R PAY, MM SALMON, D MCFAUL, F AMYOT, D BERGEN, M MCGEEMINNICH, L ODONNELL, P FERRISE, S SHALLOW, K AF SHOULSON, I FAHN, S OAKES, D ODOROFF, C LANG, A LANGSTON, JW LEWITT, P OLANOW, CW PENNEY, JB TANNER, C KIEBURTZ, K RUDOLPH, A PELUSIO, RM KOLLER, W OLANOW, W RODNITZKY, R FINK, JS GROWDON, JH PAULSON, G KURLAN, R FRIEDMAN, JH GANCHER, S NUTT, J RAJPUT, AH BENNETT, JB WOOTEN, GF GOETZ, C SHANNON, K BRIN, MF BRESSMAN, SB WEINER, MJ SANCHEZRAMOS, J JANKOVIC, J HOEHN, M TETRUD, J GRIMES, JD PFEIFFER, R SHULTS, C THAL, L GAUTHIER, S GOLBE, LI PERLMUTTER, JS MOSES, H REICH, SG HURTIG, HI STERN, M BARTER, R VETEREOVERFIELD, B GAUGER, L MALAPIRA, T DOBSON, J ATAMIAN, S TENNIS, M COHEN, JB DESCLOS, G HOFFMAN, E DENIO, L HUBER, S WOIKE, T ZOOG, K MENDELL, R DUDTE, K BEHR, J GARDINER, IF LANNON, M CARTER, J NORTHRUP, S KANIGAN, B TURK, M LANDOW, E SCHLICK, P MISTURA, K CARROLL, VS THELEN, JA DEMONG, C WINFIELD, L MOSKOWITZ, C INGENITO, A SHELDON, C CORNELIUS, L HEIBERG, D DUNNE, C BRADY, J KIERANS, C BELLESCANTLEBURY, L DUFF, J WEBER, H SAVOINI, D LEWIS, P KUTNER, SJ GRAY, P GLAESKE, C HOFMAN, R PAY, MM SALMON, D MCFAUL, F AMYOT, D BERGEN, M MCGEEMINNICH, L ODONNELL, P FERRISE, S SHALLOW, K TI CEREBROSPINAL-FLUID HOMOVANILLIC-ACID IN THE DATATOP STUDY ON PARKINSONS-DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Article ID MONOAMINE OXIDASE-A; BRAIN; DOPAMINE; CSF; METABOLITES AB Objectives: To determine whether cerebrospinal fluid (CSF) homovanillic acid (HVA) concentration in subjects with early, mild Parkinson's disease (PD) treated with the monoamine oxidase type B inhibitor selegiline hydrochloride differs from that of control subjects receiving placebo. Our hypothesis is that if selegiline offers neuroprotection in such patients, the HVA levels should not decrease over time as much as in those receiving placebo. A second objective was to define the kinetics of recovery of HVA concentration after discontinuation of selegiline therapy. Design: During the controlled clinical trial DATATOP (deprenyl [selegiline] and tocopherol antioxidative therapy of parkinsonism) (which examined the effects of selegiline and tocopherol in 800 subjects with early, untreated PD), the CSF HVA concentration was measured at baseline and again 4 weeks after the study end point (need for levodopa therapy) was reached and medications were withdrawn (n=265). Based on an interim analysis, the lumbar puncture protocol tvas modified, such that subjects who reached the study end point were randomly assigned an interval of 0 days or 2, 6, or 8 weeks between discontinuation of selegiline therapy and the lumbar puncture (n=215). Setting: In the hospital, after overnight bed rest and fasting. Patients: The 800 subjects with early, mild PD who participated in the DATATOP controlled clinical trial. Intervention: The four treatment arms were (1) selegiline-placebo and tocopherol-placebo, (2) selegiline-placebo and active tocopherol (2000 IU/d), (3) active selegiline hydrochloride (10 mg/d) and tocopherol-placebo, and (4) active selegiline hydrochloride (10 mg/d) and active tocopherol (2000 IU/d). Main Outcome Measure: Cerebrospinal fluid HVA concentrations. Results: The CSF HVA concentration at baseline did not correlate with disease duration or severity; the mean (+/-SD) HVA concentration was 34.7 +/- 17.0 ng/mL. In the 265 subjects who underwent analysis 4 weeks after the study end point was reached and medications were withdrawn, the decline in HVA concentration was significantly greater in subjects assigned to receive selegiline (9.2 +/- 12.7 ng/mL) than in subjects not receiving selegiline (3.2 +/- 14.4 ng/mL), indicating persistent monoamine oxidase (MAO) inhibition by selegiline. Tocopherol had no effect. Results from the modified protocol revealed that HVA concentration increased with time to approximately the same levels as determined in controls by 60 days but showed no clear final plateau level. At 0 days, HVA concentration was reduced from baseline by less than one third, indicating only partial inhibition of MAO activity by selegiline. Conclusions: Measurements of CSF HVA concentrations (1) indicate the long duration of MAO inhibition by selegiline, (2) have limited utility as a marker of severity or progression in PD, (3) indicate that selegiline does not provide sufficient MAO inhibition to test adequately the oxidative stress hypothesis of the cause of PD, and (4) lend no support for a protective role of selegiline in slowing the progression of PD. C1 NEUROL INST,NEW YORK,NY 10032. UNIV ROCHESTER,ROCHESTER,NY. COLUMBIA PRESBYTERIAN MED CTR,NEW YORK,NY 10032. TORONTO HOSP,TORONTO,ON M5T 2S8,CANADA. CALIF PARKINSON INST,SUNNYVALE,CA. SINAI HOSP,DETROIT,MI 48235. UNIV S FLORIDA,TAMPA,FL. UNIV MICHIGAN,ANN ARBOR,MI 48109. RUSH PRESBYTERIAN ST LUKES MED CTR,CHICAGO,IL 60612. UNIV KANSAS,KANSAS CITY,KS. UNIV IOWA,IOWA CITY,IA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OHIO STATE UNIV,COLUMBUS,OH 43210. ROGER WILLIAMS GEN HOSP,PROVIDENCE,RI 02908. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. UNIV SASKATCHEWAN,SASKATOON,SK,CANADA. UNIV VIRGINIA,CHARLOTTESVILLE,VA. UNIV CALGARY,CALGARY,AB,CANADA. UNIV MIAMI,MIAMI,FL 33152. BAYLOR COLL MED,HOUSTON,TX 77030. ST LUKES HOSP,DENVER,CO. OTTAWA CIVIC HOSP,OTTAWA,ON K1Y 4E9,CANADA. UNIV NEBRASKA,OMAHA,NE 68182. UNIV CALIF SAN DIEGO,SAN DIEGO,CA 92103. MCGILL UNIV,MONTREAL GEN HOSP,MONTREAL,PQ H3G 1A4,CANADA. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,NEW BRUNSWICK,NJ. WASHINGTON UNIV,ST LOUIS,MO. JOHNS HOPKINS UNIV,BALTIMORE,MD. GRAD HOSP PHILADELPHIA,PHILADELPHIA,PA 19146. UNIV PENN,PHILADELPHIA,PA 19104. RI Sanchez-Ramos, Juan/A-1188-2009 OI Sanchez-Ramos, Juan/0000-0002-3391-7857 NR 31 TC 30 Z9 30 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD MAR PY 1995 VL 52 IS 3 BP 237 EP 245 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA QK739 UT WOS:A1995QK73900007 ER PT J AU WARSHAW, AL AF WARSHAW, AL TI PANCREATIC SURGERY - A PARADIGM FOR PROGRESS IN THE AGE OF THE BOTTOM LINE SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 75th Annual Meeting of the New-England-Surgical-Society CY SEP 30-OCT 02, 1994 CL NEWPORT, RI SP NEW ENGLAND SURG SOC ID RADIATION-THERAPY; CARCINOMA; PSEUDOCYSTS; EXPERIENCE; RESECTION; NECROSIS; INFECTION; DIVISUM; HEAD RP WARSHAW, AL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,15 PARKMAN ST,WAC336,BOSTON,MA 02114, USA. NR 36 TC 19 Z9 19 U1 0 U2 2 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 MAR PY 1995 VL 130 IS 3 BP 240 EP 246 PG 7 WC Surgery SC Surgery GA QL792 UT WOS:A1995QL79200001 PM 7887789 ER PT J AU RATTNER, DW BROOKS, DC AF RATTNER, DW BROOKS, DC TI PATIENT SATISFACTION FOLLOWING LAPAROSCOPIC AND OPEN ANTIREFLUX SURGERY SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 75th Annual Meeting of the New-England-Surgical-Society CY SEP 30-OCT 02, 1994 CL NEWPORT, RI SP NEW ENGLAND SURG SOC ID REFLUX AB Objective: To compare laparoscopic (LNF) with open Nissen fundoplication (ONF) in terms of hospital charges, efficacy, and patient satisfaction. Design: A prospective, nonrandomized study with a median follow-up of 370 days. Setting: Two tertiary care university hospitals. Patients: Eighty-six patients with complications of gastroesophageal reflux who had not had previous antireflux surgery were studied. Patients chose ONF or LNF following discussion with the surgeon; 12 underwent ONF and 74 underwent LNF, of whom eight required conversion to laparotomy. Main Outcome Measures: Hospital charges, disability, satisfaction, and side effects of fundoplication. Results: Patients were demographically similar. Total charges (mean+/-SD) for LNF ($11 673+/-$4723) were significantly less than for ONF ($18 394+/-$17 264). Patients who underwent LNF returned to work sooner (10+/-3 days) than those who underwent ONF (28+/-1 days). Bloating, dysphagia, and recurrent heartburn occurred with equal frequency in both groups. Recurrent reflux occurred in four of 74 LNF patients and one of 12 ONF patients. Overall satisfaction scores were similar, irrespective of operative technique (LNF, 3.35+/-0.87; ONF, 3.50+/-0.94. Conclusions: Laparoscopic Nissen fundoplication is as effective as ONF in the treatment of complications of gastroesophageal reflux disease and appears to cost less and lead to faster recovery from surgery, but does not result in higher patient satisfaction than ONF. The most important factor in patient satisfaction is the abolition of preoperative symptoms rather than the type of operation. C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. RP RATTNER, DW (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 12 TC 121 Z9 123 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 MAR PY 1995 VL 130 IS 3 BP 289 EP 294 PG 6 WC Surgery SC Surgery GA QL792 UT WOS:A1995QL79200009 PM 7887796 ER PT J AU FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL AF FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL TI STANDARDS FOR PANCREATIC RESECTION IN THE 1990S SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 75th Annual Meeting of the New-England-Surgical-Society CY SEP 30-OCT 02, 1994 CL NEWPORT, RI SP NEW ENGLAND SURG SOC ID MORTALITY; PANCREATICODUODENECTOMY; PANCREATODUODENECTOMY; MORBIDITY; CARCINOMA; SURVIVAL AB Objective: To describe the current indications and operative outcomes of pancreatic resection. Design: Retrospective case series. Setting: Referral practice in a university hospital. Patients: Two hundred thirty-one consecutive patients undergoing pancreatoduodenectomy (PD), distal pancreatectomy (DP), or total pancreatectomy (TP) over a 44-month period. Their ages ranged from 16 to 85 years, with a mean of 54 years; 20% of the patients were 70 years old or older. Main Outcome Measures: Mortality, complications, and length of hospital stay. Results: Operative mortality was 0.4%;, (one death following DP); there were no deaths in 142 PDs or in 18 TPs. The most common complication following PD was delayed gastric emptying. Pancreatic fistula occurred in 6.3% of PD and in 9.8% of DP patients. Overall, 58% of PD, 80% of DP, and 78% of TP patients had no complications. The mean+/-SD length of hospital stay was 15+/-7, 10+/-5, and 15+/-6 days for PD, DP, and TP, respectively. Reoperation for any cause was necessary in only 1.2% (3/231). The most frequent indication for PD was pancreatic cancer (36%) followed by chronic pancreatitis (26%); for DP it was chronic pancreatitis (28%) and cystic neoplasms (27%); and for TP, chronic pancreatitis (55%). Newer indications for pancreatic resection included mucinous ductal ectasia and intraductal papillary tumors (eight cases, 4%) and metastatic tumors (eight cases, 4%). Conclusions: Current indications for pancreatic resection have expanded. These procedures are associated with a low risk for death and postoperative complications when performed in a high-volume setting. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP FERNANDEZDELCASTILLO, C (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,ACC-464,BOSTON,MA 02114, USA. NR 19 TC 283 Z9 291 U1 0 U2 2 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 MAR PY 1995 VL 130 IS 3 BP 295 EP 300 PG 6 WC Surgery SC Surgery GA QL792 UT WOS:A1995QL79200010 PM 7887797 ER PT J AU ROSES, AD SAUNDERS, AM CORDER, EH PERICAKVANCE, MA HAN, SH EINSTEIN, G HULETTE, C SCHMECHEL, DE HOLSTI, M HUANG, D RISCH, NJ HAINES, JL GOEDERT, M JAKES, R DONG, LM WEISGRABER, KH STRITTMATTER, WJ AF ROSES, AD SAUNDERS, AM CORDER, EH PERICAKVANCE, MA HAN, SH EINSTEIN, G HULETTE, C SCHMECHEL, DE HOLSTI, M HUANG, D RISCH, NJ HAINES, JL GOEDERT, M JAKES, R DONG, LM WEISGRABER, KH STRITTMATTER, WJ TI INFLUENCE OF THE SUSCEPTIBILITY GENES APOLIPOPROTEIN E-EPSILON-4 AND APOLIPOPROTEIN E-EPSILON-2 ON THE RATE OF DISEASE EXPRESSIVITY OF LATE-ONSET ALZHEIMERS-DISEASE SO ARZNEIMITTEL-FORSCHUNG/DRUG RESEARCH LA English DT Article DE ALZHEIMERS DISEASE, GENETIC LINKAGE, ONSET OF DISEASE; APOLIPOPROTEIN E, ASSOCIATION, ISOFORMS ID PRECURSOR PROTEIN GENE; AMYLOID-BETA-PEPTIDE; TYPE-4 ALLELE; E GENOTYPE; MUTATION; CORTEX; EPSILON-4; BINDING AB Apolipoprotein E-epsilon 4 (APOE4, gene; apoE4, protein) is a susceptibility gene or risk factor for Alzheimer's disease. The genetic relevance of APOE4 has been widely confirmed. The APOE gene is not a disease locus, with specific mutations causing Alzheimer disease. Allelic variations at the APOE locus affect the rate of disease progression. The association of specific inherited APOE alleles with age of onset distributions describes biological effects based on genotype. The inheritance of polymorphic genes with single amino acid differences between apoE4 and apoE3 (and between apoE3 and apoE2) at the protein level is associated with differences in the mean age of disease onset spanning almost two decades. The isoform-specific metabolism of apoE resulting in a faster rate of disease expression can now be studied with the expectation that genetically relevant processes are being investigated. There is now an opportunity to develop theories directed at the genetically relevant apoE metabolism that can significantly delay disease expression. C1 YALE UNIV,DEPT EPIDEMIOL & PUBL HLTH,NEW HAVEN,CT 06520. YALE UNIV,DEPT GENET,NEW HAVEN,CT 06520. MASSACHUSETTS GEN HOSP,MOLEC GENET UNIT,BOSTON,MA. MRC,MOLEC BIOL LAB,CAMBRIDGE,ENGLAND. UNIV CALIF SAN FRANCISCO,GLADSTONE INST CARDIOVASC DIS,SAN FRANCISCO,CA. RP ROSES, AD (reprint author), DUKE UNIV,MED CTR,JOSEPH & KATHLEEN BRYAN ALZHEIMERS DIS RES CTR,BOX 2900,DURHAM,NC 27710, USA. RI Haines, Jonathan/C-3374-2012 FU NCRR NIH HHS [RR-30]; NIA NIH HHS [AG-05128, AG-07922, U24 AG021886] NR 42 TC 28 Z9 29 U1 0 U2 0 PU ECV-EDITIO CANTOR VERLAG MEDIZIN NATURWISSENSCHAFTEN PI AULENDORF PA BANDELSTOCKWEG 20, POSTFACH 1255, D-88322 AULENDORF, GERMANY SN 0004-4172 J9 ARZNEIMITTEL-FORSCH JI Arzneimittelforschung PD MAR PY 1995 VL 45-1 IS 3A BP 413 EP 417 PG 5 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA QR747 UT WOS:A1995QR74700014 PM 7763336 ER PT J AU NITSCH, RM WURTMAN, RJ GROWDON, JH AF NITSCH, RM WURTMAN, RJ GROWDON, JH TI REGULATION OF PROTEOLYTIC PROCESSING OF THE AMYLOID BETA-PROTEIN PRECURSOR BY FIRST MESSENGERS - A NOVEL POTENTIAL APPROACH FOR THE TREATMENT OF ALZHEIMERS-DISEASE SO ARZNEIMITTEL-FORSCHUNG/DRUG RESEARCH LA English DT Article DE ALZHEIMERS DISEASE; BETA-AMYLOID PRECURSOR PROTEIN, REGULATION OF PROTEOLYTIC PROCESSING; MUSCARINIC RECEPTORS; SEROTONINERGIC RECEPTORS ID KINASE-C; RECEPTOR SUBTYPES; RELEASE; DERIVATIVES; PEPTIDE; ACTIVATION; HYDROLYSIS; SECRETION; CELLS; DISTINCT AB Amyloid deposits in Alzheimer's disease brains consist of aggregated amyloid beta-peptides (A beta) which are derived by proteolytic processing of the amyloid beta-protein precursor (APP). Proteolytic APP processing can be regulated by the activity of neuronal cell surface receptors including the muscarinic m1 and m3, the serotoninergic 5-HT2 and 5-HT1C, vasopressin and bradykinin receptor subtypes. Receptor stimulation with appropriate agonists rapidly increases the rates of release of the alpha-secretase processing product APP(s) which is cleaved within the A beta domain and thus is a non-amyloidogenic derivative. Moreover, stimulation of m1 receptors also decreases the formation of A beta, a secreted potentially amyloidogenic and possibly neurotoxic APP fragment. Similar biochemical events occur in stimulation experiments of fresh rat brain slices suggesting that neuronal activity may be involved in regulating APP processing in mammalian brain. Activation of non-amyloidogenic APP processing and inhibition of amyloidogenic processing pathways by subtype-specific agonists of muscarinic, serotoninergic or peptidergic receptors provides a novel approach for the pharmacological modulation of APP processing in Alzheimer's disease. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. NR 42 TC 18 Z9 18 U1 0 U2 2 PU ECV-EDITIO CANTOR VERLAG MEDIZIN NATURWISSENSCHAFTEN PI AULENDORF PA BANDELSTOCKWEG 20, POSTFACH 1255, D-88322 AULENDORF, GERMANY SN 0004-4172 J9 ARZNEIMITTEL-FORSCH JI Arzneimittelforschung PD MAR PY 1995 VL 45-1 IS 3A BP 435 EP 438 PG 4 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA QR747 UT WOS:A1995QR74700018 PM 7763340 ER PT J AU ROSOW, CE AF ROSOW, CE TI NEWER OPIOID AGONISTS SO BAILLIERES CLINICAL ANAESTHESIOLOGY LA English DT Article RP ROSOW, CE (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 0 TC 3 Z9 3 U1 0 U2 0 PU BAILLIERE TINDALL PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0950-3501 J9 BAILLIERE CLIN ANAES JI Baillieres Clin. Anaesthesiol. PD MAR PY 1995 VL 9 IS 1 BP 67 EP 82 DI 10.1016/S0950-3501(95)80053-0 PG 16 WC Anesthesiology SC Anesthesiology GA QT691 UT WOS:A1995QT69100006 ER PT J AU MENDEZ, MF DOSS, RC AF MENDEZ, MF DOSS, RC TI NEUROBEHAVIORAL ASPECTS OF THE DELAYED ENCEPHALOPATHY OF CARBON-MONOXIDE INTOXICATION - CASE-REPORT AND REVIEW SO BEHAVIOURAL NEUROLOGY LA English DT Note DE CARBON MONOXIDE; DEMYELINATION ID INTERVAL FORM; NEUROPSYCHIATRIC SEQUELAE; NEUROLOGIC SEQUELAE; PSYCHIC AKINESIA; FOLLOW-UP; BRAIN; TOMOGRAPHY; THERAPY; LESIONS; OXYGEN AB We report the neurobehavioral aspects of the delayed encephalopathy of carbon monoxide (CO) intoxication in a 29 year old woman and review the literature. Four weeks after CO poisoning, the patient developed a frontal lobe syndrome, visuoperceptual impairment, and diffuse white matter lesions with an otherwise normal neurological examination. In contrast, patients with the classical syndrome also have a parkinsonian state or an akinetic-mute state. The delayed encephalopathy of CO poisoning usually results from demyelination of subcortical white matter, necrosis of the globus pallidus, or both. The clinical aspects, risk factors, neurobiological features, and therapy and prognosis are discussed. C1 W LOS ANGELES VET AFFAIRS MED CTR,NEUROBEHAV UNIT 691116AF,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. ST PAUL RAMSEY MED CTR,ST PAUL,MN 55101. NR 45 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0953-4180 J9 BEHAV NEUROL JI Behav. Neurol. PD SPR PY 1995 VL 8 IS 1 BP 47 EP 52 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA QP683 UT WOS:A1995QP68300007 PM 24487403 ER PT J AU WRIGHT, JE PARDO, M SAYEEDSHAH, U ALPERIN, W ROSOWSKY, A AF WRIGHT, JE PARDO, M SAYEEDSHAH, U ALPERIN, W ROSOWSKY, A TI LEUCOVORIN AND FOLIC-ACID REGIMENS FOR SELECTIVE EXPANSION OF MURINE 5,10-METHYLENETETRAHYDROFOLATE POOLS SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE 5,L0-METHYLENETETRAHYDROFOLATE; LEUCOVORIN; FOLIC ACID; POLYGLUTAMYLATION; EMT6 MAMMARY ADENOCARCINOMA; DRUG MODULATION ID HUMAN-COLON ADENOCARCINOMA; HIGH-DOSE LEUCOVORIN; THYMIDYLATE SYNTHETASE; METHOTREXATE POLYGLUTAMATES; BIOCHEMICAL DETERMINANTS; CALCIUM LEUCOVORIN; ANTITUMOR-ACTIVITY; CYTO-TOXICITY; 5-FLUOROURACIL; SYNTHASE AB Mice bearing subcutaneously implanted EMT6 mammary adenocarcinoma were treated with leucovorin or folic acid by continuous subcutaneous infusion or bolus intraperitoneal injection. (6R)-5 ,10-Methyleneterrahydrofolate pools in cytosolic extracts of the tumor, marrow, and gut were measured by analysis of the ternary complex with thymidylate synthase (5,10-methylenetetrahydrofolate : dUMP C-methyltransferase, EC 2.1.1.45) and 5-fluoro-2'-deoxyuridylate, and the polyglutamate distribution in the (6R)-5,10-methylenetetrahydrofolate pool was analyzed by native gel electrophoresis. Bolus intraperitoneal administration of either leucovorin or folic acid caused dose-dependent expansion of the (6R)-5,10-methylenetetrahydrofolate pool in the tumor, but not in the marrow or gut. For example, the AUC (0-5 hr) in the tumor increased from a baseline value of 8.2 to 20 nmol/mg protein hr after a bolus dose of 1.5 mmol/kg of leucovorin or folic acid, whereas the increase in marrow and gut was 2- to 4-fold lower. Continuous subcutaneous infusion at the same total dosage over 3 days gave AUC (0-96 hr) values of 134 nmol/mg protein.hr for controls as compared with 347 nmol/mg protein.hr for the leucovorin group and 254 nmol/mg protein hr for the folic acid group. In contrast to bolus treatment, the increase in (6R)-5,10-methylenetetrahydrofolate in the marrow and small intestine with both leucovorin and folic acid infusion was similar to the increase in the tumor. Thus, intraperitoneal bolus injection was tumor selective, but subcutaneous continuous infusion was not. Longer-chain polyglutamates of (6R)-5,10-methylenetetrahydrofolate in the tumor after bolus treatment with 0.375 and 0.75 mmol/kg of leucovorin or folic acid increased relative to controls. At higher doses of 1.5 and 2.25 mmol/kg, an increase was observed only in the mono/diglutamate fraction. In marrow, on the other hand, the mono/diglutamate fraction, but not the longer-chain polyglutamates, increased at all doses. In the constant infusion regimen, longer-chain polyglutamates increased in all three tissues, though in gut and marrow the mono/diglutamate fraction increased more than in tumor. Leucovorin and folic acid were converted to (6R)-5, 10-methylenetetrahydrofolate more efficiently but less selectively during a 3-day subcutaneous infusion than after an intraperitoneal bolus. Longer-chain polyglutamates were selectively increased in tumor by both regimens of leucovorin administration. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP WRIGHT, JE (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P01-CA19589] NR 39 TC 4 Z9 5 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAR 1 PY 1995 VL 49 IS 5 BP 677 EP 685 DI 10.1016/0006-2952(94)00507-I PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QM055 UT WOS:A1995QM05500012 PM 7534077 ER PT J AU RUBINSTEIN, JT AF RUBINSTEIN, JT TI THRESHOLD FLUCTUATIONS IN AN N-SODIUM CHANNEL MODEL OF THE NODE OF RANVIER SO BIOPHYSICAL JOURNAL LA English DT Article ID MYELINATED NERVE-FIBERS; AUDITORY-NERVE; CURRENTS; CELLS AB Computer simulations of stochastic single-channel open-close kinetics are applied to an N sodium channel model of a node of Ranvier. Up to 32,000 voltage-gated sodium channels have been simulated with modified amphibian sodium channel kinetics. Poststimulus time histograms are obtained with 1000 monophasic pulse stimuli, and measurements are made of changes in the relative spread of threshold (RS) with changes in the model parameters. RS is found to be invariant with pulse durations from 100 mu s to 3 ms. RS is approximately of inverse proportion to root N. It decreases with increasing temperature and is dependent on passive electrical properties of the membrane as well as the single-channel conductance. The simulated RS and its independence of pulse duration is consistent with experimental results from the literature. Thus, the microscopic fluctuations of single, voltage-sensitive sodium channels in the amphibian peripheral node of Ranvier are sufficient to account for the macroscopic fluctuation of threshold to electrical stimulation. C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,COCHLEAR IMPLANT RES LAB,BOSTON,MA 02114. FU NIDCD NIH HHS [DC00361] NR 30 TC 118 Z9 118 U1 1 U2 3 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD MAR PY 1995 VL 68 IS 3 BP 779 EP 785 PG 7 WC Biophysics SC Biophysics GA QH944 UT WOS:A1995QH94400006 PM 7756544 ER PT J AU KUHNHALLEK, I SAGE, DR STEIN, L GROELLE, H FINGEROTH, JD AF KUHNHALLEK, I SAGE, DR STEIN, L GROELLE, H FINGEROTH, JD TI EXPRESSION OF RECOMBINATION ACTIVATING GENES (RAG-1 AND RAG-2) IN EPSTEIN-BARR VIRUS-BEARING B-CELLS SO BLOOD LA English DT Article ID LATENT MEMBRANE-PROTEIN; ACUTE LYMPHOBLASTIC-LEUKEMIA; NUCLEAR ANTIGEN-1; BURKITT-LYMPHOMA; CHROMOSOME-TRANSLOCATION; V(D)J RECOMBINATION; MOLECULAR-CLONING; LYMPHOCYTES-B; REGION GENES; KAPPA-B AB Recombination activating genes 1 and 2 (RAG-1 and RAG-2), are the only lymphoid-specific genes required for the site-directed recombination reaction leading to generation of B-cell receptors and T-cell receptors (TCRs). RAGs are normally expressed during a narrow window of precursor lymphocyte development. RAG expression was examined in Epstein-Barr virus (EBV)-infected B cells. No steady-state RAG RNA was found in EBV immortalized cells, including newly established B lymphoblastoid cell lines derived from precursor lymphocytes that transcribed RAGs at the time of infection. RAG RNAs were detected in some endemic (EBV(+)) and also in some sporadic (EBV(-)) Burkitt's lymphoma lines that had been infected with EBV in vitro. The RAG(+), EBV(+) Burhitt's lines were unusual in that they were SlgM(+) (one was SlgG(+), SlgM(-)), CD10(+), and lacked terminal deoxynucleotidyl transferase. In EBV(+) Burkitt's lymphoma lines, transcription of virus latent membrane protein-1 (LMP-1) was correlated with downregulation of RAG-1 and RAG-2. Conversely, absence of LMP-1 in clones of EBV(+) tumor lines was associated with increased RAG transcription. Translocation of c-mye into V(D)J loci has been observed in endemic Burkitt's lymphomas, and heptamer-nonamer recombination signal sequences have been identified at some chromosomal breakpoints. Association of RAG transcription with EBV infection raises the possibility that, under certain conditions, virus might predispose to aberrant V(D)J recombination reactions. (C) 1995 by The American Society of Hematology. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [P30 AI28691]; PHS HHS [R29 A126835] NR 83 TC 43 Z9 44 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 1 PY 1995 VL 85 IS 5 BP 1289 EP 1299 PG 11 WC Hematology SC Hematology GA QJ435 UT WOS:A1995QJ43500019 PM 7858259 ER PT J AU PAIETTA, E ANDERSEN, J RACEVSKIS, J ASHIGBI, M CASSILETH, P WIERNIK, PH AF PAIETTA, E ANDERSEN, J RACEVSKIS, J ASHIGBI, M CASSILETH, P WIERNIK, PH TI MODULATION OF MULTIDRUG-RESISTANCE IN DE-NOVO ADULT ACUTE MYELOID-LEUKEMIA - VARIABLE EFFICACY OF REVERTING AGENTS IN-VITRO SO BLOOD REVIEWS LA English DT Review ID P-GLYCOPROTEIN; CLINICAL-SIGNIFICANCE; CELLS; EXPRESSION; CYTOTOXICITY; PHENOTYPE; MDR-1 AB The efficacy of verapamil and cyclosporine A as modulators of P-glycoprotein, the multidrug resistance (MDR1) gene product, was studied in leukemic blast cells from 56 patients with de novo acute myeloid leukemia (AML) in vitro. Rhodamine(123) dye-efflux was measured bow cytometrically as a cellular parameter reflecting P-glycoprotein activity, While dye-efflux was measurable in 3/4 of the cases, the capacity of the P-glycoprotein inhibitors varied substantially among patients, In 23 patients, P-glycoprotein function was completely inhibited by the resistance modulators, whereas in 17 patients neither verapamil nor cyclosporine had any reverting effect on dye-efflux at concentrations even 10-times higher than achievable in vivo, Cells with a drug-sensitive rhodamine(123)-pump effluxed more efficiently (p = 0.0016) and contained significantly higher levels of MDR1 specific RNA transcripts (p = 0.0002), as determined by quantitative PCR, than cells exhibiting an efflux process that could not be inhibited, However, flow cytometric evaluation of the staining of gated blast cells,vith the anti-P-glycoprotein antibody, 4E3,16, revealed no difference in P-glycoprotein expression between modulator-sensitive and -insensitive cases (p = 0.86), indicating disproportionate translation of MDR1 mRNA, In leukemic cell populations with increased P-glycoprotein function that could be inhibited, significantly more blasts expressed the progenitor cell antigen, CD34 (median 83%), than was the case in leukemias with P-glycoprotein activity that could not be inhibited (median 7%) (p = 0.0001), The present study demonstrates that a substantial fraction of AML patients constitutively display a drug-efflux mechanism suggestive of P-glycoprotein activity, However, in many of those patients rhodamine(123)-efflux from blast cells in vitro was not sensitive to classical P-glycoprotein inhibitors. C1 ALBERT EINSTEIN CANC CTR,BRONX,NY. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. UNIV MIAMI,MIAMI,FL 33152. EASTERN COOPERAT ONCOL GRP,DENVER,CO. RP PAIETTA, E (reprint author), MONTEFIORE MED CTR,DEPT ONCOL,111 E 210TH ST,BRONX,NY 10467, USA. FU NCI NIH HHS [CA23318, CA14958, CA21115] NR 34 TC 18 Z9 18 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0268-960X J9 BLOOD REV JI Blood Rev. PD MAR PY 1995 VL 9 IS 1 BP 47 EP 52 DI 10.1016/0268-960X(95)90039-X PG 6 WC Hematology SC Hematology GA QR478 UT WOS:A1995QR47800006 PM 7540903 ER PT J AU ELIAS, AD AYASH, LJ WHEELER, C SCHWARTZ, G TEPLER, I GONIN, R MCCAULEY, M MAZANET, R SCHNIPPER, L FREI, E ANTMAN, KH AF ELIAS, AD AYASH, LJ WHEELER, C SCHWARTZ, G TEPLER, I GONIN, R MCCAULEY, M MAZANET, R SCHNIPPER, L FREI, E ANTMAN, KH TI PHASE-I STUDY OF HIGH-DOSE IFOSFAMIDE, CARBOPLATIN AND ETOPOSIDE WITH AUTOLOGOUS HEMATOPOIETIC STEM-CELL SUPPORT SO BONE MARROW TRANSPLANTATION LA English DT Article DE HIGH-DOSE ICE; STEM CELL SUPPORT ID BONE-MARROW SUPPORT; VP-16 PLUS IFOSFAMIDE; TUBULAR NEPHROTOXICITY; SOLID TUMORS; CANCER; EPIPODOPHYLLOTOXIN; TRANSPLANTATION; MALIGNANCIES; CHEMOTHERAPY; LYMPHOMAS AB More effective high-dose combination regimens are needed which have broad cytotoxic activity, steep dose-response relations and non-overlapping non-hematologic toxicities (to allow administration of full doses of each agent), This study was designed to define the dose-limiting toxicities and maximum tolerated doses of ifosfamide, carboplatin and etoposide (ICE) with hematopoietic stem cell support. Ifosfamide and carboplatin were initially fixed at 75% and 80% of the single agent maximum tolerated doses, respectively, and etoposide added to the combination, After the dose-limiting toxicity of etoposide was reached, its dose was fixed and ifosfamide and carboplatin were individually dose escalated as tolerated, All agents were given by 96h continuous infusion (days -7 to -3), Autologous marrow, with or without peripheral blood progenitor cells, was reinfused on day 0, Forty eight adults with advanced malignancies were enrolled in cohorts of three to five patients, At the maximum tolerated doses of ifosfamide 16 g/m(2), carboplatin 1.8 g/m(2) and etoposide 1.2 g/m(2), renal toxicity precluded further dose escalation, Two patients died of organ (renal, CNS) toxicity (4%), Renal toxicity was particularly prominent in patients with prior cisplatin exposure, An early chemotherapy-stopping rule was developed, supported by pharmacologic analysis, which resulted in immediate discontinuation of ifosfamide and carboplatin if the serum creatinine, monitored twice daily during chemotherapy, exceeded 1.5 mg/dl and was >0.5 mg/dl above baseline, High-dose ICE is well tolerated if serum creatinines are carefully monitored during chemotherapy administration, The early chemotherapy-stopping rule may enhance safety of the regimen but requires validation by additional correlation with pharmacokinetic data for each of the chemotherapeutic agents, The ICE regimen is active and should be evaluated in phase II trials of patients with small-cell lung, ovarian and germ cell carcinomas, and lymphomas. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. RP ELIAS, AD (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA13849] NR 33 TC 45 Z9 45 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 1995 VL 15 IS 3 BP 373 EP 379 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA QP545 UT WOS:A1995QP54500008 PM 7599561 ER PT J AU SYKES, M PEARSON, DA SZOT, GL AF SYKES, M PEARSON, DA SZOT, GL TI IL-2-INDUCED GVHD PROTECTION IS NOT INHIBITED BY CYCLOSPORINE AND IS MAXIMAL WHEN IL-2 IS GIVES OVER A 25-H PERIOD BEGINNING ON THE DAY FOLLOWING BONE-MARROW TRANSPLANTATION SO BONE MARROW TRANSPLANTATION LA English DT Article DE IL-2; GRAFT-VERSUS-HOST DISEASE PROTECTION; CYCLOSPORINE ID VERSUS-HOST DISEASE; RECOMBINANT INTERLEUKIN-2; TREATED RATS; PHASE-I; GRAFT; LEUKEMIA; IMMUNOTHERAPY; CELLS; ALLOENGRAFTMENT; SPECIFICITY AB We have recently demonstrated, in a fully MHC-mismatched murine bone marrow transplantation (BMT) model, that administration of a short course of high-dose interleukin 2 (IL-2) markedly delays the onset of graft-versus-host disease (GVHD) without compromising alloengraftment or the graft-versus-leukemia (GVL) effect of allogeneic T cells, Early timing of IL-2 administration and high dose were shown to be critical to achieve this protective effect, Although a 2.5 day course of IL-2, begun on the day of BMT, was found to confer marked protection without observable toxicity, shorter courses and a higher dose of IL-2 than 5 x 10(4) Cetus units per treatment have not been previously evaluated in this model, We now demonstrate that administration of a three-treatment course of IL-2 over a 25 h period beginning 15 h following BMT is sufficient to provide maximal GVHD protection, that increasing the IL-2 dose beyond 5 x 10(4) units per treatment does not further improve the level of GVHD protection, and that further division of IL-2 treatments to achieve more constant tissue levels does not result in improved GVHD protection, We also demonstrate that IL-2 is still protective when administered in combination with cyclosporine, These results suggest that IL-2 administered in a sufficient short course to avoid toxicity might have the potential to achieve effective GVHD prophylaxis in humans, even if given in combination with cyclosporine. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BLDG 149,BOSTON,MA 02129, USA. FU PHS HHS [R0155290, R0131158] NR 25 TC 13 Z9 13 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 1995 VL 15 IS 3 BP 395 EP 399 PG 5 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA QP545 UT WOS:A1995QP54500011 PM 7599564 ER PT J AU CUTRER, FM SCHOENFELD, D LIMMROTH, V PANAHIAN, N MOSKOWITZ, MA AF CUTRER, FM SCHOENFELD, D LIMMROTH, V PANAHIAN, N MOSKOWITZ, MA TI SUPPRESSION BY THE SUMATRIPTAN ANALOG, CP-122,288 OF C-FOS IMMUNOREACTIVITY IN TRIGEMINAL NUCLEUS CAUDALIS INDUCED BY INTRACISTERNAL CAPSAICIN SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE CP-122,288; TRIGEMINOVASCULAR SYSTEM; CAPSAICIN; C-FOS EXPRESSION; 5-HT1B/D AGONIST; SUMATRIPTAN ANALOG; MIGRAINE; HEADACHE; INTRACISTERNAL ID RAT SPINAL-CORD; TRANSCRANIAL DOPPLER; EXPRESSION; STIMULATION; PROTEIN; MIGRAINE; NEURONS; BLOOD; ATTACKS AB 1 The effects of an intravenously administered sumatriptan analogue were examined on c-fos-like immunoreactivity (c-fos-LI), a marker of neuronal activation, evoked within trigeminal nucleus caudalis (TNC) and other brain stem regions 2 h after intracisternal injection of the irritant, capsaicin (0.1 mi, 0.1 mM), in pentobarbitone-anaesthetized Hartley guinea-pigs. 2 C-fos-LI was assessed in eighteen serial sections (50 mu m) using a polyclonal antiserum. A weighted average, reflecting total expression within lamina I, II0 of TNC was obtained from three representative levels (i.e., at -0.225 mm, -2.475 mm and -6.975 mm.) 3 Capsaicin caused significant labelling within lamina I, II0, a region containing axonal terminations of small unmyelinated C-fibres, as well as within the nucleus of the solitary tract, area postrema and medial reticular nucleus. A similar distribution of positive cells was reported previously after intracisternal injection of other chemical irritants such as autologous blood or carrageenin. 4 Pretreatment with a conformationally restricted sumatriptan analogue (with some selectivity for 5-HT1B and 5-HT1D receptor subtypes) CP-122,288, reduced the weighted average by approximately 50-60% (P<0.05) in lamina I, II0 at greater than or equal to 100 pmol kg(-1), i.v., but did not decrease cell number within area postrema, nucleus of the solitary tract or medial reticular nucleus. A similar pattern was reported previously following sumatriptan, dihydroergotamine or CP-93,129 administration after noxious meningeal stimulation. 5 We conclude that modifications at the amino-ethyl side chain of sumatriptan dramatically enhance the suppression of c-fos expression within TNC, a finding consistent with its remarkable potency against neurogenic plasma protein extravasation within dura mater. CP-122,288 and related analogues may serve as an important prototype for drug development in migraine and related headaches. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR BIOSTAT,BOSTON,MA 02114. RI Moskowitz, Michael/D-9916-2011 FU NINDS NIH HHS [NS 21558] NR 22 TC 26 Z9 26 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD MAR PY 1995 VL 114 IS 5 BP 987 EP 992 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QK718 UT WOS:A1995QK71800012 PM 7780655 ER PT J AU ROSENBAUM, JF POLLOCK, RA OTTO, MW POLLACK, MH AF ROSENBAUM, JF POLLOCK, RA OTTO, MW POLLACK, MH TI INTEGRATED TREATMENT OF PANIC DISORDER SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article; Proceedings Paper CT 1995 Symposium on Coping with Anxiety: Integrated Approaches to Treatment, at the Annual Meeting of the American-Psychiatric-Association CY MAY 20-25, 1995 CL MIAMI, FL SP AMER PSYCHIAT ASSOC ID ANXIETY DISORDERS; FOLLOW-UP; SHORT-TERM; BENZODIAZEPINE TREATMENT; NORADRENERGIC FUNCTION; BEHAVIORAL-INHIBITION; HEALTHY-SUBJECTS; DOUBLE-BLIND; PERSONALITY-DISORDERS; PSYCHIATRIC-DISORDERS AB Epidemiological studies suggest that about 3.5% of the adult United States population meet criteria for panic disorder, and that an additional 2-5% suffer from agoraphobia with or without panic. Both biological and behavioral models have been proposed to elucidate the nature of this disorder. The authors review research findings regarding these models, as well as pharmacological and cognitive-behavioral treatment approaches. The complexity of factors contributing to the disorder suggests the need for an integrated treatment approach involving considerations of combination drug therapy and psychosocial interventions. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,DIV OUTPATIENT PSYCHIAT,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 122 TC 7 Z9 7 U1 4 U2 4 PU MENNINGER FOUNDATION PI TOPEKA PA BOX 829, TOPEKA, KS 66601 SN 0025-9284 J9 B MENNINGER CLIN JI Bull. Menninger Clin. PD SPR PY 1995 VL 59 IS 2 SU A BP A4 EP A26 PG 23 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA QY293 UT WOS:A1995QY29300002 PM 7795571 ER PT J AU SHERIDAN, RL WEBER, JM PETERSON, HF TOMPKINS, RG AF SHERIDAN, RL WEBER, JM PETERSON, HF TOMPKINS, RG TI CENTRAL VENOUS CATHETER SEPSIS WITH WEEKLY CATHETER CHANGE IN PEDIATRIC BURN PATIENTS - AN ANALYSIS OF 221 CATHETERS SO BURNS LA English DT Article AB To document the risk of catheter er sepsis associated with central venous catheter changes every 7 days in paediatric burn patients, an analysis of data collected prospectively on 234 such catheters was performed. During an 18-month period there were 301 acutely burned children admitted to a regional paediatric burn Facility of whom 53, with an average burn size of 42 per cent TBSA, required 234 central venous catheters. A central venous catheter management protocol was followed which included catheter changes every 7 days. IF insertion sites were clean and uninflamed, catheters were replaced by guidewire and the original catheter tip was semiquantitatively cultured. Catheters weve replaced to a new site if insertion sites appeared inflamed or catheter tips grew 15 or more colony forming units. Overall, 3.2 per cent (10.9 per cent by Centers far Disease Control definition) of central venous catheters were associated with sepsis. When catheters were replaced by guidewire from one to three times, catheter sites were used for a mean of 15.6 days without an increased rate of line sepsis. There was no difference in sepsis rates between catheters placed at a new site or replaced by guidewire. There were no deaths attributed to catheter-related sepsis. We conclude that a protocol allowing For catheter change to a new site, or replacement by guidewire, every 7 days was associated with a low risk of catheter sepsis in paediatric burn patients. RP SHERIDAN, RL (reprint author), MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 0 TC 38 Z9 38 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA LINACRE HOUSE JORDAN HILL, OXFORD, OXON, ENGLAND OX2 8DP SN 0305-4179 J9 BURNS JI Burns PD MAR PY 1995 VL 21 IS 2 BP 127 EP 129 DI 10.1016/0305-4179(95)92137-2 PG 3 WC Critical Care Medicine; Dermatology; Surgery SC General & Internal Medicine; Dermatology; Surgery GA QH068 UT WOS:A1995QH06800009 PM 7766321 ER PT J AU CHENG, EY SPRINGFIELD, DS MANKIN, HJ AF CHENG, EY SPRINGFIELD, DS MANKIN, HJ TI FREQUENT INCIDENCE OF EXTRAPULMONARY SITES OF INITIAL METASTASIS IN PATIENTS WITH LIPOSARCOMA SO CANCER LA English DT Article DE LIPOSARCOMA; SOFT TISSUE SARCOMA; METASTASIS; EXTRAPULMONARY METASTASIS ID SOFT-TISSUE SARCOMAS; CHEMOTHERAPY; EXTREMITIES; MANAGEMENT; PATTERNS AB Background. The vast majority of soft tissue sarcomas spread initially to the lungs and then to other sites. The lung has been the most carefully monitored organ system during routine surveillance for a metastasis. Liposarcoma is one of the most common soft tissue sarcomas and has been noted to have extrapulmonary sites of initial metastasis. This study was undertaken to investigate both the frequency and distinguishing features of initial extrapulmonary metastasis in patients with liposarcoma. Methods. A review of 60 patients with liposarcoma treated at the Massachusetts General Hospital (MGH) from 1971 to 1990 was performed. Survival and regression analyses were used to analyze disease free intervals and prognostic factors. Results. Metastatic disease occurred in 37% of patients and local failure in 17%. Among the subset of patients who underwent primary definitive surgery at the MGH, the incidence of local failure was 3%. An unusually high incidence of extrapulmonary site of first metastasis was found. Isolated extrapulmonary disease was the site of initial metastasis in 59% of patients. In contrast to patients with an initial pulmonary metastasis, patients with an initial extrapulmonary metastasis had a statistically significant (P = 0.001) longer disease free interval from diagnosis to first metastasis. Conclusions. Liposarcoma, in comparison with other soft tissue sarcomas, has a different pattern of metastatic spread, with a tendency toward extrapulmonary sites. In addition, patients with extrapulmonary metastases have a longer disease free interval compared with patients with pulmonary metastasis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ORTHOPAED SURG,BOSTON,MA. NR 58 TC 43 Z9 45 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAR 1 PY 1995 VL 75 IS 5 BP 1120 EP 1127 DI 10.1002/1097-0142(19950301)75:5<1120::AID-CNCR2820750511>3.0.CO;2-7 PG 8 WC Oncology SC Oncology GA QH077 UT WOS:A1995QH07700010 PM 7850710 ER PT J AU TEICHER, BA MENON, K NORTHEY, D LIU, J KUFE, DW KADDURAHDAOUK, R AF TEICHER, BA MENON, K NORTHEY, D LIU, J KUFE, DW KADDURAHDAOUK, R TI CYCLOCREATINE IN CANCER-CHEMOTHERAPY SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE CYCLOCREATINE; CREATINE KINASE; COMBINATION CHEMOTHERAPY ID ASCITES TUMOR-CELLS; CREATINE-KINASE; GROWTH; INVIVO; CIS-DIAMMINEDICHLOROPLATINUM(II); CARCINOMA; RESISTANT; INVITRO; ELEMENT; ENZYME AB Cyclocreatine, an analog of creatine, is an efficient substrate for creatine kinase, but its phosphorylated form is a poor phosphate donor in comparison with creatine phosphate. Cyclocreatine was not very cytotoxic upon 24 h of exposure of human SW2 small-cell lung cancer cells to concentrations of up to 5 mM. However, combinations of cyclocreatine (0.5 mM, 24 h) with each of four antitumor alkylating agents, cis-diamminedichloroplatinum(II), melphalan, 4-hydroperoxycyclophosphamide, and carmustine, resulted in additive to greater-than-additive cytotoxicity toward exponentially growing SW2 cells. The greatest levels of synergy were seen at higher concentrations of 4-hydroperoxycyclophosphamide and carmustine as determined by isobologram analysis. In vivo cyclocreatine (0.5 or 1 g/kg) was more effective if given i.v. rather than i.p. The longest tumor-growth delays, up to 10 days, were produced by extended regimens of cyclocreatine. Cyclocreatine was an effective addition to therapy with standard anticancer agents including cis-diamminedichloroplatinum(II), cyclophosphamide, Adriamycin, or 5-fluorouracil. No additional toxicity was observed when 10 days of cyclocreatine treatment was given with full standard-dose regimens of each drug. The resultant increases in tumor-growth delay were 1.7- to 2.4-fold as compared with those obtained for each of the drugs alone. These results indicate that cyclocreatine may be an effective single agent and an effective addition to combination chemotherapy regimens. C1 JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. AMIRA INC,CAMBRIDGE,MA 02142. RP TEICHER, BA (reprint author), DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU PHS HHS [R01-50174] NR 27 TC 22 Z9 22 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD MAR PY 1995 VL 35 IS 5 BP 411 EP 416 DI 10.1007/s002800050255 PG 6 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA QX823 UT WOS:A1995QX82300009 PM 7850923 ER PT J AU CHATTERJEE, D LIU, CJT NORTHEY, D TEICHER, BA AF CHATTERJEE, D LIU, CJT NORTHEY, D TEICHER, BA TI MOLECULAR CHARACTERIZATION OF THE IN-VIVO ALKYLATING AGENT RESISTANT MURINE EMT-6 MAMMARY-CARCINOMA TUMORS SO CANCER CHEMOTHERAPY AND PHARMACOLOGY LA English DT Article DE ANTITUMOR ALKYLATING AGENTS; IN VIVO DRUG RESISTANCE; C-JUN EXPRESSION; ERB-2 EXPRESSION; EMT-6 TUMORS ID RAS ONCOGENE EXPRESSION; SQUAMOUS-CELL CARCINOMA; JUN PROTO-ONCOGENE; C-FOS EXPRESSION; BREAST-CANCER; N-MYC; P53 MUTATIONS; ELEVATED EXPRESSION; SIGNAL TRANSDUCTION; IONIZING-RADIATION AB The expression of several early-response genes and genes associated with malignant disease was assessed in the EMT-6/parent tumor and the EMT-6/CTX and EMT-6/CDDP in vivo resistant tumor lines growing as tumors or as monolayers in culture. In the absence of treatment the levels of mRNA for the genes c-jun, c-fos, c-myc, Ha-ras and p53 were increased in the EMT-6/CTX and EMT-6/CDDP as compared with the EMT-6/parent tumor, whereas the expression of erb-2 was similar in all three tumors. Although the cells from each of the three tumors show increased expression of early response genes after exposure to cisplatin (CDDP; 100 mu M, 2 h) or 4-Hydroxyperoxycyclophosphamide (4-HC, 100 mu M, 2 h) in culture, in mRNA extracted from tumor tissue these changes are absent or very small. Both C-jun and erb-2 were detectable in liver. There was increased expression of both of these genes in the livers of tumor-bearing animals as compared with non-tumor-bearing animals. The highest expression of both c-jun and erb-2 occurred in the livers of animals bearing the EMT-6/CDDP tumor. Treatment of the animals with CDDP or cyclophosphamide, in general, resulted in increased expression of both genes at 6 h post treatment. The increased expression of these genes may impart metabolic changes in the tumors and/or hosts that contribute to the resistance of these tumors to specific antitumor alkylating agents. C1 DANA FARBER CANC INST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. FU PHS HHS [P01-38493, R01-50174] NR 87 TC 20 Z9 21 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0344-5704 J9 CANCER CHEMOTH PHARM JI Cancer Chemother. Pharmacol. PD MAR PY 1995 VL 35 IS 5 BP 423 EP 431 DI 10.1007/s002800050257 PG 9 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA QX823 UT WOS:A1995QX82300011 PM 7850925 ER PT J AU TAGHIAN, A HUANG, P AF TAGHIAN, A HUANG, P TI THE NUDE AND SCID MICE AS A TUMOR-MODEL IN EXPERIMENTAL CANCER BIOLOGY SO CANCER JOURNAL LA English DT Review ID SEVERE COMBINED IMMUNODEFICIENCY; SQUAMOUS-CELL CARCINOMAS; SUBCUTANEOUS TISSUE; XENOGRAFTS; METASTASIS; GROWTH; IRRADIATION; RADIATION; MURINE; TRANSPLANTABILITY C1 BOSTON UNIV,MED CTR,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02118. RP TAGHIAN, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB RADIAT BIOL,BOSTON,MA 02114, USA. NR 38 TC 7 Z9 7 U1 0 U2 0 PU ASSN DEVELOP COMMUN CANCEROL PI VILLEJUIF PA CANCER JOURNAL BP 8, VILLEJUIF, FRANCE SN 0765-7846 J9 CANCER J JI Cancer J. PD MAR-APR PY 1995 VL 8 IS 2 BP 52 EP 58 PG 7 WC Oncology SC Oncology GA QV667 UT WOS:A1995QV66700006 ER PT J AU CHEN, M QUINTANS, J FUKS, Z THOMPSON, C KUFE, DW WEICHSELBAUM, RR AF CHEN, M QUINTANS, J FUKS, Z THOMPSON, C KUFE, DW WEICHSELBAUM, RR TI SUPPRESSION OF BCL-2 MESSENGER-RNA PRODUCTION MAY MEDIATE APOPTOSIS AFTER IONIZING-RADIATION, TUMOR-NECROSIS-FACTOR-ALPHA, AND CERAMIDE SO CANCER RESEARCH LA English DT Note ID IRRADIATED MURINE TUMORS; PROGRAMMED CELL-DEATH; DNA FRAGMENTATION; HL-60 CELLS; DIFFERENTIATION; TRANSLOCATION; CLONING; GENE AB Recent studies have proposed that tumor necrosis factor alpha (TNF-alpha) and ionizing radiation induce apoptosis by activating hydrolysis of sphingomyelin to ceramide, Bcl-2 and a related gene, Bcl-X, inhibit several forms of apoptosis, Herein, we report that internucleosomal DNA fragmentation, characteristic of apoptosis and induced by ionizing radiation, is accompanied by concomitant decreases in Bcl-2 and Bcl-X mRNA levels in HL-60 and U-937 human leukemia cells. Apoptotic DNA fragmentation after exposure to TNF-alpha and C-2-ceramide was also associated with down-regulation of Bcl-2 mRNA in HL-60 and U-937 cells, while Bcl-X mRNA production was unaffected, These results suggest that modulation of Bcl-2 gene expression may be a target for ceramide-mediated apoptosis following exposure to ionizing radiation and TNF-alpha. Changes in Bcl-2 expression may be the basis for the interactive killing observed between radiation and TNF-alpha in some human and tumor cells. C1 UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT PATHOL,COMM IMMUNOL,CHICAGO,IL 60637. UNIV CHICAGO,DEPT MED,CHICAGO,IL 60637. UNIV CHICAGO,HOWARD HUGHES MED INST,CHICAGO,IL 60637. MEM SLOAN KETTERING CANC CTR,DEPT RADIAT THERAPY,NEW YORK,NY 10021. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,PHARMACOL LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA55241, CA42596] NR 35 TC 137 Z9 147 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1995 VL 55 IS 5 BP 991 EP 994 PG 4 WC Oncology SC Oncology GA QJ600 UT WOS:A1995QJ60000005 PM 7867010 ER PT J AU ALDERSON, LM CASTLEBERG, RL HARSH, GR LOUIS, DN HENSON, JW AF ALDERSON, LM CASTLEBERG, RL HARSH, GR LOUIS, DN HENSON, JW TI HUMAN GLIOMAS WITH WILD-TYPE P53 EXPRESS BCL-2 SO CANCER RESEARCH LA English DT Note ID PROTEIN; APOPTOSIS; LYMPHOMA; TUMORS; LINE; GENE AB Human astrocytomas frequently overexpress wild-type p53, which suggests that gliomas have evolved a mechanism to subvert p53-mediated apoptosis, bcl-2 inhibits apoptosis mediated by p53, and it is expressed in several human cancers, We therefore examined a series of human gliomas to determine whether bcl-2 is expressed and whether this expression is associated with tumors which have wild-type p53, Twenty-eight paraffin-embedded gliomas (3 WHO grade II, 13 grade III, 12 grade IV) were immunohistochemically stained for bcl-2 and p53, p53 mutations were identified with single strand conformation polymorphism and DNA sequencing, Sixteen of 28 (57%) tumors expressed bcl-2, and bcl-2 expression was associated with mild-type p53 (P < 0.01), Among gliomas which overexpressed p53, bcl-2 was positive in 7 of 7 tumors with wild-type p53 but in only 1 of 7 with mutant p53 (P < 0.01), We conclude that bcl-2 is frequently expressed in human gliomas and that expression is more common in tumors with wild-type p53. C1 MASSACHUSETTS GEN HOSP E,MOLEC NEUROONCOL LAB,NEUROL SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP E,NEUROSURG SERV,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP E,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02129. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,BOSTON,MA 02129. FU NCI NIH HHS [CA 57683]; NINDS NIH HHS [NS 01605] NR 20 TC 97 Z9 103 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 1 PY 1995 VL 55 IS 5 BP 999 EP 1001 PG 3 WC Oncology SC Oncology GA QJ600 UT WOS:A1995QJ60000007 PM 7867012 ER PT J AU NOJIMA, Y TACHIBANA, K SATO, T SCHLOSSMAN, SF MORIMOTO, C AF NOJIMA, Y TACHIBANA, K SATO, T SCHLOSSMAN, SF MORIMOTO, C TI FOCAL ADHESION KINASE (PP125(FAK)) IS TYROSINE PHOSPHORYLATED AFTER ENGAGEMENT OF ALPHA-4-BETA-1 AND ALPHA-5-BETA-1 INTEGRINS ON HUMAN T-LYMPHOBLASTIC CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID FIBRONECTIN; PROTEIN; ACTIVATION; VLA-4; DIFFERENTIATION; STIMULATION; RECEPTORS; PP125FAK AB pp125(FAK) is a novel protein tyrosine kinase associated with focal. adhesions. It has been shown that ligation of VLA beta 1 integrins on a number of cell types enhanced tyrosine phosphorylation and kinase activity of pp125(FAK). Cellular transformation by retroviral oncogene products or mitogenic neuropeptides also result in the activation of this kinase. On the basis of these observations, pp125(FAK) has been proposed to be a key regulatory molecule connecting cell adhesion, transformation, and growth. We have previously shown that ligation of VLA beta 1 integrins induced CD3-dependent T cell proliferation and stimulated tyrosine phosphorylation of a molecular mass with a 105-kDa protein (pp105). Here we report that engagement of alpha 4 beta 1 and alpha 5 beta 1 integrins by adherence to their respective ligands stimulated tyrosine phosphorylation of 105- to 120-kDa proteins (pp105 and pp120, respectively) in human H9 T-lymphoblastic cells. At least one component of the 105- to 120-kDa proteins was found to be tyrosine-phosphorylated pp125(FAK). While kinetics of adherence-dependent tyrosine phosphorylation of pp120/pp125(FAK) and pp105 are closely similar, pp105 appeared to be distinct from pp125(FAK). Given T cell costimulation induced by VLA beta 1 integrins and the putative functional role of pp125(FAK) in cell growth, tyrosine phosphorylation of these two distinct proteins may be involved in T cell activation and proliferation. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP NOJIMA, Y (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI12069, AI29530]; NIAMS NIH HHS [AR33713] NR 26 TC 45 Z9 45 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD MAR PY 1995 VL 161 IS 1 BP 8 EP 13 DI 10.1006/cimm.1995.1002 PG 6 WC Cell Biology; Immunology SC Cell Biology; Immunology GA QK252 UT WOS:A1995QK25200002 PM 7532550 ER PT J AU BASSON, CT SOLOMON, SD WEISSMAN, B MACRAE, CA POZNANSKI, AK PRIETO, F DELAFUENTE, SR PEASE, WE LEVIN, SE HOLMES, LB SEIDMAN, JG SEIDMAN, CE AF BASSON, CT SOLOMON, SD WEISSMAN, B MACRAE, CA POZNANSKI, AK PRIETO, F DELAFUENTE, SR PEASE, WE LEVIN, SE HOLMES, LB SEIDMAN, JG SEIDMAN, CE TI GENETIC-HETEROGENEITY OF HEART-HAND SYNDROMES SO CIRCULATION LA English DT Note DE HOLT-GRAM SYNDROME; CONGENITAL HEART DEFECTS; SEPTAL DEFECTS ID HOLT-ORAM SYNDROME AB Background Heart-hand syndromes compose a class of combined congenital cardiac and limb deformities. The prototypical heart-hand disorder is Holt-Gram syndrome, which is characterized by cardiac septation defects and radial ray limb deformity. We have recently mapped the Holt-Gram syndrome gene defect to the long arm of human chromosome 12 in two families. The role of this disease locus in the pathogenesis of related conditions such as heart-hand syndrome type III (cardiac conduction disease accompanied by skeletal malformations) or familial atrial septal defects is unknown. Methods and Results Clinical evaluations and genetic linkage analyses were performed in five additional kindreds with Holt-Gram syndrome and also in one kindred with heart-hand syndrome type III and one kindred with familial atrial septal defect and conduction disease. Holt-Gram syndrome in all five kindreds mapped to chromosome 12q2. These studies and previous data provide odds of greater than 10(25):1 that the Holt-Gram syndrome disease gene is at chromosome 12q2, In contrast, neither the phenotypically similar disorder heart-hand syndrome type III nor the locus responsible for a familial atrial septal defect with atrioventricular block maps to chromosome 12q2. Conclusions We demonstrate that heart-hand syndromes are genetically heterogeneous. Conditions that clinically appear to be partial phenocopies of Holt-Gram syndrome arise from distinct disease genes. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA. CHILDRENS MEM HOSP,DEPT RADIOL,CHICAGO,IL 60614. HOSP UNIV LA FE,UNIDAD GENET,VALENCIA,SPAIN. HARRISBURG HOSP,DIV CARDIOL,HARRISBURG,PA. UNIV WITWATERSRAND,SCH MED,JOHANNESBURG,SOUTH AFRICA. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,GENET & TERATOL UNIT,BOSTON,MA 02114. RI Solomon, Scott/I-5789-2013 NR 19 TC 47 Z9 49 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 MAR 1 PY 1995 VL 91 IS 5 BP 1326 EP 1329 PG 4 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QJ117 UT WOS:A1995QJ11700005 PM 7867169 ER PT J AU RODRIGUEZ, AE SANTAERA, O LARRIBAU, M FERNANDEZ, M SARMIENTO, R BALINO, NP NEWELL, JB ROUBIN, GS PALACIOS, IF AF RODRIGUEZ, AE SANTAERA, O LARRIBAU, M FERNANDEZ, M SARMIENTO, R BALINO, NP NEWELL, JB ROUBIN, GS PALACIOS, IF TI CORONARY STENTING DECREASES RESTENOSIS IN LESIONS WITH EARLY LOSS IN LUMINAL DIAMETER 24 HOURS AFTER SUCCESSFUL PTCA SO CIRCULATION LA English DT Article DE STENTS; STENOSIS; ANGIOPLASTY ID ANGIOGRAPHIC FOLLOW-UP; PALMAZ-SCHATZ STENT; CONSECUTIVE PATIENTS; ANGIOPLASTY; EXPERIENCE; SCINTIGRAPHY; PREVENTION; OCCLUSION AB Background Early loss of minimal luminal diameter (MLD) after successful percutaneous transluminal coronary angioplasty (PTCA) is associated with a higher incidence of late restenosis. Methods and Results Sixty-six patients (66 lesions) with >0.3 mm MLD loss at 24-hour on-line quantitative coronary angiography were randomized into two groups: 1, Gianturco-Roubin stent (n=33) and 2, Control, who received medical therapy only (n=33). All lesions were suitable for stenting. Baseline demographic, clinical, and angiographic characteristics were similar in the two groups. Restenosis (greater than or equal to 50% stenosis) for the overall group occurred in 32 of 66 patients (48.4%) at 3.6+/-1-month follow-up angiography. Restenosis was significantly greater in group 2 than in group 1 (75.7% versus 21.2%, P<.001). Vascular complications (21.2% versus 0%) and length of hospital stay (7.3+/-1 versus 2.4+/-0.5 days, P<.01) were higher for the stent group. Although at follow-up there were no differences in mortality or incidence of acute myocardial infarction between the two groups, patients in the control group had a higher incidence of repeat revascularization procedures (73% versus 21%, P<.001). Conclusions In patients with successful PTCA but reduced luminal diameter demonstrated by repeat angiography at 24 hours, the Gianturco-Roubin stent appears to reduce angiographic restenosis at follow-up. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. ANCHORENA HOSP,CARDIAC UNIT,BUENOS AIRES,DF,ARGENTINA. UNIV ALABAMA,CARDIAC UNIT,BIRMINGHAM,AL. NR 38 TC 89 Z9 93 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 1 PY 1995 VL 91 IS 5 BP 1397 EP 1402 PG 6 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QJ117 UT WOS:A1995QJ11700016 PM 7867179 ER PT J AU DINSMORE, RE AF DINSMORE, RE TI NONINVASIVE CORONARY ARTERIOGRAPHY - HERE AT LAST SO CIRCULATION LA English DT Editorial Material ID EMISSION COMPUTED-TOMOGRAPHY; ACUTE MYOCARDIAL-INFARCTION; ECHOCARDIOGRAPHY; FLOW C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIAC UNIT,BOSTON,MA. RP DINSMORE, RE (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV CARDIAC RADIOL,FOUNDERS 202,POB 9657,BOSTON,MA 02114, USA. NR 9 TC 6 Z9 6 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR 1 PY 1995 VL 91 IS 5 BP 1607 EP 1608 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QJ117 UT WOS:A1995QJ11700044 PM 7867205 ER PT J AU RUBIN, E WOOD, V BHARTI, A TRITES, D LYNCH, C HURWITZ, S BARTEL, S LEVY, S ROSOWSKY, A TOPPMEYER, D KUFE, D AF RUBIN, E WOOD, V BHARTI, A TRITES, D LYNCH, C HURWITZ, S BARTEL, S LEVY, S ROSOWSKY, A TOPPMEYER, D KUFE, D TI A PHASE-I AND PHARMACOKINETIC STUDY OF A NEW CAMPTOTHECIN DERIVATIVE, 9-AMINOCAMPTOTHECIN SO CLINICAL CANCER RESEARCH LA English DT Article ID DNA TOPOISOMERASE-I; CELL LUNG-CANCER; ANTITUMOR-ACTIVITY; BIOLOGICAL-ACTIVITY; CONTINUOUS INFUSION; CPT-11; DRUG; TUMORS; INHIBITION; XENOGRAFTS AB Camptothecins are the only available antitumor agents which target the nuclear enzyme topoisomerase I. 9-Amino-camptothecin (9-AC) is a water-insoluble derivative of camptothecin which has demonstrated impressive antitumor activity in preclinical models, While two other water-soluble derivatives, CPT-11 and topotecan, have successfully completed Phase I and Phase II testing, biochemical and tissue culture studies suggest that camptothecin analogues differ in characteristics which may be important in determining antitumor activity. We performed a Phase I trial of 9-AC to determine the pharmacokinetics, dose-limiting toxicity, and maximum tolerated dose of this agent when administered as a 72-h continuous i.v. infusion. Thirty-one patients with resistant solid cancers received 5-60 mu g/m(2)/h 9-AC for 72 h, repeated at 3-week intervals. The drug was administered in a vehicle containing dimethylacetamide, polyethylene glycol, and phosphoric acid, Blood samples were collected and the lactone (closed ring) form of 9-AC was quantitated. The maximum tolerated dose of 9-AC was determined to be 45 mu g/m(2)/h. Dose-limiting toxicity consisted of neutropenia. Thrombocytopenia was also prominent. There were no significant nonhematological toxicities. Minimal responses were seen in patients with gastric, colon, and non-small cell lung cancer. Although significant interpatient variation in plasma 9-AC lactone levels was observed, pooled data were fit to a two-compartment model, with a terminal half-life of 36 h. Analyses of topoisomerase protein levels in peripheral blood cells indicated decreases in topoisomerase I accompanied by increases in topoisomerase II in two of three patients. 9-AC is an active antitumor agent and may be administered safely as a 72-h infusion in patients with cancer. Although Phase II trials with a 72-h infusion of 9-AC are warranted, alternate schedules should be evaluated given the dramatic preclinical activity seen with more prolonged administrations. RP RUBIN, E (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [1U01-CA62490, K08CA01664-02] NR 52 TC 82 Z9 83 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 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD MAR PY 1995 VL 1 IS 3 BP 269 EP 276 PG 8 WC Oncology SC Oncology GA RJ527 UT WOS:A1995RJ52700004 PM 9815982 ER PT J AU CANNISTRA, SA DEFRANZO, B NILOFF, J OTTENSMEIER, C AF CANNISTRA, SA DEFRANZO, B NILOFF, J OTTENSMEIER, C TI FUNCTIONAL-HETEROGENEITY OF CD44 MOLECULES IN OVARIAN-CANCER CELL-LINES SO CLINICAL CANCER RESEARCH LA English DT Article ID LYMPHOCYTE HOMING RECEPTOR; CONFER METASTATIC BEHAVIOR; HYALURONATE RECOGNITION; ADHESION MOLECULE; SPLICE VARIANTS; PROTEINS; BINDING; FAMILY; EXPRESSION; ANTIBODIES AB We have previously shown that CD44 partly mediates ovarian cancer cell attachment to peritoneal mesothelium through recognition of mesothelial-associated hyaluronate. CD44 is a major receptor for hyaluronate and exists as a standard 90-180-kDa form (CD44H), as well as several higher molecular mass variant forms produced by alternative splicing. To determine whether functional differences exist between CD44H and its variants we have investigated the relationship between CD44 isoform expression and mesothelial adhesion in 12 ovarian cancer cell lines. Eight lines were CD44 positive (range, 83-94%) and demonstrated significant binding to mesothelium and hyaluronate, whereas two lines showed reduced CD44 levels (3-13%) and demonstrated decreased binding. Interestingly, two other lines (OVC-3 and SW626) expressed CD44 in the majority of cells (>93%) and yet bound weakly to mesothelium. Mean linear fluorescence intensity of CD44 expressed by OVC-3 and SW626 cells was approximately one-half that of strongly binding cell lines, suggesting that the ability to adhere may be partly related to CD44 surface density. However, immunoprecipitation and immunoblot analyses revealed that standard CD44H represented only 23-31% of total CD44 in weakly binding cells, with the majority of species being comprised of CD44 variants. Indirect immunofluorescence of OVC-3 and SW626 cells confirmed the presence of CD44 variants containing exons v3, v6, and v9. In contrast, CD44H represented the majority (75-86%) of total CD44 expressed by strongly binding cell lines such as CAOV-3 and UPN36T. Transfection of CD44H cDNA into weakly binding OVC-3 cells restored significant mesothelial binding which was partly blocked by anti-CD44 antibody. These data suggest that the expression of CD44 is necessary but not sufficient for mediating attachment of ovarian cancer cells to mesothelium. Although CD44 variants may constitute the major CD44 species in certain ovarian cancer cell lines, it appears that these CD44 species are not always capable of mediating significant binding to mesothelium or hyaluronate. Rather, an adequate level of CD44H is the critical determinant of binding in this system. The role of CD44 variants in the process of ovarian cancer metastasis will require further investigation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. RI Ottensmeier, Christian/E-8131-2012 OI Ottensmeier, Christian/0000-0003-3619-1657 FU NCI NIH HHS [CA 60670] NR 32 TC 38 Z9 38 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1078-0432 J9 CLIN CANCER RES JI Clin. Cancer Res. PD MAR PY 1995 VL 1 IS 3 BP 333 EP 342 PG 10 WC Oncology SC Oncology GA RJ527 UT WOS:A1995RJ52700011 PM 9815989 ER PT J AU KURIAN, MS DELACUESTA, RS WANECK, GL MACLAUGHLIN, DT MANGANARO, TF DONAHOE, PK AF KURIAN, MS DELACUESTA, RS WANECK, GL MACLAUGHLIN, DT MANGANARO, TF DONAHOE, PK TI CLEAVAGE OF MULLERIAN-INHIBITING SUBSTANCE ACTIVATES ANTIPROLIFERATIVE EFFECTS IN-VIVO SO CLINICAL CANCER RESEARCH LA English DT Article ID TRANSFORMING GROWTH-FACTOR; HUMAN OVARIAN-CANCER; DUCT REGRESSION; OOCYTE MEIOSIS; SERTOLI CELLS; COLONY GROWTH; TUMOR-GROWTH; INVITRO; BOVINE; IDENTIFICATION AB Mullerian inhibiting substance (MIS), an inhibitor of growth and development of the female reproductive ducts in male fetuses, requires precise proteolytic cleavage to yield its biologically active species. Human plasmin is now used to cleave and, thereby, activate immunoaffinity purified recombinant human MIS at its monobasic arginine-serine site at residues 427-428. To avoid the need for exogenous enzymatic cleavage and to simplify purification, we created an arginine-arginine dibasic cleavage site (MIS RR) using site-directed mutagenesis to change the serine at position 428 (AGC) to an arginine (cGC). The mutant cDNA was then stably transfected into a MIS-responsive ocular melanoma cell line, OM431, followed by cloning for amplified expression to test its biological activity in vitro and in vivo. Media from each clone were assayed for production of MIS RR by a sensitive ELISA for hole-MIS, and high- and low-producing clones were selected for further study. Media from the highest MIS RR producer caused Mullerian duct regression in an organ culture bioassay. Other transfections were done with an empty vector (pcDNAI Neo) or a construct lacking the leader sequence and thus failing to secrete MIS, to serve as controls. The OM431 clones containing the MIS RR mutant were growth inhibited in monolayer culture. The high- and low-producing MIS RR OM431 clones, along with transfected OM431 controls, were injected into the tail veins of immunosuppressed severe combined immunodeficiency mice for in vivo analyses. Four to 6 weeks later, pulmonary metastases were counted in uniformly inflated lungs, OM431 clones containing the more easily cleaved MIS RR displayed a significant dose-dependent reduction in pulmonary metastases when compared to the lungs of animals given injections of OM431 clones containing empty vector, leaderless MIS, or wild-type MIS that requires activation by plasmin cleavage. Since the purification protocol of MIS RR is less complicated than that for wild-type MIS, which requires subsequent enzymatic activation, MIS RR can be used for scale-up production with increased yields for further therapeutic trials against MIS-sensitive tumors. C1 MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LABS, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, SURG IMMUNOL LAB, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, DIV GYNECOL ONCOL, BOSTON, MA USA. HARVARD UNIV, SCH MED, DEPT SURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT OBSTET & GYNECOL, BOSTON, MA 02114 USA. FU NCI NIH HHS [CA17393]; NICHD NIH HHS [HD 30812]; NIGMS NIH HHS [GM46467] NR 53 TC 15 Z9 16 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 1078-0432 EI 1557-3265 J9 CLIN CANCER RES JI Clin. Cancer Res. PD MAR PY 1995 VL 1 IS 3 BP 343 EP 349 PG 7 WC Oncology SC Oncology GA RJ527 UT WOS:A1995RJ52700012 PM 9815990 ER PT J AU EZEKOWITZ, RAB EICHBAUM, Q AF EZEKOWITZ, RAB EICHBAUM, Q TI CHRONIC GRANULOMATOUS-DISEASE - PATHOGENESIS AND MANAGEMENT SO CLINICAL IMMUNOTHERAPEUTICS LA English DT Article ID NEUTROPHIL CYTOCHROME-B; RECOMBINANT INTERFERON-GAMMA; CHROMOSOMAL LOCATION; PHAGOCYTE FUNCTION; NADPH OXIDASE; ABSENCE; GENE; EXPRESSION; CLONING; FORMS AB Chronic granulomatous disease is a rare disorder of phagocyte oxidative metabolism. The disease is characterised by recurrent infections in childhood that require prolonged courses of antimicrobial therapy. Adjunctive therapy with interferon-gamma has been shown to reduce the frequency and severity of infections. Combined use of daily prophylactic antibiotics and thrice weekly therapy with interferon-gamma is an effective and well tolerated treatment that reduces the risk of serious infection. We also update the progress that defines the molecular basis of the disease. C1 CHILDRENS HOSP,DIV INFECT DIS,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. RP EZEKOWITZ, RAB (reprint author), CHILDRENS HOSP,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02116, USA. NR 40 TC 0 Z9 0 U1 0 U2 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 1172-7039 J9 CLIN IMMUNOTHER JI Clin. Immunother. PD MAR PY 1995 VL 3 IS 3 BP 184 EP 190 PG 7 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA QL202 UT WOS:A1995QL20200002 ER PT J AU BARCHIESI, F HOLLIS, RJ MCGOUGH, DA SCALISE, G RINALDI, MG PFALLER, MA AF BARCHIESI, F HOLLIS, RJ MCGOUGH, DA SCALISE, G RINALDI, MG PFALLER, MA TI DNA SUBTYPES AND FLUCONAZOLE SUSCEPTIBILITIES OF CANDIDA-ALBICANS ISOLATES FROM THE ORAL CAVITIES OF PATIENTS WITH AIDS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; RESISTANT CANDIDA; THERAPY; VIRUS; INDIVIDUALS; BIOTYPES AB Sixty-two Candida albicans isolates from the oral cavities of 28 patients with AIDS who were receiving fluconazole therapy were typed by restriction endonuclease analysis followed by pulsed-field gel electrophoresis; these isolates were then tested for fluconazole susceptibility by a standard broth dilution method. Sequential isolates (range, 2-4) were evaluated for 22 patients; only one isolate was evaluated for six patients. DNA subtyping revealed a total of 37 different DNA subtypes. Twelve (54.5%) of 22 patients with multiple episodes of oropharyngeal candidiasis were infected with a single DNA subtype throughout the observation period. Ten (45.5%) of 22 patients with multiple episodes of oropharyngeal candidiasis were infected with two or three DNA subtypes during the observation period. In vitro susceptibility tests revealed that MICs of fluconazole ranged from less than or equal to 0.125 mu g/mL to 64 mu g/mL, with an MIC(50) of 0.5 mu g/mL and an MIC(90) of 4 mu g/mL. A significant increase in the MICs (fourfold or greater) of fluconazole for sequential C. albicans isolates was found for 66.6% of the patients infected with a single DNA subtype and for 50% of the patients infected with multiple DNA subtypes. Despite a limited number of patients and isolates, our data suggest that C. albicans isolates that are susceptible to fluconazole at MICs of greater than or equal to 8 mu g/mL in vitro will be less susceptible in vivo to standard doses (100-200 mg/d) of this drug. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV IOWA,COLL MED,DEPT PATHOL,SPECIAL MICROBIOL LAB,IOWA CITY,IA. UNIV ANCONA,IST MALATTIE INFETT & MED PUBBL,ANCONA,ITALY. RP BARCHIESI, F (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,SAN ANTONIO,TX 78284, USA. NR 23 TC 57 Z9 57 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1995 VL 20 IS 3 BP 634 EP 640 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA QL159 UT WOS:A1995QL15900026 PM 7756488 ER PT J AU EAVEY, RD BERTERO, MDCC THORNTON, AR HERRMANN, BS JOSEPH, JM GLIKLICH, RE KRISHNAMOORTHY, KS TODRES, ID AF EAVEY, RD BERTERO, MDCC THORNTON, AR HERRMANN, BS JOSEPH, JM GLIKLICH, RE KRISHNAMOORTHY, KS TODRES, ID TI FAILURE TO CLINICALLY PREDICT NICU HEARING-LOSS SO CLINICAL PEDIATRICS LA English DT Article ID BRAIN-STEM RESPONSES; INTENSIVE-CARE NURSERY; HIGH-RISK INFANTS; AUDITORY-NERVE; FOLLOW-UP; PRETERM INFANTS; AUDIOMETRY; DEAFNESS; NEWBORNS; NOISE AB Neonatal intensive care unit (NICU) survivors demonstrate handicapping sensorineural hearing loss up to 50 times more frequently than normal newborns, yet little is known about the etiology of the hearing loss. Theoretically accurate identification and triage of a particular infant based on a clinical profile would be useful. Forty NICU graduates of The Massachusetts General Hospital were selected for a detailed retrospective chart review evaluating prenatal, perinatal, and NICU medical conditions and treatment. Twenty-three patients identified with hearing loss and 17 infants with normal hearing were compared clinically. Univariate and multivariate analysis was performed on a subpopulation of patients (20 with hearing loss and 16 with normal hearing). A history of ventilation was associated with hearing loss (P=.0023), but this factor was not absolute. No other clinical parameters were convincingly linked to hearing loss. We conclude that reliance on risk factors is an inadequate clinical method to select a patient for a hearing test and that each NICU survivor deserves audiometric evaluation. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT AUDIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DIV NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,DIV INTENS CARE,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP EAVEY, RD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 46 TC 14 Z9 16 U1 1 U2 1 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD MAR PY 1995 VL 34 IS 3 BP 138 EP 145 DI 10.1177/000992289503400304 PG 8 WC Pediatrics SC Pediatrics GA QM648 UT WOS:A1995QM64800004 PM 7774140 ER PT J AU BOLAND, GW LEE, MJ CATS, AM FERRARO, MJ MATTHIA, AR MUELLER, PR AF BOLAND, GW LEE, MJ CATS, AM FERRARO, MJ MATTHIA, AR MUELLER, PR TI CLOSTRIDIUM-DIFFICILE COLITIS - CORRELATION OF CT FINDINGS WITH SEVERITY OF CLINICAL-DISEASE SO CLINICAL RADIOLOGY LA English DT Article ID PSEUDOMEMBRANOUS COLITIS AB Clinical records and abdominal CT scans from 64 patients with documented Clostridium difficile disease were reviewed to determine if any correlation existed between CT findings of colitis and severity of clinical disease. Clostridium difficile disease was documented with stool toxin titre levels and CT scans were performed within 3 days of stool sample. Clinical disease severity was estimated by tabulating the degree of fever, WBC count, frequency and duration of diarrhoea. Thirty-nine of 64 patients showed CT evidence of colitis of which 28/39 showed evidence of focal colitis and 11/39 had pancolitis. CT findings suggesting colitis included colonic wall thickening (39 patients), nodular mucosal thickening (11 patients), the 'accordion pattern' (3 patients), pericolonic oedema (27 patients) and ascites (10 patients). Twenty-five of 64 patients showed no CT evidence of colitis. The clinical severity of disease did not statistically differ (P < 0.05) between patients with CT evidence of colitis and those without colitis. The only CT finding that correlated with clinical severity of disease was nodular mucosal thickening which was found with significantly (P < 0.05) more frequency in patients with a WBC count > 11000 mm(3). CT changes with Cl. difficile disease correlate poorly with the clinical severity. This and negative findings do not exclude the disease. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 8 TC 29 Z9 29 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9260 J9 CLIN RADIOL JI Clin. Radiol. PD MAR PY 1995 VL 50 IS 3 BP 153 EP 156 DI 10.1016/S0009-9260(05)83045-4 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QM459 UT WOS:A1995QM45900004 PM 7889703 ER PT J AU RAUCH, SL BAER, L COSGROVE, GR JENIKE, MA AF RAUCH, SL BAER, L COSGROVE, GR JENIKE, MA TI NEUROSURGICAL TREATMENT OF TOURETTES-SYNDROME - A CRITICAL-REVIEW SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; LIMBIC LEUKOTOMY; BASAL GANGLIA; FOLLOW-UP; GILLES; CINGULOTOMY; PIMOZIDE; SCALE AB Some patients with Tourette's syndrome (TS) remain disabled despite conventional treatment. Recently, neurosurgical procedures have been reported to be potentially effective interventions for such intractable cases. Clinicians are now being asked to make recommendations to patients about these candidate operations. This review explores the reported experience with neurosurgical treatment of TS to assess critically the evidence regarding risks and benefits. Toward that end, the rationale for the various procedures and the relevant neuroanatomy are outlined and recommendations for patient selection and management of future cases are discussed. We reviewed all available published reports on this subject and two unpublished cases, totaling 36 patients. Although a variety of operations have been used to treat TS, there is limited evidence pertaining to the risks or benefits of any surgical procedure. Neurosurgical treatment of TS remains experimental, since there is only anecdotal experience with these operations. Furthermore, there is no compelling evidence that any neurosurgical procedure is superior to all others. If these experimental neurosurgeries are to continue, guidelines should be developed regarding patient and operation selection, and interdisciplinary assessment committees should implement such guidelines at institutions where these operations are performed. Moreover, future cases should be prospectively studied using contemporary technologies to assess lesion placement and size and validated clinical instruments to characterize patients and assess outcome, including adverse effects. (C) 1995 by W.B. Saunders Company C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,OBSESS COMPULS DISORDERS CLIN & RES UNIT,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 78 TC 49 Z9 54 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0010-440X J9 COMPR PSYCHIAT JI Compr. Psychiat. PD MAR-APR PY 1995 VL 36 IS 2 BP 141 EP 156 DI 10.1016/S0010-440X(95)90109-4 PG 16 WC Psychiatry SC Psychiatry GA QM110 UT WOS:A1995QM11000007 PM 7758300 ER PT J AU SHEPHERD, KE FAULKNER, CS THAL, GD LEITER, JC AF SHEPHERD, KE FAULKNER, CS THAL, GD LEITER, JC TI ACUTE, SUBACUTE, AND CHRONIC HISTOLOGIC EFFECTS OF SIMULATED ASPIRATION OF A 0.7-PERCENT SUCRALFATE SUSPENSION IN RATS SO CRITICAL CARE MEDICINE LA English DT Article DE SUCRALFATE; PULMONARY ASPIRATION; ASPIRATION PNEUMONITIS; LUNG INJURY; CARDIOPULMONARY EMERGENCIES; CRITICAL ILLNESS; HISTOLOGY; LUNGS ID PULMONARY ASPIRATION; GASTROINTESTINAL HEMORRHAGE; GASTRIC CONTENTS; PNEUMONITIS; DISEASE; RISK AB Objective: To assess the acute (4-hr), subacute (7-day), and chronic (al-day) effects of simulated aspiration of a 0.7% sucralfate suspension in rats. Design: Prospective, multigroup trial in which rats were randomized to various simulated aspiration groups. Setting: Experimental animal laboratory. Subjects: Forty-five Sprague-Dawley rats. Interventions: Simulated aspiration was induced by single, direct, tracheal instillation of 2 mL/kg of either room air, sucralfate, or normal saline. Measurements and Main Results: Lung histologic changes were assessed using a quantitative numerical scoring scale. There was an increase in bronchiolar inflammation in rats undergoing acute, simulated sucralfate aspiration compared with controls. There were no significant differences (p > .05) in any other features at any time interval studied (two-way analysis of variance). Conclusions: Even though significant inflammatory airway lesions were produced in this acute model, these abnormalities resolved without evidence of subacute or chronic histologic progression, It remains to be determined if this pattern is unique to this specific experimental model or if it can be extrapolated to critically ill patients. C1 DARTMOUTH COLL,SCH MED,DEPT PHYSIOL,LEBANON,NH. DARTMOUTH COLL,SCH MED,DEPT MED,LEBANON,NH. DARTMOUTH COLL,SCH MED,DEPT PATHOL,LEBANON,NH. RP SHEPHERD, KE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA, USA. NR 22 TC 6 Z9 6 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0090-3493 J9 CRIT CARE MED JI Crit. Care Med. PD MAR PY 1995 VL 23 IS 3 BP 532 EP 536 DI 10.1097/00003246-199503000-00019 PG 5 WC Critical Care Medicine SC General & Internal Medicine GA QL468 UT WOS:A1995QL46800019 PM 7874906 ER PT J AU DUNN, MK MERCOLA, M MOORE, DD AF DUNN, MK MERCOLA, M MOORE, DD TI CYCLOPAMINE, A STEROIDAL ALKALOID, DISRUPTS DEVELOPMENT OF CRANIAL NEURAL CREST CELLS IN XENOPUS SO DEVELOPMENTAL DYNAMICS LA English DT Article DE CYCLOPAMINE; CRANIAL NEURAL CREST; CARTILAGE; CELL DEATH; XENOPUS; TERATOGENESIS ID CENTRAL-NERVOUS-SYSTEM; RETINOIC ACID; LAEVIS; DIFFERENTIATION; SPECIFICITY; EXPRESSION AB Cyclopamine is a steroidal alkaloid which causes limb and craniofacial defects in many vertebrate species, We have used Xenopus laevis as a model system to characterize the defects caused by cyclopamine at the cellular level, The most dramatic consequence of cyclopamine treatment in the Xenopus embryo is a defect in formation of craniofacial cartilage, Much of this cartilage is absent in treated animals, As in avian and mammalian species, Xenopus craniofacial cartilage is derived primarily from cells of the cranial neural crest. Grafting experiments show that development of the cartilaginous derivatives of the cranial neural crest is impaired after cyclopamine treatment, and this is at least partially due to a direct effect on presumptive crest cells, A culture system was used to determine the cellular response to the drug, Cyclopamine did not block the initial emigration of cells from a neural plate explant, However, cell death is seen in treated cultures after 4 days, Trunk neural crest cells and transformed cell lines are resistant to cyclopamine, We therefore conclude that cyclopamine specifically causes death of cranial neural crest cells and that lethality is likely to account for the teratogenic effects of this compound. (C) 1995 Wiley-Liss, Inc. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP DUNN, MK (reprint author), HARVARD UNIV,SCH MED,DEPT CELL BIOL,25 SHATTUCK ST,BOSTON,MA 02115, USA. FU NICHD NIH HHS [HD28460] NR 31 TC 25 Z9 25 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 1058-8388 J9 DEV DYNAM JI Dev. Dyn. PD MAR PY 1995 VL 202 IS 3 BP 255 EP 270 PG 16 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA QN660 UT WOS:A1995QN66000004 PM 7780175 ER PT J AU FINEGOOD, DT SCAGLIA, L BONNERWEIR, S AF FINEGOOD, DT SCAGLIA, L BONNERWEIR, S TI DYNAMICS OF BETA-CELL MASS IN THE GROWING RAT PANCREAS - ESTIMATION WITH A SIMPLE MATHEMATICAL-MODEL SO DIABETES LA English DT Article ID ENDOCRINE PANCREAS; B-CELLS; DIABETES-MELLITUS; INSULIN-SECRETION; PREGNANCY; GROWTH; DEATH; SOMATOSTATIN; EXOCRINE; ISLETS AB The growth and development of the endocrine pancreas has been studied for many years, but questions remain concerning the regulation of the mass of insulin-producing beta-cells both in the normal growing pancreas and during the pathogenesis of diabetes, The homeostatic control of beta-cell mass in both normal and pathophysiological conditions is based on the balance of cell proliferation, cell growth, and cell death, To gain insight into the relative contribution of each of these dynamic processes, we first mathematically analyzed the data available on the components involved in the maintenance of beta-cell mass, including rates of replication, beta-cell volume, and the beta-cell mass itself, at various ages in normal Sprague-Dawley rats. Then these data were combined in a simple mass balance equation to construct a mathematical model of the dynamics of the beta-cell mass in the normal growing rat pancreas, Such a model has allowed us to infer the contributions of fluxes that cannot be measured, i.e., neogenesis and cell death, to the known mass of beta-cells. Another important contribution of this model is to raise unanswered questions concerning the control of the balance of cell death and cell renewal in the endocrine pancreas. C1 JOSLIN DIABET CTR,ELLIOT P JOSLIN RES LABS,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV ALBERTA,DEPT MED,EDMONTON,AB,CANADA. UNIV ALBERTA,DEPT PHYSIOL,EDMONTON,AB,CANADA. FU NIDDK NIH HHS [DK-35449, DK-36836, DK-44523] NR 43 TC 430 Z9 448 U1 0 U2 10 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD MAR PY 1995 VL 44 IS 3 BP 249 EP 256 DI 10.2337/diabetes.44.3.249 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QZ334 UT WOS:A1995QZ33400001 PM 7883109 ER PT J AU ELHASHIMY, M ANGELICO, MC MARTIN, BC KROLEWSKI, AS WARRAM, JH AF ELHASHIMY, M ANGELICO, MC MARTIN, BC KROLEWSKI, AS WARRAM, JH TI FACTORS MODIFYING THE RISK OF IDDM IN OFFSPRING OF AN IDDM PARENT SO DIABETES LA English DT Article ID DEPENDENT DIABETES-MELLITUS; MATERNAL AGE; GENETIC-HETEROGENEITY; PREGNANCY; MOTHERS; COMPLICATIONS; RELATIVES; CHILDREN; DISEASE; STATE AB Offspring of mothers with insulin-dependent diabetes mellitus (IDDM) have a much lower risk of IDDM than do offspring of diabetic fathers, and this risk is particularly low for offspring born to diabetic mothers over the age of 25 years. To determine whether increasing maternal age also protects the offspring of IDDM fathers from IDDM, we surveyed 367 IDDM fathers (IDDM onset before age 35) who first came to the Joslin Clinic (Boston, MA) between 1945 and 1969. Of the 840 offspring of these men, IDDM developed in 28 before the age of 20, giving a cumulative risk of 5.1 +/- 1.0% (means +/- SE). Because this is similar to the result of our earlier study of IDDM fathers, the two groups were combined to give 1,084 offspring, 39 having IDDM (cumulative risk of IDDM 5.4 +/- 0.9% by age 20), for comparison with our cohort of 1,391 offspring of 739 IDDM mothers. In that cohort, IDDM developed in 20 offspring before the age of 20 years, giving a cumulative risk of 2.1 +/- 0.5%. The risk of diabetes in offspring was higher if the parent's IDDM was diagnosed before age 11 than if it was diagnosed later: 9.3 compared with 4.0% (P = 0.006) for the offspring of IDDM fathers and 2.7 compared with 1.8% for the offspring of IDDM mothers (P = 0.06). In the families in which the father's IDDM was diagnosed after age 11, a protective effect of maternal age greater than or equal to 25, similar to that in families of IDDM mothers, seems to be present, However, in families in which the father's IDDM was diagnosed before age 11, the effect of maternal age seems to be in the opposite direction: the incidence rate doubled for the offspring born to nondiabetic mothers aged greater than or equal to 25 years. In contrast, no effect of paternal age was found, regardless of which parent had IDDM. Our findings, although challenging to explain, have immediate implications for counseling families in which one parent has IDDM. C1 JOSLIN DIABET CTR,EPIDEMIOL & GENET SECT,BOSTON,MA 02215. NR 27 TC 24 Z9 24 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 MAR PY 1995 VL 44 IS 3 BP 295 EP 299 DI 10.2337/diabetes.44.3.295 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QZ334 UT WOS:A1995QZ33400009 PM 7883117 ER PT J AU WAKISAKA, M HE, Q SPIRO, MJ SPIRO, RG AF WAKISAKA, M HE, Q SPIRO, MJ SPIRO, RG TI GLUCOSE ENTRY INTO RAT MESANGIAL CELLS IS MEDIATED BY BOTH NA+-COUPLED AND FACILITATIVE TRANSPORTERS SO DIABETOLOGIA LA English DT Article DE NA+-COUPLED GLUCOSE TRANSPORTER; FACILITATIVE GLUCOSE TRANSPORTERS; MESANGIAL CELLS; GLOMERULOPATHY; PHLORHIZIN ID IV COLLAGEN PRODUCTION; MESSENGER-RNA; HEXOSE-TRANSPORT; SUGAR-TRANSPORT; XENOPUS-LAEVIS; COTRANSPORTER; KIDNEY; EXPRESSION; PROTEIN; SODIUM AB Since previous studies from our laboratory have demonstrated that increased glucose consumption by cultured rat mesangial cells is accompanied by an accelerated production of type IV and type VI collagen, we have now examined the manner by which glucose is transported into these cells. A progressive stimulation of glucose uptake by the mesangial cells was observed with increasing concentrations of NaCl so that at 145 mmol/l about twice as much glucose entered the cells as in its absence (substituted by choline chloride). Moreover, since phlorizin inhibited the NaCl-promoted uptake of glucose and this salt was found to increase the accumulation of alpha-methylglucoside in a manner which could not be duplicated by KCl or mannitol, both Na+-coupled and facilitative glucose transporters appeared to be present in the cells. K-m values of 1.93 mmol/l and 1.36 mmol/l were determined for the co-transport and facilitated transport pathways, respectively, with their V-max being 29.5 and 18.0 nmol . mg protein(-1). h(-1). Both uptake activities were found to be down-regulated by exposure of the cells to high glucose and furthermore the Na+-dependent transport could no longer be detected after about 12 passages of the cells. Hybridization of mesangial cell mRNA with cDNA probes revealed transcripts for the Na+/glucose co-transporter as well as GLUT1 and to a lesser extent GLUT4. The identification of the co-transporter in these non-polarized cells is pertinent to an understanding of the intracellular signals which can lead to the development of the diabetic glomerular lesions; in the hyperglycaemic state this carrier provides an additional route for accelerated glucose entry and furthermore by the attendant increase in Na+ flux may bring about an alteration in the ionic composition of the cell. C1 JOSLIN DIABET CTR,ELLIOT P JOSLIN RES LAB,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-31315]; NIDDK NIH HHS [DK-17477] NR 44 TC 47 Z9 53 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD MAR PY 1995 VL 38 IS 3 BP 291 EP 297 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QH749 UT WOS:A1995QH74900007 PM 7758875 ER PT J AU HOWARITZ, JH AF HOWARITZ, JH TI SERUM TUMOR-MARKERS - IMPLICATIONS OF DISCORDANT RESULTS SO DISEASE MARKERS LA English DT Editorial Material ID PROSTATE-SPECIFIC ANTIGEN; CARCINOEMBRYONIC ANTIGEN; STANDARDIZATION; IMMUNOASSAYS; GONADOTROPIN; ASSAYS RP HOWARITZ, JH (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,PATHOL & LAB MED SERV 113,LOS ANGELES,CA, USA. NR 12 TC 0 Z9 0 U1 0 U2 0 PU ASFRA PI EDAM PA VOORHAVEN 33, 1135 BL EDAM, NETHERLANDS SN 0278-0240 J9 DIS MARKERS JI Dis. Markers PD MAR PY 1995 VL 12 IS 2 BP 81 EP 83 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; Pathology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine; Pathology GA QV431 UT WOS:A1995QV43100001 PM 7614784 ER PT J AU LYNCH, RD TKACHUKROSS, LJ MCCORMACK, JM MCCARTHY, KM ROGERS, RA SCHNEEBERGER, EE AF LYNCH, RD TKACHUKROSS, LJ MCCORMACK, JM MCCARTHY, KM ROGERS, RA SCHNEEBERGER, EE TI BASOLATERAL BUT NOT APICAL APPLICATION OF PROTEASE RESULTS IN A RAPID RISE OF TRANSEPITHELIAL ELECTRICAL-RESISTANCE AND FORMATION OF ABERRANT TIGHT JUNCTION STRANDS IN MDCK CELLS SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Article DE TIGHT JUNCTION; PROTEASE; ABERRANT TJ STRANDS; POLARITY ID MEMBRANE CYTOSKELETAL COMPLEX; HT-29 ADENOCARCINOMA CELLS; KIDNEY EPITHELIAL-CELLS; EXTRACELLULAR CALCIUM; OCCLUDING JUNCTIONS; ZONULA-OCCLUDENS; IDENTIFICATION; ZO-1; POLYPEPTIDE; INHIBITORS AB In the presence of Ca2+ application of trypsin to the basolateral surface of confluent MDCK cell monolayers with formed tight junctions (TJ), induces the formation of basolaterally oriented aberrant TJ strands, Induction of aberrant TJ strands is accompanied by an increase in transepithelial electrical resistance (TER), up to 90%, which upon addition of trypsin inhibitor is maintained for up to 1 h. Thereafter TER returns slowly to baseline values. Under similar conditions, application of trypsin to the apical surface has little or no effect on either TER or the number of aberrant TJ strands, Confocal microscopy of monolayers, immunostained for ZO-1, revealed that this TJ associated cytoplasmic protein, extended below the TJ along the basolateral surface following brief exposure to trypsin. Removing Ca2+ after treatment of the monolayer with basolaterally applied trypsin resulted, after 20 min, in the increased partitioning of TJ particles onto the E fracture face, of both normal and aberrant TJ strands. Like the TJ strands themselves, therefore, aberrant strands may be linked to cytoskeletal elements. Aberrant TJ strands do not form when monolayers, maintained in low Ca2+ medium, are exposed to trypsin, suggesting that under these conditions TJ precursors, and/or trypsin-sensitive proteins regulating TJ strand assembly are sequestered in a vesicular compartment that is inaccessible to exogenous trypsin. Prolonged exposure of the apical surface of an established, polarized epithelium with intact TJ to trypsin, had Little effect on TJ integrity and did not induce aberrant strands. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM SCI & PHYSIOL,BOSTON,MA 02115. UNIV MASSACHUSETTS,DEPT BIOL SCI,LOWELL,MA. FU NHLBI NIH HHS [HL25822] NR 37 TC 28 Z9 28 U1 0 U2 0 PU WISSENSCHAFTLICHE VERLAG GMBH PI STUTTGART 10 PA BIRKENWALDSTRASSE 44 POSTFACH 105339, W-7000 STUTTGART 10, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD MAR PY 1995 VL 66 IS 3 BP 257 EP 267 PG 11 WC Cell Biology SC Cell Biology GA QM105 UT WOS:A1995QM10500005 PM 7774611 ER PT J AU CONLON, K OSBORNE, J MORIMOTO, C ORTALDO, JR YOUNG, HA AF CONLON, K OSBORNE, J MORIMOTO, C ORTALDO, JR YOUNG, HA TI COMPARISON OF LYMPHOKINE SECRETION AND MESSENGER-RNA EXPRESSION IN THE CD45RA(+) AND CD45RO(+) SUBSETS OF HUMAN PERIPHERAL-BLOOD CD4(+) AND CD8(+) LYMPHOCYTES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE T CELLS; CD45RA(+); CD45RO(+); LYMPHOKINES ID T-CELL CLONES; TUMOR-NECROSIS-FACTOR; FUNCTIONAL SUBSETS; INTERFERON-GAMMA; MESSENGER-RNA; DIFFERENTIATION; PROFILES; CD4+CD45RA+; ACTIVATION; ANTIBODY AB Flow cytometric analysis of human peripheral blood T lymphocytes demonstrated that the majority of the CD4(+) cells were CD29(+) or CD45RO(+) ''mature'' cells while the CD8(+) cells were primarily CD45R4(+) ''naive'' cells. After an initial separation into CD4(+) and CD8(+) cells and a secondary separation into CD45 subsets, lymphokine secretion was assessed after phorbol 12-myristate 13-acetate and ionomycin or fixed anti-CD3 stimulation. Within the respective CD45 subsets, CD4(+) cells produced more interleukin (IL)-2, IL-4, and IL-6; but the CD8(+) cells secreted more interferon-gamma and granulocyte/macrophage-colony-stimulating factor. Tumor necrosis factor-alpha secretion was similar in the matched CD45 subsets. Northern analysis revealed a parallel pattern of lymphokine mRNA expression in the four lymphocyte subsets. These results suggest that human CD8(+) peripheral blood lymphocytes have a significant capacity to secrete lymphokines, and that the low lymphokine production observed in unseparated CD8(+) cells reflects the higher percentage of less functional CD45RA(+) cells. C1 NCI,FREDERICK CANC RES & DEV CTR,BIOL RESPONSE MODIFIERS PROGRAM,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. PROGRAM RESOURCES INC DYNCORP,BIOL CARCINOGENESIS & DEV PROGRAM,FREDERICK,MD. DANA FARBER CANC INST,DIV TUMOR IMMUNOL,CAMBRIDGE,MA. NR 31 TC 49 Z9 51 U1 0 U2 3 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD MAR PY 1995 VL 25 IS 3 BP 644 EP 648 DI 10.1002/eji.1830250303 PG 5 WC Immunology SC Immunology GA QY507 UT WOS:A1995QY50700002 PM 7705392 ER PT J AU KALLED, SL SIVA, N STEIN, H REINHERZ, EL AF KALLED, SL SIVA, N STEIN, H REINHERZ, EL TI THE DISTRIBUTION OF CD10 (NEP-24.11, CALLA) IN HUMANS AND MICE IS SIMILAR IN NONLYMPHOID ORGANS BUT DIFFERS WITHIN THE HEMATOPOIETIC SYSTEM - ABSENCE ON MURINE T-LYMPHOID AND B-LYMPHOID PROGENITORS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE CD10; LYMPHOID PROGENITORS ID ACUTE LYMPHOBLASTIC-LEUKEMIA; NEUTRAL ENDOPEPTIDASE 24.11; HUMAN-BONE MARROW; ANTIGEN CALLA; MONOCLONAL-ANTIBODY; CONVERTING ENZYME; HUMAN-NEUTROPHILS; SUBSTANCE-P; CELL-LINES; ENKEPHALINASE AB Prior studies in the human have implied an important function for CD10 (CALLA, neutral endopeptidase 24.11) in early lymphoid development. To examine the role of this ectoenzyme in an experimental system, a rat mAb specific for mouse CD10, termed R103, was generated. Immunohistological and flow cytometric analyses indicate that the distribution of CD10 in non-lymphoid anatomical compartments is virtually identical in human and mouse. However, CD10 expression within the hematopoietic system is strikingly different. In contrast to human spleen, lymph node and thymus, the corresponding mouse organs contain no detectable CD10(+) cells. Mouse granulocytes, unlike human granulocytes, also lack CD10 expression. Five-color flow cytometric studies of adult bone marrow (BM) from C57BL/6 and BALB/c mice with mAb specific for CD43, B220, HSA, BP-1 and immunoglobulin M fail to detect any significant number of CD10(+) cells at pro-B, pre-B or B cell stages. In addition, lymphoid cells in both (rIL-7) independent and rIL-7-dependent in vitro pro-B cell cultures lack CD10 expression. Consistent with this result, CD10 mRNA is not detected. Unlike the AA4.1(+) population from day 13 and 14 fetal liver, the CD10(+) subset is unable to reconstitute T and B lymphoid compartments in RAG-2(-/-) mice. Nevertheless, mouse CD10 is readily found on BM stromal elements known to support early B lineage lymphoid development. Given the common expression of CD10 on human and mouse BM stromal elements, this enzyme may have an important function in the stromal cell-dependent phase of hematopoiesis. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. FREE UNIV BERLIN,KLINIKUM STEGLITZ,INST PATHOL,W-1000 BERLIN,GERMANY. RP KALLED, SL (reprint author), DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA49232] NR 60 TC 17 Z9 18 U1 0 U2 3 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD MAR PY 1995 VL 25 IS 3 BP 677 EP 687 DI 10.1002/eji.1830250308 PG 11 WC Immunology SC Immunology GA QY507 UT WOS:A1995QY50700007 PM 7705396 ER PT J AU CONLON, K LLOYD, A CHATTOPADHYAY, U LUKACS, N KUNKEL, S SCHALL, T TAUB, D MORIMOTO, C OSBORNE, J OPPENHEIM, J YOUNG, H KELVIN, D ORTALDO, J AF CONLON, K LLOYD, A CHATTOPADHYAY, U LUKACS, N KUNKEL, S SCHALL, T TAUB, D MORIMOTO, C OSBORNE, J OPPENHEIM, J YOUNG, H KELVIN, D ORTALDO, J TI CD8(+) AND CD45RA(+) HUMAN PERIPHERAL-BLOOD LYMPHOCYTES ARE POTENT SOURCES OF MACROPHAGE INFLAMMATORY PROTEIN 1-ALPHA, INTERLEUKIN-8 AND RANTES SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article DE MACROPHAGE INFLAMMATORY PROTEIN 1-ALPHA; RANTES; INTERLEUKIN-8; CD45RA; CD45RO ID TUMOR-NECROSIS-FACTOR; T-CELL CLONES; MOLECULAR-CLONING; CYTOKINE FAMILY; GENE-EXPRESSION; HUMAN CD4+; ACTIVATION; IDENTIFICATION; MIP-1-ALPHA; MIP-1-BETA AB The chemokines macrophage inflammatory protein 1 alpha. (MIP 1 alpha), interleukin-8 (IL-8) and RANTES are potent regulators of leukocyte trafficking. Examination of chemokine secretion by human peripheral blood lymphocytes after stimulation with anti-CD3 or phorbol 12, 13 myristate acetate and ionomycin showed CD8(+) cells were the dominant source of MIP 1 alpha and RANTES. Although production of MLP 1 alpha and IL-8 were similar in pharmacologically stimulated CD4(+) CD45RA(+), CD4(+) CD45RO(+), and CD8(+) CD45RA(+) cells, the largest amounts of MIP 1 alpha and RANTES were secreted by CD8(+) CD45RO(+) lymphocytes. A parallel pattern of prolonged chemokine mRNA expression for at least 18 h after activation was observed in the T cell subsets. These results confirm that human T lymphocytes have a unique capacity for secretion of these three chemokines. In addition, CD8(+) cells have an unrecognized role in recruiting cells to sites of inflammation, and adult human CD45RA(+) cells have a physiologically significant secretory capacity. C1 NCI,FREDERICK CANC RES & DEV CTR,EXPTL IMMUNOL LAB,FREDERICK,MD 21702. NCI,FREDERICK CANC RES & DEV CTR,MOLEC IMMUNOREGULAT LAB,BIOL RESPONSE MODIFIERS PROGRAM,FREDERICK,MD 21702. PRINCE HENRY HOSP,DEPT INFECT DIS,LITTLE BAY,NSW 2036,AUSTRALIA. UNIV MICHIGAN,DEPT PATHOL,ANN ARBOR,MI 48109. GENENTECH CORP,DEPT IMMUNOL,S SAN FRANCISCO,CA 94080. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NCI,FREDERICK CANC RES & DEV CTR,DYNCORP,PRI,FREDERICK,MD 21702. NR 28 TC 106 Z9 107 U1 0 U2 1 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD MAR PY 1995 VL 25 IS 3 BP 751 EP 756 DI 10.1002/eji.1830250319 PG 6 WC Immunology SC Immunology GA QY507 UT WOS:A1995QY50700018 PM 7535702 ER PT J AU WATSON, A ENSOR, E SYMES, A WINTER, J KENDALL, G LATCHMAN, D AF WATSON, A ENSOR, E SYMES, A WINTER, J KENDALL, G LATCHMAN, D TI A MINIMAL CGRP GENE PROMOTER IS INDUCIBLE BY NERVE GROWTH-FACTOR IN ADULT-RAT DORSAL-ROOT GANGLION NEURONS BUT NOT IN PC12 PHEOCHROMOCYTOMA CELLS SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE NERVE GROWTH FACTOR; CGRP; DNA TRANSFECTION; GENE REGULATION; SENSORY NEURON ID HELIX-LOOP-HELIX; CALCITONIN-GENE; SENSORY NEURONS; PHEOCHROMOCYTOMA CELLS; LUNG-CARCINOMA; REPORTER GENE; EXPRESSION; RNA; SEQUENCES; BINDING AB The calcitonin/CGRP gene is transcribed in thyroid C cells and some neuronal cells but not in other cell types. Although the promoter sequences mediating gene activity in thyroid C cells have been extensively studied, the elements responsible for promoter activity in neuronal cells and its stimulation by nerve growth factor (NGF) have not previously been defined. We report the first use of the calcium phosphate procedure to successfully transfect adult rat dorsal root ganglion neurons, which naturally express the calcitonin/calcitonin gene-related peptide (CGRP) in an NGF-inducible manner. This method was used to characterize the elements in the calcitonin/CGRP promoter which are responsible for its basal activity and NGF inducibility in DRG neurons and in PC12 cells, a neuronally derived cell line which does not naturally express the calcitonin/CGRP gene. Although the sequences required for basal activity are similar in each cell type, we show that a minimal calcitonin/CGRP promoter is NGF-responsive in dorsal root ganglion cells, but that upstream sequences are required for such inducibility in PC12 cells. C1 UCL, SCH MED, DEPT MOLEC PATHOL, LONDON W1P 6DB, ENGLAND. MASSACHUSETTS GEN HOSP, MOLEC NEUROBIOL LAB, 149, 13TH ST, BOSTON, MA 02129 USA. SANDOZ INST MED RES, LONDON WC1E 6BN, ENGLAND. RI Symes, Aviva/S-7471-2016 OI Symes, Aviva/0000-0003-2557-9939 NR 41 TC 33 Z9 33 U1 0 U2 1 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0953-816X J9 EUR J NEUROSCI JI Eur. J. Neurosci. PD MAR 1 PY 1995 VL 7 IS 3 BP 394 EP 400 DI 10.1111/j.1460-9568.1995.tb00335.x PG 7 WC Neurosciences SC Neurosciences & Neurology GA QR634 UT WOS:A1995QR63400006 PM 7773437 ER PT J AU LATHAN, CE WALL, CW HARRIS, LR AF LATHAN, CE WALL, CW HARRIS, LR TI HUMAN EYE-MOVEMENT RESPONSE TO Z-AXIS LINEAR ACCELERATION - THE EFFECT OF VARYING THE PHASE-RELATIONSHIPS BETWEEN VISUAL AND VESTIBULAR INPUTS SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE LINEAR ACCELERATION; OPTOKINETIC; OTOLITHS; VISUAL VESTIBULAR INTERACTION; SENSORY CONFLICT MODEL; HUMAN ID DYNAMIC CHARACTERISTICS; OPTOKINETIC NYSTAGMUS; VIEWING DISTANCE; SQUIRREL-MONKEY; MOTION; ROTATION; CAT; NUCLEI; PERCEPTION; OTOLITHS AB We investigated the effect of systematically varying the phase relationship between 0.5-Hz sinusoidal z-axis optokinetic (OKN) and linear acceleration stimuli upon the resulting vertical eye movement responses of five humans. Subjects lay supine on a linear sled which accelerated them sinusoidally along their z-axis at 0.4 g peak acceleration (peak velocity 1.25 m/s). A high-contrast, striped z-axis OKN stimulus moving sinusoidally at 0.5 Hz, 70 degrees/s peak velocity was presented either concurrently or with the acceleration stimulus or alone. Subjects' vertical eye movements were recorded using scleral search coils. When stimuli were paired in the naturally occurring relationship (e.g., visual stripes moving upward paired with downward physical acceleration), the response was enhanced over the response to the visual stimulus presented alone. When the stimuli were opposed (e.g., visual stripes moving upward during upward physical acceleration, a combination that does not occur naturally), the response was not significantly different from the response to the visual stimulus presented alone. Enhancement was maximized when the velocities of the visual and motion stimuli were in their normal phase relationship, while the response took intermediate values for other phase relationships. The phase of the response depended upon the phase difference between the two inputs. We suggest that linear self-motion processing looks at agreement between the two stimuli - a sensory conflict model. C1 MASSACHUSETTS EYE & EAR INFIRM, BOSTON, MA 02114 USA. MIT, DEPT BRAIN & COGNIT SCI, CAMBRIDGE, MA 02139 USA. YORK UNIV, DEPT PSYCHOL, TORONTO, ON M3J 1P3, CANADA. FU NIGMS NIH HHS [T32-GM07484] NR 45 TC 14 Z9 14 U1 0 U2 0 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0014-4819 EI 1432-1106 J9 EXP BRAIN RES JI Exp. Brain Res. PD MAR PY 1995 VL 103 IS 2 BP 256 EP 266 PG 11 WC Neurosciences SC Neurosciences & Neurology GA QR636 UT WOS:A1995QR63600008 PM 7789433 ER PT J AU LEWIS, JD WINTER, HS AF LEWIS, JD WINTER, HS TI INTESTINAL AND HEPATOBILIARY DISEASES IN HIV-INFECTED CHILDREN SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; ADENOVIRUS INFECTION; DIARRHEA; AIDS; GLOBULIN; INFANT AB Children with HIV disease and gastrointestinal disease should be evaluated for enteric pathogens. Bacterial, protozoal, and viral agents can cause chronic diarrhea, abdominal pain, gastrointestinal bleeding, and contribute to growth retardation. This article presents an approach to the evaluation of the HIV-infected child with gastrointestinal symptoms. Therapeutic and nutritional interventions are discussed with emphasis on the multidisciplinary approach required to initiate successful management. C1 BOSTON UNIV,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,CHILDRENS HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 27 TC 13 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD MAR PY 1995 VL 24 IS 1 BP 119 EP 132 PG 14 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QH188 UT WOS:A1995QH18800007 PM 7729856 ER PT J AU KATKOV, WN DIENSTAG, JL AF KATKOV, WN DIENSTAG, JL TI HEPATITIS VACCINES SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Article ID B SURFACE-ANTIGEN; C VIRUS-INFECTION; HUMORAL IMMUNE-RESPONSE; HEALTH-CARE WORKERS; PRE-S-REGION; NON-A; UNITED-STATES; POSTTRANSFUSION HEPATITIS; GENETIC-REGULATION; VIRAL-HEPATITIS AB The 1980s represented a decade of breakthroughs for the development of hepatitis vaccines. Plasma-derived and then recombinant hepatitis B vaccines were developed and introduced, killed hepatitis A vaccine was developed, and the virologic tools were discovered with which to lay the groundwork for a vaccine against hepatitis C. Even as the focus of the 1990s shifts toward antiviral therapy of chronic viral hepatitis, we cannot afford to neglect the importance of prevention by vaccination. Better vaccines and improved vaccination strategies for preventing hepatitis A and B will continue to demand research investment, and the most meager toehold will have to be exploited and pursued aggressively if a practical, effective hepatitis C vaccine is to be developed. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP KATKOV, WN (reprint author), UNIV CALIF LOS ANGELES,SCH MED,10833 LE CONTE AVE,LOS ANGELES,CA 90024, USA. NR 90 TC 14 Z9 15 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD MAR PY 1995 VL 24 IS 1 BP 147 EP 159 PG 13 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QH188 UT WOS:A1995QH18800009 PM 7729858 ER PT J AU CHEN, SY ZANI, C KHOURI, Y MARASCO, WA AF CHEN, SY ZANI, C KHOURI, Y MARASCO, WA TI DESIGN OF A GENETIC IMMUNOTOXIN TO ELIMINATE TOXIN IMMUNOGENICITY SO GENE THERAPY LA English DT Article DE GENE THERAPY; IMMUNOTOXIN; ANTIBODY, AIDS ID HUMAN MONOCLONAL-ANTIBODY; HIV-INFECTED CELLS; PSEUDOMONAS EXOTOXIN; A-CHAIN; EXPRESSION; THERAPY; MELANOMA; CANCER; COMPLEXES; TOXICITY AB Host antibody response to toxin molecules is a major obstacle to the use of immunotoxins as efficacious agents in the treatment of human cancer and other diseases. In this study, a genetic form of immunotoxin has been designed which should eliminate toxin immunogenicity by replacing the toxin protein moitey with weakly immunogenic or nonimmunogenic plasmid DNA. A recombinant bifunctional fusion protein, which consists of a human antibody Fab targeting moiety [directed against gp 120, the envelope glycoprotein of human immunodeficiency virus (HIV)-1] and a human DNA binding moiety (protamine), is used as a gene carrier. Toxin plasmid DNAs expressing the catalytic fragment of Pseudomonas exotoxin A (PEA) statically interact with the fusion proteins to form soluble protein-DNA complexes. The complexes are specifically transferred into HIV-1-infected cells by receptor-mediated endocytosis, resulting in selective killing of the target cells. These 'genetic immunotoxins' may have significant advantages over protein immunotoxins for the treatment of a variety of human diseases. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI31783, AI33802] NR 35 TC 50 Z9 55 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0969-7128 J9 GENE THER JI Gene Ther. PD MAR PY 1995 VL 2 IS 2 BP 116 EP 123 PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity; Research & Experimental Medicine GA QK782 UT WOS:A1995QK78200005 PM 7719928 ER PT J AU ENG, C MULLIGAN, LM SMITH, DP HEALEY, CS FRILLING, A RAUE, F NEUMANN, HPH PFRAGNER, R BEHMEL, A LORENZO, MJ STONEHOUSE, TJ PONDER, MA PONDER, BAJ AF ENG, C MULLIGAN, LM SMITH, DP HEALEY, CS FRILLING, A RAUE, F NEUMANN, HPH PFRAGNER, R BEHMEL, A LORENZO, MJ STONEHOUSE, TJ PONDER, MA PONDER, BAJ TI MUTATION OF THE RET PROTOONCOGENE IN SPORADIC MEDULLARY-THYROID CARCINOMA SO GENES CHROMOSOMES & CANCER LA English DT Article ID MULTIPLE ENDOCRINE NEOPLASIA; LINE AB Medullary thyroid carcinoma (MTC) occurs sporadically or as part of the inherited cancer syndrome multiple endocrine neoplasia (MEN) type 2. in MEN 2A, germline missense mutations are found in one of five cysteine codons within exons 10 and 11 in the extracellular domain of the RET protooncogene. In MEN 2B, germline mutations occur in codon 918 (exon 16) within the catalytic core of the tyrosine kinase domain. To determine if RET mutations similar to those in MEN 2A and 28 play a role in the pathogenesis of sporadic MTC, we analysed 71 sporadic tumours comprising 68 primary rumours and three cell lines, for mutations in RET exons 10, 11, and 16. We found that 23% of sporadic MTC had RET codon 918 mutations, while only 3% had exon 10 mutations, and none had mutations in exon 11. We found no exon 16 mutations in MTC from 14 MEN 2A cases. Thus, exon 10 and 11 mutations, commonly found in familial MTC and MEN 2A, rarely occur in sporadic MTC; somatic mutation of RET codon 918 appears to play a role in the tumourigenesis of a significant minority of sporadic MTC but not MEN 2A tumours. In addition to their biological interest, these findings may have some clinical application in determining whether a patient presenting with isolated MTC is truly sporadic or is part of an inherited cancer syndrome. C1 UNIV CAMBRIDGE,DEPT PATHOL,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE CB2 1QP,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV MED ONCOL,BOSTON,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV CANC EPIDEMIOL & CONTROL,BOSTON,MA. QUEENS UNIV,DEPT PAEDIAT,KINGSTON,ON,CANADA. QUEENS UNIV,DEPT PATHOL,KINGSTON,ON,CANADA. UNIV HAMBURG,KRANKENHAUS EPPENDORF,CHIRURG KLIN,W-2000 HAMBURG,GERMANY. UNIV HEIDELBERG,MED KLIN & POLIKLIN,HEIDELBERG,GERMANY. UNIV FREIBURG,INNERE MED NEPHROL ABT 6,FREIBURG,GERMANY. KARL FRANZENS UNIV GRAZ,DEPT GEN & EXPTL PATHOL,GRAZ,AUSTRIA. KARL FRANZENS UNIV GRAZ,DEPT MED BIOL & HUMAN GENET,GRAZ,AUSTRIA. OI Eng, Charis/0000-0002-3693-5145 NR 16 TC 143 Z9 147 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 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD MAR PY 1995 VL 12 IS 3 BP 209 EP 212 DI 10.1002/gcc.2870120308 PG 4 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA QE724 UT WOS:A1995QE72400007 PM 7536460 ER PT J AU FLETCHER, JA LONGTINE, J WALLACE, K MENTZER, SJ SUGARBAKER, DJ AF FLETCHER, JA LONGTINE, J WALLACE, K MENTZER, SJ SUGARBAKER, DJ TI CYTOGENETIC AND HISTOLOGIC-FINDINGS IN 17 PULMONARY CHONDROID HAMARTOMAS - EVIDENCE FOR A PATHOGENETIC RELATIONSHIP WITH LIPOMAS AND LEIOMYOMAS SO GENES CHROMOSOMES & CANCER LA English DT Article ID CHROMOSOME; REARRANGEMENT; TISSUE; TUMORS; LUNG AB Pulmonary chondroid hamartomas (PCH) are benign tumors that contain mesenchymal and epithelial components. In this series, we identified clonal chromosome aberrations in mesenchymal cells from 10 of 17 PCH. Chromosome band 12q15 was rearranged most frequently (N = 4), and one case had a t(12;14)(q15;q24) that was identical cytogenetically to the characteristic translocation in uterine leiomyomas. Histologic review revealed diverse mesenchymal populations, including undifferentiated cells, cartilage, adipose tissue, and smooth muscle, in most of the PCH. These findings suggest that PCH result from neoplastic transformation of a primitive mesenchymal cell that differentiates along chondroid, adipose, and smooth muscle pathways. (C) 1995 Wiley-Liss, Inc. C1 BRIGHAM & WOMENS HOSP,DIV THORAC SURG,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL ONCOL,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 SURG,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1K11CA01498-03] NR 13 TC 47 Z9 47 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-2257 J9 GENE CHROMOSOME CANC JI Gene Chromosomes Cancer PD MAR PY 1995 VL 12 IS 3 BP 220 EP 223 DI 10.1002/gcc.2870120310 PG 4 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA QE724 UT WOS:A1995QE72400009 PM 7536462 ER PT J AU MILNE, GT HO, T WEAVER, DT AF MILNE, GT HO, T WEAVER, DT TI MODULATION OF SACCHAROMYCES-CEREVISIAE DNA DOUBLE-STRAND BREAK REPAIR BY SRS2 AND RAD51 SO GENETICS LA English DT Article ID YEAST; MUTATIONS; PROTEIN; RECOMBINATION; HELICASE; GENES; TRANSFORMATION; SUPPRESSORS; MUTANTS; ALLELE AB RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KIRAD52) and RAD51 (KRAD51) but failed to suppress either a rad52 Delta or a ra51 Delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 Delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively. 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. NR 33 TC 47 Z9 48 U1 0 U2 0 PU GENETICS PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202 SN 0016-6731 J9 GENETICS JI Genetics PD MAR PY 1995 VL 139 IS 3 BP 1189 EP 1199 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA QJ968 UT WOS:A1995QJ96800007 PM 7768432 ER PT J AU RAUCH, SL RENSHAW, PF AF RAUCH, SL RENSHAW, PF TI CLINICAL NEUROIMAGING IN PSYCHIATRY SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID MAGNETIC-RESONANCE SPECTROSCOPY; POSITRON EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; DRUG-NAIVE SCHIZOPHRENICS; DOPAMINE D2 RECEPTORS; HUMAN VISUAL-CORTEX; COMPUTED-TOMOGRAPHY; ALZHEIMERS-DISEASE; CONTRAST-MEDIA; NEUROPSYCHIATRIC DISORDERS AB The practical aspects of contemporary neuroimaging techniques relevant to clinical psychiatry are reviewed. In particular, the structural imaging modalities of computed axial tomography (CT) and magnetic resonance imaging (MRI) are described and compared. Likewise, functional neuroimaging modalities including the nuclear imaging techniques of positron emission tomography (PET) and single photon emission computed tomography (SPECT), as well as the newer magnetic resonance techniques of functional magnetic resonance imaging (fMRI) and magnetic resonance spectroscopy (MRS), are reviewed. Although structural imaging techniques are most useful for ruling out medical etiologies of mental status disturbances, functional neuroimaging techniques currently have an adjunctive role in the evaluation of dementia and seizure disorders and show promise for the evaluation of primary psychiatric disorders in the future. Specific guidelines are suggested regarding the use of these neuroimaging studies. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MCLEAN HOSP,CTR BRAIN IMAGING,BELMONT,MA 02178. FU NCI NIH HHS [5T32CA09362-11] NR 92 TC 31 Z9 31 U1 0 U2 4 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD MAR-APR PY 1995 VL 2 IS 6 BP 297 EP 312 DI 10.3109/10673229509017151 PG 16 WC Psychiatry SC Psychiatry GA QQ062 UT WOS:A1995QQ06200001 PM 9384916 ER PT J AU SUMMERGRAD, P LANGMANDORWART, N KLEINMAN, S AF SUMMERGRAD, P LANGMANDORWART, N KLEINMAN, S TI FAILURE OF MANAGED CARE OR FAILURE TO MANAGE THE CARE SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article C1 BLUE CROSS SHIELD MASSACHUSETTS,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SUMMERGRAD, P (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,FRUIT STREET,BOSTON,MA 02114, USA. NR 10 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 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD MAR-APR PY 1995 VL 2 IS 6 BP 341 EP 346 DI 10.3109/10673229509017155 PG 6 WC Psychiatry SC Psychiatry GA QQ062 UT WOS:A1995QQ06200005 PM 9384920 ER PT J AU LEHNER, LA BURGESS, JF AF LEHNER, LA BURGESS, JF TI TEACHING AND HOSPITAL PRODUCTION - THE USE OF REGRESSION ESTIMATES SO HEALTH ECONOMICS LA English DT Article; Proceedings Paper CT 1st Annual Health-Economics-Committee Northeast Regional Research Symposium CY SEP 03, 1992 CL NEWPORT, RI SP US DEPT VET AFFAIRS, HLTH ECON COMM DE PRODUCTION; REGRESSION ANALYSIS; LABOR REQUIREMENTS; PROSPECTIVE PAYMENT SYSTEM; TEACHING HOSPITALS; MEDICAL EDUCATION ID PROSPECTIVE PAYMENT; COSTS; SPECIFICATION; VARIABLES; ERRORS; SYSTEM AB Medicare's Prospective Payment System pays U.S. teaching hospitals for the indirect costs of medical education based on a regression coefficient in a cost function. In regression studies using health care data, it is common for explanatory variables to be measured imperfectly, yet the potential for measurement error is often ignored. In this paper, U.S. Department of Veterans Affairs data is used to examine issues of health care production estimation and the use of regression estimates like the teaching adjustment factor. The findings show that measurement error and persistent multicollinearity confound attempts to have a large degree of confidence in the precise magnitude of parameter estimates. RP LEHNER, LA (reprint author), US DEPT VET AFFAIRS,MANAGEMENT SCI GRP,200 SPRINGS RD,BEDFORD,MA 01730, USA. NR 25 TC 9 Z9 9 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 1057-9230 J9 HEALTH ECON JI Health Econ. PD MAR-APR PY 1995 VL 4 IS 2 BP 113 EP 125 DI 10.1002/hec.4730040204 PG 13 WC Economics; Health Care Sciences & Services; Health Policy & Services SC Business & Economics; Health Care Sciences & Services GA QV095 UT WOS:A1995QV09500004 PM 7613596 ER PT J AU GABA, DM HOWARD, SK AF GABA, DM HOWARD, SK TI SITUATION AWARENESS IN ANESTHESIOLOGY SO HUMAN FACTORS LA English DT Article ID SIMULATED CRITICAL INCIDENTS; ANESTHETIC MISHAPS; OPERATING-ROOM; PERFORMANCE; MANAGEMENT; ENVIRONMENT; WORKLOAD; SKILLS; ERROR AB Situation awareness has primarily been confined to the aviation field. We believe that situation awareness is an equally important characteristic in the complex, dynamic, and risky field of anesthesiology. We describe three aspects of situations of which the decision maker must remain aware: subtle cues, evolving situations, and special knowledge elements. We provide examples of real or simulated anesthesia situations in which situation awareness is clearly involved in the provision of optimal patient care, and we map the elements of situation awareness onto a cognitive process model of the anesthesiologist. Finally, we consider how situation awareness can be further investigated and taught in this medical domain using anesthesia simulators and analyses of real cases. The study of situation awareness in anesthesiology may provide a good example of the wider application of the concept of situation awareness to nonaerospace environments. C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. STANFORD UNIV, MED CTR, SCH MED, STANFORD, CA 94305 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. RP GABA, DM (reprint author), VET ADM MED CTR, ANESTHESIA SERV 112A, PALO ALTO, CA 94304 USA. OI Howard, Steven/0000-0001-6475-1792 NR 45 TC 132 Z9 135 U1 1 U2 8 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0018-7208 J9 HUM FACTORS JI Hum. Factors PD MAR PY 1995 VL 37 IS 1 BP 20 EP 31 DI 10.1518/001872095779049435 PG 12 WC Behavioral Sciences; Engineering, Industrial; Ergonomics; Psychology, Applied; Psychology SC Behavioral Sciences; Engineering; Psychology GA RL735 UT WOS:A1995RL73500003 PM 7790008 ER PT J AU GRABBE, S BEISSERT, S SCHWARZ, T GRANSTEIN, RD AF GRABBE, S BEISSERT, S SCHWARZ, T GRANSTEIN, RD TI DENDRITIC CELLS AS INITIATORS OF TUMOR IMMUNE-RESPONSES - A POSSIBLE STRATEGY FOR TUMOR-IMMUNOTHERAPY SO IMMUNOLOGY TODAY LA English DT Editorial Material ID COLONY-STIMULATING FACTOR; ANTIGEN-PRESENTING CELLS; EPIDERMAL LANGERHANS CELLS; MOUSE BONE-MARROW; COMPLEX CLASS-II; ULTRAVIOLET-RADIATION; ANTITUMOR IMMUNITY; NECROSIS-FACTOR; CLONAL ANERGY; LYMPHOCYTES-T AB Since all T-cell-mediated immune responses require antigen presentation, antigen-presenting cells (APCs) may be of central importance for the generation and regulation of tumor immunity. This article describes approaches used to induce tumor immunity via modulation of the presentation of tumor antigen, either by tumor-antigen-exposed dendritic cells or by tumor cells engineered to act as APCs. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. RP GRABBE, S (reprint author), UNIV MUNSTER,LUDWIG BOLTZMANN INST CELL BIOL & IMMUNOBIOL SKIN,DEPT DERMATOL,D-48149 MUNSTER,GERMANY. RI Schwarz, Thomas/A-9148-2010 FU NIAMS NIH HHS [AR 40667] NR 59 TC 260 Z9 266 U1 0 U2 1 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 MAR PY 1995 VL 16 IS 3 BP 117 EP 121 DI 10.1016/0167-5699(95)80125-1 PG 5 WC Immunology SC Immunology GA QK065 UT WOS:A1995QK06500001 PM 7718082 ER PT J AU MOZDZIERZ, GJ AF MOZDZIERZ, GJ TI GREETINGS SO INDIVIDUAL PSYCHOLOGY-THE JOURNAL OF ADLERIAN THEORY RESEARCH & PRACTICE LA English DT Editorial Material C1 LOYOLA UNIV,STRITCH SCH MED,MAYWOOD,IL 60153. RP MOZDZIERZ, GJ (reprint author), US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,PSYCHOL SERV 116B,ROOSEVELT RD & 5TH AVE,HINES,IL 60141, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV TEXAS PRESS PI AUSTIN PA BOX 7819, AUSTIN, TX 78713-7819 SN 0277-7010 J9 INDIV PSYCHOL JI Individ. Psychol.- J. Adlerian Theory Res. Pract. PD MAR PY 1995 VL 51 IS 1 BP 1 EP 3 PG 3 WC Psychology SC Psychology GA RQ189 UT WOS:A1995RQ18900001 ER PT J AU LAWRENCE, O RACHIE, N QURESHI, N BOMSZTYK, K SIBLEY, CH AF LAWRENCE, O RACHIE, N QURESHI, N BOMSZTYK, K SIBLEY, CH TI DIPHOSPHORYL LIPID-A FROM RHODOBACTER-SPHAEROIDES TRANSIENTLY ACTIVATES NF-KAPPA-B BUT INHIBITS LIPOPOLYSACCHARIDE INDUCTION OF KAPPA-LIGHT-CHAIN AND OCT-2 IN THE B-CELL LYMPHOMA LINE-70Z/3 SO INFECTION AND IMMUNITY LA English DT Article ID SURFACE-IMMUNOGLOBULIN EXPRESSION; DNA-BINDING SUBUNIT; RHODOPSEUDOMONAS-SPHAEROIDES; GENE-TRANSCRIPTION; NONTOXIC LIPOPOLYSACCHARIDE; CONSERVED SEQUENCE; FATTY-ACIDS; PROTEIN; ENHANCER; CD14 AB Lipopolysaccharide (LPS) is implicated in much of the pathophysiology associated with gram-negative septic shock One approach to this serious clinical problem is to develop new drugs that antagonize the action of toxic LPS. A model system to study LPS action and test for potential antagonists is readily provided by LPS regulation of the kappa gene in the murine B-cell line 70Z/3. Rhodobacter sphaeroides diphosphoryl lipid A (RsDPLA) effectively blocked toxic LPS induction of kappa light-chain immunoglobulin expression in 70Z/3 cells. Induction of kappa expression by LPS is dependent on the activation of at least two transcription factors, Oct-2 and NF-KB. RsDPLA completely repressed the long-term activation of NF-KB observed after 24 h of Salmonella typhosa LPS treatment and antagonized activation of oct-2 mRNA expression. However, RsDPLA was not an inert competitor of LPS. RsDPLA alone strongly activated NP KB binding activity by 30 min but not beyond 9 h of treatment. It also induced a small increase in oct-a mRNA levels. RsDPLA is not simply a weak agonist; we found no graded increase in kappa expression with increasing RsDPLA concentrations up to 50 mu g/ml. The NF-KB complexes activated by RsDPLA and S. typhosa LPS were both composed of the p50-p65 heterodimer. These results suggest that the physiological LPS receptor(s) on B cells transmits qualitatively different signals depending on the nature of the binding ligand and that the fatty acyl groups of LPS play an important role in activating signal transduction. C1 UNIV WASHINGTON,DEPT GENET,SEATTLE,WA 98195. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,COLL AGR & LIFE SCI,DEPT BACTERIOL,MADISON,WI 53706. FU NIAID NIH HHS [AI08626]; NIGMS NIH HHS [GM50870, GM45134] NR 50 TC 12 Z9 12 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD MAR PY 1995 VL 63 IS 3 BP 1040 EP 1046 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QJ524 UT WOS:A1995QJ52400043 PM 7868225 ER PT J AU KOZIEL, H KOZIEL, MJ AF KOZIEL, H KOZIEL, MJ TI PULMONARY COMPLICATIONS OF DIABETES-MELLITUS - PNEUMONIA SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Review ID GRAM-NEGATIVE BACILLI; PNEUMOCYSTIS-CARINII PNEUMONIA; BRONCHOALVEOLAR MACROPHAGE DEFENSE; INSULIN-DEPENDENT DIABETICS; PNEUMOCOCCAL PNEUMONIA; NOSOCOMIAL PNEUMONIA; RESPIRATORY-TRACT; UNITED-STATES; PARAPNEUMONIC EFFUSIONS; STAPHYLOCOCCUS-AUREUS AB Diabetes mellitus is often identified as an independent risk factor for developing lower respiratory tract infections. Pulmonary infections, such as those caused by Mycobacterum tuberculosis, mucor, Staphylococcus aureus, and gram-negative bacteria may occur with an increased frequency whereas infections due to Streprococcus pneumoniae, Legionella, and influenza may be associated with increased morbidity and mortality. The predisposition to lower respiratory tract infections may represent alterations in pulmonary host defenses at several levels. The purpose of this article is to review the spectrum of pulmonary infections encountered in the diabetic patient, focusing on predisposing defects in pulmonary host defense, highlighting characteristic clinical features, and discussing diagnostic approaches, therapeutic interventions, and prophylaxis in this patient population. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP KOZIEL, H (reprint author), NEW ENGLAND DEACONESS HOSP,DEPT MED,DIV PULM & CRIT CARE MED,PALMER 108,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 209 TC 101 Z9 107 U1 2 U2 4 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD MAR PY 1995 VL 9 IS 1 BP 65 EP 96 PG 32 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QN083 UT WOS:A1995QN08300006 PM 7769221 ER PT J AU TOLKOFFRUBIN, NE RUBIN, RH AF TOLKOFFRUBIN, NE RUBIN, RH TI THE INFECTIOUS-DISEASE PROBLEMS OF THE DIABETIC RENAL-TRANSPLANT RECIPIENT SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID POLYMORPHONUCLEAR LEUKOCYTES; EXTERNAL OTITIS; RISK-FACTORS; MUCORMYCOSIS; MELLITUS; EPIDEMIOLOGY; MANAGEMENT; FOOT AB Approximately 30% of patients with end stage renal disease who undergo transplantation develop renal failure as a result of their long-standing diabetes mellitus. Therefore, diabetics warrant special attention in considering the infectious disease problems associated with transplantation. The three categories that should be considered in infections affecting the diabetic renal transplant recipient are discussed in this article. C1 MASSACHUSETTS GEN HOSP,CAPD UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,CTR EXPTL PHARMACOL & THERAPEUT,DIV HLTH SCI & TECHNOL,BOSTON,MA. RP TOLKOFFRUBIN, NE (reprint author), MASSACHUSETTS GEN HOSP,HEMODIALYSIS UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 44 TC 9 Z9 10 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD MAR PY 1995 VL 9 IS 1 BP 117 EP 130 PG 14 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QN083 UT WOS:A1995QN08300008 PM 7769213 ER PT J AU TIERNEY, MR BAKER, AS AF TIERNEY, MR BAKER, AS TI INFECTIONS OF THE HEAD AND NECK IN DIABETES-MELLITUS SO INFECTIOUS DISEASE CLINICS OF NORTH AMERICA LA English DT Article ID MALIGNANT EXTERNAL OTITIS; INTRAOCULAR-LENS IMPLANTATION; PARS-PLANA VITRECTOMY; RHINOCEREBRAL MUCORMYCOSIS; POSTOPERATIVE ENDOPHTHALMITIS; CATARACT-EXTRACTION; AMPHOTERICIN-B; MANAGEMENT; DIAGNOSIS; THERAPY AB Patients with diabetes mellitus exhibit particular susceptibility to three severe infections of the head and neck: rhinocerebral mucormycosis, postoperative endophthalmitis, and malignant otitis externa. Rhinocerebral mucormycosis is an extensive life-threatening infection beginning in the nasal passages and sinuses and extending often into the orbit and the cerebrum. Endophthalmitis, which is infection of the vitrealcontents, can occur secondary to bacteremia, trauma, or postoperatively. Invasive external otitis or malignant otitis externa is an invasive infection beginning in the adjacent soft tissue and into bone. It is usually secondary to Pseudomonas aeruginosa and occurs almost exclusively in diabetics. These will all be discussed in this article. C1 MASSACHUSETTS EYE & EAR INFIRM,INFECT DIS SERV,BOSTON,MA 02114. RP TIERNEY, MR (reprint author), VET ADM MED CTR,W ROXBURY BROCKTON DIV,INFECT DIS UNIT,940 BELMONT AVE,BROCKTON,MA 02401, USA. NR 82 TC 28 Z9 30 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0891-5520 J9 INFECT DIS CLIN N AM JI Infect. Dis. Clin. North Am. PD MAR PY 1995 VL 9 IS 1 BP 195 EP 216 PG 22 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA QN083 UT WOS:A1995QN08300013 PM 7769218 ER PT J AU ATHANASOULIS, CA KAUFMAN, JA ROBERTS, A STRUYVEN, J YAMADA, R ZEITLER, E ZOLLIKOFER, CL AF ATHANASOULIS, CA KAUFMAN, JA ROBERTS, A STRUYVEN, J YAMADA, R ZEITLER, E ZOLLIKOFER, CL TI CONTROVERSIES IN VASCULAR IMAGING AND INTERVENTION - A PANEL DISCUSSION SO INTERNATIONAL ANGIOLOGY LA English DT Review AB Purpose: To express for educational purposes, different and often opposing views on controversial topics of current interest in vascular radiology. And to explore whether or not consensus can be reached on any of these controversial issues. Method: Panel discussion among experts in the field. With the help of a moderator, controversial topics were introduced for discussion. For each topic the moderator underscored the principal issue and asked relevant questions. All panelists were asked to express their views on all issues. The following issues were discussed: Atherectomy vs balloon angioplasty; Balloon angioplasty vs stents; Digital vs analog Imaging; TIPS as an emergency procedure; Regional thrombolysis; MRA vs conventional angiography; Laser angioplasty; Carbon dioxide angiography; Lymphangiography vs CT; The training of surgeons in angiography. The panelists were urged to avoid extensive references to the literature but rather to express their own personal opinions based on experience and practice. For each topic an attempt was made to arrive at consensus. Results: Ten issues were presented for debate and discussion. Despite divergent opinions it was possible and relatively painless to reach consensus on seven controversies. On the remaining issues the panelists agreed to disagree. However even when there was disagreement certain trends became apparent. Local considerations and resource availability accounted for varied approaches to the solution of certain controversies. Conclusions: A panel discussion among experts may be a useful way to address controversies for educational purposes. Despite divergence of opinions consensus may be reached, or in absence of consensus general trends may become apparent. RP ATHANASOULIS, CA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,FRUIT ST,BOSTON,MA 02181, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU EDIZIONI MINERVA MEDICA PI TURIN PA CORSO BRAMANTE 83-85 INT JOURNALS DEPT., 10126 TURIN, ITALY SN 0392-9590 J9 INT ANGIOL JI Int. Angiol. PD MAR PY 1995 VL 14 IS 1 BP 24 EP 31 PG 8 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QZ196 UT WOS:A1995QZ19600005 PM 7658101 ER PT J AU TEUTSCH, M HIGER, M WANG, D WORTIS, HW AF TEUTSCH, M HIGER, M WANG, D WORTIS, HW TI INDUCTION OF CD5 ON B-CELLS AND T-CELLS IS SUPPRESSED BY CYCLOSPORINE-A, FK-520 AND RAPAMYCIN SO INTERNATIONAL IMMUNOLOGY LA English DT Article DE IMMUNOPHILINS; NFAT(P); THYMUS-INDEPENDENT 2 TYPE ID ANTIGEN RECEPTOR COMPLEX; MOUSE LYMPHOCYTES-T; FACTOR-ALPHA GENE; P70 S6 KINASE; MEMBRANE GLYCOPROTEIN; SIGNAL-TRANSDUCTION; NUCLEAR FACTOR; ACTIVATION; SURFACE; EXPRESSION AB The expression of CD5 can be induced on murine B-2 cells by anti-lgM, a recognized analog of thymus-independent 2 type (TI-2) antigen. Given that cyclosporin A (CsA) sensitivity is a distinguishing feature of TI-2 type B cell activation, we asked whether the in vitro induction of CD5 on B cells by anti-mu is CsA sensitive. We report that anti-mu induced CD5 expression on B-2 cells was inhibited by CsA as well as FK-520 and rapamycin. When L-685,818, a FK-520 and rapamycin antagonist, was added to anti-mu stimulated B cell cultures containing FK-520 or rapamycin, but not CsA, suppression was abrogated and complete induction of CD5 was seen. When we used either CD4(+)CD8(+) thymocytes or peripheral T cells activated by phorbol ester and ionomycin, the cell surface induction of CD5 was also partially blocked by CsA, FK-520 and rapamycin. Moreover, in both B and T cells, the same immunosuppressive drugs did not affect constitutive CD5 expression but only blocked de novo induction. To determine the level of CD5 regulation, we activated T cells using phorbol myristate acetate (PMA)/ionomycin and report that CD5 induction was sensitive to actinomycin D (AcD). Similarly, the induction of CD5 on anti-mu activated B cells was blocked by AcD. In addition, T cells that were activated by PMA/ionomycin expressed more abundant CD5 mRNA than CsA or FK-520 treated cells. Based on the CsA-sensitive regulation of CD5 we thought that the CsA-sensitive nuclear factor of activated T cells (NFAT) might be involved in CD5 regulation. We report evidence by Western blot analysis that NFAT, is expressed by both resting and TI activated B cells but apparently not CD4(+)CD8(+)CD5(+) thymocytes. We conclude that in both B and T cells the induction of CD5 requires transcriptional regulation, and that the inhibition of CD5 expression by the immunosuppressive drugs CsA, FK-520 and rapamycin requires drug-immunophilin complex formation. C1 TUFTS UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NIAID NIH HHS [R01AI15803, P01AI33180, 1F32AI0918301] NR 75 TC 26 Z9 26 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 MAR PY 1995 VL 7 IS 3 BP 381 EP 392 DI 10.1093/intimm/7.3.381 PG 12 WC Immunology SC Immunology GA QQ041 UT WOS:A1995QQ04100005 PM 7540861 ER PT J AU POLANSKI, M VERMEULEN, MW WU, JY KARNOVSKY, ML AF POLANSKI, M VERMEULEN, MW WU, JY KARNOVSKY, ML TI MURAMYL DIPEPTIDE MIMICRY IN THE REGULATION OF MURINE MACROPHAGE ACTIVATION BY SEROTONIN SO INTERNATIONAL JOURNAL OF IMMUNOPHARMACOLOGY LA English DT Note ID BINDING-SITES; ADJUVANT ACTIVITY; INTERFERON-GAMMA; GENE-EXPRESSION; SLEEP FACTORS; PEPTIDES; MOUSE; PEPTIDOGLYCAN; STIMULATION; MODULATION AB Muramyl peptides (MPs) are regulators of macrophage function. That the activities of MPs may be mediated by serotonin (5-HT) is supported by earlier work that demonstrated specific binding sites for MPs an macrophages that competitively bind 5-HT. Both mediators were also shown to enhance the production of superoxide anion (an antibacterial agent) by these cells. We now report on two additional macrophage activation phenomena affected by 5-HT: phagocytosis and induction of tumor necrosis factor alpha (TNF) mRNA. Serotonin acts as a muramyl peptide-like agonist by increasing phagocytosis of tubercle bacilli by murine peritoneal macrophages, and as a partial agonist/antagonist in the induction of mRNA for tumor necrosis factor. These observations provide further evidence for a serotonergic involvement in some of the physiological responses to MPs. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PULM & CRIT CARE UNIT,BOSTON,MA 02115. FU NHLBI NIH HHS [HL46966]; NIAID NIH HHS [AI03260] NR 42 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 0192-0561 J9 INT J IMMUNOPHARMACO JI Int. J. Immunopharmacol. PD MAR PY 1995 VL 17 IS 3 BP 225 EP & DI 10.1016/0192-0561(94)00097-8 PG 0 WC Immunology; Pharmacology & Pharmacy SC Immunology; Pharmacology & Pharmacy GA QX700 UT WOS:A1995QX70000010 PM 7558518 ER PT J AU MROZEK, K ARTHUR, DC KARAKOUSIS, CP KODURU, PRK LEBEAU, MM PETTENATI, MJ TANTRAVAHI, R MROZEK, E PEREZMESA, C RAO, UNM FRANKEL, SR DAVEY, FR BLOOMFIELD, CD AF MROZEK, K ARTHUR, DC KARAKOUSIS, CP KODURU, PRK LEBEAU, MM PETTENATI, MJ TANTRAVAHI, R MROZEK, E PEREZMESA, C RAO, UNM FRANKEL, SR DAVEY, FR BLOOMFIELD, CD TI DER(16)T(1-16) IS A NONRANDOM SECONDARY CHROMOSOME ABERRATION IN MANY TYPES OF HUMAN NEOPLASIA, INCLUDING MYXOID LIPOSARCOMA, RHABDOMYOSARCOMA AND PHILADELPHIA-CHROMOSOME-POSITIVE ACUTE LYMPHOBLASTIC-LEUKEMIA SO INTERNATIONAL JOURNAL OF ONCOLOGY LA English DT Article DE KARYOTYPING; CHROMOSOME TRANSLOCATION; LIPOSARCOMA; RHABDOMYOSARCOMA; ACUTE LYMPHOBLASTIC LEUKEMIA; PERIPHERAL PRIMITIVE NEUROEPITHELIAL TUMOR ID ROUND CELL TUMORS; PRIMITIVE NEUROECTODERMAL TUMOR; HUMAN BREAST-CANCER; EWINGS-SARCOMA; SOFT-TISSUE; CYTOGENETIC ANALYSIS; TRANSLOCATION T(11-22)(Q24-Q12); PERIPHERAL NEUROEPITHELIOMA; MYELODYSPLASTIC SYNDROMES; FLOW-CYTOMETRY AB An unbalanced translocation between chromosomes 1 and 16, der(16)t(1;16), resulting in trisomy 1q and loss of genetic material from 16q, has been thus far suggested to constitute a nonrandom secondary abnormality in two types of closely related solid tumors - Ewing sarcoma and peripheral primitive neuroepithelial tumor (PNET). We report on three cases of soft tissue tumors, a myxoid liposarcoma, a PNET and a rhabdomyosarcoma, and four cases of hematologic disorders, two acute lymphoblastic leukemias (ALL), an acute mixed leukemia and a refractory anemia, that in addition to primary chromosome abnormalities displayed the presence of the der(16)t(1;16). All three cases of acute leukemia were Philadelphia (Ph) chromosome-positive and all displayed both lymphoid and myeloid antigens. Our results and review of the literature indicate that the occurrence of der(16)t(1;16) is not limited to Ewing sarcoma and PNET, but that acquisition of this abnormality may represent a more general pathway of clonal evolution in several different tumor types including Ph chromosome-positive ALL, myxoid liposarcoma, rhabdomyosarcoma, breast cancer, endometrial adenocarcinoma, myelodysplastic syndromes, acute myeloid leukemia, retinoblastoma, and Wilms' tumor. C1 ROSWELL PK CANC INST,DEPT SURG ONCOL,BUFFALO,NY 14263. ROSWELL PK CANC INST,DEPT PATHOL,BUFFALO,NY 14263. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. N SHORE UNIV HOSP,DEPT LABS,MANHASSET,NY 11030. UNIV CHICAGO,MED CTR,CHICAGO,IL 60637. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT PEDIAT,WINSTON SALEM,NC 27157. DANA FARBER CANC INST,BOSTON,MA 02115. SUNY HLTH SCI CTR,SYRACUSE,NY 13210. RP MROZEK, K (reprint author), ROSWELL PK CANC INST,DIV MED,CYTOGENET RES LAB,CARLTON HOUSE,ROOM A 420,ELM & CARLTON ST,BUFFALO,NY 14263, USA. RI Mrozek, Krzysztof/A-3142-2008; Mrozek, Ewa/E-3708-2011 NR 71 TC 23 Z9 23 U1 0 U2 0 PU INT JOURNAL ONCOLOGY PI ATHENS PA C/O PROFESSOR D A SPANDIDOS, EDITORIAL OFFICE, 1, S MERKOURI ST, ATHENS 116 35, GREECE SN 1019-6439 J9 INT J ONCOL JI Int. J. Oncol. PD MAR PY 1995 VL 6 IS 3 BP 531 EP 538 PG 8 WC Oncology SC Oncology GA QJ135 UT WOS:A1995QJ13500003 PM 21556567 ER PT J AU BURSELL, SE CLERMONT, AC OREN, B KING, GL AF BURSELL, SE CLERMONT, AC OREN, B KING, GL TI THE IN-VIVO EFFECT OF ENDOTHELINS ON RETINAL CIRCULATION IN NONDIABETIC AND DIABETIC RATS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE ENDOTHELIN-1; ENDOTHELIN-3; RETINAL HEMODYNAMICS; DIABETES; RATS ID VASCULAR SMOOTH-MUSCLE; ELEVATED GLUCOSE-LEVELS; PROTEIN-KINASE-C; VASOCONSTRICTOR PEPTIDE; DIACYLGLYCEROL ACCUMULATION; MICROVASCULAR PERICYTES; FLUORESCEIN ANGIOGRAPHY; CELLULAR MECHANISM; CELLS; RECEPTOR AB Purpose. The endothelins are potent vasoactive peptides. This study was performed to characterize the in vivo effects of the endothelin peptides on the retinal circulation in nondiabetic and diabetic rats. Methods. The video fluorescein angiography methodology was used to quantitate retinal hemodynamic responses to endothelin-1 (ET-1) and endothelin-3 (ET-3) in rats. A total of 99 rats were used for these experiments. Video fluorescein angiography recordings were performed before and at different times after intravitreal injection of different concentrations of ET-1 and ET-3 in nondiabetic and diabetic rats. Vascular diameters and retinal circulation times were determined using computer-assisted image analysis of the recorded angiograms. Results. The maximal response to ET-1 was observed at 15 minutes after intravitreal injection and was maintained for as long as 30 minutes after injection. Subsequent data measured at 15 minutes after intravitreal injection showed significant prolongation of retinal circulation times and retinal artery constriction. For example, at a concentration of 10(-7) M, the retinal circulation time increased by 270% +/- 121% of the baseline value. In contrast, 10(-7) M ET-3 injection showed a 52% +/- 29.5% increase in circulation time compared to baseline. In diabetic animals, 10(-7) M ET-1 injection showed a blunted response (only 26% +/- 8% of baseline) compared to the same ET-1 injected concentration in nondiabetic rats. Conclusions. The rat retinal circulation shows a pronounced retinal response to ET-1 intravitreal injection. The response to ET-3 is significantly less than it is to ET-1, and in diabetic animals there was also a significant blunting of the retinal response to ET-1. The blunted response to ET-3 is consistent with the lower affinity of retinal vessel ET-1 receptors to ET-3. The blunted ET-1 response in diabetic rats is consistent with previously reported results, demonstrating resistance to ET-1 action in retinal pericytes exposed to high glucose. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP BURSELL, SE (reprint author), JOSLIN DIABET CTR,BEETHAM EYE INST,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY09178] NR 45 TC 84 Z9 85 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR PY 1995 VL 36 IS 3 BP 596 EP 607 PG 12 WC Ophthalmology SC Ophthalmology GA QL942 UT WOS:A1995QL94200012 PM 7890491 ER PT J AU FINI, ME GIRARD, MT MATSUBARA, M BARTLETT, JD AF FINI, ME GIRARD, MT MATSUBARA, M BARTLETT, JD TI UNIQUE REGULATION OF THE MATRIX METALLOPROTEINASE, GELATINASE-B SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE MATRIX METALLOPROTEINASE; COLLAGENASE; TUMOR PROMOTOR; TRANSFORMING GROWTH FACTOR; CORNEA ID TRANSFORMING GROWTH-FACTOR; CULTURED HUMAN KERATINOCYTES; FACTOR-BETA; IV COLLAGENASE; GELATINOLYTIC ENZYMES; MAJOR ROLE; EXPRESSION; TISSUE; FIBROBLASTS; RABBIT AB Purpose. The matrix metalloproteinase (MMP), gelatinase B, is expressed by both corneal cell types found at the epithelial-stromal tissue interface, the site of basement membrane repair in the healing cornea. This study investigates the relative regulation of gelatinase B compared to other MMPs in response to agents related to those found in the corneal repair environment or in corneal ulcers. Methods. A culture model of corneal cells isolated from rabbit was used. Results. Gelatinase B is the major MMP expressed by corneal epithelial cells, whereas stromal fibroblasts produce gelatinase B along with three other MMPs: collagenase, stromelysin, and gelatinase A. Phorbol-12-myristate 13-acetate (PMA) stimulates gelatinase B mRNA. and protein synthesis by corneal cells, which is similar to its effect on the other MMPs. Stimulation occurs, at least partially, at the transcriptional level. PMA-stimulated MMP expression follows biphasic kinetics, with the major effect on collagenase, stromelysin, and gelatinase A occurring during the late component. In contrast, the major gelatinase B response occurs during the early component. Transforming growth factor-beta (TGF-beta) has no effect on constitutive expression of gelatinase B by fibroblasts; however, expression stimulated by PMA is enhanced. In contrast, constitutive expression of collagenase and stromelysin is inhibited by TGF-beta. However, in the presence of PMA, the initial inhibitory effect of TGF-beta is reversed after treatment. Conclusion. Gelatinase B expression is regulated differently from other corneal MMPs. This provides a mechanism for control of basement membrane repair independent of repair processes in the stroma. C1 HARVARD UNIV, SCH MED, DEPT DERMATOL, BOSTON, MA USA. RP FINI, ME (reprint author), MASSACHUSETTS GEN HOSP, CUTANEOUS BIOL RES CTR, CNY3, 13TH ST, BOSTON, MA 02129 USA. FU NEI NIH HHS [EY08408, EY09828]; NIAMS NIH HHS [AR42981] NR 42 TC 78 Z9 84 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR PY 1995 VL 36 IS 3 BP 622 EP 633 PG 12 WC Ophthalmology SC Ophthalmology GA QL942 UT WOS:A1995QL94200015 PM 7890493 ER PT J AU OTTO, MW POLLACK, MH FAVA, M UCCELLO, R ROSENBAUM, JF AF OTTO, MW POLLACK, MH FAVA, M UCCELLO, R ROSENBAUM, JF TI ELEVATED ANXIETY SENSITIVITY INDEX SCORES IN PATIENTS WITH MAJOR DEPRESSION - CORRELATES AND CHANGES WITH ANTIDEPRESSANT TREATMENT SO JOURNAL OF ANXIETY DISORDERS LA English DT Article; Proceedings Paper CT 26th Annual Association-for-Advancement-of-Behavior-Therapy Convention CY NOV 18-21, 1993 CL ATLANTA, GA SP ASSOC ADV BEHAV THERAPY ID PANIC DISORDER; QUESTIONNAIRE; PERSONALITY; ALPRAZOLAM; STATE AB Anxiety sensitivity has proven to be a valuable concept for understanding panic-related disorders. Norms now exist for the Anxiety Sensitivity Index (ASI) for patients with anxiety disorders and control samples, but anxiety sensitivity has not been well studied in depressed patients. We examined ASI scores in two samples of depressed patients and found elevations in die mid 20s (25.2), similar to scores for individuals with nonpanic anxiety disorders, including social phobia, generalized anxiety disorder, and obsessive-compulsive disorder. Among depressive symptoms, ASI scores were most strongly linked with dysfunctional attitudes and the severity of somatic symptoms. ASI scores decreased following treatment with antidepressant medication (fluoxetine) to levels comparable to control norms. Clinical and methodological implications of these findings are discussed. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP OTTO, MW (reprint author), MASSACHUSETTS GEN HOSP,BEHAV THERAPY UNIT,WACC-815,BOSTON,MA 02114, USA. NR 28 TC 96 Z9 98 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0887-6185 J9 J ANXIETY DISORD JI J. Anxiety Disord. PD MAR-APR PY 1995 VL 9 IS 2 BP 117 EP 123 DI 10.1016/0887-6185(94)00035-2 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QM219 UT WOS:A1995QM21900003 ER PT J AU VANDERMEER, TJ MENCONI, MJ OSULLIVAN, BP LARKIN, VA WANG, HL SOFIA, M FINK, MP AF VANDERMEER, TJ MENCONI, MJ OSULLIVAN, BP LARKIN, VA WANG, HL SOFIA, M FINK, MP TI ACUTE LUNG INJURY IN ENDOTOXEMIC PIGS - ROLE OF LEUKOTRIENE B-4 SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE RESPIRATORY DISTRESS SYNDROME; ADULT; ENDOTOXINS; CHEMILUMINESCENCE; LIPOPOLYSACCHARIDE; EICOSANOIDS; NEUTROPHIL ID BRONCHOALVEOLAR LAVAGE FLUID; RECEPTOR ANTAGONIST; PORCINE MODEL; INHIBITION; ARDS; LIPOPOLYSACCHARIDE; NEUTROPHILS; METABOLISM; ACTIVATION; INCREASES AB The role of leukotriene B-4 (LTB(4)) in the pathogenesis of acute lung injury was examined in endotoxemic pigs. In a preliminary study, the activity and specificity of an LTB(4)-receptor antagonist, LY-306669, were evaluated. In vitro, LY-306669 completely blocked the functional upregulation of phagocyte opsonin receptors induced by LTB(4) but had a much smaller effect on opsonin receptor upregulation induced by platelet-activating factor. In pigs, treatment with LY-306669 prevented leukopenia induced by injection of authentic LTB(4) but had no effect on the hematologic or hemodynamic effects of PAF or U-48816, a thromboxane-A(2) mimetic. In a second study, pigs received an intravenous priming dose of lipopolysaccharide (LPS) at time (t) = -18 h and were randomized to receive 1) no further treatment (n = 5), 2) LPS (250 mu g/kg over 1 h beginning at t = 0 h) and LY-306669 (10 mg/kg bolus and 3 mg . kg(-1). h(-1) infusion beginning at t = -15 min) (n = 7), or 3) LPS and vehicle (n = 6). Treatment with LY-306669 significantly ameliorated LPS-induced hypoxemia, pulmonary edema, and alveolitis. These data suggest that LTB(4) is an important mediator of pulmonary dysfunction and transendothelial migration of neutrophils in LPS-induced acute lung injury. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. UNIV MASSACHUSETTS,MED CTR,DEPT PEDIAT,WORCESTER,MA 01655. LILLY CORP CTR,LILLY RES LABS,INDIANAPOLIS,IN 46285. FU NIGMS NIH HHS [GM-07806-1, R01-GM37631-07] NR 32 TC 25 Z9 27 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD MAR PY 1995 VL 78 IS 3 BP 1121 EP 1131 PG 11 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA QP826 UT WOS:A1995QP82600048 PM 7775306 ER PT J AU ALON, R KASSNER, PD CARR, MW FINGER, EB HEMLER, ME SPRINGER, TA AF ALON, R KASSNER, PD CARR, MW FINGER, EB HEMLER, ME SPRINGER, TA TI THE INTEGRIN VLA-4 SUPPORTS TETHERING AND ROLLING IN FLOW ON VCAM-1 SO JOURNAL OF CELL BIOLOGY LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; MEMORY T-CELLS; HIGH ENDOTHELIAL VENULES; L-SELECTIN; MONOCLONAL-ANTIBODIES; P-SELECTIN; CYTOPLASMIC DOMAINS; LYMPHOCYTE BINDING; PLASMA FIBRONECTIN; HOMING RECEPTOR AB Selectins have previously been shown to tether a flowing leukocyte to a vessel wall and mediate rolling. Here, we report that an integrin, VLA-4, can also support tethering and rolling. Blood T lymphocytes and alpha 4 integrin-transfected cells can tether in shear flow, and then roll, through binding of the integrin VLA-4 to purified VCAM-1 on the wall of a flow chamber. VLA-4 transfectants showed similar tethering and rolling on TNF-stimulated endothelium. Tethering efficiency, rolling velocity, and resistance to detachment are related to VCAM-1 density. Tethering and rolling did not occur on ICAM-1, fibronectin, or fibronectin fragments, and tethering did not require integrin activation or the presence of an alpha 4 cytoplasmic domain. Arrest of rolling cells on VCAM-1 occurred spontaneously, and/or was triggered by integrin activating agents Mn2+, phorbol ester, and mAb TS2/16. These agents, and the alpha 4 cytoplasmic domain, promoted increased resistance to detachment. Together the results show that VLA-4 is a versatile integrin that can mediate tethering, rolling, and firm arrest on VCAM-1. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NHLBI NIH HHS [HL48675]; NIGMS NIH HHS [GM46526] NR 77 TC 558 Z9 561 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD MAR PY 1995 VL 128 IS 6 BP 1243 EP 1253 DI 10.1083/jcb.128.6.1243 PG 11 WC Cell Biology SC Cell Biology GA QN288 UT WOS:A1995QN28800021 PM 7534768 ER PT J AU SQUIRES, LA KRISHNAMOORTHY, KS NATOWICZ, MR AF SQUIRES, LA KRISHNAMOORTHY, KS NATOWICZ, MR TI DELAYED MYELINATION IN INFANTS AND YOUNG-CHILDREN - RADIOGRAPHIC AND CLINICAL CORRELATES SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID WHITE-MATTER; MATURATION; BRAIN AB Magnetic resonance imaging (MRI) is the best method for assessing myelination in infants and young children. Although delayed myelination is a common neuroradiologic diagnosis, there are few or no data regarding the reliability of this diagnosis or radiographic and clinical findings in cohorts of such patients. We evaluated the cranial MRI scans of 109 patients from age 0 to 36 months, without knowledge of any patient's age or previous clinical or radiologic diagnosis. For each cranial MRI, seven neuroradiologic landmarks were evaluated and established criteria used to assess the state of myelination. We found that in 12 of 109 patients, delayed myelination was misdiagnosed, whereas the diagnosis of delayed myelination was missed in four other patients. Lack of familiarity with the myelination milestones of infancy was the most common reason for a misdiagnosis of delayed myelination. Failure to recognize delayed myelination was due to a failure to appreciate the forceps minor as a landmark. Overall, the diagnosis of delayed myelination was inaccurately applied or missed in 15% of the patients in this series. Of the 14 patients identified as having delayed myelination, 10 had other central nervous system structural abnormalities seen on MRI, most commonly cortical atrophy. Developmental delay was the most common clinical correlate of delayed myelination and was documented in 12 of the 14 patients. To increase the reliability of neuroradiologic assessments in young children, we propose that central nervous system myelin maturation be evaluated and expressed as a myelination age equivalent, analogous to the assessment of pediatric bone age using conventional radiographs. Further, prospective studies of infants and young children with delayed myelination are needed to learn the full clinical spectrum of this common neuroradiologic diagnosis. C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,WALTHAM,MA 02254. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 27 TC 14 Z9 15 U1 0 U2 1 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON ST, PO BOX 620, LCD 1, HAMILTON ON L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD MAR PY 1995 VL 10 IS 2 BP 100 EP 104 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA QL978 UT WOS:A1995QL97800005 PM 7540191 ER PT J AU TROLL, GF AF TROLL, GF TI REGIONAL OPHTHALMIC ANESTHESIA - SAFE TECHNIQUES AND AVOIDANCE OF COMPLICATIONS SO JOURNAL OF CLINICAL ANESTHESIA LA English DT Article DE ANESTHESIA, OPHTHALMIC, REGIONAL; SURGERY, EYE, OPHTHALMIC AB In the last decade, anesthesiologists have become increasingly involved in administering regional eye block, while providing care for patients undergoing ophthalmic surgery. This article describes the two major approaches to regional eye block, namely retrobulbar and peribulbar, with special consideration given to relevant orbital anatomy and technical guidelines. Potential complications, ocular and systemic, with their risk factors, are reviewed. Anesthesiologists wishing to acquire skill in administering safe regional blockade are encouraged to familiarize themselves with regional anatomy and specific guidelines suggested herein. RP TROLL, GF (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT ANESTHESIA,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 23 Z9 25 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN PI WOBURN PA 225 WILDWOOD AVE #UNITB PO BOX 4500, WOBURN, MA 01801-2084 SN 0952-8180 J9 J CLIN ANESTH JI J. Clin. Anesth. PD MAR PY 1995 VL 7 IS 2 BP 163 EP 172 DI 10.1016/0952-8180(95)90001-M PG 10 WC Anesthesiology SC Anesthesiology GA QP805 UT WOS:A1995QP80500015 PM 7598928 ER PT J AU KLIBANSKI, A BILLER, BMK SCHOENFELD, DA HERZOG, DB SAXE, VC AF KLIBANSKI, A BILLER, BMK SCHOENFELD, DA HERZOG, DB SAXE, VC TI THE EFFECTS OF ESTROGEN ADMINISTRATION ON TRABECULAR BONE LOSS IN YOUNG-WOMEN WITH ANOREXIA-NERVOSA SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID MINERAL DENSITY; HYPERPROLACTINEMIC AMENORRHEA; EATING DISORDERS; ADOLESCENT GIRLS; OSTEOPOROSIS; OSTEOPENIA; MASS; BULIMIA; FRACTURES AB To study the effects of prolonged anorexia nervosa on bone density (BD) and to determine whether estrogen administration prevents bone loss in women with this disorder, 48 amenorrheic women with anorexia nervosa (mean age, 23.7 yr) were randomized to receive estrogen and progestin replacement (n = 22) or no replacement (n = 26). Clinical variables, biochemical indices, and spinal trabecular BD were measured every 6 months for a mean of 1.5 yr. Initial mean BD (130 +/- 27 mg K2HPO4/cm(3), +/- 1 so) was significantly (P < 0.001) less than normal (176 +/- 26 mg K2HPO4/cm(3)) and less than 2 SD below normal in 21 of the 48 women. Forty-four women completed the study (19 in the estrogen group and 25 in the control group). The mean duration of follow-up was comparable in the estrogen-treated (1.57 +/- 0.89 yr) us. the control group (1.41 +/- 0.69 yr). The estrogen-treated group had no significant change in BD compared with the control group; however, there was a 4.0% increase in mean BD in patients with an initial ideal body weight of less than 70% who were treated with estrogen. In contrast, control patients with comparably low initial weight had a 20.1% decrease in BD. Women in the control group with spontaneous resumption of menses, all of whom had an initial percent ideal body weight of greater than 70%, had a 19.3% increase in bone mass. It is concluded that: 1) estrogen replacement cannot prevent progressive osteopenia in young women with anorexia nervosa; 2) a subset of patients may have improved BD with estrogen and progestin administration depending on initial body weight; and 3) recovery from anorexia nervosa is associated with significantly improved BD. C1 MASSACHUSETTS GEN HOSP, GEN CLIN RES CTR, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, PSYCHIAT SERV, EATING DISORDERS UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP KLIBANSKI, A (reprint author), MASSACHUSETTS GEN HOSP, MED SERV, NEUROENDOCRINE UNIT, GRJ 10, BOSTON, MA 02114 USA. FU NICHD NIH HHS [HD-21204]; NIDDK NIH HHS [DK-08330]; NIMH NIH HHS [MH3-8333] NR 38 TC 282 Z9 286 U1 2 U2 8 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD MAR PY 1995 VL 80 IS 3 BP 898 EP 904 DI 10.1210/jc.80.3.898 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QM008 UT WOS:A1995QM00800036 PM 7883849 ER PT J AU GRINSPOON, S CLEMMONS, D SWEARINGEN, B KLIBANSKI, A AF GRINSPOON, S CLEMMONS, D SWEARINGEN, B KLIBANSKI, A TI SERUM INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN-3 LEVELS IN THE DIAGNOSIS OF ACROMEGALY SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID IGF-I; RADIOIMMUNOASSAY; PLASMA AB Insulin-like growth factor-binding protein-3 (IGFBP-3) is a GH-dependent protein that binds insulin-like growth factor-I (IGF-I) in the circulation and modulates its action at the tissue level. Because IGFBP-3 is a stable and specific marker of somatotroph function, we hypothesized that it would be a useful biochemical marker in the diagnosis of patients with acromegaly and the assessment of surgical cure. We, therefore, investigated the sensitivity of serum IGFBP-3 levels to detect GH excess in 44 patients with clinical acromegaly and pathologically confirmed somatotroph adenomas, including a cohort of 18 patients with untreated disease evaluated before transsphenoidal surgery and medical therapy. IGFBP-3 levels were compared to IGF-I and random GH levels before and after transsphenoidal surgery. Concordance among IGFBP-3, IGF-I, and GH suppressibility by glucose was also determined. In addition, the response of IGFBP-3 to glucose suppression was investigated. All 18 patients with untreated acromegaly had elevated serum IGFBP-3 levels, ranging from 4,186-10,026 mu g/L (mean +/- SD, 6566 [plusm] 1800 mu g/L). There was no overlap with the age-adjusted normative ranges (P = 0.0001 in patients 18-55 yr old and P = 0.0176 in patients >55 yr old) or with the levels obtained in age-comparable controls (P = 0.0001). In 11% of untreated patients with clinical findings of acromegaly and a pathologically confirmed adenoma, IGFBP-3 levels were elevated, although GH was suppressed to less than 2 mu g/L with glucose. In these patients, IGF-I levels were either normal or minimally elevated and considered nondiagnostic. IGFBP-3 and IGF-I levels were correlated in patients with untreated acromegaly (r = 0.650; P = 0.0162) and after transsphenoidal surgery (r = 0.644; P = 0.0001). Neither IGF-I nor IGFBP-3 correlated with random GH levels before surgery. However, both IGF-I (r = 0.471; P = 0.0001) and IGFBP-3 (r = 0.259; P = 0.041) correlated with random GH levels in patients studied more than 1 month after transsphenoidal surgery. IGFBP-3 and IGF-I levels were concordant with GH suppressibility by glucose (P = 0.0039) and IGFBP-3 decreased with glucose suppression in 7 of 10 patients. These data indicate that IGFBP-3 is a sensitive physiological marker of somatotroph function and is concordant with glucose suppression and IGF-I levels before and after transsphenoidal surgery. Therefore, serum IGFBP-3 levels may be of use as a biochemical marker of GH excess in patients with suspected acromegaly and to determine cure after transsphenoidal surgery. C1 MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROSURG, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. UNIV N CAROLINA, DIV ENDOCRINOL, CHAPEL HILL, NC 27599 USA. FU NCRR NIH HHS [RR-01066]; NIA NIH HHS [AG-02331]; NIADDK NIH HHS [R32-AM-07028-18] NR 16 TC 80 Z9 81 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 MAR PY 1995 VL 80 IS 3 BP 927 EP 932 DI 10.1210/jc.80.3.927 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QM008 UT WOS:A1995QM00800040 PM 7533774 ER PT J AU SAYEGH, R AWWAD, JT MAXWELL, C LESSEY, B ISAACSON, K AF SAYEGH, R AWWAD, JT MAXWELL, C LESSEY, B ISAACSON, K TI ALPHA(2)-MACROGLOBULIN PRODUCTION BY THE HUMAN ENDOMETRIUM SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GROWTH-FACTOR-BETA; ALPHA-2-MACROGLOBULIN SYNTHESIS; EMBRYO IMPLANTATION; HORMONAL-REGULATION; BINDING-PROTEIN; STROMAL CELLS; EXPRESSION; CULTURE; INTERLEUKIN-1-BETA; PROGESTERONE AB alpha(2)-Macroglobulin (A2M) is a broad spectrum plasma protease inhibitor previously described in uterine effluents and recently demonstrated to bind and possibly modulate the functions of cytokines. As cytokines, proteases, and protease inhibitors are important in implantation and endometrial physiology, we sought to investigate and characterize the pattern of production of A2M in the endometrium. Endometrial tissues from different phases of the menstrual cycle were analyzed for A2M production. Tissues were incubated in methionine-free Minimum Essential Medium with [S-35]methionine for 12 h at 37 C in 5% CO2. Conditioned media were immunoprecipitated with a polyclonal antibody to human A2M. Recovered proteins were resolved under reducing and nonreducing conditions by 5% sodium dodecyl sulfate-polyacrylamide gel electrophoresis and analyzed by autoradiography. Immunohistochemistry was performed on both cryostat sections of OCT-embedded tissue and formalin-fixed paraffin-embedded tissue. The intensity of staining was evaluated, and a histochemical score was assigned. Comparisons between histochemical scores were performed using the nonparametric Wilcoxon rank sum test. Immunoprecipitation with A2M antibody yielded a single 320-kilodalton protein band under nonreducing conditions and a single 182-kilodalton band under reducing conditions. Both physical and immunological properties of the recovered protein were consistent with A2M. A2M was identified in all endometrial samples and represented approximately 2% of the total radiolabeled proteins produced. Immunohistochemical analysis revealed prominent stromal, but no glandular, staining for A2M throughout the menstrual cycle. The stromal staining in secretory endometrial samples was significantly more intense than that in proliferative samples. In the proliferative phase, staining was more intense in the spongiosum and basalis layers, and less intense in the superficial compactum layer. In the secretory phase, it remained very intense in the spongiosum, but less so in the basalis layer. These findings indicate that A2M is predominantly produced by the stromal component of endometrial tissue. This production is menstrual cycle dependent, with zonal differences in A2M expression within the endometrium, which may indicate a functional significance relevant to the process of implantation that merits further investigation. C1 UNIV N CAROLINA, SCH MED, DEPT OBSTET & GYNECOL, CHAPEL HILL, NC 27599 USA. RP SAYEGH, R (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, VINCENT MEM OBSTET & GYNECOL SERV, 511 FRUIT ST, BOSTON, MA 02114 USA. NR 46 TC 15 Z9 15 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 MAR PY 1995 VL 80 IS 3 BP 1021 EP 1026 DI 10.1210/jc.80.3.1021 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA QM008 UT WOS:A1995QM00800055 PM 7533769 ER PT J AU ALARCON, C LEAHY, JL SCHUPPIN, GT RHODES, CJ AF ALARCON, C LEAHY, JL SCHUPPIN, GT RHODES, CJ TI INCREASED SECRETORY DEMAND RATHER THAN A DEFECT IN THE PROINSULIN CONVERSION MECHANISM CAUSES HYPERPROINSULINEMIA IN A GLUCOSE-INFUSION RAT MODEL OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PC2; PC3; CARBOXYPEPTIDASE-H; PROINSULIN; PANCREATIC ISLETS; DIABETES ID NEUROPEPTIDE-PROCESSING ENZYME; BETA-CELL DYSFUNCTION; PANCREATIC-ISLETS; CARBOXYPEPTIDASE-H; SUBTILISIN FAMILY; STORED INSULIN; MESSENGER-RNA; ATT-20 CELLS; ATT20 CELLS; PC2 AB Hyperproinsulinemia in non-insulin-dependent diabetes mellitus (NIDDM) is due to an increased release of proinsulin from pancreatic beta cells. This could reside in increased secretory demand placed on the beta cell by hyperglycemia or in the proinsulin conversion mechanism. In this study, biosynthesis of the proinsulin conversion enzymes (PC2, PC3, and carboxypeptidase-H [CP-H]) and proinsulin, were examined in islets isolated from 48-h infused rats with 50% (wt/vol) glucose (hyperglycemic, hyperinsulinemic, and increased pancreatic proinsulin to insulin ratio), 20% (wt/vol) glucose (normoglycemic but hyperinsulinemic), and 0.45% (wt/vol) saline (controls). A decrease in the islet content of PC2, PC3, and CP-H from hyperglycemic rats was observed. This reduction did not correlate with any deficiency in mRNA levels or biosynthesis of PC2, PC3, CP-H, or proinsulin. Furthermore, proinsulin conversion rate was comparable in islets from hyperglycemic and control rats. However, in islets from hyperglycemic rats an abnormal increased proportion of proinsulin was secreted, that was accompanied by an augmented release of PC2, PC3 and CP-H. Stimulation of the beta cell's secretory pathway by hyperglycemia, resulted in proinsulin being prematurely secreted from islets before its conversion could be completed. Thus, hyperproinsulinemia induced by chronic hyperglycemia likely results from increased beta cell secretory demand, rather than a defect in the proinsulin processing enzymes per se. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,EP JOSLIN RES LAB,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. TUFTS UNIV,NEW ENGLAND MED CTR,DEPT ENDOCRINOL DIABET METAB & MOLEC MED,BOSTON,MA 02111. FU NIDDK NIH HHS [DK-38543, DK-36836] NR 46 TC 71 Z9 73 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 MAR PY 1995 VL 95 IS 3 BP 1032 EP 1039 DI 10.1172/JCI117748 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200018 PM 7883951 ER PT J AU NAKAMURA, H KIM, DK PHILBIN, DM PETERSON, MB DEBROS, F KOSKI, G BONVENTRE, JV AF NAKAMURA, H KIM, DK PHILBIN, DM PETERSON, MB DEBROS, F KOSKI, G BONVENTRE, JV TI HEPARIN-ENHANCED PLASMA PHOSPHOLIPASE A(2) ACTIVITY AND PROSTACYCLIN SYNTHESIS IN PATIENTS UNDERGOING CARDIAC-SURGERY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PHOSPHOLIPIDS; POLYMORPHONUCLEAR LEUKOCYTES, SIGNAL TRANSDUCTION; CARDIOPULMONARY BYPASS; THROMBOXANE; PROTAMINE ID CARDIOPULMONARY BYPASS; COMPLEMENT ACTIVATION; PROTAMINE REVERSAL; PULMONARY VASOCONSTRICTION; HEMODYNAMIC-RESPONSES; ENDOTHELIAL-CELLS; MESANGIAL CELLS; THROMBOXANE; PURIFICATION; GENERATION AB Although eicosanoid production contributes to physiological and pathophysiological consequences of cardiopulmonary bypass (CPB), the mechanisms accounting for the enhanced eicosanoid production have not been defined. Plasma phospholipase A(2) (PLA(2)) activity, 6-keto-prostaglandin F-1 alpha (6-keto-PGF(1 alpha)), and thromboxane B-2 (TXB(2)) levels were measured at various times during cardiac surgery. Plasma PLA(2) activity increased after systemic heparinization, before CPB. This was highly correlated with concurrent increases in plasma 6-keto-PGF(1 alpha). TXB(2) concentrations did not increase with heparin administration but did increase significantly after initiation of CPB. High plasma PLA(2) activity, 6-keto-PGF(1 alpha), and TXB(2) concentrations were measured throughout the CPB period. Protamine, administered to neutralize the heparin, caused an acute reduction of both plasma PLA(2) activity and plasma 6-keto-PGF(1 alpha), but no change in plasma TXB(2) concentrations. Thus the ratio of TXB(2) to 6-keto-PGF(1 alpha) increased significantly after protamine administration. Enhanced plasma PLA(2) activity was also measured in patients with lower doses of heparin used clinically for nonsurgical applications. Human plasma PLA(2) was identified as group II PLA(2) by its sensitivity to deoxycholate and dithiothreitol, its substrate specificity, and its elution characteristics on heparin affinity, chromatography. Heparin addition to PMNs in vitro resulted in dose-dependent increases in cellular PLA(2) activity and release of PLA(2). The PLA(2) released from the PMN had characteristics similar to those of post-heparin plasma PLA(2). In conclusion, plasma PLA(2) activity and 6-keto-PGF(1 alpha) concentrations are markedly enhanced with systemic heparinization. Part of the anticoagulant and vasodilating effects of heparin may be due to increased plasma prostacyclin (PGI(2)) levels. In addition the pulmonary vasoconstriction sometimes associated with protamine infusion during cardiac surgery might be due to decreased plasma PLA(2) activity, with an associated increased TXB(2)/6-keto-PGF(1 alpha) ratio. C1 MASSACHUSETTS GEN HOSP,MED SERV LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,HK BEECHER MEM RES LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,CARDIAC ANESTHESIA GRP,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. TUFTS UNIV,SCH MED,NEW ENGLAND MED CTR,PEDIAT INTENS CARE UNIT,BOSTON,MA 02111. FU NIDDK NIH HHS [DK-38452, DK-39773]; NINDS NIH HHS [NS-10828] NR 51 TC 30 Z9 32 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 MAR PY 1995 VL 95 IS 3 BP 1062 EP 1070 DI 10.1172/JCI117752 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200022 PM 7883954 ER PT J AU WENZEL, UO FOUQUERAY, B BISWAS, P GRANDALIANO, G CHOUDHURY, GG ABBOUD, HE AF WENZEL, UO FOUQUERAY, B BISWAS, P GRANDALIANO, G CHOUDHURY, GG ABBOUD, HE TI ACTIVATION OF MESANGIAL CELLS BY THE PHOSPHATASE INHIBITOR VANADATE - POTENTIAL IMPLICATIONS FOR DIABETIC NEPHROPATHY SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE PLATELET-DERIVED GROWTH FACTOR; HUMAN KIDNEY; TYROSINE PHOSPHORYLATION; PROTEIN KINASE C; PHOSPHOLIPASE C ID PROTEIN TYROSINE PHOSPHATASES; FIBROBLAST GROWTH-FACTOR; DNA-SYNTHESIS; MESSENGER-RNAS; RAT ADIPOCYTES; PDGF RECEPTOR; FACTOR-BETA; KINASE-C; EXPRESSION; KIDNEY AB The metalion vanadate has insulin-like effects and has been advocated for use in humans as a therapeutic modality for diabetes mellitus. However, since vanadate is a tyrosine phosphatase inhibitor, it may result in undesirable activation of target cells. We studied the effect of vanadate on human mesangial cells, an important target in diabetic nephropathy. Vanadate stimulated DNA synthesis and PDGF B chain gene expression. Vanadate also inhibited total tyrosine phosphatase activity and stimulated tyrosine phosphorylation of a set of cellular proteins. Two chemically and mechanistically dissimilar tyrosine kinase inhibitors, genistein and herbimycin A, blocked DNA synthesis induced by vanadate. Vanadate also stimulated phospholipase C and protein kinase C. Downregulation of protein kinase C abolished vanadate-induced DNA synthesis. Thus, vanadate-induced mitogenesis is dependent on tyrosine kinases and protein kinase C activation. The most likely mechanism for the effect of vanadate on these diverse processes involves the inhibition of cellular phosphotyrosine phosphatases. These studies demonstrating that vanadate activates mesangial cells may have major implications for the therapeutic potential of vanadate administration in diabetes. Although vanadate exerts beneficial insulin-like effects and potentiates the effect of insulin in sensitive tissue, it may result in undesirable activation of other target cells, such as mesangial cells. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX. UNIV HOSP TEXAS,DEPT MED,DIV NEPHROL,SAN ANTONIO,TX 78284. RI Grandaliano, Giuseppe/G-2963-2012 FU NIDDK NIH HHS [DK-43988, DK-33665] NR 50 TC 31 Z9 32 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 MAR PY 1995 VL 95 IS 3 BP 1244 EP 1252 DI 10.1172/JCI117774 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200044 PM 7883973 ER PT J AU FEENER, EP NORTHRUP, JM AIELLO, LP KING, GL AF FEENER, EP NORTHRUP, JM AIELLO, LP KING, GL TI ANGIOTENSIN-II INDUCES PLASMINOGEN-ACTIVATOR INHIBITOR-1 AND INHIBITOR-2 EXPRESSION IN VASCULAR ENDOTHELIAL AND SMOOTH-MUSCLE CELLS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE ANGIOTENSIN II; PLASMINOGEN ACTIVATOR INHIBITOR; ENDOTHELIAL CELL; VASCULAR SMOOTH MUSCLE CELLS; GENE EXPRESSION ID PROTEIN-KINASE-C; GROWTH-FACTOR-BETA; PHORBOL ESTER; CONVERTING ENZYME; MYOCARDIAL-INFARCTION; MESSENGER-RNA; GENE-EXPRESSION; HEART-FAILURE; INSULIN; SYSTEM AB Angiotensin II (AII)- and Arg(8)-vasopressin (AVP)-regulated gene expression in vascular cells has been reported to contribute to vascular homeostasis and hypertrophy. In this report, AVP-induced expression of plasminogen activator inhibitor (PAI)-2 mRNA in rat microvessel endothelial (RME) cells was identified using differential mRNA display. Further characterization of vasoactive peptide effects on PAI expression revealed that AII stimulated a 44.8+/-25.2-fold and a 12.4+/-3.2-fold increase in PAI-2 mRNA in RME cells and rat aortic smooth muscle cells (RASMC), respectively. AII also stimulated a 10- and 48-fold increase in PAI-1 mRNA in RME cells and RASMC, respectively. These AII effects mere inhibited by either Sar(1), Ile(8)-angiotensin or the AT(1) antagonist DuP 735, but mere not significantly altered in the presence of the AT(2) antagonist PD123319. AII stimulation of RASMC and RME cells also significantly increased both PAI-1 protein and PAI activity released to the culture medium. Inhibition of protein kinase C completely blocked PMA-stimulated induction of PAI-2 mRNA in both cell types and inhibited the AII-stimulated increase in RASMC by 98.6+/-2.8% In contrast, protein kinase C inhibition only partially decreased the AII-stimulated PAI-2 expression in RME cells by 68.8+/-11.1%, suggesting that a protein kinase C-independent mechanism contributes to a 6.9+/-1.5-fold AII induction of PAI-2 expression in endothelial cells. AII and PMA also stimulated protein tyrosine phosphorylation in RME cells, and the tyrosine kinase inhibitor genistein partially blocked their induction of PAI-2 mRNA. These findings suggest that AII may regulate plasminogen activation in the vasculature by inducing both PAI-1 and PAI-2 expression. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,DEPT MED,BEETHAM EYE INST,BOSTON,MA 02215. RP FEENER, EP (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,JOSLIN DIABET CTR,DEPT MED,DIV RES,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-23811-06, DK-36836, P30 DK036836] NR 56 TC 218 Z9 222 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 MAR PY 1995 VL 95 IS 3 BP 1353 EP 1362 DI 10.1172/JCI117786 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200056 PM 7883982 ER PT J AU ANTONETTI, DA REYNET, C KAHN, CR AF ANTONETTI, DA REYNET, C KAHN, CR TI INCREASED EXPRESSION OF MITOCHONDRIAL-ENCODED GENES IN SKELETAL-MUSCLE OF HUMANS WITH DIABETES-MELLITUS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE MITOCHONDRIA; INSULIN; ELECTRON TRANSPORT; OXIDATIVE PHOSPHORYLATION; MICE ID CYTOCHROME-C-OXIDASE; THYROID-HORMONE; POINT MUTATION; TRANSCRIPTION; NUCLEAR; DNA; INSULIN; REPLICATION; SUBUNIT AB Screening subtraction libraries from normal and type II diabetic human skeletal muscle, we identified four different mitochondrially encoded genes which were increased in expression in diabetes. The genes were cytochrome oxidase I, cytochrome oxidase III, NADH dehydrogenase IV, and 12s rRNA, all of which are located on the heavy strand of the mitochondrial genome. There was a 1.5- to 2.2-fold increase in the expression of these mRNA molecules relative to total RNA in both type I and type II diabetes as assessed by Northern blot analyses. Since there was similar to 50% decrease in mitochondrial DNA. copy number as estimated by Southern blot analyses, mitochondrial gene expression increased similar to 2.5-fold when expressed relative to mitochondrial DNA copy number. For cytochrome oxidase I similar changes in mitochondrial gene expression were observed in muscle of nonobese diabetic and ob/ob mice, models of type I and type II diabetes, respectively. By contrast there was no change or a slight decrease in expression of cytochrome oxidase 7a, a nuclear-encoded subunit of cytochrome oxidase, and the expression of mitochondrial transcription factor 1 in human skeletal muscle did not change with type I or type II diabetes. The increased mitochondrial gene expression may contribute to the increase in mitochondrial respiration observed in uncontrolled diabetes. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. FU NIDDK NIH HHS [2 T32 DK 07337, DK 33201] NR 36 TC 91 Z9 91 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD MAR PY 1995 VL 95 IS 3 BP 1383 EP 1388 DI 10.1172/JCI117790 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200060 PM 7533791 ER PT J AU CHELEN, CJ FANG, Y FREEMAN, GJ SECRIST, H MARSHALL, JD HWANG, PT FRANKEL, LR DEKRUYFF, RH UMETSU, DT AF CHELEN, CJ FANG, Y FREEMAN, GJ SECRIST, H MARSHALL, JD HWANG, PT FRANKEL, LR DEKRUYFF, RH UMETSU, DT TI HUMAN ALVEOLAR MACROPHAGES PRESENT ANTIGEN INEFFECTIVELY DUE TO DEFECTIVE EXPRESSION OF B7 COSTIMULATORY CELL-SURFACE MOLECULES SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Note DE ALVEOLAR MACROPHAGES; B7; ANTIGEN PRESENTATION; CD28; ANERGY ID T-CELL; LANGERHANS CELLS; DENDRITIC CELLS; CLONAL ANERGY; TOLERANCE; CD28; INDUCTION; RESPONSES; RECEPTOR; PROLIFERATION AB Alveolar macrophages, resident phagocytic cells in the lung that derive from peripheral blood monocytes, are paradoxically ineffective in presenting antigen to T cells. We found that antigen presentation by alveolar macrophages could be restored by the addition of anti-CD28 mAb to cultures of T cells and macrophages, indicating that costimulation by alveolar macrophages via the CD28 pathway was defective. In addition, we found that alveolar macrophages activated with IFN-gamma faded to express B7-1 or B7-2 antigens, which normally ligate CD28 on T cells and provide a costimulatory signal required for the activation of T cells. These observations are the first to demonstrate the inability of a ''professional'' antigen-presenting cell type to effectively express the costimulatory molecules B7-1 and B7-2. Inasmuch as immune reactions within the lung are inevitably associated with inflammatory injury to pulmonary tissue, these observations suggest that reduced expression of B7-1 and B7-2 by alveolar macrophages may be advantageous, as a critical mechanism involved in the induction of peripheral tolerance to the abundance of antigens to which mucosal tissues are continuously exposed. C1 STANFORD UNIV,LUCILE SALTER PACKARD CHILDRENS HOSP,DEPT PEDIAT,DIV ALLERGY IMMUNOL & RESP MED,STANFORD,CA 94305. STANFORD UNIV,LUCILE SALTER PACKARD CHILDRENS HOSP,DEPT PEDIAT,DIV CRIT CARE MED,STANFORD,CA 94305. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. FU NIAID NIH HHS [R01AI26322, KO7AI01026, R01AI24571] NR 41 TC 110 Z9 116 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 MAR PY 1995 VL 95 IS 3 BP 1415 EP 1421 DI 10.1172/JCI117796 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA QM012 UT WOS:A1995QM01200066 PM 7533793 ER PT J AU COLOMBO, AL BARCHIESI, F MCGOUGH, DA RINALDI, MG AF COLOMBO, AL BARCHIESI, F MCGOUGH, DA RINALDI, MG TI COMPARISON OF E-TEST AND NATIONAL-COMMITTEE-FOR-CLINICAL-LABORATORY-STANDARDS BROTH MACRODILUTION METHOD FOR AZOLE ANTIFUNGAL SUSCEPTIBILITY TESTING SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID FUNGAL-INFECTIONS; MULTICENTER EVALUATION; AGAR DILUTION; FLUCONAZOLE; TRANSPLANTATION; MICRODILUTION; YEASTS AB The use of Etest strips for antimicrobial susceptibility testing is a new and promising method with broad applications in microbiology. Since these strips contain a predefined continuous gradient of a drug, it is possible to obtain a reproducible, quantitative MIC reading. We performed a prospective and double-blinded study to compare the Etest and National Committee for Clinical Laboratory Standards (Villanova, Pa.) broth macrodilution methods for determining the MICs of fluconazole, itraconazole, and ketoconazole for 100 clinical isolates (25 Candida albicans, 25 Cryptococcus neofarmans var, neoformans, 20 Torulopsis [Candida] glabrata, 15 Candida tropicalis, and 15 Candida parapsilosis). The Etest method was performed according to the manufacturer's instructions, and the reference method was performed according to National Committee for Clinical Laboratory Standards document M27-P guidelines. Despite differences between results for some species-drug combinations, Etest and macrobroth MICs were, in general, in good agreement. The MIC agreement rates for the two methods, within +/-1 dilution, were 71% for ketoconazole, 80% for fluconazole, and 84% for itraconazole. According to our data, Etest has potential utility as an alternative method. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV ANCONA,IST MALATTIE INFETT & MED PUBBL,ANCONA,ITALY. RP COLOMBO, AL (reprint author), ESCOLA PAULISTA MED,DISCIPLINA DOENCAS INFECCIOSAS & PARASITARIAS,RUA BOTUCATU 740,BR-04023062 SAO PAULO,BRAZIL. NR 25 TC 106 Z9 116 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD MAR PY 1995 VL 33 IS 3 BP 535 EP 540 PG 6 WC Microbiology SC Microbiology GA QG830 UT WOS:A1995QG83000005 PM 7751353 ER PT J AU KRISHER, KK HOLDRIDGE, NB MUSTAFA, MM RINALDI, MG MCGOUGH, DA AF KRISHER, KK HOLDRIDGE, NB MUSTAFA, MM RINALDI, MG MCGOUGH, DA TI DISSEMINATED MICROASCUS-CIRROSUS INFECTION IN PEDIATRIC BONE-MARROW TRANSPLANT RECIPIENT SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note ID IMMUNOCOMPROMISED HOST; SCOPULARIOPSIS AB Microascus cirrosus Curzi and its associated anamorphic state, Scopulariopsis, were recovered from the cutaneous lesion of a 12-year-old male who had undergone an autologous bone marrow transplantation for acute myelogenous leukemia. Histopathology sections from the biopsied lesion demonstrated septate hyphae consistent with a fungal etiology. Radiographic studies of the lungs subsequent to progression of the lesion revealed a consolidation in the right upper lobe suggesting a primary focus of infection. While M. cirrosus is fairly abundant in nature and widely distributed in stored grains in North America, this is, to our knowledge, the first reported human infection by this species. Salient characteristics for the identification of this dematiaceous ascomycete, M. cirrosus, will be presented. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KRISHER, KK (reprint author), CHILDRENS MED CTR,1935 MOTOR ST,DALLAS,TX 75235, USA. NR 12 TC 25 Z9 25 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD MAR PY 1995 VL 33 IS 3 BP 735 EP 737 PG 3 WC Microbiology SC Microbiology GA QG830 UT WOS:A1995QG83000043 PM 7751387 ER PT J AU BIEDERMAN, J THISTED, RA GREENHILL, LL RYAN, ND AF BIEDERMAN, J THISTED, RA GREENHILL, LL RYAN, ND TI ESTIMATION OF THE ASSOCIATION BETWEEN DESIPRAMINE AND THE RISK FOR SUDDEN-DEATH IN 5-YEAR-OLD TO 14-YEAR-OLD CHILDREN SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID RIGHT CORONARY-ARTERY; TRICYCLIC ANTIDEPRESSANTS; FUNCTIONAL CONSEQUENCES; DEPRESSED-PATIENTS; LEFT SINUS; ADOLESCENTS; DISEASE; VALSALVA; ADULTS; CANCER AB Background: Four cases of sudden death in children 12 years or younger during desipramine treatment were identified between 1986 and 1992. We evaluated whether these events support the hypothesis that exposure to therapeutic doses of desipramine contributes to the risk for sudden death in otherwise healthy children. Method: The National Center for Health Statistics provided the baseline number of sudden unexplained deaths in children 5 to 14 years old. Data from the National Disease and Therapeutic Index were used to estimate the exposure to desipramine in children in the same age group. Since two of the four deaths were identified by 1987, we used the post-1987 experience as if it were a prospective period in which a causal association could be examined. Results: The number of sudden deaths in desipramine-exposed children did not increase from 1986 to 1992 despite a marked increase in exposure. By using 4 to 6 months as the average lifetime of a desipramine prescription and a baseline rate of sudden death of 4.2 deaths/million/year in this population, the post-1987 period would account for 162,000 to 242,000 person-years of desipramine exposure. Although not statistically significant, this level of exposure corresponds to a relative risk of 2.1 (95% CI = 0.5 to 15) to 3.1 (95% CI = 0.8 to 22). Conclusion: Although, based on our estimates, the evidence for an association between desipramine and sudden death in children aged 5 to 14 years appears weak, replication of our findings is needed with a more precise numerator (total number of deaths) and denominator (the appropriate conversion from drug appearance to actual exposure) before a firm conclusion on this subject can be drawn. Until then, even if remote, the possibility of an association between desipramine and sudden death in children stresses the importance of assessing risks and benefits when desipramine is used in pediatric patients. C1 UNIV CHICAGO,DEPT STAT,CHICAGO,IL. NEW YORK STATE PSYCHIAT INST & HOSP,DIV CHILD & ADOLESCENT PSYCHIAT,NEW YORK,NY. UNIV PITTSBURGH,SCH MED,WESTERN PSYCHIAT INST & CLIN,PITTSBURGH,PA. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC-725,FRUIT ST,BOSTON,MA 02114, USA. RI Thisted, Ronald/B-1985-2008 NR 32 TC 63 Z9 63 U1 1 U2 2 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 MAR PY 1995 VL 56 IS 3 BP 87 EP 93 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA QN897 UT WOS:A1995QN89700001 PM 7883735 ER PT J AU TRAMO, MJ LOFTUS, WC THOMAS, CE GREEN, RL MOTT, LA GAZZANIGA, MS AF TRAMO, MJ LOFTUS, WC THOMAS, CE GREEN, RL MOTT, LA GAZZANIGA, MS TI SURFACE-AREA OF HUMAN CEREBRAL-CORTEX AND ITS GROSS MORPHOLOGICAL SUBDIVISIONS - IN-VIVO MEASUREMENTS IN MONOZYGOTIC TWINS SUGGEST DIFFERENTIAL HEMISPHERE EFFECTS OF GENETIC-FACTORS SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID BRAIN; MAMMALS; APART AB We measured the surface area of the cerebral cortex and its gross morphological subdivisions in 10 pairs of monozygotic twins. Cortical surface area was estimated in vivo using magnetic resonance imaging and three-dimensional computer models of the intra- and extrasulcal pial surface. The means and standard deviations of regional (e.g., gyral), lobar, hemisphere, and total cortical surface area were tabulated for the entire population of 20 young, right-handed adults (10 females, 10 males). To determine whether genotypic differences were associated with morphometric differences, analyses of variance were carried out on each measure across unrelated twin pairs (genotype factor) and within co-twins (birth order factor). Across unrelated pairs, there was wide variation in regional cortical surface area for the left hemisphere (normalized by total cortical surface area, p less than or equal to 0.0001) but not for the right hemisphere (normalized, p = 0.12). More variation in lobar surface area was also observed for the left hemisphere (normalized, p = 0.05) than for the right (normalized, p = 0.48). Within co-twins, no significant variation in regional surface area or lobar surface area was found for the left or right hemisphere. Although normalized regional and lobar surface area in the left hemisphere differed across unrelated pairs, overall left hemisphere surface area normalized by total cortical surface area did not (p = 0.73). Total cortical surface area normalized by body weight varied across unrelated pairs (p = 0.001) but not within co-twins (p = 0.39). The effects observed across unrelated pairs were not attributable to sex differences. These results suggest: 1) both the total area and folding of the cortical surface are heavily influenced by genetic factors in humans; and 2) the cerebral hemispheres may be differentially affected by genetic influences on cortical morphogenesis, with the language-dominant left cerebral cortex under stronger genetic control than the right. C1 MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. UNIV CALIF DAVIS, DAVIS, CA 95616 USA. DARTMOUTH COLL SCH MED, LEBANON, NH USA. RP TRAMO, MJ (reprint author), HARVARD UNIV, SCH MED, DEPT NEUROBIOL, 220 LONGWOOD AVE, BOSTON, MA 02115 USA. NR 52 TC 60 Z9 60 U1 1 U2 5 PU MIT PRESS PI CAMBRIDGE PA 55 HAYWARD ST JOURNALS DEPT, CAMBRIDGE, MA 02142 SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD SPR PY 1995 VL 7 IS 2 BP 292 EP 302 DI 10.1162/jocn.1995.7.2.292 PG 11 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA QX770 UT WOS:A1995QX77000011 PM 23961829 ER PT J AU PROVENZALE, JM BARBORIAK, DP TAVERAS, JM AF PROVENZALE, JM BARBORIAK, DP TAVERAS, JM TI EXERCISE-RELATED DISSECTION OF CRANIOCERVICAL ARTERIES - CT, MR, AND ANGIOGRAPHIC FINDINGS SO JOURNAL OF COMPUTER ASSISTED TOMOGRAPHY LA English DT Article DE ARTERIES, CRANIOCERVICAL; BRAIN, BLOOD FLOW; HYPOTENSION; MAGNETIC RESONANCE IMAGING; COMPUTED TOMOGRAPHY; ANGIOGRAPHY ID INTERNAL CAROTID-ARTERY; VERTEBRAL ARTERIES; CEREBRAL-ARTERIES; INFARCTION; STROKE; INJURY; NECK AB Objective: Our goal was to demonstrate the spectrum of neuroradiologic (CT, MR, and angiographic) findings in craniocervical arterial dissection (CAD) related to exercise or sporting activities and compare the diagnostic utility of CT, MRI, and MR angiography (MRA). Materials and Methods: The neuroradiologic examinations of 11 patients with CAD was performed: CT was performed in 10 patients, cranial MRI in 9, cranial and cervical MRA in 4, and contrast angiography in 10. The CT examinations were assessed for the presence of an infarction or a hyperdense artery (consistent with intraluminal thrombus), MRI examinations for the presence of infarction or abnormal periarterial signal, and contrast angiograms for arterial stenosis or occlusion, luminal irregularity, pseudoaneurysm, intimal flap, or distal branch occlusions. Results: Computed tomography demonstrated infarction in four patients. At contrast angiography, a dissection was found in the artery supplying the region of infarction in all cases. A hyperdense artery was found by CT in two patients, which correlated with dissection of the artery or its parent artery on contrast angiography. Cranial MRI findings were seen in six patients (infarction in five, periarterial signal abnormality in five). Dissection was confirmed in all four patients with abnormal periarterial signal who underwent contrast angiography. Two patients with abnormal intracranial periarterial signal had corresponding abnormalities on MRA. False-negative cranial and cervical MRI and MRA studies were performed in one patient because the imaging volumes used for the cervical and intracranial MR examinations did not overlap. Four patients with normal intracranial arterial signal had dissection in the neck demonstrated by contrast angiography. Conclusion: Neuroradiologic findings of CAD can include infarction, a hyperdense artery on CT, abnormal periarterial signal on MRI, and a narrowed arterial signal column on MRA. Computed tomography is an insensitive screening examination. Proper use of MRI and MRA involves examination of both the head and the neck with overlapping imaging volumes of the two regions. C1 SHIELDS HLTH CARE,BROCKTON,MA. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP PROVENZALE, JM (reprint author), DUKE UNIV,MED CTR,DEPT RADIOL,DURHAM,NC 27710, USA. NR 25 TC 39 Z9 39 U1 0 U2 0 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 MAR-APR PY 1995 VL 19 IS 2 BP 268 EP 276 DI 10.1097/00004728-199503000-00019 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QN282 UT WOS:A1995QN28200019 PM 7890854 ER PT J AU WALTMANN, E SKOBE, Z GOLDHABER, P AF WALTMANN, E SKOBE, Z GOLDHABER, P TI ENDOMEMBRANOUS MINERALIZATION IN TISSUE-CULTURE USING A DEFINED MEDIUM SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 FAC CHIRURG DENT,STRASBOURG,FRANCE. FORSYTH DENT CTR,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD MAR PY 1995 VL 74 IS 3 BP 936 EP 936 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QX162 UT WOS:A1995QX16201489 ER PT J AU SHANETZKY, B HORVITZ, D SMORODINSKY, N GANESHKUMAR, N WEISS, E AF SHANETZKY, B HORVITZ, D SMORODINSKY, N GANESHKUMAR, N WEISS, E TI CHARACTERIZATION OF F-NUCLEATUM PK1594 ADHESION OF MONOCLONAL-ANTIBODIES AND SIMPLE SUGARS SO JOURNAL OF DENTAL RESEARCH LA English DT Meeting Abstract C1 TEL AVIV UNIV,SCH DENT MED,IL-69978 TEL AVIV,ISRAEL. FORSYTH DENT CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC DENTAL RESEARCH PI ALEXANDRIA PA 1619 DUKE ST, ALEXANDRIA, VA 22314 SN 0022-0345 J9 J DENT RES JI J. Dent. Res. PD MAR PY 1995 VL 74 IS 3 BP 962 EP 962 PG 1 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA QX162 UT WOS:A1995QX16201672 ER PT J AU VENKATARAMAN, L BURAKOFF, SJ SEN, RJ AF VENKATARAMAN, L BURAKOFF, SJ SEN, RJ TI FK506 INHIBITS ANTIGEN RECEPTOR-MEDIATED INDUCTION OF C-REL IN B-LYMPHOID AND T-LYMPHOID CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID NF-KAPPA-B; SURFACE IG RECEPTOR; CYCLOSPORINE-A; INTERLEUKIN-2 PROMOTER; LYMPHOCYTES-T; ACTIVATION GENES; ALPHA-GENE; TAX GENE; CALCINEURIN; EXPRESSION AB Stimulation of B and T cells via the antigen receptor, by phorbol ester or by phorbol ester and ionomycin, leads to nuclear translocation of the inducible transcription factor NF-kappa B, comprising the p50 and p65 rel-related polypeptides. In this report we show that c-rel is a component of the antigen receptor-induced kappa B binding proteins in both B and T cells. Whereas NF-kappa B can be induced by phorbol ester alone, optimal induction of c-rel requires stimulation by both phorbol ester and ionomycin, the dual signal that is necessary for proliferation of untransformed lymphocytes. Furthermore, c-rel induction is blocked by the immunosuppressive drug FK506 that is known to inhibit B and T cell activation. c-rel-dependent transactivation of the interleukin-2 receptor alpha chain (IL-2R alpha) promoter is augmented by coexpression of calcineurin, suggesting the involvement of a calcineurin-dependent intracellular pathway. Our results identify c-rel as a target of immunosuppressive agents and illustrate the similarity of activation pathways in both B and T cells. C1 BRANDEIS UNIV,ROSENSTIEL BASIC MED SCI RES CTR,DEPT BIOL,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 41 TC 82 Z9 84 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 MAR 1 PY 1995 VL 181 IS 3 BP 1091 EP 1099 DI 10.1084/jem.181.3.1091 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA QH747 UT WOS:A1995QH74700025 PM 7532676 ER PT J AU THAIK, CM SEMIGRAN, MJ GINNS, L WAIN, JC DEC, GW AF THAIK, CM SEMIGRAN, MJ GINNS, L WAIN, JC DEC, GW TI EVALUATION OF ISCHEMIC-HEART-DISEASE IN POTENTIAL LUNG-TRANSPLANT RECIPIENTS SO JOURNAL OF HEART AND LUNG TRANSPLANTATION LA English DT Article; Proceedings Paper CT 14th Annual Meeting and Scientific Sessions of the International-Society-for-Heart-and-Lung-Transplantation CY MAR 23-26, 1994 CL VENICE, ITALY SP INT SOC HEART & LUNG TRANSPLANTAT AB Background: The prevalence of coronary artery disease in potential lung transplant recipients has not been extensively studied. Given the limited donor supply, a high degree of sensitivity for detecting occult disease is essential. Methods: This retrospective study examined both the clinical indications for coronary angiography and the extent of coronary arteriosclerotic disease in 105 consecutive potential lung transplant candidates. Results: Fifty-one patients (49%) underwent angiography to either exclude asymptomatic atherosclerosis (n = 46) or define the extent of known symptomatic ischemic heart disease (n = 5). The perceived risk of occult disease according to a semiquantitative coronary risk assessment score that included hypertension, hyperlipidemia, diabetes, smoking, a family history of coronary artery disease, and electrocardiographic or echocardiographic abnormalities influenced the decision to perform angiography: 4 of 44 patients (9%) with two or fewer risk factors underwent angiography versus 42 of 56 patients (75%) with more than two risk factors (p less-than-or-equal-to 0.05). A higher risk factor score also correlated with angiographic evidence of coronary artery disease. In the 46 patients without symptoms who were studied, two hemodynamically significant but unsuspected coronary lesions were identified. Six other patients without symptoms had noncritical (<50%) lesions. Among the five patients with angina or a prior myocardial infarction, coronary angiography showed either minimal atherosclerosis (n = 2) or non-life threatening anatomy (n = 3). Angiographic findings did not exclude any patient from transplant listing. Conclusion: Coronary angiography appears most useful in patients without symptoms with multiple coronary risk factors and in a subset of patients who might otherwise be excluded from lung transplantation because of a history of symptomatic cardiovascular disease. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULFINCH 211,BOSTON,MA 02114. NR 0 TC 19 Z9 20 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1053-2498 J9 J HEART LUNG TRANSPL JI J. Heart Lung Transplant. PD MAR-APR PY 1995 VL 14 IS 2 BP 257 EP 266 PG 10 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery; Transplantation SC Cardiovascular System & Cardiology; Respiratory System; Surgery; Transplantation GA QQ927 UT WOS:A1995QQ92700008 PM 7779844 ER PT J AU KOLLIAS, N GILLIES, R MUCCINI, JA UYEYAMA, RK PHILLIPS, SB DRAKE, LA AF KOLLIAS, N GILLIES, R MUCCINI, JA UYEYAMA, RK PHILLIPS, SB DRAKE, LA TI A SINGLE-PARAMETER, OXYGENATED HEMOGLOBIN, CAN BE USED TO QUANTIFY EXPERIMENTAL IRRITANT-INDUCED INFLAMMATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Article DE ERYTHEMA; SKIN; POLARIZED PHOTOGRAPHY ID SODIUM LAURYL SULFATE; PATCH-TEST RESPONSES; REFLECTANCE MEASUREMENTS; BIOENGINEERING METHODS; CONTACT-DERMATITIS; HUMAN MELANIN; SKIN; ERYTHEMA; QUANTIFICATION; INVIVO AB To quantify the dose-response relation of irritant-induced erythema, we examined inflammation in human skin after application of an irritant, using perpendicular polarized photography and diffuse reflectance spectroscopy as compared to clinical visual scoring, The ventral forearms of 11 healthy subjects were patch-tested for 24 h under occlusion in hm chambers with five concentrations of the irritant sodium lauryl sulfate, The tested sites and three control sites were evaluated clinically for erythema at 24, 48, and 72 h after occlusion, photographed using standard and perpendicular polarized photography, and measured by diffuse reflectance spectroscopy, Ah photographs were evaluated for erythema by three investigators, Diffuse reflectance spectra were analyzed, and changes in apparent oxyhemoglobin and deoxyhemoglobin concentrations were estimated, Clinical and photographic assessments of erythema yielded similar linear dose-response relations, A linear dose-response relation, with no minimum threshold, also was obtained for changes in the apparent oxyhemoglobin concentration with increasing irritant dose, whereas the apparent deoxyhemoglobin concentrations were unchanged with increasing dose, These results show that diffuse reflectance spectroscopy permits the characterization of irritant-induced inflammation in terms of a single parameter, the apparent concentration of oxyhemoglobin, and that irritant-induced inflammation primarily involves the capillaries and the superficial arterial plexus. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. RP KOLLIAS, N (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,MGH BHX 630,BOSTON,MA 02114, USA. NR 25 TC 34 Z9 35 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAR PY 1995 VL 104 IS 3 BP 421 EP 424 DI 10.1111/1523-1747.ep12666001 PG 4 WC Dermatology SC Dermatology GA QJ121 UT WOS:A1995QJ12100023 PM 7861012 ER PT J AU CACCIOLA, JS ALTERMAN, AI RUTHERFORD, MJ SNIDER, EC AF CACCIOLA, JS ALTERMAN, AI RUTHERFORD, MJ SNIDER, EC TI TREATMENT RESPONSE OF ANTISOCIAL SUBSTANCE-ABUSERS SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID DIAGNOSTIC INTERVIEW SCHEDULE; SEEKING COCAINE ABUSERS; PERSONALITY-DISORDER; ALCOHOLICS; PSYCHOPATHOLOGY; FOLLOW; SEVERITY; VALIDITY; ADDICTS AB We evaluated the relationship of antisociality to 7-month treatment response in 224 alcohol- and/or cocaine-dependent men. Subjects with and without a DSM-III antisocial personality disorder (ASPD) responded similarly and positively to treatment in a number of functional domains, including substance use. A more detailed analysis comparing subjects with ASPD, subjects meeting adult but not childhood ASPD criteria (A-ASPD), and subjects meeting neither adult nor childhood ASPD criteria (pure non-ASPD) revealed similar and positive responses to treatment among the three groups. The antisocial groups had more cocaine and alcohol use at the baseline evaluation, but at 7-month follow-up, they had levels of use not significantly different than the pure non-ASPD group. The findings suggest that an ASPD diagnosis or an adult antisocial lifestyle, at least as measured by DSM-III criteria, does not predict short-term treatment response. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,PENN VET AFFAIRS CTR STUDIES ADDICT,PHILADELPHIA,PA. VET AFFAIRS MED CTR,PENN VET AFFAIRS CTR STUDIES ADDICT,PHILADELPHIA,PA. NR 29 TC 67 Z9 67 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAR PY 1995 VL 183 IS 3 BP 166 EP 171 DI 10.1097/00005053-199503000-00007 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QM559 UT WOS:A1995QM55900007 PM 7891063 ER PT J AU CHEYETTE, SR CUMMINGS, JL AF CHEYETTE, SR CUMMINGS, JL TI ENCEPHALITIS LETHARGICA - LESSONS FOR CONTEMPORARY NEUROPSYCHIATRY SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID PARKINSONS-DISEASE; DEPRESSION; DOPAMINE; DISORDER AB Encephalitis lethargica (von Economo's encephalitis), pandemic from 1917 to 1926, opened a window on the study of behavioral consequences of infection-induced subcortical disorder. Widely varying acute manifestations included extra-pyramidal disorders, myoclonus, eye movement disorders, paralyses, delirium, mood changes, inverted diurnal rhythms, and catatonia. Major pathological changes involved the substantia nigra, globus pallidus, and hypothalamus. A symptom-free recovery period was often followed by postencephalitic disturbances, typically parkinsonism in adults and conduct disorder in children. Occurrence of depression, mania, obsessive-compulsive disorder, and hyperactivity in post-encephalitic patients anticipated current concepts of the role of the basal ganglia in mood, personality, and obsessional syndromes. Observations of deferred onset and ''tardy'' hyperkinesias presaged current theories of the pathophysiology of tardive dyskinesia. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA. RP CHEYETTE, SR (reprint author), UNIV CALIF LOS ANGELES,SCH MED,REED NEUROL RES CTR,DEPT NEUROL,710 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. NR 82 TC 46 Z9 46 U1 3 U2 7 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 SPR PY 1995 VL 7 IS 2 BP 125 EP 134 PG 10 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QV776 UT WOS:A1995QV77600001 PM 7626955 ER PT J AU HINKIN, CH VANGORP, WG MANDELKERN, MA GEE, M SATZ, P HOLSTON, S MARCOTTE, TD EVANS, G PAZ, DH ROPCHAN, JR QUINONES, N KHONSARY, A BLAHD, WH AF HINKIN, CH VANGORP, WG MANDELKERN, MA GEE, M SATZ, P HOLSTON, S MARCOTTE, TD EVANS, G PAZ, DH ROPCHAN, JR QUINONES, N KHONSARY, A BLAHD, WH TI CEREBRAL METABOLIC CHANGE IN PATIENTS WITH AIDS - REPORT OF A 6-MONTH FOLLOW-UP USING POSITRON-EMISSION-TOMOGRAPHY SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID IMMUNODEFICIENCY-VIRUS INFECTION; BLOOD-BRAIN-BARRIER; DEMENTIA COMPLEX; NEUROPSYCHOLOGICAL FINDINGS; ASYMPTOMATIC SUBJECTS; HIV-1 INFECTION; HOMOSEXUAL MEN; ALZHEIMER TYPE; HTLV-III; PERFORMANCE AB The authors examined change in cerebral metabolic function over time by using PET in HIV-infected individuals diagnosed with AIDS. Ten subjects with AIDS received [F-18]2-fluoro-2-deoxy-D-glucose PET scans and completed a comprehensive neuropsychological battery. The scan and test battery were repeated after 6 months. Over time, the subjects showed increased relative basal ganglia metabolism as well as increased parietal lobe metabolism. There were no statistically significant changes in neuropsychological performance. These results suggest that PET may be move sensitive than traditional neuropsychological evaluation to subtle central nervous system changes in AIDS. C1 W LOS ANGELES DEPT VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF IRVINE,DEPT PHYS,IRVINE,CA 92717. RP HINKIN, CH (reprint author), UNIV CALIF LOS ANGELES,SCH MED,NPI,ROOM C8-747,760 WESTWOOD PLAZA,LOS ANGELES,CA 90024, USA. NR 47 TC 48 Z9 49 U1 2 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SPR PY 1995 VL 7 IS 2 BP 180 EP 187 PG 8 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA QV776 UT WOS:A1995QV77600007 PM 7626961 ER PT J AU CARROLL, RS ZHANG, JP DASHNER, K SAR, M WILSON, EM BLACK, PM AF CARROLL, RS ZHANG, JP DASHNER, K SAR, M WILSON, EM BLACK, PM TI ANDROGEN RECEPTOR EXPRESSION IN MENINGIOMAS SO JOURNAL OF NEUROSURGERY LA English DT Article DE MENINGIOMA; ANDROGEN RECEPTOR; NEOPLASM; NORTHERN BLOT ANALYSIS; IMMUNOCYTOCHEMISTRY ID SEX STEROID-RECEPTORS; PROGESTERONE RECEPTORS; ESTROGEN-RECEPTOR; BINDING-ACTIVITY; BREAST-CANCER; TRANSCRIPTIONAL ACTIVATION; HORMONE RECEPTORS; RIBONUCLEIC-ACID; DNA; GROWTH AB The predominance of meningiomas in females, the accelerated growth of these tumors during the luteal phase of the menstrual cycle and during pregnancy, and the association between meningiomas and breast cancer have led to a number of studies examining the potential role of steroids in the growth of meningiomas. The possibility that androgens play a role in meningioma proliferation has been suggested by a small number of investigators. The aim of this study was to examine the expression of androgen receptor messenger ribonucleic acid (mRNA) and correlate it using immunochemistry with the nuclear localization of androgen receptor in a large number of meningiomas. Thirty-nine meningiomas were examined by Northern blot analysis for the presence of measurable amounts of androgen receptor mRNA and eight of these were analyzed by immunohistochemistry for receptor protein. Sixty-seven percent of the meningiomas expressed androgen receptor mRNA. There was a marked predominance of women among the patients whose tumors expressed androgen receptor; 69% were women and 31% were men. The immunohistochemical data correlated with Northern blot analysis of mRNA. The staining was predominantly nuclear, suggesting that the androgen receptor resides in a location that can activate gene expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. UNIV N CAROLINA,SCH MED,DEPT CELL BIOL & ANAT,CHAPEL HILL,NC 27599. UNIV N CAROLINA,SCH MED,DEPT PEDIAT & BIOCHEM,CHAPEL HILL,NC 27599. RP CARROLL, RS (reprint author), BRIGHAM & WOMENS HOSP,221 LONGWOOD AVE,ROOM 121,BOSTON,MA 02115, USA. NR 67 TC 28 Z9 31 U1 0 U2 1 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 MAR PY 1995 VL 82 IS 3 BP 453 EP 460 DI 10.3171/jns.1995.82.3.0453 PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA QJ311 UT WOS:A1995QJ31100011 PM 7861224 ER PT J AU HEYDARI, AR CONRAD, CC RICHARDSON, A AF HEYDARI, AR CONRAD, CC RICHARDSON, A TI EXPRESSION OF HEAT-SHOCK GENES IN HEPATOCYTES IS AFFECTED BY AGE AND FOOD RESTRICTION IN RATS SO JOURNAL OF NUTRITION LA English DT Article DE LIVER; FOOD RESTRICTION; RATS; HEAT SHOCK PROTEINS; UBIQUITIN ID GLUCOSE-REGULATED PROTEIN; UBIQUITIN MESSENGER-RNA; DIETARY RESTRICTION; TRANSCRIPTIONAL REGULATION; HSP70-LIKE PROTEIN; CELLS; STRESS; FAMILY; LIVER; FIBROBLASTS AB The objective of this study was to determine how food restriction altered the age-related changes in the basal and heat-induced expression of heat shock genes (hsc70, grp78, and ubiquitin) by hepatocytes isolated from young (4 to 6 mo old) and old (26 to 28 mo old) male Fischer 344 rats. The basal levels of the mRNA transcripts for hsc70 and ubiquitin were similar for hepatocytes isolated from young and old rats fed with free access to the diet (control) or from rats fed a restricted diet (40% restriction of food intake). However, the induction of the mRNA transcripts for hsc70 and ubiquitin by a heat shock (42.5 degrees C for 30 min) was significantly higher for hepatocytes isolated from old rats fed the restricted diet compared with old rats fed with free access to the diet. The changes in hsc70 mRNA levels were paralleled by similar changes in hsc70 transcription by isolated nuclei; therefore, the greater induction of hsc70 expression by food restriction results from changes in the transcription of hsc70 gene. In contrast with hsc70 and ubiquitin, the basal levels of grp78 were reduced with age and by food restriction. Therefore, the effect of aging and food restriction on the basal and heat-induced expression of heat shock genes varies considerably from gene to gene. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP HEYDARI, AR (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX 78284, USA. FU NIA NIH HHS [AG01548]; NIEHS NIH HHS [ES06277] NR 35 TC 42 Z9 44 U1 0 U2 3 PU AMER INST NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-3166 J9 J NUTR JI J. Nutr. PD MAR PY 1995 VL 125 IS 3 BP 410 EP 418 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QL021 UT WOS:A1995QL02100002 PM 7876915 ER PT J AU BILLINGS, JA AF BILLINGS, JA TI DEPRESSION SO JOURNAL OF PALLIATIVE CARE LA English DT Article ID CANCER-PATIENTS; MEDICALLY ILL; METHYLPHENIDATE; PAIN; ANTIDEPRESSANT; SYMPTOMS; PSYCHOSTIMULANTS; AMITRIPTYLINE; MANAGEMENT; MOOD C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,COMMUNITY HLTH PLAN,CAMBRIDGE,MA 02138. RP BILLINGS, JA (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 47 TC 9 Z9 9 U1 0 U2 1 PU CENTER BIOETHICS CLIN RES INST MONTREAL PI MONTREAL PA 110 PINE AVE W, MONTREAL PQ H2W 1R7, CANADA SN 0825-8597 J9 J PALLIATIVE CARE JI J. Palliative Care PD SPR PY 1995 VL 11 IS 1 BP 48 EP 54 PG 7 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA RA228 UT WOS:A1995RA22800009 PM 7751987 ER PT J AU LOSTY, PD SUEN, HC MANGANARO, TF DONAHOE, PK SCHNITZER, JJ AF LOSTY, PD SUEN, HC MANGANARO, TF DONAHOE, PK SCHNITZER, JJ TI PRENATAL HORMONAL-THERAPY IMPROVES PULMONARY COMPLIANCE IN THE NITROFEN-INDUCED CDH RAT MODEL SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article; Proceedings Paper CT 41st Annual International Congress of the British-Association-of-Paediatric-Surgeons CY JUN 29-JUL 01, 1994 CL ROTTERDAM, NETHERLANDS SP BRIT ASSOC PAEDIAT SURGEONS DE CONGENITAL DIAPHRAGMATIC HERNIA; PRENATAL THERAPY; LUNG MECHANICS; LUNG MATURATION; NITROFEN ID CONGENITAL DIAPHRAGMATIC-HERNIA; THYROTROPIN-RELEASING-HORMONE; THYROID-HORMONES; PREMATURE-INFANTS; SURGICAL REPAIR; LUNG MATURATION; NEWBORN RATS; SURFACTANT; HYPOPLASIA; SURVIVAL AB Neonates with congenital diaphragmatic hernia (CDH) experience a high mortality despite intensive medical and surgical management. The associated pulmonary hypoplasia is accompanied by an underlying biochemical deficiency that bears similarity to respiratory distress syndrome (RDS) in the premature newborn. Using therapies extrapolated from those used to treat RDS, the authors have previously shown correction of the immature pulmonary biochemical indices in the nitrofen rat CDH model. This study investigates the functional and histological outcome of prenatal hormone therapy on CDH rats. Compared with saline-treated CDH controls, dexamethasone-treated CDH animals achieved significant Increases in lung distensibility (P = .0006) and functional residual capacity (P = .004); CDH rats treated with combined dexamethasone and thyrotropin-releasing hormone (TRH) showed improved functional residual capacity (p = .043) and alveolar stability (P = .025); CDH animals treated with TRH alone (TRH-CDH) showed no improvement in any parameter tested. Histologically, the lungs from dexamethasone- and dexamethasone-TRH-treated CDH animals showed changes that included narrow septal walls, increased air saccule size, and thinning of the pulmonary interstitium compared with the lungs of saline or TRH-CDH rats, which were developmentally arrested at the canalicular State. Lung weights and lung weight-body weights ratios were similar in all CDH rats, confirming that treatment did hbt impair pulmonary growth. These results support the potential clinical use of prenatal pharmacological therapies to treat human fetuses with prenatally diagnosed CDH. Copyright (C) 1995 by W.B. Saunders Company C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT SURG SERV,PEDIAT SURG RES LABS,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. NR 56 TC 52 Z9 53 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 MAR PY 1995 VL 30 IS 3 BP 420 EP 426 DI 10.1016/0022-3468(95)90046-2 PG 7 WC Pediatrics; Surgery SC Pediatrics; Surgery GA QM211 UT WOS:A1995QM21100011 PM 7760234 ER PT J AU SCAVONE, C SCANLON, C MCKEE, M NATHANSON, JA AF SCAVONE, C SCANLON, C MCKEE, M NATHANSON, JA TI ATRIAL-NATRIURETIC-PEPTIDE MODULATES SODIUM AND POTASSIUM-ACTIVATED ADENOSINE-TRIPHOSPHATASE THROUGH A MECHANISM INVOLVING CYCLIC-GMP AND CYCLIC GMP-DEPENDENT PROTEIN-KINASE SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID CAMP-REGULATED PHOSPHOPROTEIN; COLLECTING DUCT CELLS; RENAL TUBULE CELLS; NA-K-ATPASE; NEURONAL PHOSPHOPROTEIN; PHOSPHATASE INHIBITOR-1; GUANYLATE-CYCLASE; RAT-KIDNEY; DOPAMINE; DARPP-32 AB Prior studies indicate that the natriuretic effects of atrial natriuretic peptide (ANP) are due, in part, to an inhibition of the passive movement of sodium ions from tubular lumen through apical cation channels into renal tubular epithelium. The present work demonstrates that ANP also exerts a potent inhibitory effect on the active pumping of sodium ions by renal tubular sodium and potassium-activated adenosine triphosphatase (Na, K-ATPase). This action of ANP is relatively long lasting, is due to a change in enzyme V-max and is specific for ouabain-sensitive activity. Enzyme modulation occurs with an EC(50) for ANP of 0.1 nM, is independent of intracellular [Na+] and is associated with an increase in tissue cyclic GMP (cGMP), but not cyclic AMP (cAMP). Modulation of Na, K-ATPase by ANP is mimicked by 8-bromo-cGMP and okadaic acid (OA) and is blocked by KT 5823, a selective inhibitor of cGMP-dependent protein kinase (PKG), but not by KT 5720, a selective inhibitor of cyclic AMP-dependent protein kinase (PKA), which suggests that the action of ANP on the sodium pump involves cGMP-mediated changes in protein phosphorylation. Regulation of renal Na, K-ATPase activity also occurs with nitric oxide-generating compounds, such as nitroglycerin and sodium nitroprusside (SNP). However, the ability of ANP to modulate Na, K-ATPase does not appear to involve this latter pathway because the effects of ANP on the sodium pump cannot be blocked by either N-omega-nitro-L-arginine, an inhibitor of NO synthase, or hemoglobin, which blocks NO through binding. Taken together, the present data indicate that the natriuretic effects of ANP occur, not only by regulation of sodium entry through amiloride-sensitive cation channels, but also by modulation of the active pumping of sodium by tubular epithelial Na, K-ATPase. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,NEUROPHARMACOL RES LAB,BOSTON,MA 02114. OI Scavone, Cristoforo/0000-0002-1206-0882 FU NEI NIH HHS [EY05077] NR 44 TC 58 Z9 59 U1 0 U2 1 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 MAR PY 1995 VL 272 IS 3 BP 1036 EP 1043 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA QL995 UT WOS:A1995QL99500011 PM 7891313 ER PT J AU GUCCIONE, AA ANDERSON, JJ ANTHONY, JM MEENAN, RF AF GUCCIONE, AA ANDERSON, JJ ANTHONY, JM MEENAN, RF TI THE CORRELATES OF HEALTH PERCEPTIONS IN RHEUMATOID-ARTHRITIS SO JOURNAL OF RHEUMATOLOGY LA English DT Article DE HEALTH PERCEPTIONS; RHEUMATOID ARTHRITIS; HEALTH STATUS ID IMPACT MEASUREMENT SCALES; WORK DISABILITY; PSYCHOLOGICAL DISTRESS; DISEASE; MORTALITY; WOMEN AB Objective, Although measures of health perceptions have been routinely incorporated into assessments of individuals with rheumatoid arthritis (RA), the relationships of other characteristics of these individuals to their health perceptions is not fully understood. We describe the cross sectional associations of sociodemographic, disease, and functional status characteristics with perceived health in individuals with RA. Methods, This description was generated through a 2-phase secondary data analysis using 2 statistical approaches: recursive partitioning of the sample and standard multivariate logistic regression techniques. Results. Both methodological approaches identified education, race, depression, and physical activity as important correlates of self-assessed health in RA. Each approach, in its own way, also identified an interactive effect between physical activity and education and between depression and race in these models. Conclusion, An individual's sociodemographic, disease, and functional status characteristics form a complex model of the correlates of health perceptions of individuals with RA. C1 HARVARD UNIV,SCH MED,DEPT ORTHOPAED,BOSTON,MA. UNIV BOSTON HOSP,BOSTON,MA 02118. BOSTON UNIV,SCH PUBL HLTH,BOSTON,MA. BOSTON UNIV,MASSACHUSETTS GEN HOSP,DEPT MED,PHYS THERAPY SERV,BOSTON,MA 02114. RP GUCCIONE, AA (reprint author), BOSTON UNIV,MASSACHUSETTS GEN HOSP,CTR ARTHRITIS,PHYS THERAPY SERV,15 PARKMAN ST WAC128,BOSTON,MA 02114, USA. FU NIA NIH HHS [K01 AG00567]; NIAMS NIH HHS [AR20613] NR 28 TC 11 Z9 12 U1 0 U2 3 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 MAR PY 1995 VL 22 IS 3 BP 432 EP 439 PG 8 WC Rheumatology SC Rheumatology GA QP817 UT WOS:A1995QP81700010 PM 7783057 ER PT J AU DICKERSON, RN MANZO, CB CHARLAND, SL SETTLE, RG STEIN, TP KUHL, DA RAJTER, JJ AF DICKERSON, RN MANZO, CB CHARLAND, SL SETTLE, RG STEIN, TP KUHL, DA RAJTER, JJ TI THE EFFECT OF INSULIN-LIKE GROWTH-FACTOR-I ON PROTEIN-METABOLISM AND HEPATIC RESPONSE TO ENDOTOXEMIA IN PARENTERALLY FED RATS SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID ACUTE PHASE RESPONSE; ENERGY-METABOLISM; SKELETAL-MUSCLE; SEPTIC RATS; FACTOR-I; 3-METHYLHISTIDINE; NUTRITION; NITROGEN; SEPSIS; EXPRESSION AB To determine the influence of insulin-like growth factor-1 (IGF-1) on nitrogen loss and hepatic response to critical illness, 34 male Sprague-Dawley rats (190-230 g) were randomized to receive parenteral nutrition (PN) only (Ctrl), PN plus continuous infusion of Escherichia coli 026:B6 lipopolysaccharide at 6 mg/kg/day (LPS), or PN plus LPS plus rhIGF-1 (IGF-1) at 3 mg/kg/day for 48 hr. Prior to randomization, all animals underwent iv cannulation and 30 hr of adaptation to PN. All animals received isocaloric and isonitrogenous PN (glucose 170 kcal/kg/day and nitrogen 1.1 g/kg/day) and were kept NPO except for water ad libitum, [N-15]glycine was infused in all animals for determination of liver fractional synthetic rate. Cumulative nitrogen balance during endotoxemia was significantly different from each other (+72 +/- 42, -217 +/- 131, -114 +/- 137 mg/kg/48 hr for the Ctrl, LPS, and IGF-1 groups, respectively; ANOVA, P < 0.001). Endotoxin significantly increased the urinary 3-methylhistidine/creatinine ratio (0.24 +/- 0.05, 0.55 +/- 0.12, 0.48 +/- 0.17 for the Ctrl, LPS, and IGF-1 groups, respectively; ANOVA, P < 0.001); however, IGF-1 did not significantly reduce the ratio. Endotoxin induced a significant increase in liver fractional synthetic rate (29 +/- 8, 56 +/- 18, 64 +/- 12%/day for the Ctrl, LPS, and IGF-1 groups, respectively; ANOVA, P < 0.01) and depressed hepatic cytochrome P450 concentration (0.54 +/- 0.19, 0.22 +/- 0.07, 0.19 +/- 0.07 nmol/mg protein, respectively; ANOVA, P < 0.05) and ethoxycoumarin O-deethylase (ECOD) activity (103 +/- 73, 29 +/- 13, 17 +/- 11, pmol/mg/min, respectively; ANOVA, P < 0.01); however, rhIGF-1 did not significantly alter these hepatic variables during endotoxin infusion. Recombinant human insulin-like growth factor-1 significantly improved nitrogen balance without compromising hepatic response as measured by liver fractional synthetic rate, cytochrome P450 concentration, and ECOD activity in endotoxemic parenterally fed rats. (C) 1995 Academic Press, Inc. C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA COLL PHARM & SCI,PHILADELPHIA,PA. UNIV MED & DENT NEW JERSEY,CAMDEN,NJ. RP DICKERSON, RN (reprint author), UNIV TENNESSEE,DEPT CLIN PHARM,26 S DUNLAP ST,MEMPHIS,TN 38163, USA. RI Dickerson, Roland/C-5185-2008 FU NIDDK NIH HHS [1R15DK46545-01] NR 37 TC 20 Z9 20 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD MAR PY 1995 VL 58 IS 3 BP 260 EP 266 DI 10.1006/jsre.1995.1041 PG 7 WC Surgery SC Surgery GA QL031 UT WOS:A1995QL03100002 PM 7885022 ER PT J AU JELLINEK, MS AF JELLINEK, MS TI PROFESSIONAL IDENTITY - MAY THE FORCE BE WITH US ... ALWAYS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JELLINEK, MS (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,15 PARKMAN ST,ACC725,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAR PY 1995 VL 34 IS 3 BP 387 EP 388 DI 10.1097/00004583-199503000-00026 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA QK025 UT WOS:A1995QK02500026 PM 7896682 ER PT J AU WEISSMAN, NJ NIDORF, SM GUERRERO, JL WEYMAN, AE PICARD, MH AF WEISSMAN, NJ NIDORF, SM GUERRERO, JL WEYMAN, AE PICARD, MH TI OPTIMAL STAGE DURATION IN DOBUTAMINE STRESS ECHOCARDIOGRAPHY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CORONARY-ARTERY DISEASE; ACUTE MYOCARDIAL-INFARCTION; PRESSURE-VOLUME; PERICARDIUM; PERFORMANCE; INFUSION AB Objectives. This study attempted to determine the benefit of a 5-min dobutamine stress echocardiographic stage versus a 3-min stage in a canine model. Background. Dobutamine stress echocardiography, as currently performed, uses a variety of different protocols. Among the many aspects of dobutamine stress echocardiographic protocols that vary is stage duration. Because dobutamine has specific pharmacodynamics, it is possible that stages of different durations may have different cardiovascular effects. Methods. Paired dobutamine stress echocardiograms were obtained in 10 open chest instrumented dogs. The stage duration for the initial dobutamine stress echocardiogram was randomly allocated to either 3 or 5 min, and all hemodynamic and echocardiographic variables were allowed to return to baseline before the second dobutamine stress echocardiogram was obtained using the alternative stage duration. At each stage, heart rate, systolic blood pressure, coronary how, myocardial wall thickness and left ventricular cavity area were recorded. Cavity obliteration, hypotension, ventricular tachycardia or a maximal dose of 40 mu g/kg body weight per min served as the dobutamine stress echocardiographic end point. Results. At baseline, no difference was detected between the 3- or 5-min protocols for heart rate, systolic blood pressure, rate-pressure product, coronary blood how, wall thickness or percent area change. Heart rate, systolic blood pressure and coronary flow increased more by the 10-mu g/kg per min dose with the 5-min protocol than with the 3-min protocol. The dobutamine stress echocardiographic end points were achieved at a lower doubt-amine dose (15.0 +/- 4.1 vs. 11.0 +/- 2.1 mu g/kg per min [mean +/- SD], p = 0.01) with the longer stage duration. Conclusions. In this canine model, a longer stage produced a greater hemodynamic effect at a lower peak dose. Thus, extending stage duration in clinical dobutamine stress echocardiography may achieve equivalent physiologic stress at lower doses and contribute to the optimization of dobutamine stress echocardiographic protocols. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP WEISSMAN, NJ (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC ULTRASOUND LAB,CARDIAC UNIT,VBK 508,FRUIT ST,BOSTON,MA 02114, USA. RI Guerrero, Jorge/I-3666-2015; OI Guerrero, Jorge/0000-0003-4315-7318; Picard, Michael/0000-0002-9264-3243 NR 26 TC 28 Z9 30 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1995 VL 25 IS 3 BP 605 EP 609 DI 10.1016/0735-1097(94)00450-5 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QJ480 UT WOS:A1995QJ48000008 PM 7860903 ER PT J AU LEVINE, RA AF LEVINE, RA TI EXERCISE-INDUCED REGURGITATION IN MITRAL-VALVE PROLAPSE - IS IT A NEW DISEASE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material ID SYSTOLIC-MURMUR SYNDROME; FOLLOW-UP; DIAGNOSIS; ABNORMALITIES; PREVALENCE; SIZE; ECHOCARDIOGRAPHY; COMPLICATIONS; MORPHOLOGY; PATHOLOGY C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,NONINVAS CARDIAC LAB,BOSTON,MA 02114. NR 61 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1995 VL 25 IS 3 BP 700 EP 702 DI 10.1016/0735-1097(94)00566-9 PG 3 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QJ480 UT WOS:A1995QJ48000021 PM 7860916 ER PT J AU HORNBERGER, LK SANDERS, SP SAHN, DJ RICE, MJ SPEVAK, PJ BENACERRAF, BR MCDONALD, RW COLAN, SD AF HORNBERGER, LK SANDERS, SP SAHN, DJ RICE, MJ SPEVAK, PJ BENACERRAF, BR MCDONALD, RW COLAN, SD TI IN-UTERO PULMONARY-ARTERY AND AORTIC GROWTH AND POTENTIAL FOR PROGRESSION OF PULMONARY OUTFLOW TRACT OBSTRUCTION IN TETRALOGY OF FALLOT SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID CONGENITAL HEART-DISEASE; LEFT-VENTRICULAR HYPOPLASIA; CARDIAC DOPPLER FLOW; FETAL ECHOCARDIOGRAPHY; PRENATAL-DIAGNOSIS; FETUS; STENOSIS; LIFE; DYSFUNCTION; LIMITATIONS AB Objectives. This study was designed to define patterns of pulmonary artery and aortic growth in fetuses with tetralogy of Fallot and to determine the potential for in utero progression of right ventricular outflow tract obstruction. Background. Despite an abundance of reports documenting the prenatal diagnosis of tetralogy of Fallot, there is little information about its course in utero. Methods. Pulmonary artery and ascending aortic diameters were measured from prenatal and postnatal echocardiograms of 16 fetuses with tetralogy of Fallot, initially studied at 23.6 +/- 6.0 (mean +/- SD) weeks of gestation. Fetuses were classified retrospectively as having mild and severe tetralogy of Fallot according to whether the pulmonary artery circulation was (severe, n = 5) or was not (mild, n = 11) ductus arteriosus dependent at birth. Results. Initial main pulmonary artery diameter was small for gestational age in 9 fetuses, large in 2 and normal in 5 compared with data from 57 gestational age-adjusted normal fetal studies; it was significantly smaller in the group with severe tetralogy of Fallot (p = 0.05). The initial main pulmonary artery/aortic diameter ratio was also smaller for the group with severe tetralogy of Fallot (0.50 +/- 0.15 vs. 0.73 +/- 0.14 in the group with mild tetralogy of Fallot, p = 0.01). Initial aortic and branch pulmonary artery diameters tended to be normal or near normal for age. In eight fetuses serially studied, main and branch pulmonary artery growth was normal or reduced during prenatal follow-np, Pulmonary artery growth was most reduced in two fetuses in the group with severe tetralogy of Fallot, resulting in pulmonary artery hypoplasia at birth, Two fetuses with valvular pulmonaly atresia at birth had previously shown anterograde pulmonary outflow in midgestation, suggesting progression of pulmonaly outflow obstruction. Conclusions. The postnatal spectrum of pulmonary artery size in tetralogy of Fallot can be attributed to variable patterns of growth in utero. Main pulmonary artery size, main pulmonary artery/aortic diameter ratio and pattern of pulmonary artery growth may be predictive of the severity of postnatal pulmonary outflow obstruction. Pulmonary atresia can develop in utero in some fetuses with tetralogy of Fallot. C1 CLIN GENOLIER,ALDO CASTANEDA INST CONGENITAL HEART DIS,GENOLIER,SWITZERLAND. OREGON HLTH SCI UNIV,CLIN CARE CTR CONGENITAL HEART DIS,DEPT CARDIOL,PORTLAND,OR 97201. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. RP HORNBERGER, LK (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT CARDIOL,300 LONGWOOD AVE,BOSTON,MA 02115, USA. OI Sanders, Stephen/0000-0003-3521-4044 NR 27 TC 80 Z9 85 U1 0 U2 2 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 1 PY 1995 VL 25 IS 3 BP 739 EP 745 DI 10.1016/0735-1097(94)00422-M PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QJ480 UT WOS:A1995QJ48000028 PM 7860923 ER PT J AU TAN, AU COHEN, AH LEVINE, BS AF TAN, AU COHEN, AH LEVINE, BS TI RENAL AMYLOIDOSIS IN A DRUG-ABUSER SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE AMYLOIDOSIS; DRUG ABUSE; NEPHROTIC SYNDROME; COLCHICINE ID FAMILIAL MEDITERRANEAN FEVER; PRIMARY SYSTEMIC AMYLOIDOSIS; COLCHICINE THERAPY; TRANSPLANTATION; DIMETHYLSULFOXIDE; EXPERIENCE; SURVIVAL AB Drug abusers, particularly those who inject drugs s.c. (''skin popping''), may develop amyloidosis, Chronic infections are thought to play a pathogenetic role in this setting. A patient is presented who had a history of ''skin popping'' cocaine and heroin and developed nephrotic syndrome, with an elevated serum creatinine and a creatinine clearance of 61 ml/min. Renal biopsy demonstrated amyloidosis. Treatment with colchicine was initiated, and proteinuria decreased to near normal levels after 12 months, Concomitant with the decrease in proteinuria, creatinine clearance improved, although a repeat renal biopsy failed to show any significant improvement in amyloid burden. These observations suggest that colchicine may be a useful treatment in reversing the proteinuria of renal amyloidosis associated with drug abuse. Furthermore, clinical improvement may occur before any demonstrable regression in the amyloidosis. C1 W LOS ANGELES VET AFFAIRS MED CTR,DEPT MED,LOS ANGELES,CA 90073. CEDARS SINAI MED CTR,DEPT MED,LOS ANGELES,CA 90048. CEDARS SINAI MED CTR,DEPT PATHOL,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. NR 25 TC 19 Z9 20 U1 0 U2 1 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 MAR PY 1995 VL 5 IS 9 BP 1653 EP 1658 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA QM947 UT WOS:A1995QM94700003 PM 7780053 ER PT J AU GRAY, RJ AF GRAY, RJ TI TESTS FOR VARIATION OVER GROUPS IN SURVIVAL-DATA SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION LA English DT Article DE CENSORED FAILURE TIME DATA; CORRELATED DATA; COUNTING PROCESSES; PROPORTIONAL HAZARDS ID COX REGRESSION-MODEL; LIKELIHOOD; RESIDUALS AB When survival data can be divided into natural groups, such as in a clinical trial with patients from a number of different institutions, the question arises whether effects are different for the different groups. For situations where one is concerned with a random pattern of variation over groups, this article proposes testing the null hypothesis of no variation using statistics based on the sums of martingale residuals over subjects within groups. These tests are closely related to the locally most powerful tests of Liang for testing for variation across a large number of strata. The tests are applied to data from a lung cancer trial conducted by the Eastern Cooperative Oncology Group. RP GRAY, RJ (reprint author), HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115, USA. NR 14 TC 22 Z9 22 U1 0 U2 0 PU AMER STATIST ASSN PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0162-1459 J9 J AM STAT ASSOC JI J. Am. Stat. Assoc. PD MAR PY 1995 VL 90 IS 429 BP 198 EP 203 PG 6 WC Statistics & Probability SC Mathematics GA QH030 UT WOS:A1995QH03000021 ER PT J AU GRILLO, HC DONAHUE, DM MATHISEN, DJ WAIN, JC WRIGHT, CD AF GRILLO, HC DONAHUE, DM MATHISEN, DJ WAIN, JC WRIGHT, CD TI POSTINTUBATION TRACHEAL STENOSIS - TREATMENT AND RESULTS SO JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY LA English DT Article ID TRACHEOESOPHAGEAL FISTULA; SUBGLOTTIC LARYNGEAL; RECONSTRUCTION; RESECTION; COMPLICATIONS; TRACHEOSTOMY; MANAGEMENT; INJURY; LASER AB A total of 503 patients underwent 521 tracheal resections and reconstructions for postintubation stenosis from 1965 through 1992. Fifty-three had had prior attempts at surgical resection, 51 others had undergone various forms of tracheal or laryngeal repair, and 45 had had laser treatment. There were 251 cuff lesions, 178 stomal lesions, 38 at both levels, and 36 of indeterminate origin. Sixty-two patients with major laryngeal injuries required complete resection of anterior cricoid cartilage and anastomosis of trachea to thyroid cartilage, and 117 had tracheal anastomosis to the cricoid. A cervical approach was used in 350, cervicomediastinal in 145, and transthoracic in 8. Length of resection was 1.0 to 7.5 cm. Forty-nine had laryngeal release to reduce anastomotic tension. A total of 471 patients (93.7%) had good (87.5%) or satisfactory (6.2%) results. Eighteen of 37 whose operation failed underwent a second reconstruction. Eighteen required postoperative tracheostomy or T-tube insertion for extensive or multilevel disease. Twelve died (2.4%). The most common complication, suture line granulations (9.7%), has almost vanished with the use of absorbable sutures. Wound infection occurred in 15 (3%) and glottic dysfunction in 11 (2.2%). Five had postoperative innominate artery hemorrhage. Resection and reconstruction offer optimal treatment for postintubation tracheal stenosis. C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP GRILLO, HC (reprint author), MASSACHUSETTS GEN HOSP,GEN THORAC SURG UNIT,BOSTON,MA 02114, USA. NR 24 TC 211 Z9 233 U1 0 U2 16 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 MAR PY 1995 VL 109 IS 3 BP 486 EP 493 DI 10.1016/S0022-5223(95)70279-2 PG 8 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA QM203 UT WOS:A1995QM20300009 PM 7877309 ER PT J AU SHEPHERD, KE FAULKNER, CS BROWN, EN AF SHEPHERD, KE FAULKNER, CS BROWN, EN TI ELASTIN FIBER ANALYSIS IN ACUTE DIFFUSE LUNG INJURY CAUSED BY SMOKE-INHALATION SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article DE ADULT RESPIRATORY DISTRESS SYNDROME; ELASTIN FIBERS; LUNG INJURY; POTASSIUM HYDROXIDE PREPARATIONS; PNEUMONIA; PNEUMONIA DIAGNOSIS; SMOKE INHALATION ID RESPIRATORY-DISTRESS SYNDROME; MECHANICALLY VENTILATED PATIENTS; PROTECTED SPECIMEN BRUSH; BRONCHOALVEOLAR LAVAGE; NECROTIZING PNEUMONIA; NOSOCOMIAL PNEUMONIA; PULMONARY INFECTIONS; INTUBATED PATIENTS; DIAGNOSIS; SPECIFICITY AB Objective: The evaluation of various techniques to diagnose or exclude ventilator-associated bacterial pneumonia has been a focus of much research. One such technique involves elastin fiber detection. It has been inferred from previous work that 40% potassium hydroxide preparations of respiratory secretions that demonstrate elastin fibers have a 100% specificity in diagnosing bacterial pneumonia in intubated, mechanically ventilated patients without acute diffuse lung injury. The purpose of this investigation was to ascertain if elastin fibers might be detected in respiratory secretions in acute, diffuse lung injury in the absence of pneumonia (i.e., assess specificity). Design: An animal model using a standardized smoke inhalation protocol to cause acute, diffuse lung injury was used. Materials and Methods: Respiratory secretions collected from the endotracheal tubes from eight sheep that underwent the standardized smoke inhalation protocol and were examined with 40% potassium hydroxide. Histologic data were obtained from autopsy to diagnose or exclude lung injury and pneumonia. Measurements and Main Results: We found six (false) positive elastin fiber preparations in the absence of histologic pneumonia. Specificity was 0.25. Conclusions: We concluded that seeing these results, given a true specificity of 0.99 inferred from previous work, is highly improbable with a probability of 2.74 x 10(-7). Thus, elastin fiber analysis is likely to be highly nonspecific for diagnosing pneumonia in the setting of acute diffuse lung injury. C1 DARTMOUTH COLL,HITCHCOCK MED CTR,DEPT PATHOL,LEBANON,NH 03756. RP SHEPHERD, KE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 37 TC 2 Z9 2 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 Inf. Crit. Care PD MAR PY 1995 VL 38 IS 3 BP 375 EP 378 DI 10.1097/00005373-199503000-00014 PG 4 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA RD561 UT WOS:A1995RD56100014 PM 7897720 ER PT J AU SHERIDAN, RL HURLEY, J SMITH, MA RYAN, CM BONDOC, CC QUINBY, WC TOMPKINS, RG BURKE, JF AF SHERIDAN, RL HURLEY, J SMITH, MA RYAN, CM BONDOC, CC QUINBY, WC TOMPKINS, RG BURKE, JF TI THE ACUTELY BURNED HAND - MANAGEMENT AND OUTCOME BASED ON A 10-YEAR EXPERIENCE WITH 1047 ACUTE HAND BURNS SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article ID EXCISION AB Optimal hand function has a very positive impact on the quality of survival after burn injury, Over a 10-year period, 659 patients with 1047 acutely burned hands were managed at the Sumner Redstone Burn Center of the Massachusetts General Hospital. Our approach to acutely burned hands emphasizes ranging and splinting throughout hospitalization, prompt sheet autograft wound closure as soon as practical, and the selective use of axial pin fixation and flaps. This approach is associated with normal function in 97% of those with superficial injuries and 81% of those with deep dermal and full-thickness injuries requiring surgery. Although only 9% of those with injuries involving the extensor mechanism, joint capsule, or bone had normal functional outcomes, 90% were able to independently perform activities of daily living. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02114. RP SHERIDAN, RL (reprint author), MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. NR 30 TC 61 Z9 61 U1 1 U2 6 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Inf. Crit. Care PD MAR PY 1995 VL 38 IS 3 BP 406 EP 411 DI 10.1097/00005373-199503000-00022 PG 6 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA RD561 UT WOS:A1995RD56100022 PM 7897728 ER PT J AU BROMLEY, B BENACERRAF, BR AF BROMLEY, B BENACERRAF, BR TI THE RESOLVING NUCHAL FOLD IN 2ND TRIMESTER FETUSES - NOT NECESSARILY REASSURING SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Note ID DOWNS-SYNDROME; HYGROMA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 6 TC 12 Z9 12 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 MAR PY 1995 VL 14 IS 3 BP 253 EP 255 PG 3 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA QJ073 UT WOS:A1995QJ07300014 PM 7760473 ER PT J AU BARRY, MJ AF BARRY, MJ TI CORRELATION OF AMERICAN-UROLOGICAL-ASSOCIATION SYMPTOM INDEX WITH OBSTRUCTIVE AND NONOBSTRUCTIVE PROSTATISM - COMMENT SO JOURNAL OF UROLOGY LA English DT Editorial Material RP BARRY, MJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA, 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 0022-5347 J9 J UROLOGY JI J. Urol. PD MAR PY 1995 VL 153 IS 3 BP 679 EP 679 PN 1 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA QF630 UT WOS:A1995QF63000036 ER PT J AU IINUMA, S BACHOR, R FLOTTE, T HASAN, T AF IINUMA, S BACHOR, R FLOTTE, T HASAN, T TI BIODISTRIBUTION AND PHOTOTOXICITY OF 5-AMINOLEVULINIC ACID-INDUCED PPIX IN AN ORTHOTOPIC RAT BLADDER-TUMOR MODEL SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; AMINOLEVULINIC ACID; PROTOPORPHYRINS; PHOTOCHEMOTHERAPY ID PHOTODYNAMIC THERAPY; CLINICAL-EXPERIENCE; CARCINOMA; PHOTOSENSITIZERS; PROTOPORPHYRIN; PHTHALOCYANINE; FLUORESCENCE; PORPHYRINS; CANCER; CELLS AB 5-Aminolevulinic acid (ALA) is a precursor of heme biosynthesis. In the penultimate step of this biosynthesis, protoporphyrin IX (PpIX), an effective photosensitizer, is generated. In this study, the biodistribution and photodynamic effect of ALA-induced PpIX were investigated in an orthotopic rat bladder tumor model. A quantitative comparison of PpIX biodistribution by extraction and fluorescence spectroscopy following intravenous and intravesical administration of ALA was made. The tumor to normal bladder wall ratio was 2:1 at 4 hours for both delivery modes. Fluorescence microscopy demonstrated predominantly cellular rather than stromal PpIX fluorescence. Phototoxicity, evaluated 4 hours after ALA administration, was light dose-dependent with the most efficient tumor necrosis being observed upon 150 J/cm.(2) of 630 nm. irradiation. These data suggest that optimized photodynamic therapy with ALA-induced PpIX may be an alternative treatment for superficial bladder carcinoma. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT UROL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 18 TC 55 Z9 57 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAR PY 1995 VL 153 IS 3 BP 802 EP 806 DI 10.1016/S0022-5347(01)67726-7 PN 1 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA QF630 UT WOS:A1995QF63000084 PM 7861543 ER PT J AU RIVITZ, SM GELLER, SC HAHN, C WALTMAN, AC AF RIVITZ, SM GELLER, SC HAHN, C WALTMAN, AC TI TREATMENT OF ACUTE MESENTERIC VENOUS THROMBOSIS WITH TRANSJUGULAR INTRAMESENTERIC UROKINASE INFUSION SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Discussion DE PORTAL VEIN, THROMBOLYSIS; PORTAL VEIN, THROMBOSIS; THROMBOSIS, VENOUS; VEINS, MESENTERIC ID PORTAL-VEIN THROMBOSIS C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. RP RIVITZ, SM (reprint author), MASSACHUSETTS GEN HOSP,DIV VASC RADIOL,POB 9657,BOSTON,MA 02114, USA. NR 12 TC 52 Z9 54 U1 0 U2 1 PU SOC CARDIOVASCULAR INTERVENTIONAL RADIOLOGY PI FAIRFAX PA 10201 LEE HWY, SUITE 160, FAIRFAX, VA 22030-2224 SN 1051-0443 J9 J VASC INTERV RADIOL JI J. Vasc. Interv. Radiol. PD MAR-APR PY 1995 VL 6 IS 2 BP 219 EP 223 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA QR539 UT WOS:A1995QR53900010 PM 7787355 ER PT J AU CONTE, MS CHOUDHRY, RP SHIRAKOWA, M FALLON, JT BIRINYI, LK AF CONTE, MS CHOUDHRY, RP SHIRAKOWA, M FALLON, JT BIRINYI, LK TI ENDOTHELIAL-CELL SEEDING FAILS TO ATTENUATE INTIMAL THICKENING IN BALLOON-INJURED RABBIT ARTERIES SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID RESTENOSIS FOLLOWING ANGIOPLASTY; VASCULAR GRAFTS; SMOOTH-MUSCLE; CORONARY ANGIOPLASTY; SAPHENOUS-VEIN; CANINE MODEL; HOLY-GRAIL; HYPERPLASIA; PROLIFERATION; PREVENTION AB Background: Restenosis of arteries or bypass grafts after vascular reconstruction is a common clinical entity that significantly limits long-term patency. This process, termed intimal hyperplasia (IH), is characterized by smooth muscle cell proliferation in the intima and subsequent accumulation of intercellular matrix. This study was designed to test the hypothesis that endothelial cell (EC) seeding of acutely injured arteries accelerates reendothelialization of the flow surface and limits the development of IH. Methods: ECs were harvested from jugular veins of New Zealand white rabbits (n = 13) and were amplified in tissue culture. Each animal subsequently underwent bilateral balloon catheter injury of the iliofemoral arteries; one side was immediately seeded with cultured autologous ECs at supraconfluent density, whereas the contralateral vessel served as a nonseeded control. Animals were killed 33 +/- 5 days after balloon injury. Intimal thickening was quantitated on histologic sections of vessels (three sections per vessel, total of 60 sections) and percent endothelialization was assessed by SEM; measurements were obtained by use of computer-aided morphometry performed by a blinded observer. Data were analyzed by use of a paired t test for comparison between seeded and control vessels. Results: Seeded vessels exhibited a greater degree of reendothelialization (93.9% +/- 7.6% of the surface) than their unseeded counterparts (65.1% +/- 22.5%, p < 0.01). Intimal cross-sectional area and the ratio of intimal area to medial area were not significantly different between seeded and control vessels (intima: 0.32 +/- 0.19 vs 0.37 +/- 0.11 mm(2), p = 0.28; intimal area to medial area ratio: 0.84 +/- 0.35 vs 1.02 +/- 0.2, p = 0.24). Conclusions: We conclude that seeding with autologous venous ECs accelerated restoration of the endothelial monolayer but failed to attenuate IK in balloon-injured rabbit arteries. Further studies are necessary to determine the functional properties of seeded endothelium and to examine the effect of EC seeding on intimal thickening in other clinically relevant models. C1 BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-43771]; NIGMS NIH HHS [T32GM07560] NR 36 TC 35 Z9 35 U1 0 U2 1 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 MAR PY 1995 VL 21 IS 3 BP 413 EP 421 DI 10.1016/S0741-5214(95)70283-0 PG 9 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA QL648 UT WOS:A1995QL64800009 PM 7877223 ER PT J AU HARDWICKE, MA SCHAFFER, PA AF HARDWICKE, MA SCHAFFER, PA TI CLONING AND CHARACTERIZATION OF HERPES-SIMPLEX VIRUS TYPE-1 ORIL - COMPARISON OF REPLICATION AND PROTEIN-DNA COMPLEX-FORMATION BY ORIL AND ORIS SO JOURNAL OF VIROLOGY LA English DT Article ID ORIGIN-BINDING-PROTEIN; GENE-PRODUCT; S-COMPONENT; UL9 PROTEIN; SEQUENCE; MOLECULES; ANATOMY; IDENTIFICATION; POPULATIONS; EXPRESSION AB The herpes simplex virus type 1 genome contains three origins of DNA replication: two copies of oriS and one copy of oriL. Although oriS has been characterized extensively, characterization of oriL has been severely limited by the inability to amplify oriL sequences in an undeleted form in Escherichia coli. We report the successful cloning of intact oriL sequences in an E. coli strain, SURE, which contains mutations in a series of genes involved in independent DNA repair pathways shown to be important in the rearrangement and deletion of DNA containing irregular structures such as palindromes. The oriL-containing clones propagated in SURE cells contained no deletions, as determined by Southern blot hybridization and DNA sequence analysis, and were replication competent in transient DNA replication assays. Deletion of 400 bp of flanking sequences decreased the replication efficiency of oriL twofold in transient assays, demonstrating a role for flanking sequences in enhancing replication efficiency. Comparison of the replication efficiencies of an 822-bp oriS-containing plasmid and an 833-bp oriL-containing plasmid demonstrated that the kinetics of replication of the two plasmids were similar but that the oriL-containing plasmid replicated 60 to 70% as efficiently as the oriS-containing plasmid at both early and late times after infection dth herpes simplex virus type 1. The virus-specified origin-binding protein (OBP) and a cellular factor(s) (OF-1) have been shown in gel mobility shift experiments to bind specific sequences in oriS (C. E. Dabrowski, P. Carmillo, and P. A. Schaffer, Mol. Cell. Biol. 14:2545-2555, 1994; C. E. Dabrowski and P. A. Schaffer, J. Virol. 65:3140-3154 1991). Although the nucleotides required for the binding of OBP to PBP binding site I in oriL and oriS are the same, a single nucleotide difference distinguishes OBP binding site III in the two origins. The nucleotides adjacent to oriS sites I and III have been shown to be important for the binding of OF-1 to oriS site I. Several nucleotide differences exist in these sequences in oriL and oriS. Despite these minor nucleotide differences, the protein-DNA complexes that formed with oriL and oriS sites I and III were indistinguishable when extracts of infected and uninfected cells were used as the source pf protein. Furthermore, the results of competition analysis suggest that the proteins involved in protein-DNA complex formation with sites I and III of the two origins are likely the same. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [F32AI08878, R01AI28537] NR 41 TC 27 Z9 27 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 MAR PY 1995 VL 69 IS 3 BP 1377 EP 1388 PG 12 WC Virology SC Virology GA QG073 UT WOS:A1995QG07300001 PM 7853470 ER PT J AU BERGELSON, JM MOHANTY, JG CROWELL, RL JOHN, NFS LUBLIN, DM FINBERG, RW AF BERGELSON, JM MOHANTY, JG CROWELL, RL JOHN, NFS LUBLIN, DM FINBERG, RW TI COXSACKIEVIRUS B3 ADAPTED TO GROWTH IN RD CELLS BINDS TO DECAY-ACCELERATING FACTOR (CD55) SO JOURNAL OF VIROLOGY LA English DT Note ID RHABDOMYOSARCOMA CELLS; NORMAL INDIVIDUALS; CELLULAR RECEPTOR; MEASLES-VIRUS; COMPLEMENT; MEMBRANE; PROTEIN; HELA; INFECTION; CLONING AB A coxsackievirus B3 (CB3) isolate adapted to growth in RD cells shows an alteration in cell tropism as a result of its capacity to bind a 70-kDa cell surface molecule expressed on these cells, We now show that this molecule is the complement regulatory protein, decay-accelerating factor (DAF) (CD55), Anti-DAF antibodies prevented CB3 attachment to the cell surface. Radiolabeled CB3 adapted to growth in RD cells bound to CHO cells transfected with human DAF, whereas CB3 (strain Nancy), the parental strain, did not bind to DAF transfectants. These results indicate that growth of CB3 in RD cells selected for a virus strain that uses DAF for cell surface attachment, C1 HAHNEMANN UNIV,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19102. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. RP BERGELSON, JM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,JIMMY FUND 409,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI 03771, AI 31628, AI 34580] NR 25 TC 151 Z9 155 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAR PY 1995 VL 69 IS 3 BP 1903 EP 1906 PG 4 WC Virology SC Virology GA QG073 UT WOS:A1995QG07300064 PM 7531780 ER PT J AU ROBERTSON, MJ MANLEY, TJ PICHERT, G CAMERON, C COCHRAN, KJ LEVINE, H RITZ, J AF ROBERTSON, MJ MANLEY, TJ PICHERT, G CAMERON, C COCHRAN, KJ LEVINE, H RITZ, J TI FUNCTIONAL CONSEQUENCES OF APO-1/FAS (CD95) ANTIGEN EXPRESSION BY NORMAL AND NEOPLASTIC HEMATOPOIETIC-CELLS SO LEUKEMIA & LYMPHOMA LA English DT Review DE CD95; APO-1; FAS; APOPTOSIS; PROGRAMMED CELL DEATH AB Murine monoclonal antibody (mAb) 7C11 binds to the same cell surface epitope as anti-APO-1 and anti-Fas and reacts specifically with cells transfected with a cDNA encoding the human Fas antigen. Furthermore, incubation with 7C11 causes death of hematopoietic cell lines that express APO-1/Fas but not APO-1/Fas-negative cell lines. 7C11 therefore recognizes the human APO-1/Fas (CD95) antigen, a 40 to 50 kDa cell surface glycoprotein that can trigger apoptosis or programmed cell death, Expression of APO-1/Fas antigen by normal and neoplastic hematopoietic cells was determined by flow cytometry using 7C11. APO-1/Fas is expressed by similar to 30 to 40% of resting peripheral blood T cells, B cells, and monocytes and by similar to 5% of resting NK cells and thymocytes. It was not detected on granulocytes, erythrocytes, or platelets. Approximately 80 to 90% of activated T cells, B cells, and thymocytes express APO-1/Fas, as do the majority of activated NK cells. Perturbation of APO-1/Fas by 7C11 does not affect the viability of resting lymphocytes or monocytes. In contrast, activated T cells and NK cells undergo apoptosis within 3 hours of exposure to 7C11. Other mAb that stimulate T cells or NK cells do not cause rapid induction of programmed cell death. APO-1/Fas antigen is expressed by many cell lines of lymphoid and myeloid lineage. However, this antigen was detected on neoplastic cells from only one of 69 patients with acute myeloid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, chronic lymphocytic leukemia, or multiple myeloma. Only 3 out of 25 tumor samples from patients with non-Hodgkin's lymphoma were found to express APO-1/Fas. All three of these lymphomas harbored the bcl-2-Ig fusion gene associated with the chromosomal translocation t(14;18). Conversely, only 27% of lymphomas that possessed the bcl-2-Ig gene were found to express the APO-1/Fas antigen. Like normal activated lymphocytes, leukemia and lymphoma cells that expressed APO-1/Fas antigen were found to undergo apoptosis in vitro after incubation with 7C11. The APO-1/Fas antigen appears to regulate the growth of normal hematopoietic cells, and the marked upregulation of this antigen on activated normal lymphocytes contrasts sharply with the absence of APO-1/Fas on neoplastic cells of hematopoietic lineage. Defects in the apoptotic signal delivered through this antigen might contribute to the pathogenesis of hematopoietic neoplasms. Thus, the gene encoding APO-1/Fas can be considered a novel type of tumor suppressor gene, just as bcl-2 can be considered a cellular proto-oncogene. RP ROBERTSON, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,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-01730, CA-41619] NR 0 TC 95 Z9 96 U1 0 U2 0 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PD MAR PY 1995 VL 17 IS 1-2 BP 51 EP 61 DI 10.3109/10428199509051703 PG 11 WC Oncology; Hematology SC Oncology; Hematology GA QJ899 UT WOS:A1995QJ89900007 PM 7539660 ER PT J AU SEIDEN, MV SCHLOSSMAN, R ANDERSEN, J FREEMAN, A ROBERTSON, M SOIFFER, R FREEDMAN, A MAUCH, P RITZ, J NADLER, L ANDERSON, KC AF SEIDEN, MV SCHLOSSMAN, R ANDERSEN, J FREEMAN, A ROBERTSON, M SOIFFER, R FREEDMAN, A MAUCH, P RITZ, J NADLER, L ANDERSON, KC TI MONOCLONAL ANTIBODY-PURGED BONE-MARROW TRANSPLANTATION THERAPY FOR MULTIPLE-MYELOMA SO LEUKEMIA & LYMPHOMA LA English DT Article DE MULTIPLE MYELOMA; BONE MARROW TRANSPLANTATION AB This report describes the clinical characteristics, treatment associated toxicity, and follow-up of fifty-eight patients with plasma cell-dyscrasias treated with high dose chemotherapy and total body irradiation (TBI) at a single institution. Following TBI, 36 patients received anti-B cell monoclonal antibody (MoAb)-treated autologous bone marrow, 21 patients received anti-CD6 cell MoAb-treated allogeneic bone marrow to deplete T cells, and one patient received unpurged bone marrow from a syngeneic donor, Evaluation after high dose chemotherapy and bone marrow transplantation (BMT) demonstrated 26 complete responses (CR), 26 partial responses (PR), 2 non-responders, 1 not yet evaluated, and three toxic deaths. Fourteen of 36 patients who underwent autologous BMT are alive free from progression at 18 (range 5 to 68) months post transplant (post-BMT); of these, 11 remain in continuous complete response at 16 (range 5 to 68) months post-BMT. Seven of 21 patients who underwent allogeneic BMT are alive free from progression at 30 (range 4 to 44) months post-BMT; of these, three patients remain in continuous complete response at 43 (range 33 to 45) months post-BMT, These data suggest that high dose chemotherapy with TBI followed by MoAb purged BM can be performed with acceptable toxicity and high tumor response rates. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA06516, CA50947]; NIAID NIH HHS [AI29530] NR 0 TC 26 Z9 27 U1 0 U2 2 PU HARWOOD ACAD PUBL GMBH PI READING PA C/O STBS LTD, PO BOX 90, READING, BERKS, ENGLAND RG1 8JL SN 1042-8194 J9 LEUKEMIA LYMPHOMA JI Leuk. Lymphoma PD MAR PY 1995 VL 17 IS 1-2 BP 87 EP 93 DI 10.3109/10428199509051707 PG 7 WC Oncology; Hematology SC Oncology; Hematology GA QJ899 UT WOS:A1995QJ89900011 PM 7773166 ER PT J AU WEDEEN, VJ WEISSKOFF, RM REESE, TG BEACHE, GM PONCELET, BP ROSEN, BR DINSMORE, RE AF WEDEEN, VJ WEISSKOFF, RM REESE, TG BEACHE, GM PONCELET, BP ROSEN, BR DINSMORE, RE TI MOTIONLESS MOVIES OF MYOCARDIAL STRAIN-RATES USING STIMULATED ECHOES SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article DE CARDIAC MRI; GATING TECHNIQUES; STRAIN ID HEART AB We present methods to acquire and analyze NMR movies of myocardial strain rates in which cardiac motion is suppressed and the histories of strain rates are accurately defined for each voxel of myocardial tissue. By means of stimulated echoes, the myocardial strain-rate tenser is phase-encoded at progressive delays in the cardiac cycle while the slice-select and spatial encoding of the image acquisition are performed at a constant cardiac delay. In these data, every image shows the identical myocardial tissue, and the anatomic configuration of the heart appears motionless. The myocardial strain-rate data, however, indicate the state of motion which existed in this slice at the time of the velocity phase-encoding, and these data evolve with the progressive delay as a movie. Using echo-planar MRI, motionless movies of myocardial strain rate of four to eight cardiac delays are obtained in a breath-hold. As an application, a quantitative characterization of cardiac mechanical synchrony is accomplished by principal component analysis (PCA) of the time series of strain rates. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. FU NHLBI NIH HHS [3-R01 HL-39810] NR 12 TC 24 Z9 24 U1 0 U2 2 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 MAR PY 1995 VL 33 IS 3 BP 401 EP 408 DI 10.1002/mrm.1910330313 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QK086 UT WOS:A1995QK08600012 PM 7760707 ER PT J AU KWONG, KK WANKE, I DONAHUE, KM DAVIS, TL ROSEN, BR AF KWONG, KK WANKE, I DONAHUE, KM DAVIS, TL ROSEN, BR TI EPI IMAGING OF GLOBAL INCREASE OF BRAIN MR SIGNAL WITH BREATH-HOLD PRECEDED BY BREATHING O-2 SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note DE EPI; BRAIN MRI; BREATH-HOLD; O-2 ID BLOOD OXYGENATION; TIME AB Brain MR signal has been observed to decrease during cessation of breathing due to the increase of deoxyhemoglobin in the blood. However, for both animal and human studies, we have demonstrated that if the subjects breathed 100% oxygen in advance of apnea for a short time, T-2*-weighted MR brain signal increased when breathing was stopped for a period of 30-60 s. This demonstrates the possibility of measuring responses to hemodynamic change throughout the entire brain with a single respiratory perturbation in a rapid, reliable, and robust manner. C1 HARVARD MIT,DIV HLTH SCI & TECHNOL,BOSTON,MA. RP KWONG, KK (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR NMR 2301,DEPT RADIOL,BLDG 19,13TH ST,BOSTON,MA 02129, USA. NR 17 TC 32 Z9 32 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 MAR PY 1995 VL 33 IS 3 BP 448 EP 452 DI 10.1002/mrm.1910330322 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QK086 UT WOS:A1995QK08600021 PM 7760716 ER PT J AU KWONG, KK AF KWONG, KK TI FUNCTIONAL MAGNETIC-RESONANCE-IMAGING WITH ECHO-PLANAR IMAGING SO MAGNETIC RESONANCE QUARTERLY LA English DT Review DE FUNCTIONAL MAGNETIC RESONANCE IMAGING; T-1 WEIGHTED PERFUSION; T-2 AND T-2(ASTERISK) WEIGHTED OXYGENATION CHANGE; BLOOD OXYGENATION LEVEL DEPENDENT; BRAIN VEIN PROBLEM; INFLOW ARTIFACTS ID HUMAN VISUAL-CORTEX; HUMAN BRAIN ACTIVITY; BLOOD OXYGENATION; ARTERIAL WATER; MOTOR CORTEX; RAT-BRAIN; SENSORY STIMULATION; PHOTIC-STIMULATION; SIGNAL CHANGES; TRANSIT-TIME AB In this report, a review is made of the mechanism behind the functional MRI (fMRI) signals and the advances made in many different areas of fMRI. Such areas include understanding and compensating for artifacts specific to fMRI, postprocessing of fMRI images, the application of fMRI to areas of interest in neuroscience, some interesting new glimpses on the frontiers of studying hemodynamics and metabolic responses, and the effort to combine fMRI results with magnetoencephalography (MEG) and electroencephalography (EEG). C1 HARVARD UNIV, SCH MED, BOSTON, MA USA. RP MASSACHUSETTS GEN HOSP, CTR NMR 2301,MGH,DEPT RADIOL,BLDG 149, 13TH ST, BOSTON, MA 02129 USA. NR 172 TC 166 Z9 168 U1 2 U2 10 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0899-9422 J9 MAGN RESON QUART JI Magn. Reson. Q. PD MAR PY 1995 VL 11 IS 1 BP 1 EP 20 PG 20 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA QW111 UT WOS:A1995QW11100001 PM 7612421 ER PT J AU FORE, WW AF FORE, WW TI NONINSULIN-DEPENDENT DIABETES-MELLITUS - THE PREVENTION OF COMPLICATIONS SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID DISEASE AB Because of the Diabetes Complications and Control Trial, the standard of diabetes mellitus is changing. The emphasis should be placed on the prevention of complications, ana the glucose control and redirection of risk factors should be started before they occur. Noninsulin-dependent diabetes mellitus offers many opportunities and challenges to the primary care physician, and approaches are reviewed and discussed. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,JOSLIN CTR DIABET WILLS & JEFFERSON,PHILADELPHIA,PA 19107. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MED,DIV ENDOCRINOL,PHILADELPHIA,PA 19107. NR 11 TC 14 Z9 19 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1995 VL 79 IS 2 BP 287 EP 298 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA QN027 UT WOS:A1995QN02700005 PM 7877391 ER PT J AU APPLEBY, J AF APPLEBY, J TI MANAGEMENT OF THE ABNORMAL PAPANICOLAOU SMEAR SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Article ID IMMUNODEFICIENCY-VIRUS-INFECTION; CERVICAL INTRAEPITHELIAL NEOPLASIA; PAP SMEAR; BACTERIAL VAGINOSIS; SEROPOSITIVE WOMEN; CANCER DETECTION; CERVICOGRAPHY; RISK; COLPOSCOPY; PREVENTION AB This article briefly reviews the natural history and epidemiology of cervical neoplasia and discusses the strengths and weaknesses of cytologic screening. The authors also review systems of reporting cytology results and outline approaches to management of the abnormal smear, including management of infectious, inflammatory, atypical, and remalignant changes. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP APPLEBY, J (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN MED,SAN ANTONIO,TX 78284, USA. NR 68 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1995 VL 79 IS 2 BP 345 EP 360 PG 16 WC Medicine, General & Internal SC General & Internal Medicine GA QN027 UT WOS:A1995QN02700009 PM 7877395 ER PT J AU LYNN, RB FRIEDMAN, LS AF LYNN, RB FRIEDMAN, LS TI IRRITABLE-BOWEL-SYNDROME - MANAGING THE PATIENT WITH ABDOMINAL-PAIN AND ALTERED BOWEL HABITS SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Review ID FUNCTIONAL GASTROINTESTINAL DISORDERS; INTESTINAL MOTILITY; PSYCHOLOGICAL TREATMENT; MYOELECTRIC ACTIVITY; COLONIC MOTILITY; MANNING CRITERIA; CONTROLLED TRIAL; UNITED-STATES; TRANSIT-TIME; STOOL WEIGHT AB Irritable bowel syndrome is a common complex of syndromes thought to be generated by a motility or sensory disturbance of the gastrointestinal tract. It is a frequent cause of chronic abdominal pain and altered bowel habits. Patients who seek medical attention for irritable bowel syndrome often do so because of psychosocial factors. Therapy remains largely empirical, directed toward the relief of symptoms in the context of a supportive physician-patient relationship. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,DEPT MED,PHILADELPHIA,PA 19107. HARVARD UNIV,SCH MED,BOSTON,MA. FU NIDDK NIH HHS [DK02094] NR 107 TC 11 Z9 12 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 MAR PY 1995 VL 79 IS 2 BP 373 EP 390 PG 18 WC Medicine, General & Internal SC General & Internal Medicine GA QN027 UT WOS:A1995QN02700011 PM 7877397 ER PT J AU OKEEFE, M HUNT, DK AF OKEEFE, M HUNT, DK TI ASSESSMENT AND TREATMENT OF IMPOTENCE SO MEDICAL CLINICS OF NORTH AMERICA LA English DT Review ID NOCTURNAL PENILE TUMESCENCE; VACUUM CONSTRICTION DEVICE; NEGATIVE-PRESSURE DEVICE; ERECTILE IMPOTENCE; SEXUAL DYSFUNCTION; BRACHIAL INDEX; BULBOCAVERNOSUS REFLEX; VASCULOGENIC IMPOTENCE; DUPLEX ULTRASONOGRAPHY; ARTERIOGENIC IMPOTENCE AB Impotence is a common problem but is often neglected or inappropriately assessed and treated. Assessment should be focused toward causes of impotence that have specific treatments: psychogenic, drug induced, hormonal, and vascular. Specific treatments available are sexual counseling, medication adjustment, hormone therapy, and vascular surgery. When impotence is neuropathic, of mixed etiology and/or unresponsive to disease-specific treatments, therapy should be determined by patient preference. Options include vacuum erection devices, penile self-injection therapy, and penile prosthesis. There is less evidence supporting the use of yohimbine, topical nitrates, or minoxidil. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. RP OKEEFE, M (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,OFF AMBULATORY CARE 11C,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 104 TC 18 Z9 18 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0025-7125 J9 MED CLIN N AM JI Med. Clin. N. Am. PD MAR PY 1995 VL 79 IS 2 BP 415 EP 434 PG 20 WC Medicine, General & Internal SC General & Internal Medicine GA QN027 UT WOS:A1995QN02700013 PM 7877399 ER PT J AU TOMERA, JF LILFORD, K AF TOMERA, JF LILFORD, K TI COMODULATION BETWEEN ACETYLCHOLINESTERASE AND CYCLIC-NUCLEOTIDE SIGNAL-TRANSDUCTION SYSTEMS IN BURN TRAUMA SO METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY LA English DT Article DE ACHE; BURN TRAUMA; CYCLIC AMP; CYCLIC GMP; SIGNAL TRANSDUCTION; MULTIVARIATE ANALYSIS; VECTORIAL ANALYSIS ID MULTIPLE-REGRESSION; 16S ACETYLCHOLINESTERASE; MULTIVARIATE INFLUENCE; GASTROCNEMIUS-MUSCLE; INOSITOL PHOSPHATES; SKELETAL-MUSCLE; RISK FACTOR; MECHANISMS; MOUSE; ENDOTOXIN AB Signal transduction systems (sts(s)) and acetylcholinesterase (AChE) levels ill skeletal muscle distantly located from the site of large body surface area (BSA) burns are due to the systemic effects of burn trauma. Evaluating the guanylate and adenylate cyclase sts(s), by measuring adenosine 3':5'-phosphate (cyclic AMP) and guanosine 3':5'-phosphate (cyclic GMP) by radioimmunoassay with polymorphic forms of AChE demonstrated that the various systems (i.e., cyclic GMP and AChE) interact while under the duress of burn trauma. This trauma emanates from large skin bunts (30-50% BSA) that have induced a chronic burn trauma response at postburn day 21. This study showed that a system, with a minimum of 2 components, regulated cyclic AMP levels. This paper provides insight into our current understanding of the effects of burn burn trauma on cellular signalling and discusses some of the potential implications of recent findings on long term rehabilitative care. C1 SHRINERS BURN INST,ANESTHESIA SERV,CLIN PHARMACOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA. NR 52 TC 7 Z9 7 U1 0 U2 0 PU J R PROUS SA PI BARCELONA PA APARTADO DE CORREOS 540, 08080 BARCELONA, SPAIN SN 0379-0355 J9 METHOD FIND EXP CLIN JI Methods Find. Exp. Clin. Pharmacol. PD MAR PY 1995 VL 17 IS 2 BP 89 EP 105 PG 17 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA RB860 UT WOS:A1995RB86000002 PM 7674703 ER PT J AU SHIEH, HL HANSEN, H ZHU, JW RIEDEL, H AF SHIEH, HL HANSEN, H ZHU, JW RIEDEL, H TI DIFFERENTIAL PROTEIN-KINASE-C LIGAND REGULATION DETECTED IN-VIVO BY A PHENOTYPIC YEAST ASSAY SO MOLECULAR CARCINOGENESIS LA English DT Article DE DRUG SCREENING; INDOLACTAM V; MEZEREIN; PHORBOL ESTER TUMOR PROMOTER; SACCHAROMYCES CEREVISIAE ID PHORBOL ESTER RECEPTOR; TUMOR PROMOTERS; SACCHAROMYCES-CEREVISIAE; SYNTHETIC ANALOGS; CATALYTIC DOMAINS; ACTIVATION; BINDING; REGIONS; ALPHA; AUTOPHOSPHORYLATION AB The molecular dissection of protein kinase C (PKC) action has been based in part on time-consuming functional assays such as the mouse skin model for testing the tumor promoter activity of phorbol esters and related PKC activators. To help overcome the limitations imposed by the complexity of such assays, we developed the yeast Saccharomyces cerevisiae as an alternative, rapid, and simple experimental system. This model has a specific phenotype, an increase in the cell doubling time, that is proportional to the level of enzymatic activity of expressed mammalian PKC isoforms. We used this phenotype to assay and compare the regulation of native bovine PKC alpha and mutants in the conserved regulatory region C1 in vivo by various activators: two diterpenes, the phorbol ester phorbol-12-myristate-13-acetate (PMA) and mezerein, and the indole alkaloid indolactam V. We found that PMA activated PKC mutants lacking either Cys-rich, zinc finger-like repeat of the conserved region C1 to comparably reduced levels, whereas indolactam V activated native PKC alpha but none of the mutants at normal doses. in contrast, mezerein activated native PKC alpha and a mutant lacking the second Cys repeat equally well but mutants lacking the first Cys repeat of C1 at a greatly reduced level. These differential responses were supported by the observed in vitro PKC catalytic activities. Therefore, PMA regulates PKC alpha activity comparably well via either Cys repeat, whereas mezerein regulation predominantly occurs via the first Cys repeat of C1. Indolactam V activation was less potent, it was greatly reduced in the absence of either Cys repeat, and displayed no preference. We introduce this phenotypic assay as a rapid and general screen for the PKC-activating or possibly inhibitory potential of drug candidates and to identify the PKC regulatory sites involved in these interactions. (C) 1995 Wiley-Liss, Inc. C1 JOSLIN DIABET CTR,MOLEC BIOL SECT,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. NR 70 TC 33 Z9 33 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0899-1987 J9 MOL CARCINOGEN JI Mol. Carcinog. PD MAR PY 1995 VL 12 IS 3 BP 166 EP 176 DI 10.1002/mc.2940120308 PG 11 WC Biochemistry & Molecular Biology; Oncology SC Biochemistry & Molecular Biology; Oncology GA QR271 UT WOS:A1995QR27100007 PM 7893369 ER PT J AU REDMOND, JMT MCKENNA, MJ FEINGOLD, M AHMAD, BK AF REDMOND, JMT MCKENNA, MJ FEINGOLD, M AHMAD, BK TI SENSORY TESTING IS DIFFERENT IN LABORATORY PERSONNEL COMPARED WITH PAID VOLUNTEERS SO MUSCLE & NERVE LA English DT Note ID THRESHOLDS C1 HENRY FORD HOSP,DEPT NEUROL,NEUROPHYSIOL LAB,DETROIT,MI 48202. HENRY FORD HOSP,DEPT MED,DETROIT,MI 48202. HENRY FORD HOSP,DIV BIOSTAT RES EPIDEMIOL & COMP,DETROIT,MI 48202. MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,BOSTON,MA 02114. OI McKenna, Malachi/0000-0002-6564-7011 NR 6 TC 3 Z9 3 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 MAR PY 1995 VL 18 IS 3 BP 351 EP 352 DI 10.1002/mus.880180316 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA QH827 UT WOS:A1995QH82700015 PM 7870117 ER PT J AU EZEKOWITZ, RAB AF EZEKOWITZ, RAB TI AGALACTOSYL IGC AND MANNOSE-BINDING PROTEINS - BIOCHEMICAL NICETY OR PATHOPHYSIOLOGICAL PARADIGM SO NATURE MEDICINE LA English DT Editorial Material ID COMPLEMENT PATHWAY; CLASSICAL PATHWAY; ASSOCIATION; PATTERN; DEFECT; FORMS; CLQ C1 CHILDRENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. RP EZEKOWITZ, RAB (reprint author), HARVARD UNIV,CHILDRENS HOSP,DEPT PEDIAT,DIV HEMATOL & INFECT DIS,BOSTON,MA 02115, USA. NR 20 TC 4 Z9 4 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD MAR PY 1995 VL 1 IS 3 BP 207 EP 208 DI 10.1038/nm0395-207 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA QX559 UT WOS:A1995QX55900022 PM 7585032 ER PT J AU GREEN, RC BENJAMIN, S CUMMINGS, JL AF GREEN, RC BENJAMIN, S CUMMINGS, JL TI FELLOWSHIP PROGRAMS IN BEHAVIORAL NEUROLOGY SO NEUROLOGY LA English DT Review ID NEUROPSYCHIATRY AB We sent a behavioral neurology fellowship questionnaire to each of the training directors of 160 neurology residency programs throughout the world, seeking information about programs offering advanced training in behavioral neurology (or similar fellowships in cognitive neurology, neurobehavior, or cognitive neuroscience). Response rate was 100%. Thirty-four respondents reported active fellowship programs in behavioral neurology, and 28 additional respondents indicated that a behavioral neurology fellowship was planned. Nine of the 34 programs (26.5%) defined themselves as exclusively or predominantly concerned with dementia and age-related neurobehavioral disorders. Directors of the 34 active fellowship programs estimated that their combined programs had graduated 199 fellows and were currently training fifty. Most fellowships concentrated on outpatient clinical training, with teaching required by 78.1% and research required by 81.8%. Specialty certification for behavioral neurology was favored by over 75% of behavioral neurology fellowship training directors but by only 30% of training directors in residency programs without behavioral neurology fellowships. Behavioral neurology training programs have grown dramatically in response to an increased recognition of the academic interest in and the clinical needs for these services. C1 EMORY UNIV,SCH MED,DEPT NEUROL,NEUROBEHAV PROGRAM,ATLANTA,GA 30322. UNIV MASSACHUSETTS,MED CTR,DEPT PSYCHIAT,NEUROPSYCHIAT PROGRAM,WORCESTER,MA 01655. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,BEHAV NEUROSCI SECT,LOS ANGELES,CA 90073. RP GREEN, RC (reprint author), EMORY UNIV,WESLEY WOODS CTR,NEUROBEHAV PROGRAM,1841 CLIFTON RD NE,ATLANTA,GA 30329, USA. FU NIA NIH HHS [P30AG10130] NR 10 TC 2 Z9 2 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 MAR PY 1995 VL 45 IS 3 BP 412 EP 415 PN 1 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA QM902 UT WOS:A1995QM90200002 PM 7898686 ER PT J AU GILLIAM, FG CHIAPPA, KH AF GILLIAM, FG CHIAPPA, KH TI SIGNIFICANCE OF SPONTANEOUS EPILEPTIFORM ABNORMALITIES ASSOCIATED WITH A PHOTOPAROXYSMAL RESPONSE SO NEUROLOGY LA English DT Article ID PHOTOSENSITIVITY AB Spontaneous epileptiform abnormalities (SEAs) are reported to occur in up to 65% of patients with a photoparoxysmal response (PPR). Although the PPR is usually assumed to indicate primary generalized epilepsy, the clinical significance of associated SEAs is not known. We conducted the first study designed to correlate seizure classification with type of SEA in photosensitive patients. We examined seizure classifications and SEAs in 115 consecutive patients who had a PPR. A PPR was the only epileptiform abnormality in 47 patients (41%). Twenty-seven patients (24%) had focal SEAs and 41 (36%) had only generalized SEAs. Seventeen patients (15%) had partial seizures and 40 (35%) had only generalized seizures. Seizure classification was strongly associated with type of SEA ip < 0.0001). Patients with focal SEAs tended to have partial seizures, while patients with generalized SEAs tended to have only generalized tonic-clonic or absence seizures. Also, the presence of SEAs was significantly associated with a history of seizures (p < 0.0001), compared with patients who had a PPR but no SEAs. Although the PPR is often presumed to signify primary generalized epilepsy, most patients with a PPR and focal SEAs have partial seizures. C1 MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LAB,BOSTON,MA 02114. NR 14 TC 8 Z9 8 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 MAR PY 1995 VL 45 IS 3 BP 453 EP 456 PN 1 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA QM902 UT WOS:A1995QM90200011 PM 7898695 ER PT J AU HUANG, Q ZHOU, D SAPP, E AIZAWA, H GE, P BIRD, ED VONSATTEL, JP DIFIGLIA, M AF HUANG, Q ZHOU, D SAPP, E AIZAWA, H GE, P BIRD, ED VONSATTEL, JP DIFIGLIA, M TI QUINOLINIC ACID-INDUCED INCREASES IN CALBINDIN-D-28K IMMUNOREACTIVITY IN RAT STRIATAL NEURONS IN-VIVO AND IN-VITRO MIMIC THE PATTERN SEEN IN HUNTINGTONS-DISEASE SO NEUROSCIENCE LA English DT Article ID INTRACELLULAR CALCIUM HOMEOSTASIS; GLUTAMATE NEUROTOXICITY; DENDRITIC TRANSPORT; HIPPOCAMPAL-NEURONS; NERVOUS-SYSTEM; SPINY NEURONS; PARVALBUMIN; GROWTH; EXCITOTOXINS; EXPRESSION AB In Huntington's disease striatal neurons undergo marked changes in dendritic morphology and coincidently exhibit an increase in immunoreactive calbindin D-28k (calbindin), a cytosolic calcium-binding protein which is highly abundant in these neurons. Previous studies in the rat striatum have shown that excitotoxic injury, which is linked to a rise in intracellular Ca2+, mimics many of the neurochemical and neuropathological characteristics of Huntington's disease. We speculated, therefore, that the apparent increase in calbindin labeling in Huntington's disease spiny neurons may signal the response to an excitotoxic process. To investigate this possibility, we compared the cellular features of calbindin immunoreactivity in grade 1-4 Huntington's disease cases with those seen in rat striatal neurons in vivo and in vitro following treatment with N-methyl-D-aspartate (NMDA) receptor agonist, quinolinic acid. In human post mortem control cases calbindin immunoreactivity was seen primarily in the somata and proximal dendrites of striatal neurons. In the Huntington's disease cases, calbindin labeling was markedly increased throughout the second and third order dendrites and in spines, and this change was more prevalent in advanced cases (grades 3-4). In the rat brain, two weeks after intrastriatal injection of quinolinic acid (6-20 ng), surviving medium-spiny neurons in the transition zone around the lesion core exhibited a marked increase in calbindin immunoreactivity similar to that seen in Huntington's disease spiny neurons. In more peripheral areas away from the lesion and on the contralateral unlesioned side, calbindin immunostaining was confirmed to somata and proximal dendrites. In situ hybridization histochemistry with an S-35-labeled oligonucleotide probe showed no change or a decrease in calbindin mRNA levels in neurons within the transition zone, suggesting that the observed increase in calbindin staining was not the result of increased transcription. In 12 day old postnatal striatal cultures, 2-6 h exposures to quinolinic acid (0.5 mM) significantly increased the length of neurites exhibiting calbindin immunoreactivity when compared to untreated controls. This effect was blocked by the selective NMDA receptor blocker (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), indicating that an NMDA receptor-mediated mechanism contributed to the change in staining pattern. Results in rats suggest that the subcellular redistribution of calbindin immunoreactivity observed in Huntington's disease spiny neurons may be related to an NMDA receptor-induced excitotoxic process. An increased availability of calbindin protein at dendrites and spines may reflect a greater demand far Ca2+ buffering precipitated by an abnormal rise in intracellular Ca2+. C1 MASSACHUSETTS GEN HOSP, CELLULAR NEUROBIOL LAB, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, MOLEC PATHOL LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. FU NINDS NIH HHS [NS09349, NS16367] NR 44 TC 54 Z9 55 U1 2 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0306-4522 EI 1873-7544 J9 NEUROSCIENCE JI Neuroscience PD MAR PY 1995 VL 65 IS 2 BP 397 EP 407 DI 10.1016/0306-4522(94)00494-P PG 11 WC Neurosciences SC Neurosciences & Neurology GA QL039 UT WOS:A1995QL03900007 PM 7777157 ER PT J AU MULLENIX, PJ DENBESTEN, PK SCHUNIOR, A KERNAN, WJ AF MULLENIX, PJ DENBESTEN, PK SCHUNIOR, A KERNAN, WJ TI NEUROTOXICITY OF SODIUM-FLUORIDE IN RATS SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE FLUORIDE; NEUROTOXICITY; CENTRAL NERVOUS SYSTEM ID ANIMAL DEVELOPMENTAL NEUROTOXICITY; GROWTH-HORMONE SECRETION; SEXUAL DIMORPHISM; BEHAVIORAL ACTS; TIME STRUCTURE; QUANTITATIVE COMPARABILITY; PATTERN-RECOGNITION; HIPPOCAMPUS; BRAIN; SOMATOSTATIN AB Fluoride (F) is known to affect mineralizing tissues, but effects upon the developing brain have not been previously considered. This study in Sprague-Dawley rats compares behavior, body weight, plasma and brain F levels after sodium fluoride (NaF) exposures; during late gestation, at weaning or in adults. For prenatal exposures, dams received injections (SC) of 0.13 mg/kg NaF or saline on gestational days 14-18 or 17-19. Weanlings received drinking water containing 0, 75, 100, or 125 ppm F for 6 or 20 weeks, and 3 month-old adults received water containing 100 ppm F for 6 weeks. Behavior was tested in a computer pattern recognition system that classified acts in a novel environment and quantified act initiations, total times and time structun:s. Fluoride exposures caused sex- and dose-specific behavioral deficits with a common pattern. Males were most sensitive to prenatal day 17-19 exposure, whereas females were more sensitive to weanling and adult exposures. After fluoride ingestion, the severity of the effect on behavior increased directly with plasma F levels and F concentrations in specific brain regions. Such association is important considering that plasma levels in this rat model (0.059 to 0.640 ppm F) are similar to those reported in humans exposed to high levels of fluoride. C1 FORSYTH RES INST,DEPT TOXICOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. EASTMAN DENT CTR,DEPT PEDIAT DENT,ROCHESTER,NY 14621. IOWA STATE UNIV SCI & TECHNOL,VET DIAGNOST LAB,AMES,IA 50011. NR 52 TC 170 Z9 188 U1 1 U2 18 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 MAR-APR PY 1995 VL 17 IS 2 BP 169 EP 177 DI 10.1016/0892-0362(94)00070-T PG 9 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA QG587 UT WOS:A1995QG58700010 PM 7760776 ER PT J AU KINOSIAN, B JEEJEEBHOY, KN AF KINOSIAN, B JEEJEEBHOY, KN TI WHAT IS MALNUTRITION - DOES IT MATTER SO NUTRITION LA English DT Article; Proceedings Paper CT Conference on The Skeleton in the Hospital Closet - 20 Years Later: Malnutrition in Patients with GI Disease, Cancer and AIDS/10th World Congress of Gastroenterology CY OCT 01-07, 1994 CL LOS ANGELES, CA SP NUTRITION ID GASTROINTESTINAL SURGERY; NUTRITIONAL-STATUS; CLINICAL JUDGMENT; PROGNOSTIC INDEX; MEDICAL PATIENTS; IMMUNITY; IMPACT; RISK C1 UNIV TORONTO,ST MICHAELS HOSP,DEPT MED,TORONTO,ON M5B 1W8,CANADA. RP KINOSIAN, B (reprint author), UNIV PENN,VET AFFAIRS MED CTR,DEPT MED,MED SERV,PHILADELPHIA,PA 19104, USA. NR 24 TC 10 Z9 10 U1 0 U2 2 PU NUTRITION PI SYRACUSE PA PO BOX 920, SYRACUSE, NY 13210-0920 SN 0899-9007 J9 NUTRITION JI Nutrition PD MAR-APR PY 1995 VL 11 IS 2 SU S BP 196 EP 197 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QY255 UT WOS:A1995QY25500003 PM 7626900 ER PT J AU HAYES, BH SHORE, JW WESTFALL, CT HARRIS, GJ AF HAYES, BH SHORE, JW WESTFALL, CT HARRIS, GJ TI MANAGEMENT OF ORBITAL AND PERIORBITAL ARTERIOVENOUS-MALFORMATIONS SO OPHTHALMIC SURGERY AND LASERS LA English DT Article ID THERAPEUTIC EMBOLIZATION; VASCULAR MALFORMATIONS; ANGIOGRAPHY; LESIONS; FACE; HEAD AB Arteriovenous malformations (AVMs) of the orbit are progressively enlarging communications between arteries and veins that bypass normal capillary beds. In contrast to arteriovenous fistulas (AVFs), AVMs are congenital lesions with multiple large feeding arteries, a central nidus, and numerous dilated draining veins. Management of AVMs of the orbit may be difficult due to the threat of hemorrhage, vascular occlusion during treatment, and collateral damage to surrounding organs. We managed AVM of the orbit and periorbital tissues in four patients. Neuroimaging studies, clinical decision making, operative experience, and longterm postoperative results were retrospectively reviewed. Four cases of AVM of the orbit and periorbital tissues were successfully treated with preoperative embolization and subsequent excision of the central nidus of the AVM. There was no evidence of recurrence in any of the cases over follow up ranging from 2 to 5 years. We conclude that identification of all arterial feeders, from both internal and external carotid systems, is critical in developing a therapeutic plan. AVMs may be treated by surgical excision alone, or embolization alone. However, in the hands of an experienced interventional neuroradiologist and an appropriately chosen surgical team, most AVMs can and should be treated by a combined approach of preoperative embolization followed by surgical excision of the vascular mass. The goal of therapy is closure of the low-resistance shunt. C1 MED COLL WISCONSIN,ORBITAL & OCULOPLAST SECT,MILWAUKEE,WI 53226. MASSACHUSETTS EYE & EAR INFIRM,EYE PLAST & ORBIT SERV,BOSTON,MA 02114. WILFORD HALL USAF MED CTR,DEPT OPHTHALMOL,LACKLAND AFB,TX 78236. RP HAYES, BH (reprint author), EGLIN HOSP,DEPT OPHTHALMOL,SGHSE,EGLIN AFB,FL 32542, USA. NR 22 TC 22 Z9 23 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD MAR-APR PY 1995 VL 26 IS 2 BP 145 EP 152 PG 8 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA QQ880 UT WOS:A1995QQ88000012 PM 7596543 ER PT J AU BIANCHIMARZOLI, S RIZZO, JF BRANCATO, R LESSELL, S AF BIANCHIMARZOLI, S RIZZO, JF BRANCATO, R LESSELL, S TI QUANTITATIVE-ANALYSIS OF OPTIC DISC CUPPING IN COMPRESSIVE OPTIC NEUROPATHY SO OPHTHALMOLOGY LA English DT Article ID NERVE DAMAGE; GLAUCOMA; ATROPHY; PALLOR AB Purpose: Cupping of the optic disc, a characteristic sign of glaucoma, has been anecdotally described in association with compressive optic neuropathy. The aim of this study is to perform a masked, controlled, and quantitative measurement of the optic disc cup to determine if compressive lesions of the afferent visual pathway were associated with increased cupping. Methods: The ratio of cup area:disc area of 29 patients with intracranial lesions impinging on the optic nerves and the chiasm (14 with pituitary adenomas, 7 with meningiomas, 6 with craniopharyngiomas, and 2 with aneurysms) was compared with those of 20 age-matched control subjects. The areal ratios were derived planimetrically from hand-drawn images of magnified stereophotographs. Patients were divided into three groups based on the degree of laterality of visual compromise, Uninvolved eyes served as an internal control for patients with unilateral disease. Results: The median ratio of cup area:disc area was 0.37 for all eyes with visual compromise (n = 51) and 0.10 for control eyes, which was statistically significant (P = 0.0001). The median intereye difference in the ratio of cup area:disc area was 0.13 for patients with unilateral lesions and 0.04 for control subjects. This difference also was statistically significant (P = 0.0001). Conclusions: The finding of intereye asymmetry in patients with unilateral optic nerve compression is convincing evidence that the enlarged cup is an acquired feature. Several types of compressive lesions of the anterior visual pathway can be associated with increased cupping of the optic disc in the absence of increased intraocular pressure. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. UNIV MILAN,HS RAFFAELE,DEPT OPHTHALMOL & VISUAL SCI,MILAN,ITALY. NR 27 TC 53 Z9 56 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1995 VL 102 IS 3 BP 436 EP 440 PG 5 WC Ophthalmology SC Ophthalmology GA QL484 UT WOS:A1995QL48400018 PM 7891982 ER PT J AU CEISLER, EJ BILYK, JR RUBIN, PAD BURKS, WR SHORE, JW AF CEISLER, EJ BILYK, JR RUBIN, PAD BURKS, WR SHORE, JW TI RESULTS OF MULLEROTOMY AND LEVATOR APONEUROSIS TRANSPOSITION FOR THE CORRECTION OF UPPER EYELID RETRACTION IN GRAVES-DISEASE SO OPHTHALMOLOGY LA English DT Article ID SURGICAL-TREATMENT; MARGINAL MYOTOMY; MUSCLE EXCISION; RECESSION; OPHTHALMOPATHY; SCLERA AB Background: Upper eyelid retraction in Graves disease may cause functional morbidity and aesthetic deformity. Surgery to correct thyroid-related upper eyelid retraction may result in temporal undercorrection with failure to eliminate lateral eyelid retraction, leading in turn to a poor eyelid contour postoperatively. Methods: In 1984, one of the authors developed a new procedure for correcting moderate to severe upper eyelid retraction associated with Graves disease. The surgical technique consists of a Mullerotomy and recession of the levator aponeurosis combined with medial transposition of the lateral horn of the levator aponeurosis. The procedure was performed on 37 patients (72 eyelids). Muller's muscle was used as the spacer to set the eyelid height, Transposition of the levator aponeurosis allowed adjustment of eyelid contour. Results: Thirty patients (58 eyelids) had excellent results, six (13 eyelids) had good results, and one (1 eyelid) had a poor result. No patient required re-operation for asymmetry, unacceptable contour, or malposition. Only one eyelid had significant overcorrection, and only one eyelid had significant undercorrection, requiring further surgery, The most frequent unwanted effects were high eyelid crease (24 eyelids) and residual temporal flare (6 eyelids); however, most of these were seen early in the series before the lateral levator transposition modification was added. Conclusion: This procedure allows successful and simultaneous correction of both eyelid position and contour in patients with moderate to severe thyroid-related upper eyelid retraction. C1 OPHTHALM CONSULTANTS BOSTON,BOSTON,MA 02114. OPHTHALMOL CONSULTANTS,MARGATE,FL. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,EYE PLAST & ORBIT SERV,BOSTON,MA. NR 36 TC 29 Z9 30 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAR PY 1995 VL 102 IS 3 BP 483 EP 492 PG 10 WC Ophthalmology SC Ophthalmology GA QL484 UT WOS:A1995QL48400025 PM 7891989 ER PT J AU RANDOLPH, GW FABIAN, RL DANIELS, GH AF RANDOLPH, GW FABIAN, RL DANIELS, GH TI PERITHYROID TEFLON GRANULOMA MIMICKING A THYROID-NODULE SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Note ID POLYTEF TEFLON; INJECTION; MIGRATION C1 BOSTON UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,THYROID UNIT,BOSTON,MA 02215. RP RANDOLPH, GW (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 11 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD MAR PY 1995 VL 112 IS 3 BP 465 EP 468 DI 10.1016/S0194-5998(95)70286-5 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA QK715 UT WOS:A1995QK71500019 PM 7870452 ER PT J AU ROELKE, M ONUNAIN, S OSSWALD, S TROUTON, TG HARTHORNE, JW GARAN, H RUSKIN, JN AF ROELKE, M ONUNAIN, S OSSWALD, S TROUTON, TG HARTHORNE, JW GARAN, H RUSKIN, JN TI VENTRICULAR PACING-INDUCED VENTRICULAR-TACHYCARDIA IN PATIENTS WITH IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS SO PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY LA English DT Note DE VENTRICULAR PACING; VENTRICULAR TACHYCARDIA; IMPLANTABLE CARDIOVERTER DEFIBRILLATOR ID SUDDEN CARDIAC DEATH; RISK STRATIFICATION; PACEMAKERS; CIRCUMSTANCES; BRADYCARDIA; PREVALENCE; MECHANISMS AB Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 +/- 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1-16 per patient) of ventricular tachycardia that were immeadiately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monmorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia. RP ROELKE, M (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,CARDIAC UNIT,FRUIT ST,BOSTON,MA 02114, USA. NR 16 TC 11 Z9 11 U1 0 U2 1 PU FUTURA PUBL CO PI ARMONK PA 135 BEDFORD RD, PO BOX 418, ARMONK, NY 10504-0418 SN 0147-8389 J9 PACE JI PACE-Pacing Clin. Electrophysiol. PD MAR PY 1995 VL 18 IS 3 BP 486 EP 491 DI 10.1111/j.1540-8159.1995.tb02551.x PN 1 PG 6 WC Cardiac & Cardiovascular Systems; Engineering, Biomedical SC Cardiovascular System & Cardiology; Engineering GA QM374 UT WOS:A1995QM37400018 PM 7770372 ER PT J AU RAMANUJAM, T LUCHI, M SCHUMACHER, HR ZWILLICH, S CHANG, CP CALLEGARI, PE VONFELDT, JM FANG, QO WEINER, DB WILLIAMS, WV AF RAMANUJAM, T LUCHI, M SCHUMACHER, HR ZWILLICH, S CHANG, CP CALLEGARI, PE VONFELDT, JM FANG, QO WEINER, DB WILLIAMS, WV TI DETECTION OF T-CELL RECEPTORS IN EARLY RHEUMATOID-ARTHRITIS SYNOVIAL TISSUE SO PATHOBIOLOGY LA English DT Article DE RHEUMATOID ARTHRITIS; T CELL RECEPTOR; POLYMERASE CHAIN REACTION; EARLY ARTHRITIS; SYNOVIAL TISSUE; SYNOVIAL BIOPSY ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; COLLAGEN-INDUCED ARTHRITIS; MYELIN BASIC-PROTEIN; MAJOR HISTOCOMPATIBILITY COMPLEX; V-BETA USAGE; ANTIGEN RECEPTOR; RESTRICTED HETEROGENEITY; CHAIN; GENES; ANTIBODIES AB Synovial tissue is rarely available from patients with early synovitis, with the exception of synovial biopsies, However, T cell populations early in the development of synovitis may be enriched in antigen-specific cells and critical to disease pathogenesis, To investigate the T cell repertoire in early synovitis, we utilized a PCR protocol for detection of T cell receptor (TCR) transcripts present in small amounts of synovial tissue. To expand the substrate for PCR, preamplification of cDNA was performed with a 3' constant region primer plus either a mixture of variable region primers or random hexanucleotides. Utilizing this method improved the sensitivity of detection, This technique is applied here to the analysis of TCR transcripts in synovial biopsies from individuals with early rheumatoid arthritis (RA) and non-RA synovitis, TCR alpha-chain transcripts were detectable in 5/5 RA and 4/4 non-RA specimens evaluated, with beta-chain transcripts detected in 4/5 early RA and 4/4 non-RA specimens evaluated, Confirmation of transcripts by sequencing of cloned PCR products verfied the specificity of amplification. The most frequently expressed TCR V region families in early RA synovitis were V alpha 11, V alpha 14, V alpha 28, V beta 7, V beta 9 and V beta 17. Several of these V regions have previously been implicated in studies of chronic RA synovitis, J alpha and J beta region usage was similar to that seen in chronic RA, and conserved N region motifs were apparent. We Early arthritis conclude that it is possible to detect TCR transcripts in small synovial biopsies Synovial tissue from individuals with early arthritis, This technique can be applied to studies Synovial biopsy of synovitis where limited quantities of synovial tissue are available. C1 UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,INST BIOTECHNOL & ADV MOLEC MED,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. UNIV ROCHESTER,SCH MED,DEPT MED,RHEUMATOL SECT,ROCHESTER,MI. RI Weiner, David/H-8579-2014 NR 42 TC 9 Z9 9 U1 0 U2 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1015-2008 J9 PATHOBIOLOGY JI Pathobiology PD MAR-APR PY 1995 VL 63 IS 2 BP 100 EP 108 DI 10.1159/000163940 PG 9 WC Cell Biology; Pathology SC Cell Biology; Pathology GA RY038 UT WOS:A1995RY03800007 PM 8554698 ER PT J AU BELL, D AF BELL, D TI SOFT-TISSUE CHONDROMA OF THE FALLOPIAN-TUBE - COMMENTARY SO PATHOLOGY RESEARCH AND PRACTICE LA English DT Note ID TERATOMA RP BELL, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU GUSTAV FISCHER VERLAG PI STUTTGART PA WOLLGRASWEG 49 POSTFACH 72 01 43, D-70577 STUTTGART, GERMANY SN 0344-0338 J9 PATHOL RES PRACT JI Pathol. Res. Pract. PD MAR PY 1995 VL 191 IS 2 BP 178 EP 178 PG 1 WC Pathology SC Pathology GA QY595 UT WOS:A1995QY59500016 ER PT J AU GEIFMANHOLTZMAN, O HOLTZMAN, EJ VADNAIS, TJ PHILLIPS, VE CAPELESS, EL BIANCHI, DW AF GEIFMANHOLTZMAN, O HOLTZMAN, EJ VADNAIS, TJ PHILLIPS, VE CAPELESS, EL BIANCHI, DW TI DETECTION OF FETAL HLA-DQ-ALPHA SEQUENCES IN MATERNAL BLOOD - A GENDER-INDEPENDENT TECHNIQUE OF FETAL CELL IDENTIFICATION SO PRENATAL DIAGNOSIS LA English DT Article DE PRENATAL DIAGNOSIS; FETAL CELLS; FLOW CYTOMETRY; POLYMERASE CHAIN REACTION; HLA-DQA ID POLYMERASE CHAIN-REACTION; PRENATAL SEX DETERMINATION; PERIPHERAL-BLOOD; NUCLEATED ERYTHROCYTES; OLIGONUCLEOTIDE PROBES; DNA; AMPLIFICATION; CIRCULATION; DIAGNOSIS; DISEASE AB The objective of this study was to detect fetal HLA-DQa gene sequences in maternal blood. HLA-DQa genotypes of 70 pregnant women and their partners were determined for type A1. We specifically sought couples where the father, but not the mother, had genotype A1. In 12 women, maternal blood samples were flow-sorted. Candidate fetal cells were isolated and amplified by using PCR primers specific for a paternal HLA-DQa A1 allele. Fetal HLA-DQa A1 genotype was predicted from sorted cells; amniocytes or cheek swabs were used for confirmation. Six of twelve sorted samples had amplification products indicating the presence of the HLA-DQa A1 allele; 6/12 did not. Prediction of the fetal genotype was 100 per cent correct, as determined by subsequent amplification of amniocytes or cheek swabs. We conclude that paternally inherited uniquely fetal HLA-DQa gene sequences can be identified in maternal blood. This system permits the identification of fetal cells independent of fetal gender, and has the potential for non-invasive prenatal diagnosis of paternally inherited conditions. C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT PEDIAT,BOSTON,MA 02111. TUFTS UNIV NEW ENGLAND MED CTR,DEPT OBSTET,BOSTON,MA 02111. TUFTS UNIV NEW ENGLAND MED CTR,DEPT GYNECOL,BOSTON,MA 02111. TUFTS UNIV,SCH MED,BOSTON,MA 02111. MED CTR HOSP VERMONT,DEPT OBSTET & GYNECOL,DIV MATERNAL FETAL MED,BURLINGTON,VT. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. PERKIN ELMER CETUS,EMERYVILLE,CA. NR 23 TC 16 Z9 16 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0197-3851 J9 PRENATAL DIAG JI Prenat. Diagn. PD MAR PY 1995 VL 15 IS 3 BP 261 EP 268 DI 10.1002/pd.1970150309 PG 8 WC Genetics & Heredity; Obstetrics & Gynecology SC Genetics & Heredity; Obstetrics & Gynecology GA QP996 UT WOS:A1995QP99600008 PM 7784384 ER PT J AU HEIMENDINGER, J FENG, Z EMMONS, K STODDARD, A KINNE, S BIENER, L SORENSEN, G ABRAMS, D VARNES, J BOUTWELL, B AF HEIMENDINGER, J FENG, Z EMMONS, K STODDARD, A KINNE, S BIENER, L SORENSEN, G ABRAMS, D VARNES, J BOUTWELL, B TI THE WORKING WELL TRIAL - BASE-LINE DIETARY AND SMOKING BEHAVIORS OF EMPLOYEES AND RELATED WORKSITE CHARACTERISTICS SO PREVENTIVE MEDICINE LA English DT Article ID UNITED-STATES; CANCER; POLICY; MODEL AB Background. The Working Well Trial, the largest randomized worksite health promotion trial to date, tests the effects of cancer prevention and control interventions on dietary and smoking behaviors of employees and the worksite environment. The trial is a 5-year cooperative agreement conducted in 57 matched pairs of worksites in 16 states by four study centers, a coordinating center, and the National Cancer Institute. The dual aims of this paper are to: (a) present a baseline description of the dietary and smoking habits of 20,801 employees, who are predominantly blue-collar workers; and (b) describe the social and physical environments of their worksites that may facilitate or hinder health behavior changes. Methods. The self-administered baseline survey of individuals consisted of a core set of questions common across all study centers on diet and smoking. The organizational survey consisted to eight instruments administered via interviews with key informants in each worksite. Continuous variables were analyzed by a mixed linear model and binary data were analyzed by the Generalized Estimating Equation. Results. The population represented is largely male (67.5%) and blue collar (53.5%). Mean levels of fat and fiber intakes were close to the national averages (36.6% of calories as fat and 13.1 g of fiber). Smoking prevalence (25.2%) was slightly lower than the national average. The worksites had a high level of health promotion activites (42% had nutrition programs, 53% had smoking control programs), but lacked environmental support for dietary behavior change and perceived support for smoking cessation. Conclusions. These findings replicate and extend previous research results to a large sample of diverse, largely blue-collar worksites. In addition the baseline results lay a foundation for the development of new insight into the relationship between individual and organizational level variables that may interact to influence behavioral and cultural norms. (C) 1995 Academic Press, Inc. C1 FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. BROWN UNIV,MIRIAM HOSP,PROVIDENCE,RI 02912. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV MASSACHUSETTS,BOSTON,MA 02125. UNIV FLORIDA,GAINESVILLE,FL 32611. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX 77025. RP HEIMENDINGER, J (reprint author), NCI,BETHESDA,MD 20892, USA. OI Biener, Lois/0000-0002-4130-8138 FU NCI NIH HHS [UO1 CA51671, UO1 CA51686, UO1 CA51687] NR 47 TC 40 Z9 40 U1 3 U2 7 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0091-7435 J9 PREV MED JI Prev. Med. PD MAR PY 1995 VL 24 IS 2 BP 180 EP 193 DI 10.1006/pmed.1995.1032 PG 14 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA QT209 UT WOS:A1995QT20900017 PM 7597021 ER PT J AU SILVA, JA LEONG, GB FERRARI, MM AF SILVA, JA LEONG, GB FERRARI, MM TI DELUSIONAL MISIDENTIFICATION OF HEALTH-CARE PROFESSIONALS SO PSYCHIATRIC QUARTERLY LA English DT Article ID CAPGRAS SYNDROME; SUBSTITUTION; PSYCHOSIS AB Delusional misidentification of others generally involves a person misidentifying others who are emotionally and geographically proximate to that person. Health care professionals may become the objects of delusional misidentification. The present study reviews and analyzes the anglophonic literature on published reports of misidentified health care professionals and adds two new cases. Relevant issues raised when patients misidentify health care professionals are explored, particularly the danger posed by these misidentification delusions. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. CTR HLTH CARE SERV,SAN ANTONIO,TX. UNIV TEXAS,HLTH SCI CTR,DEPT PSYCHIAT,SAN ANTONIO,TX 78284. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT BIOBEHAV SCI,LOS ANGELES,CA 90024. RP SILVA, JA (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,PSYCHIAT SERV 116A,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 45 TC 3 Z9 3 U1 0 U2 0 PU HUMAN SCI PRESS INC PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013-1578 SN 0033-2720 J9 PSYCHIAT QUART JI Psychiatr. Q. PD SPR PY 1995 VL 66 IS 1 BP 51 EP 61 DI 10.1007/BF02238715 PG 11 WC Psychiatry SC Psychiatry GA QB192 UT WOS:A1995QB19200004 PM 7701020 ER PT J AU JARVIK, ME GROSS, TM ROSENBLATT, MR STEIN, RE AF JARVIK, ME GROSS, TM ROSENBLATT, MR STEIN, RE TI ENHANCED LEXICAL PROCESSING OF SMOKING STIMULI DURING SMOKING ABSTINENCE SO PSYCHOPHARMACOLOGY LA English DT Article DE ABSTINENCE; INTRUSIVE THOUGHTS; NICOTINE; PRIMING; SEMANTIC ACTIVATION; PERCEPTION; PROCESSING ID TOBACCO WITHDRAWAL; ANXIETY-STATES; THREAT CUES; NICOTINE; MEMORY; MOOD; BIAS AB In a group of heavy smokers, overnight abstinence from smoking facilitated the perception of briefly presented smoking words. Subjects in the nicotine-abstinent condition accurately identified significantly more smoking-related words than food-related or neutral words. However, a group tested in a non-abstinent condition showed no significant differences in ability to identify the three different word types. Smokers deprived of cigarettes were also significantly better able to categorize smoking words than non-abstinent subjects. These results demonstrate an abstinence-based facilitation of processing smoking-related stimuli at the semantic level, consistent with the hypothesis that smoking-related concepts are activated, or primed, during deprivation from nicotine. RP JARVIK, ME (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,WILSHIRE & SAWTELE BLVD,LOS ANGELES,CA 90073, USA. NR 23 TC 18 Z9 18 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD MAR PY 1995 VL 118 IS 2 BP 136 EP 141 DI 10.1007/BF02245831 PG 6 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA QR462 UT WOS:A1995QR46200008 PM 7617799 ER PT J AU COPELAND, PM SACKS, NR HERZOG, DB AF COPELAND, PM SACKS, NR HERZOG, DB TI LONGITUDINAL FOLLOW-UP OF AMENORRHEA IN EATING DISORDERS SO PSYCHOSOMATIC MEDICINE LA English DT Article DE AMENORRHEA; ANOREXIA NERVOSA; BULIMIA NERVOSA ID ANOREXIA-NERVOSA; BULIMIA-NERVOSA; WEIGHT; ADOLESCENTS; PREVALENCE; SECRETION; WOMEN AB The authors recruited 229 treatment-seeking anorexic and bulimic women for a prospective, longitudinal study. Telephone interviews were arranged every 3 months for at least 1 year for 225 patients. At intake, 132 subjects were menstruating, 34 subjects were taking oral contraceptives, 5 subjects had an organic cause for amenorrhea (e.g., hysterectomy), and 58 subjects were amenorrheic. Each patient met Diagnostic and Statistical Manual of Mental Disorders, third edition, revised (DSM-III-R) criteria for anorexia nervosa (AN, N = 41), bulimia nervosa (BN, N = 98), or AN/BN (N = 90), All subjects were interviewed with the Schedule for Affective Disorders and Schizophrenia-Lifetime Version, which was modified to include a section for DSM-III-R eating disorders, the Longitudinal Interval Follow-Up Evaluation, and the Structured Interview for DSM-III Personality Disorders. It was found that body weight was associated with menstrual status: those with amenorrhea had a mean percent ideal body weight (IBW, Metropolitan Life criteria) of 74 +/- 1% compared with 102 +/- 19% for menstruating patients (p < .01). Affective illness was more prevalent among patients with amenorrhea than among menstruating patients (75% vs. 56%, p < .05). Menses were regained within 1 year by 33% of amenorrheic patients. These patients gained an average of 7.3% of their IBW. Longer duration of eating disorder (p < .03) and the presence of an anxiety disorder (p < .05) were associated with persistent amenorrhea. Menses were lost within 1 year by 8% of menstruating patients. These patients lost an average of 5.0% of their IBW. In conclusion, among patients with eating disorders, low weight and affective illness were associated with amenorrhea; longer duration of eating disorder and presence of anxiety disorders were associated with persistent amenorrhea. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,EATING DISORDERS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. SALEM HOSP,SALEM,MA. RP COPELAND, PM (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,MED SERV,BOSTON,MA 02114, USA. NR 34 TC 31 Z9 33 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD MAR-APR PY 1995 VL 57 IS 2 BP 121 EP 126 PG 6 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA QP781 UT WOS:A1995QP78100004 PM 7792370 ER PT J AU GREENBERG, DB AF GREENBERG, DB TI PSYCHOTROPIC-DRUG USE IN THE MEDICALLY ILL - SILVER,PA SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP GREENBERG, DB (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD MAR-APR PY 1995 VL 36 IS 2 BP 153 EP 153 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QJ709 UT WOS:A1995QJ70900011 ER PT J AU RABINOWITZ, T AF RABINOWITZ, T TI CLINICAL CHALLENGES IN PSYCHIATRY - SLEDGE,WH, TASMAN,A SO PSYCHOSOMATICS LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SPAULDING REHABIL HOSP,BOSTON,MA. RP RABINOWITZ, T (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD MAR-APR PY 1995 VL 36 IS 2 BP 153 EP 155 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QJ709 UT WOS:A1995QJ70900012 ER PT J AU CASSEM, EH AF CASSEM, EH TI DEPRESSIVE-DISORDERS IN THE MEDICALLY ILL - AN OVERVIEW SO PSYCHOSOMATICS LA English DT Article; Proceedings Paper CT 1994 Annual Meeting of the Academy-of-Psychosomatic-Medicine CY NOV 17-20, 1994 CL PHOENIX, AZ SP Acad Psychosomat Med ID CANCER-PATIENTS; PSYCHIATRIC-DISORDERS; MENTAL-DISORDERS; MAJOR DEPRESSION; MOOD DISORDERS; PREVALENCE; DISEASE; DISTURBANCE; COMMUNITY; DIAGNOSIS AB Depressive disorders are far more serious than most people realize, and depressive disorders are disabling affected persons progressively earlier in life. Heavy utilization of medical services, extensive disability and morbidity, and high suicide risk exact a staggering economic toll in the United States annually. Depressive illness is, like pneumonia and septic shock, a dread complication of major medical illness, and depressive illness appears more frequently as the medical illness worsens; diseases affecting the brain may have the highest rates of depressive symptoms. Correctly diagnosing a depressive disorder in a medically ill patient is a clinical challenge that requires systematic, persistent clinical scrutiny. Compassion demands that depressive disorders, when diagnosed, be treated aggressively. RP CASSEM, EH (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BULLFINCH,3RD FLOOR,FRUIT ST,BOSTON,MA 02114, USA. NR 45 TC 44 Z9 44 U1 1 U2 3 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD MAR-APR PY 1995 VL 36 IS 2 BP S2 EP S10 PG 9 WC Psychiatry; Psychology SC Psychiatry; Psychology GA QJ709 UT WOS:A1995QJ70900117 PM 7724710 ER PT J AU CHEW, FS PAPPAS, CN AF CHEW, FS PAPPAS, CN TI RADIOLOGY OF DEVICES FOR FRACTURE TREATMENT IN THE EXTREMITIES SO RADIOLOGIC CLINICS OF NORTH AMERICA LA English DT Article AB This article describes the appearance and application of various mechanical devices used in the treatment of fractures. It is intended to familiarize the reader with the biologic and biomechanical principles underlying the design and application of particular devices as well as to explain and demystify some of the orthopedic vocabulary used to describe them. Once a fracture has been recognized and treatment has begun, the role of the radiologist in the management of the patient shifts from diagnosis to follow-up. The purpose of the radiologic report is no longer the detection, localization, and description of the fracture but, rather, the description of the mode and progress of treatment and surveillance for the occurrence of complications. It is therefore important for the radiologist to be familiar with the application and normal radiologic appearance of devices used in the treatment of fractures. C1 HARVARD UNIV,SCH MED,BOSTON,MA. UNIV VERMONT,COLL MED,DEPT RADIOL,BURLINGTON,VT. MED CTR HOSP VERMONT,BURLINGTON,VT. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. OI Chew, Felix/0000-0003-2711-2013 NR 26 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 0033-8389 J9 RADIOL CLIN N AM JI Radiol. Clin. N. Am. PD MAR PY 1995 VL 33 IS 2 BP 375 EP 390 PG 16 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QL462 UT WOS:A1995QL46200010 PM 7871174 ER PT J AU MITCHELL, DG OUTWATER, EK MATTEUCCI, T RUBIN, DL CHEZMAR, JL SAINI, S AF MITCHELL, DG OUTWATER, EK MATTEUCCI, T RUBIN, DL CHEZMAR, JL SAINI, S TI ADRENAL-GLAND ENHANCEMENT AT MR-IMAGING WITH MN-DPDP SO RADIOLOGY LA English DT Article DE ADRENAL GLAND, MR; MAGNETIC RESONANCE (MR), CONTRAST ENHANCEMENT ID BRONCHOGENIC-CARCINOMA; CHEMICAL-SHIFT; MASSES; CT; BIOPSY; BENIGN; DIFFERENTIATION; DISTINCTION; LESIONS; SAFETY AB PURPOSE: To determine adrenal gland enhancement with manganese (II) N,N' dipyridoxylethylenediamine-N,N'-diacetate 5,5'bis(phosphate) (DPDP) at magnetic resonance imaging. MATERIALS AND METHODS: After phase III trials, fat-suppressed, motion-compensated, T1-weighted spin-echo images (repetition time, 500 msec; echo time, 12 msec) of 13 consecutive patients were obtained at 1.5 T at one site, prior to and approximately 30 minutes after intravenous administration of 5 mu mol/kg Mn-DPDP. Images were analyzed visually and by means of region-of-interest measurements, normalized to spleen. With data added from three more sites, enhancement of three adrenal adenomas and two metastases was analyzed. RESULTS: Twenty-five of 26 adrenal glands were depicted on MR images, and all showed enhancement. Mean adrenal enhancement (38%) was comparable to mean enhancement of liver (46%), pancreas (25%), and renal cortex (58%). Adrenal cortex and medulla could not be distinguished in nonenhanced or enhanced images. All three adrenal adenomas enhanced by more than 40%, but the metastases did not enhance. CONCLUSION: Functioning adrenal tissue (glands and at least some adenomas) are enhanced with Mn-DPDP. C1 THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,PHILADELPHIA,PA 19107. GOOD SAMARITAN HOSP,DEPT RADIOL,SAN JOSE,CA. EMORY UNIV HOSP,DEPT RADIOL,ATLANTA,GA 30322. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP MITCHELL, DG (reprint author), THOMAS JEFFERSON UNIV HOSP,DEPT RADIOL,1096 MAIN BLDG,132 S 10TH ST,PHILADELPHIA,PA 19107, USA. NR 36 TC 20 Z9 20 U1 0 U2 1 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD MAR PY 1995 VL 194 IS 3 BP 783 EP 787 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QG918 UT WOS:A1995QG91800027 PM 7862979 ER PT J AU BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG NADLER, LM AF BOUSSIOTIS, VA FREEMAN, GJ GRIBBEN, JG NADLER, LM TI THE CRITICAL ROLE OF CD28 SIGNALING IN THE PREVENTION OF HUMAN T-CELL ANERGY SO RESEARCH IN IMMUNOLOGY LA English DT Article ID CTLA-4 COUNTER-RECEPTOR; HUMAN LYMPHOCYTES-T; ACTIVATION PATHWAY; COSTIMULATORY SIGNAL; ANTIGEN RECEPTOR; TYROSINE KINASE; CLONAL ANERGY; GAMMA-CHAIN; INTERLEUKIN-2; B7 C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP BOUSSIOTIS, VA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,44 BINNEY ST,BOSTON,MA 02115, USA. NR 71 TC 14 Z9 14 U1 0 U2 1 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD MAR-APR PY 1995 VL 146 IS 3 BP 140 EP 149 DI 10.1016/0923-2494(96)80247-1 PG 10 WC Immunology SC Immunology GA RP877 UT WOS:A1995RP87700003 PM 8525043 ER PT J AU SCHNEIDER, H CAI, YC CEFAI, D RAAB, M RUDD, CE AF SCHNEIDER, H CAI, YC CEFAI, D RAAB, M RUDD, CE TI MECHANISMS OF CD28 SIGNALING SO RESEARCH IN IMMUNOLOGY LA English DT Article ID T-CELL ACTIVATION; RECEPTOR TYROSINE KINASES; PHOSPHATIDYLINOSITOL 3-KINASE; MITOGENIC SIGNAL; LYMPHOCYTES-T; SH3 DOMAINS; ZETA-CHAIN; PROTEIN; CTLA-4; RAS C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP SCHNEIDER, H (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 58 TC 7 Z9 7 U1 0 U2 0 PU EDITIONS SCIENTIFIQUES ELSEVIER PI PARIS CEDEX 15 PA 141 RUE JAVEL, 75747 PARIS CEDEX 15, FRANCE SN 0923-2494 J9 RES IMMUNOL JI Res. Immunol. PD MAR-APR PY 1995 VL 146 IS 3 BP 149 EP 154 DI 10.1016/0923-2494(96)80248-3 PG 6 WC Immunology SC Immunology GA RP877 UT WOS:A1995RP87700004 PM 8525044 ER PT J AU STONE, ME AF STONE, ME TI ALLERGIES A-Z - LIPKOWITZ,M, NAVARRA,T SO RQ LA English DT Book Review RP STONE, ME (reprint author), MASSACHUSETTS GEN HOSP,TREADWELL LIB,REFERENCE SERV,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER LIBRARY ASSN PI CHICAGO PA 50 E HURON ST, CHICAGO, IL 60611 SN 0033-7072 J9 RQ JI RQ PD SPR PY 1995 VL 34 IS 3 BP 385 EP 386 PG 2 WC Information Science & Library Science SC Information Science & Library Science GA QW090 UT WOS:A1995QW09000017 ER PT J AU MUELLER, PR DAWSON, SL AF MUELLER, PR DAWSON, SL TI UNTITLED 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 MAR PY 1995 VL 12 IS 1 BP U3 EP U4 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA QR340 UT WOS:A1995QR34000001 ER PT J AU BERGER, R MEZEY, E CLANCY, KP HARTA, G WRIGHT, RM REPINE, JE BROWN, RH BROWNSTEIN, M PATTERSON, D AF BERGER, R MEZEY, E CLANCY, KP HARTA, G WRIGHT, RM REPINE, JE BROWN, RH BROWNSTEIN, M PATTERSON, D TI ANALYSIS OF ALDEHYDE OXIDASE AND XANTHINE DEHYDROGENASE OXIDASE AS POSSIBLE CANDIDATE GENES FOR AUTOSOMAL RECESSIVE FAMILIAL AMYOTROPHIC-LATERAL-SCLEROSIS SO SOMATIC CELL AND MOLECULAR GENETICS LA English DT Article ID SUPEROXIDE-DISMUTASE; CLONING; CONVERSION; PROTEIN; YEAST AB Recently, point mutations in superoxide dismutase 1 (SOD1) have been shown to lead to a subset of autosomal dominantly inherited familial amyotrophic lateral sclerosis (ALS). These findings have led to the hypothesis that defects in oxygen radical metabolism may be involved in the pathogenesis of ALS. Therefore, we decided to analyze other enzymes involved in oxygen radical metabolism for possible involvement in other forms of ALS. We report here analysis of two genes encoding the molybdenum hydroxylases aldehyde oxidase (AO) and xanthine dehydrogenase/oxidase (XDH) for involvement in ALS. Of particular interest, one gene identified as encoding aldehyde oxidase is shown to map to 2q33, a region recently shown to contain a gene responsible for a familial form of ALS with autosomal recessive inheritance (FALS-AR). The AO gene appeals to be located within 280, 000 bp of simple sequence repeat marker D2S116, which shows no recombination with the FALS-AR locus. The AO gene is highly expressed in glial cells of human spinal cord. In addition, we mapped a gene for XDH to 2p22, a region previously shown to contain a highly homologous but different form of XDH. Neither of these XDH genes appears to be highly expressed in human spinal cord. This evidence suggests that AO may be a candidate gene for FALS-AR. C1 NIH,BETHESDA,MD 20892. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. UNIV COLORADO,HLTH SCI CTR,DENVER,CO 80262. WEBB WARING INST BIOMED RES,DENVER,CO 80262. RP BERGER, R (reprint author), ELEANOR ROOSEVELT INST,DENVER,CO 80206, USA. RI Brownstein, Michael/B-8609-2009 FU NIA NIH HHS [AG00029, F32AGO5666]; NINDS NIH HHS [1PO1NS31248-01] NR 39 TC 49 Z9 52 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 MAR PY 1995 VL 21 IS 2 BP 121 EP 131 DI 10.1007/BF02255787 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA RV992 UT WOS:A1995RV99200004 PM 7570184 ER PT J AU MYERS, GA CONHAIM, RL ROSENFELD, DJ HARMS, BA AF MYERS, GA CONHAIM, RL ROSENFELD, DJ HARMS, BA TI EFFECTS OF PENTAFRACTION AND HETASTARCH PLASMA EXPANSION ON LUNG AND SOFT-TISSUE TRANSVASCULAR FLUID FILTRATION SO SURGERY LA English DT Article ID INCREASED VASCULAR PRESSURE; AWAKE SHEEP; HYPOPROTEINEMIA; RESUSCITATION; LYMPH; TRANSPORT; INFUSION; BALANCE; ALBUMIN; SHOCK AB Background. Hetastarch and pentafraction are high molecular weight starch solutions designed to augment plasma oncotic pressure. Although clinical utilization of hetastarch has been limited by reported coagulation abnormalities, pentafraction is a newer derivative that appears to have Jew adverse hemostatic effects. We examined the ability of pentafraction to modulate lung and soft tissue transvascular fluid filtration under hypoproteinemic conditions compared with hetastarch and Ringer's lactate (LR). Methods. Awake, protein-depleted sheep (n = 19) were prepared with lung and soft tissue lymph fistulas, and comparable infusions of 5% pentafraction (n = 6), 6% hetastarch (n = 6), or LR (n = 7) were administered Plasma and lymph samples were collected during 24-hour period to determine changes in protein concentrations, plasma-to-lymph oncotic gradients, and lung (Q(L)) and soft tissue (Q(S)) lymph flows. Results. Q(L) and Q(S) rose nearly twofold after protein depletion alone. LR infusion increased Q(L) and Q(S) to 8.7 +/- 1.7 and 3.1 +/- 0.6 times normoproteinemic baseline, respectively (p < 0.05). In contrast, hetastarch and pentafraction infusion limited the increase in (Q(L) to 4.2 +/- 1.1 and 4.0 +/- 0.8 times normoproteinemic baseline, respectively (p < 0.05 versus LR) and did not significantly increase as. Hetastarch and pentafraction infusions increase plasma oncotic pressure by nearly 6 mm Hg, which significantly widened the plasma-to-lymph oncotic pressure gradients above preinfusion baseline by 4.7 +/- 0.7 and 3.4 +/- 0.4 mm Hp in lung and 4.6 +/- 0.7 and 3.2 +/- 0.4 mm Hg in soft tissue, respectively (p < 0.05). Conclusions. Both hetastarch and pentafraction limit transvascular fluid filtration under hypoproteinemic conditions by augmenting plasma oncotic pressure and the plasma-to-lymph oncotic pressure gradient. Because of fewer adverse hemostatic effects pentafraction may be an improvement over current therapies in critical care fluid management. C1 UNIV WISCONSIN HOSP & CLIN,WILLIAM S MIDDLETON MEM VET ADM HOSP,DEPT SURG,MADISON,WI 53792. UNIV WISCONSIN,DEPT SURG,MADISON,WI. FU NHLBI NIH HHS [HL46236] NR 27 TC 10 Z9 10 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD MAR PY 1995 VL 117 IS 3 BP 340 EP 349 DI 10.1016/S0039-6060(05)80211-9 PG 10 WC Surgery SC Surgery GA QK689 UT WOS:A1995QK68900016 PM 7533333 ER PT J AU LEWIS, CB AF LEWIS, CB TI UNTITLED SO TOPICS IN GERIATRIC REHABILITATION LA English DT Editorial Material C1 GEORGE WASHINGTON UNIV,SCH MED & HLTH SCI,WASHINGTON,DC 20052. MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA. RP LEWIS, CB (reprint author), PHYS THERAPY SERV WASHINGTON DC INC,WASHINGTON,DC, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ASPEN PUBL INC PI FREDERICK PA 7201 MCKINNEY CIRCLE, FREDERICK, MD 21701 SN 0882-7524 J9 TOP GERIATR REHABIL JI Top. Geriatr. Rehabil. PD MAR PY 1995 VL 10 IS 3 BP R5 EP R5 PG 1 WC Gerontology; Rehabilitation SC Geriatrics & Gerontology; Rehabilitation GA QJ051 UT WOS:A1995QJ05100001 ER PT J AU MOSER, R OBERLEY, TD DAGGETT, DA FRIEDMAN, AL JOHNSON, JA SIEGEL, FL AF MOSER, R OBERLEY, TD DAGGETT, DA FRIEDMAN, AL JOHNSON, JA SIEGEL, FL TI EFFECTS OF LEAD ADMINISTRATION ON DEVELOPING RAT-KIDNEY .1. GLUTATHIONE-S-TRANSFERASE ISOENZYMES SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID INTRANUCLEAR INCLUSION-BODIES; DIETARY CALCIUM; LIVER; EXPRESSION; INDUCTION; BINDING; NEPHROTOXICITY; RESISTANCE; PRESSURE; SUBUNITS AB The effects of acute and chronic exposure to lead on glutathione S-transferase (GST) isoforms were determined in developing kidney in the rat. The ontogeny of glutathione S-transferase isoforms was characterized as were the effects of depletion of dietary calcium on glutathione S-transferase isoform profiles in control and lead-treated rats, In the acute exposure experiments, rats of 14 and 50 days of age received three daily injections of lead acetate (114 mg/kg) and in the chronic exposure studies, rats received lead acetate at doses ranging from 50 to 500 ppm in their drinking water. Lead acetate administration in these chronic studies began 1 day after conception. Acute and chronic lead exposure had similar effects, causing increases in all but one glutathione S-transferase isoform (Yb-3); these increases were markedly exacerbated by dietary calcium depletion, In all lead paradigms, GST subunits Yb-1 and Yp showed the largest increases-greater than 25-fold in rats fed a low-calcium diet, GST subunit Yb-3 showed small increases in the 14-day acute lead and the 4 week low-calcium animals and did not increase in other groups. Lead-related increases in GSTs were partially reversed by transferring animals previously receiving lead to lead-free water for a 4-week period. Kidneys of rats fed the low-calcium diet did not have detectable GST Yk, but in rats on this low-calcium diet that received 500 ppm lead; this GST isoform was found at levels comparable to those in control rats fed lab chow. (C) 1995 Academic Press. Inc. C1 UNIV WISCONSIN,WAISMAN CTR,DEPT PEDIAT,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR,DEPT BIOMOLEC CHEM,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR,DEPT PATHOL,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR,CTR ENVIRONM TOXICOL,MADISON,WI 53705. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. FU NICHD NIH HHS [HD03352]; NIEHS NIH HHS [T32 ES07015]; NINDS NIH HHS [NS24669] NR 44 TC 27 Z9 30 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAR PY 1995 VL 131 IS 1 BP 85 EP 93 DI 10.1006/taap.1995.1050 PG 9 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA QK940 UT WOS:A1995QK94000011 PM 7878682 ER PT J AU OBERLEY, TD FRIEDMAN, AL MOSER, R SIEGEL, FL AF OBERLEY, TD FRIEDMAN, AL MOSER, R SIEGEL, FL TI EFFECTS OF LEAD ADMINISTRATION ON DEVELOPING RAT-KIDNEY .2. FUNCTIONAL, MORPHOLOGIC, AND IMMUNOHISTOCHEMICAL STUDIES SO TOXICOLOGY AND APPLIED PHARMACOLOGY LA English DT Article ID GLUTATHIONE-S-TRANSFERASE; MANGANESE SUPEROXIDE-DISMUTASE; SYRIAN-HAMSTER TISSUES; ANTIOXIDANT ENZYMES; CATALYTIC ACTIVITY; MESSENGER-RNAS; CELL-NUCLEUS; NEPHROPATHY; LOCALIZATION; ISOENZYMES AB The effects of chronic lead administration on renal function and cytoarchitecture and on the immunohistochemical localization of glutathione S-transferase (GST) isoenzymes were determined. Pregnant rats were given 250 ppm lead acetate in drinking water from conception until weaning and mothers and pups received 500 ppm of lead acetate from weaning until termination at either 3 or 7 weeks of age, Light and electron microscopic studies after 3 weeks of lead administration showed tubular injury with frequent mitoses noted in proximal tubular cells and, after 7 weeks of treatment, interstitial fibrosis, characteristic intranuclear inclusions, and tubular injury characterized by both nuclear and cytoplasmic pleomorphism. Rats treated with lead for 7 weeks showed significantly lower body weights and creatinine clearances than age-matched control animals, Immunohistochemical studies of glutathione transferase subunits in control rats showed unique isoform localization in each segment of the nephron; treatment with lead caused large increases in immunoreactive protein of Yc, Yk, Yb-1, and Yp GST subunits in proximal tubules, No increases in the antioxidant enzymes copper-zinc superoxide dismutase, catalase, and glutathione peroxidase were found in lead-treated rats, but there was a diffuse lead-related increase in immunoreactive protein for manganese superoxide dismutase throughout the renal cortex. Our results demonstrate large lead-induced increases of specific isoforms of glutathione S-transferase in specific kidney cell types and show that these increases preceded irreversible renal damage. (C) 1995 Academic Press, Inc. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,PATHOL SERV,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PATHOL,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT PEDIAT,MADISON,WI 53705. UNIV WISCONSIN,SCH MED,DEPT BIOMOLEC CHEM,MADISON,WI 53705. UNIV WISCONSIN,CTR ENVIRONM TOXICOL,MADISON,WI 53705. UNIV WISCONSIN,WAISMAN CTR,MADISON,WI 53705. FU NICHD NIH HHS [HD03352]; NINDS NIH HHS [NS24969] NR 51 TC 44 Z9 45 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0041-008X J9 TOXICOL APPL PHARM JI Toxicol. Appl. Pharmacol. PD MAR PY 1995 VL 131 IS 1 BP 94 EP 107 DI 10.1006/taap.1995.1051 PG 14 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA QK940 UT WOS:A1995QK94000012 PM 7878683 ER PT J AU ANDERSON, KC AF ANDERSON, KC TI ALTERNATIVES TO BLOOD PRODUCTS SO TRANSFUSION SCIENCE LA English DT Editorial Material RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BLOOD COMPONENT LAB,BOSTON,MA 02115, USA. NR 0 TC 1 Z9 1 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0955-3886 J9 TRANSFUS SCI JI Transfus. Sci. PD MAR PY 1995 VL 16 IS 1 BP 3 EP 3 DI 10.1016/0955-3886(95)90080-2 PG 1 WC Hematology SC Hematology GA QM028 UT WOS:A1995QM02800002 ER PT J AU ANDERSON, KC AF ANDERSON, KC TI INTERNATIONAL FORUM - SOUTH-AFRICA - AUTOLOGOUS BLOOD-TRANSFUSION COMPUTER SOFTWARE PROGRAM SO TRANSFUSION SCIENCE LA English DT Editorial Material RP ANDERSON, KC (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BLOOD COMPONENT LAB,BOSTON,MA 02115, USA. NR 0 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 0955-3886 J9 TRANSFUS SCI JI Transfus. Sci. PD MAR PY 1995 VL 16 IS 1 BP 63 EP 63 PG 1 WC Hematology SC Hematology GA QM028 UT WOS:A1995QM02800007 ER PT J AU SELSTED, ME OUELLETTE, AJ AF SELSTED, ME OUELLETTE, AJ TI DEFENSINS IN GRANULES OF PHAGOCYTIC AND NON-PHAGOCYTIC CELLS SO TRENDS IN CELL BIOLOGY LA English DT Article ID CATIONIC PEPTIDE GENE; ANTIMICROBIAL PEPTIDES; SMALL-INTESTINE; PANETH CELLS; CANDIDACIDAL ACTIVITY; SALMONELLA VIRULENCE; BOVINE NEUTROPHILS; MESSENGER-RNA; HOST DEFENSE; PURIFICATION AB Antimicrobial proteins stored in lysosome-like granules of neutrophils and macrophages probably play an important role in killing phagocytosed microbes after delivery to the phagolysosome. Among the granules' antimicrobial armamentarium are defensins, peptides that kill a broad spectrum of microorganisms in vitro. Antimicrobial defensins were recently also isolated from non-phagocytic granulocytes of the mouse small intestinal epithelium, from where they are secreted into the lumen to function extracellularly. Clarification of the antimicrobial mechanisms of defensins in intracellular and extracellular environments will provide a key to understanding peptide-mediated host defence. C1 UNIV CALIF IRVINE,COLL MED,DEPT MOLEC GENET,IRVINE,CA 92717. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM,BOSTON,MA 02114. RP SELSTED, ME (reprint author), UNIV CALIF IRVINE,COLL MED,DEPT PATHOL & MICROBIOL,IRVINE,CA 92717, USA. NR 47 TC 106 Z9 109 U1 0 U2 0 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0962-8924 J9 TRENDS CELL BIOL JI Trends Cell Biol. PD MAR PY 1995 VL 5 IS 3 BP 114 EP 119 DI 10.1016/S0962-8924(00)88961-8 PG 6 WC Cell Biology SC Cell Biology GA QQ301 UT WOS:A1995QQ30100007 PM 14732166 ER PT J AU BARRY, MJ AF BARRY, MJ TI EFFECT OF DEMOGRAPHIC-FACTORS, URINARY PEAK FLOW-RATES, AND BOYARSKY SYMPTOM SCORES ON PATIENT TREATMENT CHOICE IN BENIGN PROSTATIC HYPERPLASIA - COMMENT SO UROLOGY LA English DT Note RP BARRY, MJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 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 MAR PY 1995 VL 45 IS 3 BP 405 EP 405 PG 1 WC Urology & Nephrology SC Urology & Nephrology GA QL422 UT WOS:A1995QL42200011 ER PT J AU ALROY, J KNOWLES, K SCHELLING, SH KAYE, EM ROSENBERG, AE AF ALROY, J KNOWLES, K SCHELLING, SH KAYE, EM ROSENBERG, AE TI RETARDED BONE-FORMATION IN G(M1)-GANGLIOSIDOSIS - A STUDY OF THE INFANTILE FORM AND COMPARISON WITH 2 CANINE MODELS SO VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY LA English DT Article DE RETARDED BONE FORMATION; G(M1)-GANGLIOSIDOSIS; CANINE MODEL ID GLYCOPROTEIN STORAGE DISORDER; I-CELL DISEASE; MUCOPOLYSACCHARIDOSIS-VII; MUCOLIPIDOSIS-II; COLLAGEN FIBRILS; FELINE MODEL; PATHOLOGY; GLUCURONIDASE; CARTILAGE; ASPARTYLGLYCOSAMINURIA AB The development of skeletal lesions in two canine models of G(M1)-gangliosidosis, English springer spaniels and Portuguese water dogs, has been studied and compared to osseous abnormalities in a child with the infantile form of the disease. In the canine models, skeletal dysplasia was progressive. Lesions were noted at 2 months of age and characterized by retarded endochondral ossification and osteoporosis. Older puppies had focal cartilage necrosis within lumbar vertebral epiphyses. At the cellular level, lesions were characterized by chondrocytic hypertrohy and lysosomal accumulation of storage compounds. Our studies illustrate that the skeletal lesions in both canine models are similar to those in a child with G(M1)-gangliosidosis. Furthermore, we proposed that the abnormal storage of partially degraded compounds in affected chondrocytes might explain, at least in part, the retarded bone formation noted in patients with G(M1)-gangliosidosis. C1 TUFTS UNIV,SCH MED,DEPT PEDIAT NEUROL,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. TUFTS UNIV,SCH VET MED,DEPT MED,GRAFTON,MA. RP ALROY, J (reprint author), TUFTS UNIV,SCH MED & VET MED,DEPT PATHOL,136 HARRISON AVE,BOSTON,MA 02111, USA. NR 36 TC 8 Z9 9 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0945-6317 J9 VIRCHOWS ARCH JI Virchows Arch. Int. J. Pathol. PD MAR PY 1995 VL 426 IS 2 BP 141 EP 148 PG 8 WC Pathology SC Pathology GA QZ111 UT WOS:A1995QZ11100006 PM 7757284 ER PT J AU PAULUS, W BAUR, I LISZKA, U DRLICEK, M LEIGH, I BRUCKNERTUDERMAN, L AF PAULUS, W BAUR, I LISZKA, U DRLICEK, M LEIGH, I BRUCKNERTUDERMAN, L TI EXPRESSION OF TYPE-VII COLLAGEN, THE MAJOR ANCHORING FIBRIL COMPONENT, IN NORMAL AND NEOPLASTIC HUMAN NERVOUS-SYSTEM SO VIRCHOWS ARCHIV-AN INTERNATIONAL JOURNAL OF PATHOLOGY LA English DT Article DE CHOROID PLEXUS; EXTRACELLULAR MATRIX; GLIOMAS; PITUITARY GLAND; TYPE VII COLLAGEN ID IMMUNOHISTOCHEMICAL LOCALIZATION; EPIDERMOLYSIS-BULLOSA; BASEMENT-MEMBRANE; HUMAN GLIOMAS; BRAIN-TUMORS; TISSUE; CELLS; PHENOTYPE; INVITRO AB The distribution of type VII collagen was examined in the normal human nervous system, in brain tumour biopsies and in glioma cell lines by immunohistochemistry and western blotting. In normal tissue, positivity was observed beneath choroid plexus epithelial cells and around pineal gland and pituitary gland cell nests, while other brain regions and peripheral nerves were negative. Expression was preserved in most related tumours (choroid plexus papilloma, pineoblastoma, pituitary adenoma). Scattered abnormal vessels showed neo-expression of type VII collagen in about half of the astrocytic and ependymal tumours, Glioma cells in situ were consistently negative for type VII collagen, whereas the glioblastoma cell lines were positive. Our results suggest that anchoring fibrils or at least epitopes of their major structural component are present in normal and pathological cerebral structures, indicating a unique distribution of type VII collagen in the nervous system. C1 UNIV WURZBURG,INST PATHOL,W-8700 WURZBURG,GERMANY. HOSP PSYCHIAT,DEPT PATHOL,VIENNA,AUSTRIA. LONDON HOSP,COLL MED,IMPERIAL CANC RES FUND,SKIN TUMOR LAB,LONDON E1 1BB,ENGLAND. UNIV ZURICH HOSP,DEPT DERMATOL,CH-8091 ZURICH,SWITZERLAND. RP PAULUS, W (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 23 TC 6 Z9 6 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0945-6317 J9 VIRCHOWS ARCH JI Virchows Arch. Int. J. Pathol. PD MAR PY 1995 VL 426 IS 2 BP 199 EP 202 PG 4 WC Pathology SC Pathology GA QZ111 UT WOS:A1995QZ11100013 PM 7757291 ER PT J AU XU, GF LIVINGSTON, DM KREK, W AF XU, GF LIVINGSTON, DM KREK, W TI MULTIPLE MEMBERS OF THE E2F TRANSCRIPTION FACTOR FAMILY ARE THE PRODUCTS OF ONCOGENES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE RB GENE; TRANSFORMATION; CELL CYCLE CONTROL; ANCHORAGE-INDEPENDENT GROWTH ID RETINOBLASTOMA GENE-PRODUCT; ADENOVIRUS E1A PROTEINS; LARGE T-ANTIGEN; CELL-CYCLE; SUSCEPTIBILITY GENE; TUMOR SUPPRESSOR; GROWTH SUPPRESSION; MOLECULAR-CLONING; COMPLEX-FORMATION; CARCINOMA-CELLS AB The retinoblastoma gene product (pRB) is a known tumor suppressor, capable of arresting growth in mid-to-late G(1). Part of its growth suppression action arises from interaction(s) with one or more members of the E2F family of transcription factors. These proteins most likely contribute to progression from G(0) to S phase in mammalian cells, and pRB binding most likely inhibits aspects of their suspected growth-promoting function. Given their growth-stimulating potential, we asked whether one or more E2F alleles can function as oncogenes. Uncloned pools of NIH 3T3 cells producing the PRE binding target E2F-1, E2F-2, or E2F-3 grew in semisolid medium. In addition, they grew to much higher saturation density than controls. From the study of cells producing selected E2F-1 mutant species, it appears that E2F DNA-binding function contributes to, and pRB/E2F binding suppresses, soft-agar growth. Thus, three E2F family members can act as oncogene products, suggesting that part of the normal role of pRB is to down-modulate this potential activity. RP XU, GF (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 62 TC 184 Z9 186 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 FEB 28 PY 1995 VL 92 IS 5 BP 1357 EP 1361 DI 10.1073/pnas.92.5.1357 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700024 PM 7877982 ER PT J AU DIGARD, P WILLIAMS, KP HENSLEY, P BROOKS, IS DAHL, CE COEN, DM AF DIGARD, P WILLIAMS, KP HENSLEY, P BROOKS, IS DAHL, CE COEN, DM TI SPECIFIC-INHIBITION OF HERPES-SIMPLEX VIRUS-DNA POLYMERASE BY HELICAL PEPTIDES CORRESPONDING TO THE SUBUNIT INTERFACE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CIRCULAR DICHROISM; ANALYTICAL ULTRACENTRIFUGATION; PROCESSIVITY; RATIONAL DRUG DESIGN ID FUNCTIONAL INTERACTION; UL42 PROTEIN; RIBONUCLEOTIDE REDUCTASE; ACCESSORY PROTEIN; C-TERMINUS; AUXILIARY PROTEIN; CARBOXY TERMINUS; BINDING; DOMAIN; REPLICATION AB The herpes simplex virus DNA polymerase consists of two subunits - a catalytic subunit and an accessory subunit, UL42, that increases processivity, Mutations affecting the extreme C terminus of the catalytic subunit specifically disrupt subunit interactions and ablate virus replication, suggesting that new antiviral drugs could be rationally designed to interfere with polymerase heterodimerization, To aid design, we performed circular dichroism (CD) spectroscopy and analytical ultracentrifugation studies, which revealed that a 36-residue peptide corresponding to the C terminus of the catalytic subunit folds into a monomeric structure with partial ar-helical character, Co studies of shorter peptides were consistent with a model where two separate regions of alpha-helix interact to form a hairpin-like structure, The 36-residue peptide and a shorter peptide corresponding to the C-terminal 18 residues blocked UL42-dependent long-chain DNA synthesis at concentrations that had no effect on synthesis by the catalytic subunit alone or by calf thymus DNA polymerase delta and its processivity factor, These peptides, therefore, represent a class of specific inhibitors of herpes simplex virus DNA polymerase that act by blocking accessory-subunit-dependent synthesis, These peptides or their structures may form the basis for the synthesis of clinically effective drugs. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. SMITHKLINE BEECHAM PHARMACEUT INC,DEPT MACROMOLEC SCI,KING OF PRUSSIA,PA 19406. RI Digard, Paul/B-7717-2008; Brooks, Ian/E-7052-2010; OI Digard, Paul/0000-0002-0872-9440; Brooks, Ian/0000-0002-3793-3635 FU NIAID NIH HHS [AI26077] NR 38 TC 49 Z9 52 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 FEB 28 PY 1995 VL 92 IS 5 BP 1456 EP 1460 DI 10.1073/pnas.92.5.1456 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700044 PM 7878000 ER PT J AU TAKAHASHI, H FUJIMOTO, J HANADA, S ISSELBACHER, KJ AF TAKAHASHI, H FUJIMOTO, J HANADA, S ISSELBACHER, KJ TI ACUTE HEPATITIS IN RATS EXPRESSING HUMAN HEPATITIS-B VIRUS TRANSGENES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IN VIVO TRANSFECTION; T LYMPHOCYTES; VIRAL CLEARANCE ID HEPATOMA-CELL LINE; FULMINANT-HEPATITIS; GENE-EXPRESSION; LIVER-DISEASE; VIRAL-DNA; HBV-DNA; INFECTION; HEPATOCYTES; REPLICATION; SERUM AB The molecular mechanisms responsible for hepatocyte death and the events leading to viral clearance in hepatitis B virus (HBV) infections are not well understood, Elucidation of the mechanisms involved have been complicated by the difficulty of infecting human hepatocytes with HBV in vitro and the lack of an appropriate animal model. We report an animal model of human HBV infection by in vivo transfection. We have directly introduced a replication-competent, cloned HBV construct into rat liver by using a membrane fusion-promoting cationic lipid, HBV mRNA and 3.2-kb HBV DNA were expressed in the liver by this in vivo transfection method, In the majority of rats, HBV virions and hepatitis B e antigen were found in the blood 3-7 days after transfection, after which antibody to the e antigen appeared. Two to three weeks after the transfection, glutamic-pyruvic transaminase levels were elevated in serum, hepatocyte death and lymphocyte infiltration were observed in the vicinity of the portal vein of liver, and HBV virions were no longer detected in the serum. Thus, transfection of REV into rats resulted in histological and serological changes comparable to HBV-induced acute hepatitis in humans, In contrast, no hepatocellular injury was observed in T-lymphocyte-deficient nude rats transfected with the same HBV construct, and viremia was substantially prolonged, providing direct evidence that T lymphocytes play an essential role in liver cell injury and in the clearance of HBV, This rat hepatitis model will be useful for studying pathogenesis of HBV infection. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP E,CTR CANC,TUMOR BIOL LAB,BOSTON,MA 02129. RP TAKAHASHI, H (reprint author), HARVARD UNIV,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA35711, CA57584]; NIDDK NIH HHS [NIDDK43351] NR 33 TC 37 Z9 38 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 FEB 28 PY 1995 VL 92 IS 5 BP 1470 EP 1474 DI 10.1073/pnas.92.5.1470 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700047 PM 7878002 ER PT J AU FALK, PG BRY, L HOLGERSSON, J GORDON, JI AF FALK, PG BRY, L HOLGERSSON, J GORDON, JI TI EXPRESSION OF A HUMAN ALPHA-1,3/4-FUCOSYL-TRANSFERASE IN THE PIT CELL LINEAGE OF FVB/N MOUSE STOMACH RESULTS IN PRODUCTION OF LE(B)-CONTAINING GLYCOCONJUGATES - A POTENTIAL TRANSGENIC MOUSE MODEL FOR STUDYING HELICOBACTER-PYLORI INFECTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN GASTRIC EPITHELIUM; MIGRATION; DYNAMICS; CORPUS AB Helicobacter pylori is a human pathogen associated with the development of gastric and duodenal ulcers and gastric adenocarcinoma. To test the hypothesis that the human Lewis(b) blood group antigen (Le(b)) functions as a receptor for the bacteria's adhesins and mediates its attachment to gastric pit and surface mucous cells, a human alpha-1,3/4-fucosyltransferase was expressed in these cell lineages in FVB/N transgenic mice. The fucosyltransferase directed production of the Le(b) epitope without any apparent effect on the proliferation and differentiation programs of this lineage. Moreover, clinical isolates of H, pylori bound to these cells in transgenic mice but not in their normal littermates. Binding was blocked by pretreatment of the bacteria with soluble Le(b). This mouse model could be useful for examining the molecular pathogenesis of diseases caused by H. pylori infection, Creating novel pathways for production of specific oligosaccharides in selected cell lineages of transgenic animals represents an approach for examining the role of complex carbohydrates in regulating cellular differentiation and host-microbe interactions. C1 KAROLINSKA INST,MED MICROBIAL ECOL LAB,STOCKHOLM,SWEDEN. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP FALK, PG (reprint author), ST LOUIS UNIV,SCH MED,DEPT MOLEC BIOL & PHARMACOL,ST LOUIS,MO 63110, USA. FU NIDDK NIH HHS [DK33487, DK37960] NR 14 TC 107 Z9 110 U1 1 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 FEB 28 PY 1995 VL 92 IS 5 BP 1515 EP 1519 DI 10.1073/pnas.92.5.1515 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700056 PM 7878011 ER PT J AU WU, MX DALEY, JF RASMUSSEN, RA SCHLOSSMAN, SF AF WU, MX DALEY, JF RASMUSSEN, RA SCHLOSSMAN, SF TI MONOCYTES ARE REQUIRED TO PRIME PERIPHERAL-BLOOD T-CELLS TO UNDERGO APOPTOSIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE PROGRAMMED CELL DEATH; HUMAN IMMUNODEFICIENCY VIRUS 1 GP120 ID TUMOR NECROSIS FACTOR; ACTIVATED MACROPHAGES; DEATH APOPTOSIS; INDUCE DEATH; HIV; LYMPHOCYTES; THYMOCYTES; AIDS; INFECTION AB Freshly isolated, human peripheral blood T (PET) cells are largely resistant to the apoptotic effects of anti-CD3 monoclonal antibody, ionomycin, or phorbol 12-myristate 13-acetate (PMA), We demonstrate here, however, that PET cells, including both CD4(+) and CD8(+) cell populations, can be readily induced to undergo apoptosis when cocultured with either autologous or allogeneic monocytes (Mo) in PMA-containing medium. Incubation of PET cells with Mo at a ratio of 1:1 for 18 hr resulted in maximal levels (80%) of apoptotic cell death. The mechanism whereby Mo enable PET cells to undergo apoptosis in PMA-containing medium appeared to depend on cell-cell contact or close proximity between Mo and PET cells rather than solely via soluble mediators. It was demonstrated that Mo acquire the ability to prime PET cells for apoptosis after treatment with PMA and that treated Mo maintain this ability even after fixation with formaldehyde. It was also found that once PET cells became primed for apoptosis by incubation with PMA-pretreated Mo, the primed PET cells were susceptible to apoptosis triggered not only by PMA but also by either ionomycin or by monoclonal antibody crosslinking of T-cell surface molecules such as CD4 and CD3. Interestingly, the degree of apoptosis of CD4(+) T cells by crosslinking of CD4 molecules via a combination of gp120, anti-gp120, and goat anti-mouse IgG was significantly greater for T cells primed with PMA-treated Mo than for unprimed T cells. Together, these findings reveal an important role for accessory cells in priming resting PET cells for apoptosis and suggest a possible Mo-dependent mechanism by which T cells may become primed for apoptosis in human immunodeficiency virus-infected asymptomatic individuals. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP WU, MX (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-34183]; NIAID NIH HHS [AI-12069] NR 24 TC 54 Z9 54 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 FEB 28 PY 1995 VL 92 IS 5 BP 1525 EP 1529 DI 10.1073/pnas.92.5.1525 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700058 PM 7878013 ER PT J AU TAUPIN, JL TIAN, QS KEDERSHA, N ROBERTSON, M ANDERSON, P AF TAUPIN, JL TIAN, QS KEDERSHA, N ROBERTSON, M ANDERSON, P TI THE RNA-BINDING PROTEIN TIAR IS TRANSLOCATED FROM THE NUCLEUS TO THE CYTOPLASM DURING FAS-MEDIATED APOPTOTIC CELL-DEATH SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID IDENTIFICATION; RECOGNITION AB We have determined the structure, intracellular localization, and tissue distribution of TIAR, a TIA-1-related RNA-binding protein. Two related isoforms of TIAR, migrating at 42 and 50 kDa, are expressed in primate cells, Unlike TIA-I, which is found in the granules of cytotoxic lymphocytes, TIAR is concentrated in the nucleus of hematopoietic and nonhematopoietic cells, Because TIAR can trigger DNA fragmentation in permeabilized thymocytes, it is a candidate effector of apoptotic cell death. Consistent with this possibility, we have found that the expression and intracellular localization of TIAR change dramatically during Fas-mediated apoptosis, TIAR moves from the nucleus to the cytoplasm within 30 min of Fas ligation. Redistribution of TIAR precedes the onset of DNA fragmentation and is not a nonspecific consequence of nuclear disintegration, Cytoplasmic redistribution of TIAR is mot observed during cellular activation triggered by mitogens such as concanavalin A or phytohemagglutinin, Our results suggest that cytoplasmic redistribution of TIAR may be a general feature of the apoptotic program. C1 IMMUNOGEN INC,DEPT CELL BIOL,CAMBRIDGE,MA 02139. BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL,BOSTON,MA 02115. RP TAUPIN, JL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI3360] NR 16 TC 107 Z9 111 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 FEB 28 PY 1995 VL 92 IS 5 BP 1629 EP 1633 DI 10.1073/pnas.92.5.1629 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QK077 UT WOS:A1995QK07700079 PM 7533298 ER PT J AU LEE, JO RIEU, P ARNAOUT, MA LIDDINGTON, R AF LEE, JO RIEU, P ARNAOUT, MA LIDDINGTON, R TI CRYSTAL-STRUCTURE OF THE A-DOMAIN FROM THE A-SUBUNIT OF INTEGRIN CR3 (CD11B/CD18) SO CELL LA English DT Article ID AMINO-ACID-SEQUENCE; BETA-SUBUNIT; VONWILLEBRAND-FACTOR; EXTRACELLULAR-MATRIX; ADHESION RECEPTOR; ALPHA-SUBUNIT; MONOCLONAL-ANTIBODIES; FIBRONECTIN RECEPTOR; MOLECULAR-CLONING; GLOBULAR DOMAINS AB We have determined the high resolution crystal structure of the A domain from the a chain of integrin CR3. The domain adopts a classic alpha/beta ''Rossmann'' fold and contains an unusual Mg2+ coordination site at its surface. One of the coordinating ligands is the glutamate side chain from another A domain molecule. We suggest that this site represents a general metal ion-dependent adhesion site (MIDAS) for binding protein ligands. We further propose that the beta subunits of integrins contain a MIDAS motif within a modified A domain. Our crystal structure will allow reliable models to be built for other members of the A domain superfamily and should facilitate development of novel adhesion modulatory drugs. C1 MASSACHUSETTS GEN HOSP,DEPT MED,DIV NEPHROL,LEUKOCYTE BIOL & INFLAMMAT PROGRAM,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,XRAY CRYSTALLOG LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [5P30CA0651]; NIAID NIH HHS [P01 AI-28465]; NIDDK NIH HHS [R01 DK-48549] NR 74 TC 717 Z9 721 U1 0 U2 8 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 24 PY 1995 VL 80 IS 4 BP 631 EP 638 DI 10.1016/0092-8674(95)90517-0 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QJ602 UT WOS:A1995QJ60200015 PM 7867070 ER PT J AU RORDORFNIKOLIC, T VANHORN, DJ CHEN, DX WHITE, MF BACKER, JM AF RORDORFNIKOLIC, T VANHORN, DJ CHEN, DX WHITE, MF BACKER, JM TI REGULATION OF PHOSPHATIDYLINOSITOL 3'-KINASE BY TYROSYL PHOSPHOPROTEINS - FULL ACTIVATION REQUIRES OCCUPANCY OF BOTH SH2 DOMAINS IN THE 85-KDA REGULATORY SUBUNIT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECEPTOR KINASE INSERT; PDGF RECEPTOR; SIGNAL TRANSDUCTION; INSULIN-RECEPTOR; GROWTH-FACTOR; INTACT-CELLS; PHOSPHOINOSITIDE 3-KINASE; PI 3-KINASE; PHOSPHORYLATION; BINDING AB Phosphatidylinositol 3'-kinase (PI 3'-kinase) is activated in insulin-stimulated cells by the binding of the SH2 domains in its 85-kDa regulatory subunit to insulin receptor substrate-1 (IRS-1). We have previously shown that both tyrosyl-phosphorylated IRS-l and mono-phosphopeptides containing a single YXXM motif activate PI 3'-kinase in vitro. However, activation by the monophosphopeptides was significantly less potent than activation by the multiply phosphorylated IRS-1. We now show that the increased potency of PI 3'-kinase activation by IRS-1 relative to phosphopeptide is not due to tertiary structural features IRS-l, as PI 3'-kinase is activated normally by denatured, reduced, and carboxymethylated IRS-1. Furthermore, activation of PI 3'-kinase by bis-phosphorylated peptides containing two YXXM motifs is 100-fold more potent than the corresponding mono-phosphopeptides and similar to activation by IRS-1. These data suggest that tyrosyl-phosphorylated IRS-1 or bis-phosphorylated peptides bind simultaneously to both SH2 domains of p85. However, these data cannot differentiate between an activation mechanism that requires two-site occupancy for maximal activity as opposed to one in which bivalent binding enhances the occupancy of a single activating site. To distinguish between these possibilities, we produced recombinant PI 3'-kinase containing either wild-type p85 or p85 mutated in its N-terminal, C-terminal, or both SH2 domains. We find that mutation of either SH2 domains significantly reduced phosphopeptide binding and decreased PI 3'-kinase activation by 50%, whereas mutation of both SH2 domains completely blocked binding and activation. These data provide the first direct evidence that full activation of PI 3'-kinase by tyrosylphosphorylated proteins requires occupancy of both SH2 domains in p85. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOLEC PHARMACOL,BRONX,NY 10461. BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,DIV RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02215. FU NIDDK NIH HHS [DK-44541] NR 35 TC 198 Z9 198 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 24 PY 1995 VL 270 IS 8 BP 3662 EP 3666 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QH688 UT WOS:A1995QH68800033 PM 7876105 ER PT J AU JAIN, JN BURGEON, E BADALIAN, TM HOGAN, PG RAO, A AF JAIN, JN BURGEON, E BADALIAN, TM HOGAN, PG RAO, A TI A SIMILAR DNA-BINDING MOTIF IN NFAT FAMILY PROTEINS AND THE REL HOMOLOGY REGION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ACTIVATED T-CELLS; KAPPA-B; TRANSCRIPTION FACTOR; NUCLEAR FACTOR; CYCLOSPORINE-A; C-REL; CALCINEURIN; FOS; JUN; PROMOTER AB The cyclosporin-sensitive factor NFATp cooperates with Fos and Jun family proteins to regulate transcription of the interleukin 2 gene in activated T cells. We have defined a 187-amino acid fragment of NFATp, located centrally within the protein sequence, as the minimal region required for DNA binding and for complex formation with Fos and Jun. The sequence of this region of NFATp shows a low degree of similarity to the Rel homology region. One specific short sequence in NFATp (RAHYETEG), located near the NH, terminus of the DNA-binding domain, resembles a highly conserved sequence (RFRYxCEG) that is located near the NH, terminus of the Rel homology region and that has been implicated in DNA binding by Rel family proteins. Mutational analysis demonstrates that the residues in this sequence that are identical in NFATp, and Rel family proteins contribute to DNA binding by NFATp. Further, mutation of the threonine residue in this sequence to cysteine, as in Rel proteins, confers on NFATp a sensitivity to sulfhydryl modification similar to that of Rel family proteins. The results suggest that NFATp and Rel family proteins bind to DNA using similar structural motifs. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA42471]; NIGMS NIH HHS [GM46227] NR 41 TC 120 Z9 120 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 24 PY 1995 VL 270 IS 8 BP 4138 EP 4145 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QH688 UT WOS:A1995QH68800099 PM 7876165 ER PT J AU BOWLING, AC BEAL, MF AF BOWLING, AC BEAL, MF TI BIOENERGETIC AND OXIDATIVE STRESS IN NEURODEGENERATIVE DISEASES SO LIFE SCIENCES LA English DT Review DE MITOCHONDRIA; OXIDATIVE PHOSPHORYLATION; ELECTRON TRANSPORT CHAIN; OXIDATIVE DAMAGE; FREE RADICALS; ALZHEIMERS DISEASE; PARKINSONS DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; HUNTINGTONS DISEASE ID AMYOTROPHIC-LATERAL-SCLEROSIS; MOTOR-NEURON DISEASE; SUPEROXIDE-DISMUTASE ACTIVITY; CYTOCHROME-C-OXIDASE; MITOCHONDRIAL RESPIRATORY-CHAIN; POSITRON EMISSION TOMOGRAPHY; TRANSGENIC DROSOPHILA-MELANOGASTER; ALPHA-KETOGLUTARATE DEHYDROGENASE; GLUTATHIONE-PEROXIDASE ACTIVITY; IDIOPATHIC PARKINSONS-DISEASE AB Aging is a major risk factor for several common neurodegenerative diseases, including Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and Huntington's disease (HD). Recent studies have implicated mitochondrial dysfunction and oxidative stress in the aging process and also in the pathogenesis of neurodegenerative diseases. In brain and other tissues, aging is associated with progressive impairment of mitochondrial function and increased oxidative damage. In PD, several studies have demonstrated decreased complex I activity, increased oxidative damage, and altered activities of antioxidant defense systems. Some cases of familial ALS are associated with mutations in the gene for Cu, Zn superoxide dismutase (Cu, Zn SOD) and decreased Cu, Zn SOD activity, while in sporadic ALS oxidative damage may be increased. Defects in energy metabolism and increased cortical lactate levels have been detected in HD patients. Studies of AD patients have identified decreased complex IV activity, and some patients with AD and PD have mitochondrial DNA mutations. The age-related onset and progressive course of these neurodegenerative diseases may be due to a cycling process between impaired energy metabolism and oxidative stress. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROCHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NIA NIH HHS [5P 50 AG-05134, P01 AG-11337]; NINDS NIH HHS [NS-16367] NR 255 TC 263 Z9 273 U1 2 U2 17 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0024-3205 J9 LIFE SCI JI Life Sci. PD FEB 24 PY 1995 VL 56 IS 14 BP 1151 EP 1171 DI 10.1016/0024-3205(95)00055-B PG 21 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA QJ273 UT WOS:A1995QJ27300001 PM 7475893 ER PT J AU EISENBERG, E LACROSS, S STRASSMAN, AM AF EISENBERG, E LACROSS, S STRASSMAN, AM TI THE CLINICALLY TESTED N-METHYL-D-ASPARTATE RECEPTOR ANTAGONIST MEMANTINE BLOCKS AND REVERSES THERMAL HYPERALGESIA IN A RAT MODEL OF PAINFUL MONONEUROPATHY SO NEUROSCIENCE LETTERS LA English DT Article DE EXCITATORY AMINO ACID; GLUTAMATE; CHRONIC CONSTRICTIVE INJURY; SCIATIC NERVE ID DORSAL HORN; SPINAL-CORD; PERIPHERAL MONONEUROPATHY; NEURONS; MK-801; INVOLVEMENT; NOCICEPTION; GLUTAMATE; BEHAVIORS; NERVE AB This study tested the prophylactic and therapeutic efficacy of memantine (1-amino-3,5-dimethyl-amandate), a clinically tested N-methyl-D-aspartate (NMDA) antagonist on thermal hyperalgesia in a rat model of painful mononeuropathy. Persistent hyperalgesia induced by chronic constrictive injury (CCI) to the sciatic nerve was significantly reduced for up to 14 days by prophylactic administration of memantine (3.0 mg/kg) via i.p implanted osmotic micropumps for a period of 7 days. Therapeutic i.p injections of memantine (10 mg/kg) given on post-injury days 7 and 14 completely reversed existing hyperalgesia for a short period of 1 h. These results provide evidence that memantine produces long-term prophylactic and short-term therapeutic effects on thermal hyperalgesia in a model of painful mononeuropathy. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. SPAULDING REHABIL HOSP,PAIN PROGRAM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,PAIN PHYSIOL LAB,BOSTON,MA 02129. NR 21 TC 62 Z9 62 U1 1 U2 1 PU ELSEVIER SCI PUBL 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 FEB 24 PY 1995 VL 187 IS 1 BP 17 EP 20 DI 10.1016/0304-3940(95)11326-R PG 4 WC Neurosciences SC Neurosciences & Neurology GA QP055 UT WOS:A1995QP05500005 PM 7617292 ER PT J AU KIRCHGESSNER, CU PATIL, CK EVANS, JW CUOMO, CA FRIED, LM CARTER, T OETTINGER, MA BROWN, JM AF KIRCHGESSNER, CU PATIL, CK EVANS, JW CUOMO, CA FRIED, LM CARTER, T OETTINGER, MA BROWN, JM TI DNA-DEPENDENT KINASE (P350) AS A CANDIDATE GENE FOR THE MURINE SCID DEFECT SO SCIENCE LA English DT Article ID STRAND BREAK-REPAIR; COMBINED IMMUNE-DEFICIENCY; PLASMINOGEN-ACTIVATOR GENE; PRE-B CELLS; V(D)J RECOMBINATION; PROTEIN-KINASE; HUMAN CHROMOSOME-8; INSITU HYBRIDIZATION; KU PROTEIN; POLYMERASE-BETA AB Severe combined immunodeficient (SCID) mice are deficient in a recombination process utilized in both DNA double-strand break repair and in V(D)J recombination. The phenotype of these mice involves both cellular hypersensitivity to ionizing radiation and a lack of B and T cell immunity. The catalytic subunit of DNA-dependent protein kinase, p350, was identified as a strong candidate for the murine gene SCID. Both p350 and a gene complementing the SCID defect colocalize to human chromosome 8q11. Chromosomal fragments expressing p350 complement the SCID phenotype, and p350 protein levels are greatly reduced in cells derived from SCID mice compared to cells from wild-type mice. C1 STANFORD UNIV,SCH MED,DEPT RADIAT ONCOL,STANFORD,CA 94305. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. ST JOHNS UNIV,DEPT BIOL SCI,JAMAICA,NY 11439. FU NCI NIH HHS [CA 15201, CA 37761]; NIGMS NIH HHS [GM48026] NR 70 TC 542 Z9 547 U1 0 U2 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD FEB 24 PY 1995 VL 267 IS 5201 BP 1178 EP 1183 DI 10.1126/science.7855601 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QJ237 UT WOS:A1995QJ23700041 PM 7855601 ER PT J AU LIANG, P PARDEE, AB AF LIANG, P PARDEE, AB TI ALTERNATIVES TO S-35 AS A LABEL FOR THE DIFFERENTIAL DISPLAY OF EUKARYOTIC MESSENGER-RNA - REPLY SO SCIENCE LA English DT Article RP LIANG, P (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH REGULAT,44 BINNEY ST,BOSTON,MA 02115, USA. NR 6 TC 15 Z9 16 U1 1 U2 1 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD FEB 24 PY 1995 VL 267 IS 5201 BP 1186 EP 1187 DI 10.1126/science.267.5201.1186-a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QJ237 UT WOS:A1995QJ23700044 ER PT J AU FALK, E FERNANDEZORTIZ, A AF FALK, E FERNANDEZORTIZ, A TI ROLE OF THROMBOSIS IN ATHEROSCLEROSIS AND ITS COMPLICATIONS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID LOW-DENSITY-LIPOPROTEIN; ACUTE MYOCARDIAL-INFARCTION; ACUTE CORONARY SYNDROMES; FIBROUS PLAQUES; ARTERY DISEASE; VESSEL WALL; PATHOGENESIS; LESIONS; HEPARIN; ASPIRIN AB The endothelium is intact but activated and dysfunctioning during the early phase of atherogenesis, owing to Increased endothelial permeability, many blood derived components, including hemostatic factors, are present in early as well as advanced atherosclerotic lesions, Insudated fibrin(ogen) and related degradation products and thrombin could contribute to atherogenesis by their chemotactic (attracting monocytes/macrophages) and mitogenic (stimulating cell proliferation) properties, All key cells in plaque may express thrombin receptors, indicating that thrombin may play a role in the genesis of uncomplicated atherosclerosis by mediating inflammatory and proliferative processes, Later, endothelial denudation with platelet adherence occurs over mature plaques, Then, Incorporation of microthrombi and probably platelet/thrombus derived growth factors are critical for the progressive growth of the smooth muscle cell-related plaque component, Besides transendothelial Influx and Incorporation of mural thrombi, blood products in atherosclerotic plaques may originate from hemorrhage through a ruptured plaque surface or from fragile newly formed vessels (neovascularization) frequently found at the base of advanced plaques, Rupture-related plaque progression due to luminal thrombosis and/or plaque hemorrhage is the most important mechanism underlying the unpredictable rapid progression of coronary lesions responsible for acute coronary syndromes, Both platelets and fibrin play a role In the dynamic thrombotic response to plaque rupture, There seem to be 3 main determinants for the outcome (mural or occlusive thrombosis): (1) character and extent of exposed thrombogenic materials (thrombogenic substrate); (2) degree of stenosis and surface irregularities (local flow disturbances); and (3) thrombotic-thrombolytic equilibrium at the time of rupture (systemic thrombotic propensity). Of note, the atheromatous ''gruel-like'' plaque component is dangerous, being mainly responsible for both vulnerability and thrombogenicity of atherosclerotic plaques. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP FALK, E (reprint author), ODENSE UNIV,INST FORENS MED,WINSLOWPK 17,DK-5000 ODENSE,DENMARK. RI Fernandez-Ortiz, Antonio/B-2227-2017 OI Fernandez-Ortiz, Antonio/0000-0002-3239-1910 NR 43 TC 30 Z9 31 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD FEB 23 PY 1995 VL 75 IS 6 BP B5 EP B11 DI 10.1016/0002-9149(95)80003-B PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QH854 UT WOS:A1995QH85400003 ER PT J AU PARVIN, JD MCCORMICK, RJ SHARP, PA FISHER, DE AF PARVIN, JD MCCORMICK, RJ SHARP, PA FISHER, DE TI PRE-BENDING OF A PROMOTER SEQUENCE ENHANCES AFFINITY FOR THE TATA-BINDING FACTOR SO NATURE LA English DT Article ID CRYSTAL-STRUCTURE; MINOR-GROOVE; BOX COMPLEX; TFIID BINDS; DNA; PROTEIN; ELEMENTS AB TATA-binding protein (TBP) binds the minor groove of the TATA element with the DNA bent 80 degrees towards the major groove(1-4). A constrained minicircle strategy(5) has been used to test the effect of DNA topology on the affinity of TBP for the TATA element. We report here that TBP bound to DNA which was slightly pre-bent towards the major groove with 100-fold higher affinity than unbent (linear) DNA of identical sequence and 300-foId higher affinity than DNA pre-bent towards the minor groove, Similar discrimination was observed with the holo-TFIID transcription complex. DNA topology, particularly bending, is determined by many factors including chromatin in cells and may, through changes in the affinity of the TATA factor, be important in the control of transcription. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. RI Parvin, Jeffrey/C-8955-2009 NR 19 TC 154 Z9 155 U1 1 U2 4 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 23 PY 1995 VL 373 IS 6516 BP 724 EP 727 DI 10.1038/373724a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QH928 UT WOS:A1995QH92800062 PM 7854460 ER PT J AU BENACERRAF, BR BRAMSON, R SCULLY, RE COOPERBERG, PL DOODY, DP EICHHORN, JH AF BENACERRAF, BR BRAMSON, R SCULLY, RE COOPERBERG, PL DOODY, DP EICHHORN, JH TI A ONE-MONTH-OLD GIRL WITH AN INTRAABDOMINAL MASS FOUND ON PRENATAL ULTRASONOGRAPHIC EXAMINATION - OVARIAN-CYST, PROBABLY FOLLICULAR WITH ANTENATAL TORSION, HEMORRHAGIC INFARCTION, AUTOAMPUTATION, AND IMPLANTATION ON THE MIDJEJUNAL MESENTERY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID SONOGRAPHIC DIAGNOSIS; ULTRASONIC DIAGNOSIS; MECONIUM PERITONITIS; FETAL; DUPLICATION; INUTERO; POLYHYDRAMNIOS; RESOLUTION; MANAGEMENT; FETUS C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP BENACERRAF, BR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 48 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 FEB 23 PY 1995 VL 332 IS 8 BP 522 EP 527 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA QH288 UT WOS:A1995QH28800008 ER PT J AU VANHOEK, AN WIENER, MC VERBAVATZ, JM BROWN, D LIPNIUNAS, PH TOWNSEND, RR VERKMAN, AS AF VANHOEK, AN WIENER, MC VERBAVATZ, JM BROWN, D LIPNIUNAS, PH TOWNSEND, RR VERKMAN, AS TI PURIFICATION AND STRUCTURE-FUNCTION ANALYSIS OF NATIVE, PNGASE F-TREATED, AND ENDO-BETA-GALACTOSIDASE-TREATED CHIP28 WATER CHANNELS SO BIOCHEMISTRY LA English DT Article ID RAT-KIDNEY; RADIATION INACTIVATION; MEMBRANE-PROTEIN; XENOPUS-OOCYTES; RECONSTITUTION; GLYCOPROTEINS; ERYTHROCYTES; LOCALIZATION; EXPRESSION; LIPOSOMES AB CHIP28 occurs naturally in glycosylated and nonglycosylated forms. The purpose of this study was to determine the role of glycosylation in CHIP28 structure and function. A new purification procedure based on phenylboronic acid-agarose (PEA) affinity chromatography was developed to isolate CHIP28. In purified native CHIP28 from erythrocytes, similar to 50% of CHIP28 molecules were glycosylated; each mole of glycosylated CHIP28 contained 5.4 kDa of monosaccharides consisting of 2 mol of Fuc, 8 mol of Gal, 1 mol of GalN, 13 mol of GlcN, 3 mol of Man, and 1 mol of Neu5Ac. The proportions of each monosaccharide and the sensitivity to endo-beta-galactosidase indicated that CHIP28 contained polylactosaminyl oligosaccharides. Glycosylated and nonglycosylated CHIP28 remained tightly associated when solubilized in octyl beta-D-glucoside (OG) and could not be separated by conventional chromatographic procedures. To remove the sugar moiety, CHIP28 was enzymatically deglycosylated by PNGase F and purified by Q-Sepharose anion-exchange and Erythrina cristagalli lectin chromatography. Highperformance size-exclusion chromatography revealed that native CHIP28 eluted as an apparent dimer, whereas deglycosylated CHIP28 eluted as an apparent monomer. In reconstituted proteoliposomes, deglycosylated CHIP28 had a single channel water permeability (p(f)) of 3.1 x 10(-14) cm(3)/s (10 degrees C), not different from that of 3.2 x 10(-14) cm(3)/s for native CHIP28. Circular dichroism of native and deglycosylated CHIP28 in OG revealed 45% and 48% alpha-helix, respectively; intrinsic tryptophan fluorescence showed no effects of glycosylation on tryptophan environment. Freeze-fracture electron microscopy with rotary shadowing indicated that native and deglycosylated CHIP28 assembled as tetramers in reconstituted proteoliposomes. The results establish a procedure to purify deglycosylated CHIP28 in functional form and indicate that glycosylation is required neither for the water transport function nor for the tetrameric assembly in membranes. C1 UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PHARMACEUT CHEM,SAN FRANCISCO,CA 94143. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. RP VANHOEK, AN (reprint author), UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST,DEPT MED,1246 HLTH SCI E TOWER,SAN FRANCISCO,CA 94143, USA. FU NCRR NIH HHS [RR01614]; NHLBI NIH HHS [HL51854]; NIGMS NIH HHS [GM24485] NR 39 TC 68 Z9 68 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 21 PY 1995 VL 34 IS 7 BP 2212 EP 2219 DI 10.1021/bi00007a015 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QH590 UT WOS:A1995QH59000015 PM 7532004 ER PT J AU SAWASDIKOSOL, S RAVICHANDRAN, KS LEE, KK CHANG, JH BURAKOFF, SJ AF SAWASDIKOSOL, S RAVICHANDRAN, KS LEE, KK CHANG, JH BURAKOFF, SJ TI CRK INTERACTS WITH TYROSINE-PHOSPHORYLATED P116 UPON T-CELL ACTIVATION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID SIGNAL TRANSDUCTION; SH3 DOMAINS; PROTEIN; ONCOGENE; RECEPTOR; FIBROBLASTS; KINASES AB Products of the crk oncogene are expressed in all tissues. Crk proteins are composed exclusively of Src homology 2 (SH2) and Src homology 3 (SH3) domains, and they have been implicated in intracellular signaling. For example, they participate as mediators of Ras activation during nerve growth factor stimulation of PC12 pheochromocytoma cells. We examined the role of Crk proteins during T cell receptor-mediated signaling and observed that Crk proteins specifically interact, via their SH2 domains, with a tyrosine-phosphorylated 116-kDa protein upon T cell activation. p116 may be related to the recently cloned fibroblast p130(cus) and/or p120-Cbl. In addition, we observed that GST-Crk fusion proteins and Crk-L bind, most likely via their SH3 domain, to C3G, a has guanine nucleotide exchange factor. Thus, the interaction of Crk with p116 and C3G strongly implicates Crk as a mediator of T cell receptor signaling, possibly involved in Ras activation. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SAWASDIKOSOL, S (reprint author), HARVARD UNIV,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI17258] NR 36 TC 75 Z9 75 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 17 PY 1995 VL 270 IS 7 BP 2893 EP 2896 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QG471 UT WOS:A1995QG47100004 PM 7531694 ER PT J AU PLUSKEY, S WANDLESS, TJ WALSH, CT SHOELSON, SE AF PLUSKEY, S WANDLESS, TJ WALSH, CT SHOELSON, SE TI POTENT STIMULATION OF SH-PTP2 PHOSPHATASE-ACTIVITY BY SIMULTANEOUS OCCUPANCY OF BOTH SH2 DOMAINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID SH2-CONTAINING PHOSPHOTYROSINE PHOSPHATASE; PROTEIN-TYROSINE-PHOSPHATASE; PHOSPHORYLATION; BINDING; ASSOCIATION; ACTIVATION; 3-KINASE AB Src homology 2 (SH2) domains are phosphotyrosine binding modules found within many cytoplasmic proteins. A major function of SR2 domains is to bring about the physical assembly of signaling complexes, We now show that, in addition, simultaneous occupancy of both SH2 domains of the phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) by a tethered peptide with two IRS-1-derived phosphorylation sites potently stimulates phosphatase activity. The concentration required for activation by the tethered peptide is 80-160-fold lower than either corresponding monophosphorylated peptide. Moreover, the diphosphorylated peptide stimulates catalytic activity 37-fold, compared with 9-16-fold for the monophosphorylated peptides. Mutational analyses of the SH2 domains of SH-PTP2 confirm that both SH2 domains participate in this effect. Binding studies with a tandem construct comprising the N- plus C-terminal SH2 domains show that the diphosphorylated peptide binds with 60-90-fold higher affinity than either monophosphorylated sequence. These results demonstrate that SH-PTP2 activity can be potently regulated by interacting via both of its SH2 domains with phosphoproteins having two cognate phosphorylation sites. C1 JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36836]; NIGMS NIH HHS [GM 20011] NR 25 TC 191 Z9 192 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 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 17 PY 1995 VL 270 IS 7 BP 2897 EP 2900 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QG471 UT WOS:A1995QG47100005 PM 7531695 ER PT J AU YAMADA, K CARPENTIER, JL CHEATHAM, B GONCALVES, E SHOELSON, SE KAHN, CR AF YAMADA, K CARPENTIER, JL CHEATHAM, B GONCALVES, E SHOELSON, SE KAHN, CR TI ROLE OF THE TRANSMEMBRANE DOMAIN AND FLANKING AMINO-ACIDS IN INTERNALIZATION AND DOWN-REGULATION OF THE INSULIN-RECEPTOR SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE KINASE-ACTIVITY; JUXTAMEMBRANE REGION; MEDIATED INTERNALIZATION; POLYPEPTIDE HORMONES; DIABETIC RATS; ENDOCYTOSIS; BINDING; DEGRADATION; SEQUENCE; PROTEIN AB We have characterized the internalization and downregulation of the insulin receptor and nine receptors with mutations in the transmembrane (TM) domain and/or flanking charged amino acids to define the role of this domain in receptor cycling, When expressed in Chinese hamster ovary cells, all had normal tetrameric structure and normal insulin-stimulated autophosphorylation/kinase activity, Replacement of the TM domain with that of the platelet derived growth factor receptor, insertion of 3 amino acids, and substitution of Asp for Val(938) or of Ala for either Gly(933) Or Pro(934) had no effect on internalization Replacement of the TER domain with that of c-neu or conversion of the charged amino acids on the cytoplasmic Bank to uncharged amino acids, on the other hand, resulted in a 40-60% decrease in insulin-dependent internalization rate constants, By contrast, substitution of Ala for both Gly(933) and Pro(934) increases lateral diffusion mobility and accelerates internalization rate, These changes in internalization were due to decreased or increased rates of redistribution of receptors from microvilli to the nonvillous cell surface, In all cases, receptor down-regulation and receptor-mediated insulin degradation paralleled the changes in internalization Thus, the structure of the transmembrane domain of the insulin receptor and flanking amino acids are major determinants of receptor internalization, insulin degradation, and receptor down-regulation. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. UNIV GENEVA,DEPT MORPHOL,CH-1211 GENEVA 4,SWITZERLAND. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK 36836, DK 31036] NR 51 TC 20 Z9 20 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 17 PY 1995 VL 270 IS 7 BP 3115 EP 3122 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QG471 UT WOS:A1995QG47100036 PM 7852393 ER PT J AU CARRERA, AC PARADIS, H BORLADO, LR ROBERTS, TM MARTINEZ, C AF CARRERA, AC PARADIS, H BORLADO, LR ROBERTS, TM MARTINEZ, C TI LCK UNIQUE DOMAIN INFLUENCES LCK SPECIFICITY AND BIOLOGICAL FUNCTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TYROSINE-PROTEIN-KINASE; CELL ANTIGEN RECEPTOR; ACTIVATED T-CELLS; SIGNAL TRANSDUCTION; PHOSPHATIDYLINOSITOL 3-KINASE; NUCLEAR FACTOR; BETA-CHAIN; P56LCK; EXPRESSION; P56(LCK) AB Src-family tyrosine kinases share structural and amino acid sequence homology, particularly in the catalytic domain as well as in the SH2 and SH3 domains of the regulatory region. However, each src-family member also contains a unique domain which is specific to and characteristic of each individual tyrosine kinase. These unique or specific domains may contribute to the functional specificity of each src-family kinase. To address this possibility, we analyzed the kinase activities and substrate specificities of the lymphoid src-kinase, pp56(lck), and a mutant of pp56(lck) lacking its specific domain. Our data show that both the wild type enzyme and the specific domain-deleted mutant displayed similar affinities for ATP and the non-physiological substrate denatured enolase. However, the specific domain-deleted mutant failed to phosphorylate a number of physiological substrates of pp56(lck). In addition, the ability of pp56(lck) to mediate induction of the interleukin-2 promoter was strongly impaired upon deletion of its specific domain. Thus, the unique domain is not required for the intrinsic kinase activity of pp56(lck), however, it influences substrate preference and contributes to the unique physiological function of this src-family tyrosine kinase. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CELLULAIRE & MOLEC,BOSTON,MA 02115. RP CARRERA, AC (reprint author), UNIV AUTONOMA MADRID,CSIC,CTR NACL BIOTECNOL,CAMPUS CANTOBLANCO,E-28049 MADRID,SPAIN. OI Carrera, Ana/0000-0002-3999-5434 FU NCI NIH HHS [CA 43803] NR 44 TC 25 Z9 25 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 17 PY 1995 VL 270 IS 7 BP 3385 EP 3391 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QG471 UT WOS:A1995QG47100074 PM 7531706 ER PT J AU HALEVY, O NOVITCH, BG SPICER, DB SKAPEK, SX RHEE, J HANNON, GJ BEACH, D LASSAR, AB AF HALEVY, O NOVITCH, BG SPICER, DB SKAPEK, SX RHEE, J HANNON, GJ BEACH, D LASSAR, AB TI CORRELATION OF TERMINAL CELL-CYCLE ARREST OF SKELETAL-MUSCLE WITH INDUCTION OF P21 BY MYOD SO SCIENCE LA English DT Article ID RETINOBLASTOMA GENE-PRODUCT; MYOGENIC DIFFERENTIATION; DEPENDENT KINASES; PROTEIN; EXPRESSION; E2F; P53; SUPPRESSION; ASSOCIATION; INHIBITION AB Skeletal muscle differentiation entails the coordination of muscle-specific gene expression and terminal withdrawal from the cell cycle. This cell cycle arrest in the G(0) phase requires the retinoblastoma tumor suppressor protein (Rb). The function of Rb is negatively regulated by cyclin-dependent kinases (Cdks), which are controlled by Cdk inhibitors. Expression of MyoD, a skeletal muscle-specific transcriptional regulator, activated the expression of the Cdk inhibitor p21 during differentiation of murine myocytes and in nonmyogenic cells. MyoD-mediated induction of p21 did not require the tumor suppressor protein p53 and correlated with cell cycle withdrawal. Thus, MyoD may induce terminal cell cycle arrest during skeletal muscle differentiation by increasing the expression of p21. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. COLD SPRING HARBOR LAB,HOWARD HUGHES MED INST,COLD SPRING HARBOR,NY 11724. DANA FARBER CANC INST,BOSTON,MA 02115. OI Novitch, Bennett/0000-0002-2696-3708 FU NIAMS NIH HHS [F32ARO8214-01A1]; NICHD NIH HHS [N01-HD-6-2915] NR 49 TC 1030 Z9 1039 U1 3 U2 10 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 17 PY 1995 VL 267 IS 5200 BP 1018 EP 1021 DI 10.1126/science.7863327 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QG990 UT WOS:A1995QG99000037 PM 7863327 ER PT J AU SKAPEK, SX RHEE, J SPICER, DB LASSAR, AB AF SKAPEK, SX RHEE, J SPICER, DB LASSAR, AB TI INHIBITION OF MYOGENIC DIFFERENTIATION IN PROLIFERATING MYOBLASTS BY CYCLIN D1-DEPENDENT KINASE SO SCIENCE LA English DT Article ID RETINOBLASTOMA PROTEIN; EXPRESSION; MUSCLE; P21 AB Although the myogenic regulator MyoD is expressed in proliferating myoblasts, differentiation of these cells is limited to the G(0) phase of the cell cycle. Forced expression of cyclin D1, but not cyclins A, B, or E, inhibited the ability of MyoD to transactivate muscle-specific genes and correlated with phosphorylation of MyoD. Transfection of myoblasts with cyclin-dependent kinase (Cdk) inhibitors p21 and p16 augmented muscle-specific gene expression in cells maintained in high concentrations of serum, suggesting that an active cyclin-Cdk complex suppresses MyoD function in proliferating cells. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. FU NIAMS NIH HHS [1F32AR08214-01A1] NR 33 TC 434 Z9 435 U1 1 U2 2 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD FEB 17 PY 1995 VL 267 IS 5200 BP 1022 EP 1024 DI 10.1126/science.7863328 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QG990 UT WOS:A1995QG99000038 PM 7863328 ER PT J AU BLUMENTHAL, D AF BLUMENTHAL, D TI HEALTH-CARE REFORM - PAST AND FUTURE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP BLUMENTHAL, D (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 11 TC 22 Z9 22 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 16 PY 1995 VL 332 IS 7 BP 465 EP 468 DI 10.1056/NEJM199502163320711 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA QF770 UT WOS:A1995QF77000011 PM 7824020 ER PT J AU ANDO, K GRIFFIN, JD AF ANDO, K GRIFFIN, JD TI CDK4 INTEGRATES GROWTH-STIMULATORY AND INHIBITORY SIGNALS DURING G1 PHASE OF HEMATOPOIETIC-CELLS SO ONCOGENE LA English DT Article DE HEMATOPOIESIS; CYCLINS; CELL CYCLE, INTERLEUKIN-3; CDK4; TGF-BETA-1; RETINOBLASTOMA ID RETINOBLASTOMA-SUSCEPTIBILITY GENE; D-TYPE CYCLINS; TGF-BETA; PROTEIN-KINASES; PRODUCT; EXPRESSION; PROGRESSION; SUBUNIT; ENTRY AB Proliferation of hematopoietic cells is controlled by both growth stimulatory and inhibitory cytokines acting primarily in G1, but the mechanism which integrate these disparate signals are unknown. In a myeloid cell line dependent on interleukin-3 (IL-3) for proliferation, expression of the cyclin dependent kinase Cdk4 and D-type cyclin partners, D2 and D3, in mid G1 was found to be directly related to the concentration of IL-3. TGF beta 1, which induces cell cycle arrest in mid-G1, blocked IL-3-induced expression of Cdk4, but had no effect on expression of cyclins D2 or D3. Sublines made to constitutively express Cdk4, but not lines constitutively expressing cyclins D2 or D3, were hyper responsive to IL-3 and resistant to TGF beta 1. Using an in vitro kinase assay with recombinant retinoblastoma protein (Rb) as a substrate, cyclin D2-associated kinase activity was shown to be induced in G1 by IL-3 and inhibited by TGF beta 1. Constitutive expression of Cdk4, but not cyclin D2 or D3, increased cyclin D2-associated Rb kinase activity and this activity could no longer be inhibited by TGF beta 1. Also, in vivo phosphorylation of Rb was inhibited by TGF beta 1 in wild type but not in Cdk4 lines. Cdk2 kinase activity was also decreased by TGF beta 1, and restored by overexpression of Cdk4. These results implicate Cdk4 activity as a mid G1 checkpoint sensitive to both growth stimulatory and inhibitory cytokines. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. NR 31 TC 48 Z9 48 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB 16 PY 1995 VL 10 IS 4 BP 751 EP 755 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QH612 UT WOS:A1995QH61200015 PM 7862452 ER PT J AU SOIFFER, RJ MURRAY, C RITZ, J PHILLIPS, N JACOBSOHN, D CHARTIER, S AMBROSINO, DM AF SOIFFER, RJ MURRAY, C RITZ, J PHILLIPS, N JACOBSOHN, D CHARTIER, S AMBROSINO, DM TI RECOMBINANT INTERLEUKIN-2 INFUSIONS AND DECREASED IGG2 SUBCLASS CONCENTRATIONS SO BLOOD LA English DT Article ID NATURAL-KILLER-CELLS; BONE-MARROW TRANSPLANTATION; STIMULATORY FACTOR-I; MURINE B-CELLS; INTERFERON-GAMMA; PROLONGED INFUSION; IGE PRODUCTION; ANTIBODY; INVIVO; LYMPHOCYTES AB The administration of low doses of recombinant interleukin-2 (rIL-2) in vivo to patients with malignant neoplasms has been demonstrated to selectively increase the number of circulating natural killer (NK) cells in these patients. Recent evidence from SCID mouse models suggests that IgG subclass levels can be influenced by the presence and activity of NK cells. Therefore, we sought to examine the effect of rIL-2 infusions on human serum IgG subclass concentrations. We determined serum IgG subclass concentrations in 27 cancer patients receiving low-dose rIL-2 by daily continuous intravenous infusion. Eleven of these patients had active, metastatic, nonhematologic tumors; 16 patients had received IL-2 when they were in a minimal residual disease state after autologous or allogeneic bone marrow transplantation. Samples obtained before beginning IL-2 therapy and 8 to 10 weeks into therapy were tested. Treatment with IL-2 resulted in an increase in the percentage of CD56+ NK cells from 18% to 54% (P = .0001). A significant decrease in geometric mean lgG2 concentration from 2,017 mu g/mL to 1,655 mu g/mL was noted over this time interval (P = .03). Furthermore, the geometric mean lgG2 concentration after treatment was significantly lower than that of healthy controls (P = .026). In contrast, no significant changes in serum IgG1, IgG3, or IgG4 were noted during r-IL2 infusions. Our data suggest that rIL-2 treatment selectively decreases serum lgG2 concentrations. We speculate that increased NK cells mediate downregulation of human serum IgG2. (C) 1995 by The American Society of Hematology. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA41619]; NIAID NIH HHS [AI29530, AI29623] NR 22 TC 5 Z9 5 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD FEB 15 PY 1995 VL 85 IS 4 BP 925 EP 928 PG 4 WC Hematology SC Hematology GA QG993 UT WOS:A1995QG99300009 PM 7849314 ER PT J AU KAMEOKA, J SATO, T TORIMOTO, Y SUGITA, K SOIFFER, RJ SCHLOSSMAN, SF RITZ, J MORIMOTO, C AF KAMEOKA, J SATO, T TORIMOTO, Y SUGITA, K SOIFFER, RJ SCHLOSSMAN, SF RITZ, J MORIMOTO, C TI DIFFERENTIAL CD26-MEDIATED ACTIVATION OF THE CD3 AND CD2 PATHWAYS AFTER CD6-DEPLETED ALLOGENEIC BONE-MARROW TRANSPLANTATION SO BLOOD LA English DT Article ID T-CELL ACTIVATION; DIPEPTIDYL PEPTIDASE-IV; VERSUS-HOST DISEASE; HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; IMMUNOGLOBULIN-SYNTHESIS; IMMUNOLOGICAL RECOVERY; GRAFT RECIPIENTS; RECEPTOR COMPLEX; ANTIGEN AB Patients who have undergone allogeneic bone marrow transplantation (allo-BMT) are susceptible to a variety of opportunistic infectious complications in the months to years after engraftment. Impaired in vitro T-cell functions have been documented in these patients, and these T-cell dysfunctions contribute to the prolonged immune deficiency after allo-BMT. In the present study, we examined the expression of CD26 as well as the reconstitution of CD26-mediated T-cell costimulation via the CD3 and CD2 pathways at various times in patients aged greater than 18 years after CD6-positive, T-cell depleted allo-BMT. We found that the percentage of CD26- and CD3-positive cells, as well as the levels of expression of both antigens, was lower than in normal controls during the first 4 months after CD6-depleted allo-BMT. Subsequently, the number of lymphocytes expressing CD3 and CD26 and the quantitative surface expression of CD3 and CD26 were not significantly different in patients and normal controls. Functional studies showed that CD26-mediated T-cell proliferation via the CD3 pathway was considerably improved and almost reached normal levels by 1 year, whereas recovery of CD26-mediated T-cell proliferation via the CD2 pathway was delayed for at least 2 years after CD6-depleted allo-BMT, As CD26 involvement in the regulation of human thymocyte activation is restricted preferentially to the CD3 pathway-unlike its involvement with both CD3 and CD2 pathways of peripheral T cells-our results suggest that the different effects of CD26-mediated costimulation via the CD3 and CD2 pathways after CD6-depleted allo-BMT may be a reflection of peripheral T-cell immaturity in those individuals, similar to that seen in mature medullary thymocytes or cord T lymphocytes. (C) 1995 by The American Society of Hematology, C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV HEMATOL MALIGNANCIES,BOSTON,MA. RI Ritz, Jerome/C-7929-2009 OI Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA55601]; NIAID NIH HHS [AI29530] NR 36 TC 15 Z9 15 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 FEB 15 PY 1995 VL 85 IS 4 BP 1132 EP 1137 PG 6 WC Hematology SC Hematology GA QG993 UT WOS:A1995QG99300032 PM 7849301 ER PT J AU HENDEL, RC CHEN, MH LITALIEN, GJ NEWELL, JB PAUL, SD EAGLE, KA LEPPO, JA AF HENDEL, RC CHEN, MH LITALIEN, GJ NEWELL, JB PAUL, SD EAGLE, KA LEPPO, JA TI SEX-DIFFERENCES IN PERIOPERATIVE AND LONG-TERM CARDIAC EVENT-FREE SURVIVAL IN VASCULAR-SURGERY PATIENTS - AN ANALYSIS OF CLINICAL AND SCINTIGRAPHIC VARIABLES SO CIRCULATION LA English DT Article DE CORONARY DISEASE; DIPYRIDAMOLE; SURGERY PROGNOSIS; IMAGING ID CORONARY-ARTERY DISEASE; MYOCARDIAL PERFUSION SCINTIGRAPHY; HEART-DISEASE; EXERCISE ELECTROCARDIOGRAPHY; DIPYRIDAMOLE INFUSION; WOMEN; MEN; RISK; INFARCTION; TRIALS AB Background Little information is available regarding the occurrence of perioperative and late cardiac events in women with vascular disease. The current study was performed to examine whether sex-specific differences exist in these outcomes in a large population of vascular surgery patients and to determine the value of clinical and dipyridamole thallium variables in predicting myocardial infarction and cardiac death. Methods and Results Preoperative dipyridamole thallium imaging was performed in 567 vascular surgery patients, including 380 men and 187 women. The incidence of nonfatal myocardial infarction and cardiac death was noted during the perioperative period and during a follow-up period of 50+/-5 months. Fixed and reversible thallium perfusion abnormalities were more common in men than in women (P<.001 and P=.004, respectively). Perioperative cardiac event rates were similar in men and women, 8.4% and 7.5%, respectively (P=.07). A transient thallium defect was associated with an increased risk of cardiac events by 3.9-fold in men (CI, 1.5 to 10.2) and 5.5-fold in women (CI, 1.4 to 22). Various clinical factors also were predictive of events but demonstrated substantial sex differences. For example, dipyridamole-induced ST-segment depression was strongly associated with perioperative events in men but not in women. There were 22 nonfatal myocardial infarctions and 29 cardiac deaths in men during the follow-up period, with comparable event rates noted for women. Cardiac event-free survival rates also were similar for men and women (P=.40). Multivariate analysis demonstrated that a history of heart failure was an important prognostic variable for both sexes, as was a fixed thallium defect. Significant sex differences in the predictive value of other clinical factors for late cardiac events was apparent. Conclusions The present study demonstrates that (1) thallium perfusion defects are more common in men; (2) transient thallium defects are associated with perioperative myocardial. infarction and cardiac death in both sexes; (3) long-term survival rates after vascular surgery are similar between men and women; (4) a fixed perfusion defect is predictive of late cardiac events in women, with a trend noted in men; and (5) sex-specific differences were noted with regard to the prognostic value of various clinical risk factors. Therefore, dipyridamole thallium plays a significant role in the assessment of perioperative and long-term prognosis for both male and female vascular surgery patients. On the basis of these observations, modifications in risk stratification based on sex may be appropriate for men and women with vascular disease. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. UNIV MASSACHUSETTS,MED CTR,DEPT NUCL MED,WORCESTER,MA. RP HENDEL, RC (reprint author), NORTHWESTERN UNIV,SCH MED,DEPT MED,DIV CARDIOL,250 E SUPER ST,SUITE 726,CHICAGO,IL 60611, USA. NR 36 TC 31 Z9 31 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 FEB 15 PY 1995 VL 91 IS 4 BP 1044 EP 1051 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QJ078 UT WOS:A1995QJ07800016 PM 7850940 ER PT J AU LEVINE, RA VLAHAKES, GJ LEFEBVRE, X GUERRERO, JL CAPE, EG YOGANATHAN, AP WEYMAN, AE AF LEVINE, RA VLAHAKES, GJ LEFEBVRE, X GUERRERO, JL CAPE, EG YOGANATHAN, AP WEYMAN, AE TI PAPILLARY-MUSCLE DISPLACEMENT CAUSES SYSTOLIC ANTERIOR MOTION OF THE MITRAL-VALVE - EXPERIMENTAL VALIDATION AND INSIGHTS INTO THE MECHANISM OF SUBAORTIC OBSTRUCTION SO CIRCULATION LA English DT Article DE CARDIOMYOPATHY; ECHOCARDIOGRAPHY; HYPERTROPHY ID OUTFLOW TRACT OBSTRUCTION; VENTRICULAR SEPTAL MYOTOMY; DIMENSIONAL ECHOCARDIOGRAPHIC ASSESSMENT; TERM FOLLOW-UP; HYPERTROPHIC CARDIOMYOPATHY; PRESSURE-GRADIENT; DOPPLER ECHOCARDIOGRAPHY; M-MODE; LEAFLET; REPAIR AB Background Systolic anterior motion (SAM) of the mitral valve in hypertrophic cardiomyopathy (HCM) has generally been explained by a Venturi effect related to septal hypertrophy, causing outflow tract narrowing and high velocities. Patients with HCM, however, also have primary abnormalities of the mitral apparatus, including anterior and inward or central displacement of the papillary muscles, and leaflet elongation. These findings have led to the hypothesis that changes in the mitral apparatus can be a primary cause of SAM by altering the forces acting on the mitral valve and its ability to move in response to them. Despite suggestive observations, however, it has never been prospectively demonstrated that such changes can actually cause SAM. Methods and Results To test this hypothesis in vivo, anterior papillary muscle displacement was created in 7 dogs studied by echocardiography, with controlled cardiac output and heart rate. In all 7 dogs, papillary muscle displacement caused SAM, with an outflow tract gradient (33+/-19 mm Hg) and mitral regurgitation in 6. As in patients with HCM, the mitral valve was displaced anteriorly and the coaptation point shifted toward the insertion of the leaflets, creating longer distal residual leaflets that moved anteriorly. Conclusions Primary changes in the mitral apparatus can cause SAM without septal hypertrophy. In this model, SAM appears to be determined by the ability of the leaflets to move anteriorly (papillary muscle displacement causing slack and increased residual leaflet length) and their interposition into the outflow stream by anterior displacement, determining the direction of this motion. Geometric factors observed in HCM and in patients with SAM without HCM can therefore play a primary role in causing SAM. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NON INVAS CARDIOL LAB,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC SURG UNIT,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. GEORGIA INST TECHNOL,SCH CHEM ENGN,CARDIOVASC FLUID MECH LAB,ATLANTA,GA 30332. UNIV PITTSBURGH,CHILDRENS HOSP PITTSBURGH,SCH MED,DIV PEDIAT CARDIOL,PITTSBURGH,PA. FU NHLBI NIH HHS [HL-38176] NR 72 TC 120 Z9 121 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD FEB 15 PY 1995 VL 91 IS 4 BP 1189 EP 1195 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA QJ078 UT WOS:A1995QJ07800034 PM 7850958 ER PT J AU HOSKINS, KF STOPFER, JE CALZONE, KA MERAJVER, SD REBBECK, TR GARBER, JE WEBER, BL AF HOSKINS, KF STOPFER, JE CALZONE, KA MERAJVER, SD REBBECK, TR GARBER, JE WEBER, BL TI ASSESSMENT AND COUNSELING FOR WOMEN WITH A FAMILY HISTORY OF BREAST-CANCER - A GUIDE FOR CLINICIAN SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID LINE P53 MUTATIONS; OVARIAN-CANCER; INDIVIDUALIZED PROBABILITIES; RISK; DISEASE; ONSET; PREVENTION; LINKAGE; AGE AB More women in all risk categories are seeking information regarding their individual breast cancer risk, and there is a need for their primary care clinicians to be able to assess familial risk factors for breast cancer, provide individualized risk information, and offer surveillance recommendations. Estimates of the number of women with a family history of breast cancer range from approximately 5% to 20%, depending on the population surveyed. Many of these women will not have a family history that suggests the presence of a highly penetrant breast cancer susceptibility gene. However, it small subset of such women will come from families with a striking incidence of breast and other cancers often associated with inherited mutations. The development and refinement of risk prediction models provide an epidemiologic basis for counseling women with a family history that does not appear related to a dominant susceptibility gene. In contrast, the recent isolation of BRCA1, the localization of BRCA2, and the acknowledgment that additional breast cancer susceptibility genes must exist provide a molecular basis for counseling some high-risk women. We present a guide for primary care clinicians that may be helpful in defining families as moderate or high risk, in determining individual risk in women with a family history of breast cancer based on this distinction, and for counseling women in a setting where the data necessary to design surveillance and prevention strategies are lacking. We include criteria for selecting women who may be candidates for detection of inherited mutations in breast cancer susceptibility genes. C1 UNIV PENN,MED CTR,DEPT INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT EPIDEMIOL & BIOSTAT,PHILADELPHIA,PA. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI. DANA FARBER CANC INST,BOSTON,MA. NR 63 TC 254 Z9 256 U1 1 U2 3 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 FEB 15 PY 1995 VL 273 IS 7 BP 577 EP 585 DI 10.1001/jama.273.7.577 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA QF686 UT WOS:A1995QF68600029 PM 7837392 ER PT J AU FRASER, CC SYKES, M LEE, RS SACHS, DH LEGUERN, C AF FRASER, CC SYKES, M LEE, RS SACHS, DH LEGUERN, C TI SPECIFIC UNRESPONSIVENESS TO A RETROVIRALLY-TRANSFERRED CLASS-I ANTIGEN IS CONTROLLED THROUGH THE HELPER PATHWAY SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MIXED ALLOGENEIC CHIMERAS; HEMATOPOIETIC STEM-CELLS; HUMAN GENE-THERAPY; BONE-MARROW; MONOCLONAL-ANTIBODIES; MYELOPROLIFERATIVE SYNDROME; SKIN ALLOGRAFTS; COMPLEX GENE; T-CELLS; EXPRESSION AB To investigate the potential role for gene therapy in induction of tolerance to solid organ grafts, we used a murine model based on the introduction of an allogeneic MHC class I gene (H-2K(b)) into hematopoietic cells of congenic animals differing only at the class I locus. The H-2K(b) gene was placed into a retroviral vector under the control of regulatory sequences of the myeloproliferative sarcoma virus long terminal repeat. Transplantation of H-2K(b) retrovirus-transduced autologous bone marrow into B10.AKM (K-k I-k D-q) recipients resulted in detectable levels of H-2K(b) RNA and cell surface protein in lymphoid and myeloid lineages. H-2K(b) expression was significant, although variable, in bone marrow Mac1(+) cells, in splenic B cells, and in CD4(+)/CD8(+) thymocytes 8 wk post-bone marrow transplantation. The recipients of the H-2K(b)-transduced bone marrow showed specifically delayed rejection of B10.MBR (K-b I-k D-q) skin grafts disparate only for K-b. However, B10.MBR skin grafts were rapidly rejected when grafted simultaneously with skin grafts from B10 (K-b I-b D-b) mice, a strain bearing additional third party alloantigens in association with K-b. Our experiments suggest that the hyporesponsive state induced by using the retrovirally mediated gene transfer model is characterized by the persistence of H-2K(b)-specific cytolytic T cell precursors, which may be inactive because of deficient T cell help. Tolerance to K-b induced by this approach may therefore be restricted to T helper cell lineages. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BOSTON,MA 02129. FU NHLBI NIH HHS [R01 HL48049]; NIAID NIH HHS [1RO1 AI33053] NR 49 TC 44 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 FEB 15 PY 1995 VL 154 IS 4 BP 1587 EP 1595 PG 9 WC Immunology SC Immunology GA QG208 UT WOS:A1995QG20800007 PM 7836744 ER PT J AU FRUMAN, DA BIERER, BE BENES, JE BURAKOFF, SJ AUSTEN, KF KATZ, HR AF FRUMAN, DA BIERER, BE BENES, JE BURAKOFF, SJ AUSTEN, KF KATZ, HR TI THE COMPLEX OF FK506-BINDING PROTEIN-12 AND FK506 INHIBITS CALCINEURIN PHOSPHATASE-ACTIVITY AND IGE ACTIVATION-INDUCED CYTOKINE TRANSCRIPTS, BUT NOT EXOCYTOSIS, IN MOUSE MAST-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CONNECTIVE-TISSUE-TYPE; SULFATE-E-PROTEOGLYCAN; MOLECULAR-CLONING; CYCLOSPORINE-A; SIGNAL-TRANSDUCTION; W/WV MICE; RELEASE; DIFFERENTIATION; IMMUNOPHILIN; INTRAPERITONEAL AB FK506 and cyclosporin A (CsA) are immunosuppressive agents that inhibit IL-2 production by activated T cells, but only CsA inhibits IgE activation-induced cytokine transcripts in mouse IL-3-dependent, bone marrow-derived mast cells (BMMC). We previously associated the resistance of BMMC to FK506 with a deficiency in the expression of FK506 binding protein (FKBP) 12, a molecule that forms a complex with FK506 capable of inhibiting calcineurin phosphatase activity in vitro. In this report, we establish that FKBP12 mediates FK506 inhibition of both calcineurin phosphatase activity and IgE activation-induced cytokine transcripts in a Kirsten murine sarcoma virus-immortalized mast cell line that is FKBP12 deficient. Overexpression of FKBP12 by transfection enhanced the ability of FK506 to inhibit calcineurin phosphatase activity (IC50 = 2 nM), compared with cells transfected with the expression vector alone (IC50 > 30 nM). The IC50 value for FK506 inhibition of IgE activation-induced transcripts for TNF-alpha decreased from 40 nM in vector control cells to 10 nM in FKBP12 transfectants. Similarly, the IC50 value for inhibition of IL-6 transcripts decreased from > 1000 nM in vector control cells to 35 nM in FKBP12 transfectants. In contrast, activation-elicited release of the secretory granule mediator beta-hexosaminidase was only partially inhibited by FK506 at 1000 nM, regardless of the levels of FKBP12 expressed by the cells. Thus, FKBP12 is the dominant cytosolic protein that mediates FK506 inhibition of TNF-alpha and IL-6 transcripts. C1 HARVARD UNIV,SCH MED,COMM IMMUNOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA. BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT RHEUMATOL & IMMUNOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI32101, AI22531, AI31599] NR 36 TC 37 Z9 38 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 FEB 15 PY 1995 VL 154 IS 4 BP 1846 EP 1851 PG 6 WC Immunology SC Immunology GA QG208 UT WOS:A1995QG20800035 PM 7530743 ER PT J AU LARSON, JS SCHUETZ, TJ KINGSTON, RE AF LARSON, JS SCHUETZ, TJ KINGSTON, RE TI IN-VITRO ACTIVATION OF PURIFIED HUMAN HEAT-SHOCK FACTOR BY HEAT SO BIOCHEMISTRY LA English DT Article ID HUMAN HSP70 PROMOTER; DNA-BINDING ACTIVITY; TRANSCRIPTION FACTOR; COILED-COIL; SCHIZOSACCHAROMYCES-POMBE; MOLECULAR-CLONING; PROTEIN; STRESS; YEAST; GENE AB A major regulatory step in the heat-induced transcription of heat shock protein (hsp) genes in eukaryotes is the activation of heat shock factor (HSF). In metazoans and Schizasaccharomyces pombe, HSF is present in unstressed cells but is unable to bind to its target DNA sequence element, the heat shock element (HSE). Heat induction of the DNA binding activity of HSF is a critical component required for activation of heat shock genes. Inactive HSF in extracts of non-heat shocked human cells can be heated in vitro to activate HSF, suggesting the factors required to sense temperature and activate HSF are soluble factors [Larson, J. S., Schuetz, T. J., and Kingston, R. E. (1988) Nature 335, 372-375]. We utilized the ability to purify human HSF in the active form to characterize further the in vitro activation of HSF. Here we have developed a procedure to deactivate the DNA binding ability of HSF. When purified and deactivated HSF is heated, the DNA binding ability of HSF is activated. This activation occurs most efficiently at 43 degrees C (heat shock temperature), but, in contrast to activation in the crude system, some activation of HSF is observed at 37 degrees C (non-heat shock temperature). We show that purified and deactivated HSF is similar to natural inactive HSF in both size and shape. Thus, the monomer to trimer transition that activates HSF can occur in a temperature-dependent fashion in the absence of other proteins. It is possible that these biochemical properties of HSF contribute to the ability of HSF to respond to heat in vivo. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. FU NIGMS NIH HHS [GM43901] NR 56 TC 47 Z9 48 U1 0 U2 4 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD FEB 14 PY 1995 VL 34 IS 6 BP 1902 EP 1911 DI 10.1021/bi00006a011 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QG848 UT WOS:A1995QG84800011 PM 7849050 ER PT J AU CHAKRABARTI, R MCCRACKEN, JB CHAKRABARTI, D SOUBA, WW AF CHAKRABARTI, R MCCRACKEN, JB CHAKRABARTI, D SOUBA, WW TI DETECTION OF A FUNCTIONAL PROMOTER ENHANCER IN AN INTRON-LESS HUMAN GENE ENCODING A GLUTAMINE SYNTHETASE-LIKE ENZYME SO GENE LA English DT Article DE TRANSCRIPTION; PSEUDOGENE; NUCLEOTIDE SEQUENCE; REGULATORY ELEMENT; TRANSCRIPT ID PROCESSED PSEUDOGENES; CELLS; FAMILY AB A human genomic clone, Psi GS, containing an intron-less glutamine synthetase (GS)-encoding pseudogene, was isolated by screening a human library, A sequence of 3004 bp, containing the GS coding region and both the 5' and 3' flanking sequences, was identified that exhibits all the characteristics of a processed pseudogene. The coding region shows 93% identity with the human GS cDNA (hGS) sequence and contains two frame-shifts and two termination codons. The coding sequence is flanked by a 9-bp AT repeat and a putative polyadenylation site, AATAAA, at the 3' end. Primer extension analysis and S1 nuclease mapping showed a transcription start point (tsp) 62 bp upstream from the start codon indicating a shorter untranslated region than hGS. Transfection of HeLa cells with cat constructs containing portions of the 5' flanking sequence showed the presence of a functional promoter/enhancer within 200 bp of the tsp, independent of its orientation. C1 UNIV FLORIDA,DEPT SURG,GAINESVILLE,FL 32610. UNIV FLORIDA,DEPT BIOCHEM & MOLEC BIOL,GAINESVILLE,FL 32610. UNIV FLORIDA,INTERDISCIPLINARY CTR BIOTECHNOL RES,GAINESVILLE,FL 32610. MASSACHUSETTS GEN HOSP,DEPT SURG,DIV SURG ONCOL,BOSTON,MA 02146. FU NHLBI NIH HHS [HL 44986] NR 24 TC 29 Z9 29 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0378-1119 J9 GENE JI Gene PD FEB 14 PY 1995 VL 153 IS 2 BP 163 EP 169 DI 10.1016/0378-1119(94)00751-D PG 7 WC Genetics & Heredity SC Genetics & Heredity GA QJ263 UT WOS:A1995QJ26300003 PM 7875583 ER PT J AU ROTHMAN, DL MAGNUSSON, I CLINE, G GERARD, D KAHN, CR SHULMAN, RG SHULMAN, GI AF ROTHMAN, DL MAGNUSSON, I CLINE, G GERARD, D KAHN, CR SHULMAN, RG SHULMAN, GI TI DECREASED MUSCLE GLUCOSE-TRANSPORT PHOSPHORYLATION IS AN EARLY DEFECT IN THE PATHOGENESIS OF NON-INSULIN-DEPENDENT DIABETES-MELLITUS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE C-13 NMR SPECTROSCOPY; GLYCOGEN METABOLISM; NONOXIDATIVE GLUCOSE METABOLISM ID HUMAN SKELETAL-MUSCLE; GLYCOGEN-SYNTHASE; NMR MEASUREMENT; BIOPSY SAMPLES; INCREASED RISK; WHOLE-BODY; RESISTANCE; HYPERGLYCEMIA; INVIVO; NIDDM AB Recent studies have demonstrated that reduced insulin-stimulated muscle glycogen synthesis is the major cause of insulin resistance in patients with non-insulin-dependent diabetes mellitus (NIDDM), This reduced rate has been assigned to a defect in either glucose transport or hexokinase activity, However it is unknown whether this is a primary or acquired defect in the pathogenesis of NIDDM, To examine this question, we measured the rate of muscle glycogen synthesis and the muscle glucose 6-phosphate (G6P) concentration using C-13 and P-31 NMR spectroscopy as well as oxidative and nonoxidative glucose metabolism in six lean, normoglycemic offspring of parents with NIDDM and seven age/weight-matched control subjects under hyperglycemic (approximate to 11 mM)-hyperinsulinemic (approximate to 480 pM) clamp conditions, The offspring of parents with NIDDM had a 50% reduction in total glucose metabolism, primarily due to a decrease in the nonoxidative component, The rate of muscle glycogen synthesis was reduced by 70% (P < 0.005) and muscle G6P concentration was reduced by 40% (P < 0.003), which suggests impaired muscle glucose transport/hexokinase activity. These changes were similar to those previously observed in subjects with fully developed NIDDM, When the control subjects were studied at similar insulin levels (approximate to 440 pM) but euglycemic plasma glucose concentration (approximate to 5 mM), both the rate of glycogen synthesis and the G6P concentration were reduced to values similar to the offspring of parents with NIDDM, We conclude that insulin-resistant offspring of parents with NIDDM have reduced nonoxidative glucose metabolism and muscle glycogen synthesis secondary to a defect in muscle glucose transport/hexokinase activity prior to the onset of overt hyperglycemia. The presence of this defect in these subjects suggests that it may be the primary factor in the pathogenesis of NIDDM. C1 YALE UNIV, SCH MED, DEPT INTERNAL MED, NEW HAVEN, CT 06520 USA. YALE UNIV, SCH MED, DEPT MOLEC BIOPHYS & BIOCHEM, NEW HAVEN, CT 06520 USA. JOSLIN DIABET CTR, BOSTON, MA 02215 USA. FU NIDDK NIH HHS [DK-34576, R01 DK040936, DK-45735, DK-49230] NR 40 TC 226 Z9 228 U1 0 U2 1 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 FEB 14 PY 1995 VL 92 IS 4 BP 983 EP 987 DI 10.1073/pnas.92.4.983 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QG770 UT WOS:A1995QG77000011 PM 7862678 ER PT J AU GOTTER, R GOLDMANN, WH ISENBERG, G AF GOTTER, R GOLDMANN, WH ISENBERG, G TI INTERNAL ACTIN FILAMENT DYNAMICS IN THE PRESENCE OF VINCULIN - A DYNAMIC LIGHT-SCATTERING STUDY SO FEBS LETTERS LA English DT Article DE ACTIN; VINCULIN; DYNAMIC LIGHT SCATTERING ID TALIN; NETWORKS AB Analyses of dynamic light scattering data by stretched exponential fit show that vinculin has a negligible influence on internal actin filament dynamics and actin bending stiffness which contrasts with our previous observations with talin, another actin and vinculin-binding protein from focal adhesions, The results here agree with kinetic and rheologic measurements. C1 TECH UNIV MUNICH,DEPT BIOPHYS,D-85747 GARCHING,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02129. RI Goldmann, Wolfgang/H-5572-2013 NR 17 TC 7 Z9 7 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 FEB 13 PY 1995 VL 359 IS 2-3 BP 220 EP 222 DI 10.1016/0014-5793(95)00045-B PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA QH112 UT WOS:A1995QH11200029 PM 7867804 ER PT J AU BERLIN, C BARGATZE, RF CAMPBELL, JJ VONANDRIAN, UH SZABO, MC HASSLEN, SR NELSON, RD BERG, EL ERLANDSEN, SL BUTCHER, EC AF BERLIN, C BARGATZE, RF CAMPBELL, JJ VONANDRIAN, UH SZABO, MC HASSLEN, SR NELSON, RD BERG, EL ERLANDSEN, SL BUTCHER, EC TI ALPHA-4 INTEGRINS MEDIATE LYMPHOCYTE ATTACHMENT AND ROLLING UNDER PHYSIOLOGICAL FLOW SO CELL LA English DT Article ID HIGH ENDOTHELIAL VENULES; VASCULAR ADDRESSIN; SELECTIN; ADHESION; MADCAM-1; LECAM-1; SPECIFICITY; LEUKOCYTES; MECHANISMS; EXPRESSION AB Of the several families of adhesion receptors involved in leukocyte-endoethelial cell interactions, only the selectins have been shown to initiate leukocyte interaction under physiologic shear; indeed, beta 2 (CD18) integrins responsible for neutrophil arrest are unable to engage without prior selectin-mediated rolling. In contrast, alpha 4 (CD49d) integrins are shown here to initiate lymphocyte contact (''tethering'') In vitro under shear and in the absence of a selectin contribution. The alpha 4 integrin ligands MAdCAM-1 and VCAM-1 support loose reversible interactions including rolling, as well as rapid sticking and arrest that is favored following integrin activation. Moreover, alpha 4 beta 7 mediates L-selectin (CD62L)-independent attachment of blood-borne lymphocytes to lamina propria venules in situ. Scanning electron microscopy of alpha 4 beta 7(hi) lymphoid cells reveals that, like L-selectin, alpha 4 beta 7 is highly concentrated on microvillous sites of initial cellular contact, whereas the beta 2 integrin LFA-1 is excluded from villi. Thus, alpha 4 but not beta 2 integrins can initiate leukocyte adhesion under flow, a capacity that may be in part a function of topographic presentation on microvilli. C1 VET AFFAIRS MED CTR,CTR MOLEC BIOL & MED,FOOTHILL RES CTR,PALO ALTO,CA 94304. MONTANA STATE UNIV,VET MOLEC BIOL LAB,BOZEMAN,MT 59717. UNIV MINNESOTA,DEPT LAB MED & PATHOL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT DERMATOL,MINNEAPOLIS,MN 55455. UNIV MINNESOTA,DEPT CELL BIOL & NEUROANAT,MINNEAPOLIS,MN 55455. CTR BLOOD RES,BOSTON,MA 02115. PROT DESIGN LABS,MT VIEW,CA 94043. RP BERLIN, C (reprint author), STANFORD UNIV,DEPT PATHOL,IMMUNOL & VASC BIOL LAB,STANFORD,CA 94305, USA. RI von Andrian, Ulrich/A-5775-2008; Berg, Ellen/D-9076-2014 OI Berg, Ellen/0000-0001-5149-6665 FU NIAID NIH HHS [AI19957, AI37832]; NIGMS NIH HHS [GM37734] NR 38 TC 797 Z9 808 U1 2 U2 16 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD FEB 10 PY 1995 VL 80 IS 3 BP 413 EP 422 DI 10.1016/0092-8674(95)90491-3 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA QG470 UT WOS:A1995QG47000007 PM 7532110 ER PT J AU SONGYANG, Z CARRAWAY, KL ECK, MJ HARRISON, SC FELDMAN, RA MOHAMMADI, M SCHLESSINGER, J HUBBARD, SR SMITH, DP ENG, C LORENZO, MJ PONDER, BAJ MAYER, BJ CANTLEY, LC AF SONGYANG, Z CARRAWAY, KL ECK, MJ HARRISON, SC FELDMAN, RA MOHAMMADI, M SCHLESSINGER, J HUBBARD, SR SMITH, DP ENG, C LORENZO, MJ PONDER, BAJ MAYER, BJ CANTLEY, LC TI CATALYTIC SPECIFICITY OF PROTEIN-TYROSINE KINASES IS CRITICAL FOR SELECTIVE SIGNALING SO NATURE LA English DT Article ID SUBSTRATE-SPECIFICITY; PHOSPHORYLATION; DOMAINS; INVITRO; ANTIGEN; SITES AB How do distinct protein-tyrosine kinases activate specific downstream events? Src-homology-2 (SH2) domains on tyrosine kinases or targets of tyrosine kinases recognize phosphotyrosine in a specific sequence context and thereby provide some specificity(1-3). The role of the catalytic site of tyrosine kinases in determining target specificity has not been fully investigated. Here we use a degenerate peptide library to show that each of nine tyrosine kinases investigated has a unique optimal peptide substrate. We find that the cytosolic tyrosine kinases preferentially phosphorylate peptides recognized by their own SH2 domains or closely related SH2 domains (group I; ref. 3), whereas receptor tyrosine kinases preferentially phosphorylate peptides recognized by subsets of group In SH2 domains(3). The importance of these findings for human disease is underscored by our observation that a point mutation in the RET receptor-type tyrosine kinase, which causes multiple endocrine neoplasia type 2B, results in a shift in peptide substrate specificity. C1 BETH ISRAEL HOSP,DEPT MED,DIV SIGNAL TRANSDUCT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02215. TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP,MOLEC MED LAB,BOSTON,MA 02115. UNIV MARYLAND,SCH MED,DEPT MICROBIOL & IMMUNOL,BALTIMORE,MD 21201. UNIV MARYLAND,MARYLAND BIOTECHNOL INST,CTR MED BIOTECHNOL,BALTIMORE,MD 21201. NYU,MED CTR,DEPT PHARMACOL,NEW YORK,NY 10016. COLUMBIA UNIV,DEPT BIOCHEM & MOLEC BIOPHYS,NEW YORK,NY 10032. UNIV CAMBRIDGE,DEPT PATHOL,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE CB2 1QP,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. RI Cantley, Lewis/D-1800-2014; OI Cantley, Lewis/0000-0002-1298-7653; Eng, Charis/0000-0002-3693-5145 NR 25 TC 730 Z9 737 U1 2 U2 19 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 9 PY 1995 VL 373 IS 6514 BP 536 EP 539 DI 10.1038/373536a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QF724 UT WOS:A1995QF72400063 PM 7845468 ER PT J AU VLAHAKES, GJ WARREN, RL AF VLAHAKES, GJ WARREN, RL TI TRAUMATIC RUPTURE OF THE AORTA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP VLAHAKES, GJ (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 6 TC 16 Z9 16 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD FEB 9 PY 1995 VL 332 IS 6 BP 389 EP 390 DI 10.1056/NEJM199502093320610 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA QF300 UT WOS:A1995QF30000010 PM 7824003 ER PT J AU RIEK, RP HANDSCHUMACHER, MD SUNG, SS TAN, M GLYNIAS, MJ SCHLUCHTER, MD NOVOTNY, J GRAHAM, RM AF RIEK, RP HANDSCHUMACHER, MD SUNG, SS TAN, M GLYNIAS, MJ SCHLUCHTER, MD NOVOTNY, J GRAHAM, RM TI EVOLUTIONARY CONSERVATION OF BOTH THE HYDROPHILIC AND HYDROPHOBIC NATURE OF TRANSMEMBRANE RESIDUES SO JOURNAL OF THEORETICAL BIOLOGY LA English DT Article ID PROTEIN-COUPLED RECEPTORS; HUMAN ASIALOGLYCOPROTEIN RECEPTOR; PHOTOSYNTHETIC REACTION CENTER; MULTIPLE SEQUENCE ALIGNMENT; AMINO-ACID-SEQUENCE; MEMBRANE-PROTEINS; SECONDARY STRUCTURE; 3-DIMENSIONAL STRUCTURE; STRUCTURE PREDICTION; MOLECULAR-CLONING AB An algorithm (HRG), developed to allow the pairwise comparisons of the aligned residues of several members of large gene families of polytopic integral membrane proteins is described. Using hydrophobicity scales, application of this algorithm allows the number and size of the membrane-spanning domains of bacteriorhodopsin, a polytopic protein whose structure has been partially determined, to be predicted with a high degree of accuracy (sensitivity 94%, specificity 82% for predicting the membrane embedded or extramembranous location of residues). As opposed to previously reported structure-prediction algorithms, delineation of putative transmembrane segments from connecting loops is also more clearly evident with the application of the HRG algorithm, even with proteins from widely divergent species. This indicates strong evolutionary pressure for the conservation of both the hydrophobic and hydrophilic character of residues in membrane-embedded regions of polytopic proteins, such as those of the G-protein-coupled receptor superfamily. These and other structural and functional implications evident from the application of the HRG algorithm are considered. C1 CLEVELAND CLIN FDN,RES INST,DEPT CARDIOVASC BIOL,CLEVELAND,OH 44195. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,CELLULAR & MOLEC RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. CLEVELAND CLIN FDN,RES INST,DEPT EPIDEMIOL & BIOSTAT,CLEVELAND,OH 44195. BRISTOL MYERS SQUIBB,DEPT MACROMOLEC MODELLING,PRINCETON,NJ 08543. CASE WESTERN RESERVE UNIV,DEPT PHYSIOL & BIOPHYS,CLEVELAND,OH 44106. FU NIGMS NIH HHS [GM 45985]; NINDS NIH HHS [NS 19583] NR 69 TC 28 Z9 28 U1 0 U2 0 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-5193 J9 J THEOR BIOL JI J. Theor. Biol. PD FEB 7 PY 1995 VL 172 IS 3 BP 245 EP 258 PG 14 WC Biology; Mathematical & Computational Biology SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology GA QH402 UT WOS:A1995QH40200006 PM 7715195 ER PT J AU STROHMEIER, GR REPPERT, SM LENCER, WI MADARA, JL AF STROHMEIER, GR REPPERT, SM LENCER, WI MADARA, JL TI THE A(2B) ADENOSINE RECEPTOR MEDIATES CAMP RESPONSES TO ADENOSINE RECEPTOR AGONISTS IN HUMAN INTESTINAL EPITHELIA SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NEUTROPHIL-DERIVED SECRETAGOGUE; CHLORIDE SECRETION; CELL-LINE; MOLECULAR-CLONING; CL SECRETION; T84 CELLS; ELECTROLYTE SECRETION; MESSENGER SYSTEMS; APICAL MEMBRANE; EXPRESSION AB Adenosine is thought to be a major effector in immunological stimulation of Cl- secretion in intestinal epithelia. Previous studies indicate that both apical and basolateral domains of intestinal epithelial cells possess functionally defined adenosine receptors. However, it is unclear whether the same receptor subclass is expressed, what the receptor subclass(es) is, or how the receptors signal the Cl- secretory response. We now characterize the intestinal epithelial adenosine receptor subtype using the model epithelium, T84. Both apical and basolateral adenosine receptor agonist response profiles revealed a hierarchy (ED(50)) of 5'-(N-ethylcarboxamido)adenosine > adenosine > CGS-21680. Similarly, inhibition studies revealed identical ID50 hierarchies for apical and basolateral antagonism by xanthine amine congener > 1,3-diethyl-8-phenylxanthine > aminophylline. Analyses of both agonist and antagonist pharmacological hierarchies in Chinese hamster ovary cells stably expressing the A(2b) receptor revealed these same hierarchies, Northern blots performed on RNA extracted from polarized T84 monolayers demonstrated no detectable message for A(1) or A(2a) adenosine receptor, but strong hybridization was detected for the A(2b) adenosine receptor. Subsequent Northern blots of RNA prepared from human alimentary tract revealed that A(2b) adenosine receptor message was heavily expressed throughout the colon, in the appendix, and more modestly expressed in the small intestine (ileum), Analyses of cAMP generation in T84 cells in response to adenosine indicated that the basolateral A(2b) receptor elicits Cl- secretion through this signaling pathway, Stimulation of Cl- secretion through the apical A(2b) receptor exhibited relatively small but significant increases in cAMP compared with basolateral stimulation, The protein kinase A inhibitor H-89, used at concentrations that did not affect short circuit current responses to the Ca2+-mediated agonist carbachol, effectively inhibited short circuit current elicited by either apical or basolateral adenosine, These data suggest that the major intestinal epithelial adenosine receptor is the A(2b) subclass, which is positively coupled to adenylate cyclase, Such observations have potentially important implications for the treatment of diarrheal diseases. C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA 02115. RP STROHMEIER, GR (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV GASTROINTESTINAL PATHOL,20 SHATTUCK ST,THORN 1419,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK-47662, DK-35932, DK-42125] NR 44 TC 179 Z9 179 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD FEB 3 PY 1995 VL 270 IS 5 BP 2387 EP 2394 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA QE493 UT WOS:A1995QE49300062 PM 7836474 ER PT J AU KAHN, CR AF KAHN, CR TI DIABETES - CAUSES OF INSULIN-RESISTANCE SO NATURE LA English DT Editorial Material ID SKELETAL-MUSCLE; TYROSINE KINASE; RECEPTOR; INHIBITOR; MELLITUS; HUMANS C1 JOSLIN DIABET CTR,BOSTON,MA 02215. RP KAHN, CR (reprint author), HARVARD UNIV,SCH MED,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 15 TC 70 Z9 73 U1 0 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 2 PY 1995 VL 373 IS 6513 BP 384 EP 385 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QE670 UT WOS:A1995QE67000028 PM 7830788 ER PT J AU SHIVDASANI, RA MAYER, EL ORKIN, SH AF SHIVDASANI, RA MAYER, EL ORKIN, SH TI ABSENCE OF BLOOD FORMATION IN MICE LACKING THE T-CELL LEUKEMIA ONCOPROTEIN TAL-1/SCL SO NATURE LA English DT Article ID DNA-BINDING MOTIF; CHROMOSOMAL TRANSLOCATION; ERYTHROID-DIFFERENTIATION; TARGETED MUTATION; GENE SCL; EXPRESSION; LEUKEMIA; PROTEIN; HEMATOPOIESIS; RECOMBINATION AB CHROMOSOMAL translocations associated with malignancies often result in deregulated expression of genes encoding transcription factors(1). In human T-cell leukaemias such regulators belong to diverse protein families and may normally be expressed widely (for example, Ttg-1/rbtn1, Ttg-2/rbtn2)(2'3), exclusively outside the haematopoietic system (for example, Hox11)(4), or specifically in haematopoietic cells and other selected sites (for example, tal-1/ SCL, lyl-1)(5,6). Aberrant expression within T cells is thought to interfere with programmes of normal maturation. The most frequently activated gene in acute T-cell leukaemias, tal-1 (also called SCL)(7,8), encodes a candidate regulator of haematopoietic development(9), a basic-helix-loop-helix protein(5), related to critical myogenic(10) and neurogenic(11) factors. Here we show by targeted gene disruption in mice(12) that tal-1 is essential for embryonic blood formation in vivo. With respect to embryonic erythropoiesis, tal-1 deficiency resembles loss of the erythroid transcription factor GATA-(13,14) or the LIM protein rbtn2(15). Profound reduction in myeloid cells cultured in vivo from tal-1 null yolk sacs suggests a broader defect manifest at the myelo-erythroid or multipotential progenitor cell level. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. RP SHIVDASANI, RA (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 30 TC 672 Z9 686 U1 3 U2 11 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD FEB 2 PY 1995 VL 373 IS 6513 BP 432 EP 434 DI 10.1038/373432a0 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA QE670 UT WOS:A1995QE67000057 PM 7830794 ER PT J AU ENG, C SMITH, DP MULLIGAN, LM HEALEY, CS ZVELEBIL, MJ STONEHOUSE, TJ PONDER, MA JACKSON, CE WATERFIELD, MD PONDER, BAJ AF ENG, C SMITH, DP MULLIGAN, LM HEALEY, CS ZVELEBIL, MJ STONEHOUSE, TJ PONDER, MA JACKSON, CE WATERFIELD, MD PONDER, BAJ TI A NOVEL POINT MUTATION IN THE TYROSINE KINASE DOMAIN OF THE RET PROTOONCOGENE IN SPORADIC MEDULLARY-THYROID CARCINOMA AND IN A FAMILY WITH FMTC SO ONCOGENE LA English DT Article DE MULTIPLE ENDOCRINE NEOPLASIA TYPE 2; RECEPTOR TYROSINE KINASE GENE ID MULTIPLE ENDOCRINE NEOPLASIA; PROTOONCOGENE; FEATURES AB Germline mutations within one of six codons of the RET proto-oncogene account for the majority of cases of multiple endocrine neoplasia (MEN) type 2A and type 2B and familial medullary thyroid carcinoma (FMTC). MEN 2A and FMTC mutations characterised thus far occur exclusively in the cysteine-rich domain of the extracellular region of RET. We now report a missense mutation in the intracellular tyrosine kinase domain of RET in the germline of a family with FMTC that does not have a cysteine codon mutation. In this family, the mutation, which alters GAG (GIu) to GAC (Asp) at codon 768, segregates with the FMTC phenotype. The same mutation was also detected in sporadic MTC but not in corresponding constitutional DNA, confirming that it is likely to be of pathological significance rather than a rare polymorphism. C1 UNIV CAMBRIDGE, DEPT PATHOL, CRC, HUMAN CANC GENET RES GRP, CAMBRIDGE CB2 1QP, ENGLAND. HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DEPT MED, DIV MED ONCOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DEPT MED, DIV CANC EPIDEMIOL & CONTROL, BOSTON, MA 02115 USA. QUEENS UNIV, DEPT PEDIAT, KINGSTON, ON K7L 3N6, CANADA. QUEENS UNIV, DEPT PATHOL, KINGSTON, ON K7L 3N6, CANADA. LUDWIG INST CANC RES, LONDON W1P 8BT, ENGLAND. HENRY FORD HOSP, DEPT MED, DETROIT, MI 48202 USA. UCL, DEPT BIOCHEM & MOLEC BIOL, LONDON, ENGLAND. OI Eng, Charis/0000-0002-3693-5145 NR 22 TC 248 Z9 252 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB 2 PY 1995 VL 10 IS 3 BP 509 EP 513 PG 5 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QF648 UT WOS:A1995QF64800011 PM 7845675 ER PT J AU LIU, QY YAN, YX MCCLURE, M NAKAGAWA, H FUJIMURA, F RUSTGI, AK AF LIU, QY YAN, YX MCCLURE, M NAKAGAWA, H FUJIMURA, F RUSTGI, AK TI MTS-1 (CDKN2) TUMOR-SUPPRESSOR GENE DELETIONS ARE A FREQUENT EVENT IN ESOPHAGUS SQUAMOUS CANCER AND PANCREATIC ADENOCARCINOMA CELL-LINES SO ONCOGENE LA English DT Note DE TUMOR SUPPRESSOR GENE; ESOPHAGUS CANCER; PANCREAS CANCER ID BLADDER-CANCER; CHROMOSOME-9; EXPRESSION; RETINOBLASTOMA; MUTATION; RECEPTOR; REGION AB MTS-1 is a candidate tumor suppressor gene on chromosome 9p21-22, a region frequently observed to have loss of heterozygosity in esophagus squamous cell carcinomas and pancreatic ductal adenocarcinomas. In order to determine whether MTS-1 sequences are deleted or mutated in cell lines derived from these cancers, we performed PCR amplification of MTS-1 exons 1 and 2. In this fashion, we found that 67% of esophagus squamous cancer cell lines have deletions of both exons 1 and 2, and 50% of pancreatic cancer cell lines have similar deletions. Furthermore, an additional 30% of pancreatic cancer cell lines harbored point mutations or microdeletions based on DNA sequencing. MTS-1 encodes p16, an inhibitor of cyclin-dependent kinase 4 (cdk4) which complexes with cyclin D1. Our data suggest that MTS-1 deletions and mutations may play an important role in the molecular pathogenesis of esophagus squamous cell and pancreatic cancers. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. MYRIAD GENET INC,SALT LAKE CITY,UT 84108. NR 26 TC 82 Z9 86 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD FEB 2 PY 1995 VL 10 IS 3 BP 619 EP 622 PG 4 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA QF648 UT WOS:A1995QF64800024 PM 7845688 ER PT J AU BLUMBERG, ML JOSEPH, AM FREEMAN, JR AF BLUMBERG, ML JOSEPH, AM FREEMAN, JR TI A STRATEGY FOR IMPROVING THE SUPERVISION AND PERFORMANCE OF MOONLIGHTING RESIDENTS SO ACADEMIC MEDICINE LA English DT Article ID PRACTICE GUIDELINES; HOUSE OFFICERS AB Background. In 1990 the Ambulatory Care Service of the Ralph H. Johnson Department of Veterans Affairs Medical Center, affiliated with the Medical University of South Carolina College of Medicine, developed written clinical protocols for the management of patients with certain high risk medical conditions. Method. Appropriateness of care was assessed by determining physician compliance to the protocols over a 24-month period (October 1990-September 1992). All physicians who did not comply received individualized feedback from the service chief. For the first 12 months, both staff physicians and moonlighting second- and third-year medical residents were assessed (a total of seven staff physicians and 20 residents participated in the study). For the second 12 months, only the residents were assessed. Results. The moonlighting residents were notably less consistent than the staff physicians in protocol compliance (95-100% for the staff physicians; 78-100% for the moonlighters). Additional interventions were then implemented to improve the moonlighters' utilization of the protocols. Moonlighters' compliance over the subsequent 12 months was less variable (mean compliance of 92%, SD, 3%, the first year versus 95%, SD, 8%, the second year). Conclusion. The strategy seemed to improve the supervision and performance of the moonlighting residents and promoted consistent delivery of high-quality outpatient care. C1 MED UNIV S CAROLINA,COLL MED,DEPT MED,CHARLESTON,SC. RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,AMBULATORY CARE SERV,CHARLESTON,SC. NR 10 TC 4 Z9 4 U1 0 U2 1 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD FEB PY 1995 VL 70 IS 2 BP 155 EP 157 DI 10.1097/00001888-199502000-00022 PG 3 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA QH465 UT WOS:A1995QH46500025 PM 7865044 ER PT J AU LIMMROTH, V WAEBER, C DIENER, HC AF LIMMROTH, V WAEBER, C DIENER, HC TI SUMATRIPTAN - UPDATE INFORMATION ON PHARMACOLOGY, MECHANISM OF ACTION AND CLINICAL USE SO AKTUELLE NEUROLOGIE LA German DT Article ID BLOOD-FLOW VELOCITY; GENE-RELATED PEPTIDE; RAT DURA-MATER; SUBCUTANEOUS SUMATRIPTAN; ANTIMIGRAINE DRUG; MIGRAINE ATTACKS; VASCULAR HEADACHES; CEREBRAL-ARTERIES; RECEPTORS; EFFICACY AB Sumatriptan is the first selective serotonin (5-HT) agonist, which in numerous clinical trials proved to be a potent drug in the treatment of migraine and cluster headache and received approval for these indications in several countries. It is the first anti-migraine drug to act receptor-specific and has introduced a new era of headache treatment. Initially suspected as a potent anti-migraine drug because of its ability to constrict cerebral arteries, recent evidence indicates that its beneficial effects might be due to a blockade of neurotransmitter release and neurotransmission. Besides providing the physician with another helpful tool in the treatment of headache, sumatriptan provides further insight into the pathophysiology of headache. The article reviews the current knowledge of pharmacology, mechanism and clinical trials. C1 UNIV ESSEN GESAMTHSCH,NEUROL KLIN & POLIKLIN,HUFELANDSTR 55,D-45122 ESSEN,GERMANY. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RI Waeber, Christian/A-8333-2009 OI Waeber, Christian/0000-0001-6078-0027 NR 72 TC 0 Z9 0 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0302-4350 J9 AKTUEL NEUROL JI Aktuelle Neurol. PD FEB PY 1995 VL 22 IS 1 BP 31 EP 39 DI 10.1055/s-2007-1017885 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA QJ574 UT WOS:A1995QJ57400006 ER PT J AU HARRIS, RA PROCTOR, WR MCQUILKIN, SJ KLEIN, RL MASCIA, MP WHATLEY, V WHITING, PJ DUNWIDDIE, TV AF HARRIS, RA PROCTOR, WR MCQUILKIN, SJ KLEIN, RL MASCIA, MP WHATLEY, V WHITING, PJ DUNWIDDIE, TV TI ETHANOL INCREASES GABA(A) RESPONSES IN CELLS STABLY TRANSFECTED WITH RECEPTOR SUBUNITS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE GABA; ETHANOL; CELL CULTURE; TRANSFECTION GABA; RECEPTORS ID GAMMA-AMINOBUTYRIC-ACID; GATED CHLORIDE CHANNELS; XENOPUS OOCYTES; MESSENGER-RNAS; ION CHANNELS; LONG-SLEEP; RAT-BRAIN; NEURONS; POTENTIATION; SITES AB Ethanol enhancement of GABA(A) receptor function has been found in some, but not all, studies. These results suggest the existence of ethanol-sensitive and -resistant receptors that may differ in subunit composition, although methodological differences (e,g., Cl-36(-) flux versus membrane currents) could also contribute to the different results. To examine these possibilities, we used mouse L(tk(-)) cells stably transfected with alpha(1) + beta(1) or alpha(1) + beta(1) + gamma(2L) GABA(A) receptor subunit DNAs and compared Cl-36(-) flux with whole-cell, patch-clamp measurements of GABA(A) receptor function. Both techniques detected a similar modulation of the GABA receptor by ethanol, flunitrazepam, and pentobarbital. The potentiating action of ethanol required the gamma-subunit and was maximal at a concentration of 10 mM, Similar ethanol potentiation was obtained with brief (20 msec) or long (2 sec) applications of GABA. Analysis of data obtained from individual cells expressing alpha(1) beta(1-)gamma(2L) subunits showed considerable variability in sensitivity to ethanol, particularly with concentrations of 30 and 100 mM, Ethanol potentiated GABA action if the cells were grown on coverslips coated with polylysine, but had no effect on GABA(A) receptors of cells grown on uncoated coverslips. Thus, ethanol action was influenced by the growth matrix. Taken together, these data indicate that a gamma-subunit is necessary, but not sufficient, for ethanol sensitivity in this cell system. We suggest that posttranslational processing, particularly receptor phosphorylation, may also be important and that stably transfected cells will be useful in elucidating these events. C1 UNIV COLORADO, SCH MED, DENVER VA MED CTR, ALCOHOL RES CTR, DENVER, CO USA. MERCK SHARP & DOHME LTD, NEUROSCI RES LABS, HARLOW CM20 2QR, ESSEX, ENGLAND. RP UNIV COLORADO, HLTH SCI CTR,SCH MED,DEPT PHARMACOL,C236, 4200 E 9TH AVE, DENVER, CO 80262 USA. NR 29 TC 102 Z9 104 U1 1 U2 2 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0145-6008 EI 1530-0277 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD FEB PY 1995 VL 19 IS 1 BP 226 EP 232 DI 10.1111/j.1530-0277.1995.tb01496.x PG 7 WC Substance Abuse SC Substance Abuse GA QG625 UT WOS:A1995QG62500036 PM 7771653 ER PT J AU GRACEFFO, MA OROURKE, RA HIBNER, C BOULET, AJ AF GRACEFFO, MA OROURKE, RA HIBNER, C BOULET, AJ TI THE TIME-COURSE AND RELATION OF POSITIVE SIGNAL-AVERAGED ELECTROCARDIOGRAMS BY TIME-DOMAIN AND SPECTRAL TEMPORAL MAPPING ANALYSES AFTER INFARCTION SO AMERICAN HEART JOURNAL LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; SUSTAINED VENTRICULAR-TACHYCARDIA; CORONARY-ARTERY DISEASE; HIGH-FREQUENCY COMPONENTS; BUNDLE-BRANCH BLOCK; LATE POTENTIALS; PROGNOSTIC-SIGNIFICANCE; ARRHYTHMIC EVENTS; QUANTITATIVE-ANALYSIS; NATURAL-HISTORY AB We evaluated the time course of development of positive signal-averaged electrocardiograms (SA-ECGs) by time-domain and Spectral Temporal Mapping(TM) (STM) analyses after myocardial infarction in 88 patients without bundle branch block, The incidence of positive SA-ECGs by time-domain analysis peaked at 4 to 8 weeks postinfarction whereas the peak incidence by STM analysis varied from 4 days to 4 to 10 months postinfarction. Positive time-domain SA-ECGs demonstrated a significantly reduced factor of normality (NF) compared with negative time-domain SA-ECGs by X, Z, or vector SIM analyses, but marked overlap was present for the standard deviations of positive and negative SA-ECGs in all STM leads. Chi square analysis demonstrated a significant correlation only between X-lead STM analysis and time-domain analysis; however, the two methods were markedly discordant. Although there is a statistically significant relation between time-domain and STM analyses of SA-ECGs, the two analyses are not clinically interchangeable. C1 UNIV TEXAS,HLTH SCI CTR,DIV CARDIOL,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. FU NHLBI NIH HHS [5 T32 HL07350] NR 52 TC 8 Z9 8 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1995 VL 129 IS 2 BP 238 EP 251 DI 10.1016/0002-8703(95)90004-7 PG 14 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QE518 UT WOS:A1995QE51800005 PM 7832095 ER PT J AU OSSWALD, S ROELKE, M ONUNAIN, SS TROUTON, TG SUAREZ, GES PEREZ, IE TORCHIANA, D MCGOVERN, BA GARAN, H RUSKIN, JN BROOKS, R AF OSSWALD, S ROELKE, M ONUNAIN, SS TROUTON, TG SUAREZ, GES PEREZ, IE TORCHIANA, D MCGOVERN, BA GARAN, H RUSKIN, JN BROOKS, R TI ELECTROCARDIOGRAPHIC PSEUDO-INFARCT PATTERNS AFTER IMPLANTATION OF CARDIOVERTER-DEFIBRILLATORS SO AMERICAN HEART JOURNAL LA English DT Article ID PERIOPERATIVE MYOCARDIAL-INFARCTION; NONCARDIAC SURGERY; CREATINE-KINASE; CORONARY-BYPASS; MEN AB Postoperative electrocardiographic (EGG) changes are frequently present after insertion of implantable cardioverter-defibrillators (ICD) and may mimic perioperative myocardial infarction (MI). The purpose of this study was to assess the incidence and clinical significance of postoperative ECG changes in relation to clinical, laboratory, and implantation data. In 25 (16%) of 156 patients undergoing ICD implantation, significant ECG changes (greater than or equal to 50% reduction in R-wave amplitude in greater than or equal to 3 leads or new Q waves in greater than or equal to 2 leads) were present 1 to 3 days after the operation and persisted at hospital discharge in 12 (8%). Presence of thoracotomy, the total number of induced ventricular fibrillation episodes, and the number of defibrillation shocks required during defibrillation threshold (DFT) testing correlated with postoperative ECG changes. Other factors associated with a significant R-wave loss in the lateral precordial reads included left-sided pleural effusion, lung infiltrates or atelectasis, and large defibrillator patch electrodes over the left ventricle or the lateral chest wall. Myocardial necrosis documented by elevated cardiac enzymes occurred in 6 (5%) of 151 patients without significant ECG changes and in 3 (12%) with (p value not significant). However, postoperative ECG changes associated with elevated enzymes were indistinguishable from changes unrelated to necrosis. Therefore the sensitivity and specificity of the surface ECG for detection of MI after ICD placement is poor. Multiple factors such as thoracotomy, myocardial injury from DFT testing, electric insulation, or shielding of the heart may contribute to the development of electrocardiographic pseudo-infarct patterns. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ARRHYTHMIA SERV,CARDIAC UNIT,BOSTON,MA 02114. NR 26 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 0002-8703 J9 AM HEART J JI Am. Heart J. PD FEB PY 1995 VL 129 IS 2 BP 265 EP 272 DI 10.1016/0002-8703(95)90007-1 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA QE518 UT WOS:A1995QE51800008 PM 7832098 ER PT J AU PAPAS, AS JOSHI, A BELANGER, AJ KENT, RL PALMER, CA DEPAOLA, PF AF PAPAS, AS JOSHI, A BELANGER, AJ KENT, RL PALMER, CA DEPAOLA, PF TI DIETARY MODELS FOR ROOT CARIES SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article; Proceedings Paper CT Symposium on Nutritional Aspects of Oral Health - New Perspectives, at the Joint Meeting of the IADR/AADR Nutrition-Group/Biochemistry-and-Nutrition-Section of the American-Association-of-Dental-Schools CY MAR 10, 1993 CL CHICAGO, IL SP INT ASSOC DENTAL RES, NUTR GRP, AMER ASSOC DENTAL RES, NUTR GRP DE DIET; DAIRY PRODUCTS; NUTRITION; ROOT CARIES; SUGAR ID DENTAL-CARIES; ENAMEL DEMINERALIZATION; FOOD CARIOGENICITY; CALCIUM LACTATE; SURFACE CARIES; BOVINE ENAMEL; ORAL HYGIENE; CHEESE; CHILDREN; PLAQUE AB A stepwise multiple logistic regression was computed to assess which of the nutritional variables differentiate the healthy and diseased group of participants in the Forsyth Specialized Caries Center (n = 275). Variables considered as candidates for the model included the consumption per week of sugars, starch, cheese, fruits and fruit juices, noncariogenic foods, and dairy products. Two variables-sugars nd cheese-were statistically significant by the stepwise procedure. Increased intake of sugar was associated with being in the root caries group, whereas high intake of cheese was negatively associated with root caries. Thus, cheese seems to have a protective effect after sugar intake is controlled for. Odds ratios were computed to quantify the influence of the variables. An increase of two exposures of sugar per day corresponded with an odds ratio of 1.26. The odds ratio continues to increase with sugar intake so that an increase to five exposures per day gives an odds ratio of 1.79. This model is consistent with past in vitro studies suggesting that cheese protects against caries formation when sugar intake is controlled for and that increasing frequency of sugar intake increases the odds of root caries. C1 HARVARD UNIV, SCH DENT MED, BOSTON, MA 02115 USA. BOSTON UNIV, BOSTON, MA 02215 USA. FORSYTH DENT RES CTR, BOSTON, MA USA. RP TUFTS UNIV, SCH DENT MED, 1 KNEELAND ST, SCH BOX 3, BOSTON, MA 02111 USA. FU NIDCR NIH HHS [DE-07009] NR 63 TC 25 Z9 25 U1 0 U2 0 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD FEB PY 1995 VL 61 IS 2 BP 417S EP 422S PG 6 WC Nutrition & Dietetics SC Nutrition & Dietetics GA QD951 UT WOS:A1995QD95100033 PM 7840087 ER PT J AU GOLDSTEIN, AM GORLICK, N GIBBS, D DELCASTILLO, CF AF GOLDSTEIN, AM GORLICK, N GIBBS, D DELCASTILLO, CF TI HEMOPERITONEUM DUE TO SPONTANEOUS RUPTURE OF THE UMBILICAL VEIN SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Note ID VARICES AB Portal hypertension often leads to collateralization of blood flow via variceal vessels that shunt blood from the portal to the systemic circulation. Rupture of an intra-abdominal varix is an unusual complication of portal hypertension that can lead to life-threatening hemoperitoneum. We describe a patient with portal hypertension secondary to Liver cirrhosis who presented with acute intra-abdominal hemorrhage. At laparotomy, she was found to have a rupture of the umbilical vein. The vessel was ligated, and the patient recovered uneventfully. The causes of hemoperitoneum in cirrhosis are discussed, and the previously reported cases of intra-abdominal variceal bleeding are reviewed. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP GOLDSTEIN, AM (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,15 PARKMAN ST,SUITE 464,BOSTON,MA 02114, USA. NR 13 TC 17 Z9 18 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD FEB PY 1995 VL 90 IS 2 BP 315 EP 317 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA QF747 UT WOS:A1995QF74700030 PM 7847310 ER PT J AU POTTS, JT CLAYTON, CP AF POTTS, JT CLAYTON, CP TI REPORT OF THE APM DIVERSITY SUBCOMMITTEE - REVIEW OF ISSUES AND INITIATIVES IN MINORITY RECRUITMENT AND FACULTY-DEVELOPMENT SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material ID INTERNAL-MEDICINE; FUTURE RP POTTS, JT (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114, USA. NR 8 TC 1 Z9 1 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1995 VL 98 IS 2 BP 105 EP 109 DI 10.1016/S0002-9343(99)80392-1 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA QF552 UT WOS:A1995QF55200001 ER PT J AU REEDE, JY AF REEDE, JY TI HARVARD MEDICAL-SCHOOL MINORITY FACULTY-DEVELOPMENT PROGRAM - ADDRESSING THE NEEDS OF MINORITIES IN THE BIOMEDICAL SCIENCES SO AMERICAN JOURNAL OF MEDICINE LA English DT Editorial Material C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHILDRENS HOSP,BOSTON,MA 02115. RP REEDE, JY (reprint author), HARVARD UNIV,SCH MED,MINOR FAC DEV PROGRAM,BOSTON,MA, USA. NR 7 TC 1 Z9 1 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD FEB PY 1995 VL 98 IS 2 BP 109 EP 113 DI 10.1016/S0002-9343(99)80393-3 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA QF552 UT WOS:A1995QF55200002 ER PT J AU DRAELOS, MT JACOBSON, AM WEINGER, K WIDOM, B RYAN, CM FINKELSTEIN, DM SIMONSON, DC AF DRAELOS, MT JACOBSON, AM WEINGER, K WIDOM, B RYAN, CM FINKELSTEIN, DM SIMONSON, DC TI COGNITIVE FUNCTION IN PATIENTS WITH INSULIN-DEPENDENT DIABETES-MELLITUS DURING HYPERGLYCEMIA AND HYPOGLYCEMIA SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID GLYCEMIC THRESHOLDS; GLUCOSE-LEVELS; PERFORMANCE; RESPONSES; SYMPTOMS; BRAIN; IDDM; COUNTERREGULATION; RADIOIMMUNOASSAY; DYSFUNCTION AB BACKGROUND: To determine the impact of glycemic control, gender, and other relevant parameters on cognitive function during exposure, to different blood glucose levels in patients with insulin-dependent diabetes mellitus (IDDM), we examined neuropsychologic function during experimentally induced periods of hyperglycemia and hypoglycemia. METHODS: We studied 20 men and 22 women, aged 18 to 44 years, with IDDM duration of 3 to 14 years and HbA1 values ranging from 5.8% to 18.0% (nondiabetic range 5.4% to 7.4%). We used a controlled experimental setting involving tests of sensory perceptual processing, simple motor abilities, attention, learning and memory, language, and spatial and constructional abilities at plasma glucose levels of 2.2, 5.6, 8.9, 14.4, and 21.1 mmol/L. Patients were blind to the glucose level. Tests used at each glucose level included reaction time (simple and choice), digit vigilance, trail making part B, word recall, digit sequence learning, and verbal fluency. RESULTS: All aspects of neuropsychologic function were diminished at 2.2 mmol/L when compared with basal levels of performance at 8.9 mmol/L, whereas no alterations were observed at 14.4 or 21.1 mmol/L. Tests involving associative learning, attention, and mental flexibility were the most affected during hypoglycemia. Glycemic control was not correlated with neuropsychologic function at any glucose level. Women demonstrated less of an impairment in neuropsychologic function than men at 2.2 mmol/L. CONCLUSIONS: Cognitive function in IDDM patients was generally well-preserved even at substantially elevated blood glucose levels. Deficits in all relevant areas of cognitive function occurred during hypoglycemia (2.2 mmol/L), irrespective of prior glycemic control, and women with IDDM were less cognitively impaired than men with IDDM during hypoglycemia. C1 JOSLIN DIABET CTR, PSYCHOSOCIAL UNIT, BOSTON, MA 02215 USA. NEW ENGLAND DEACONESS HOSP, BOSTON, MA 02215 USA. BRIGHAM & WOMENS HOSP, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA USA. UNIV PITTSBURGH, SCH MED, PITTSBURGH, PA USA. WESTERN PSYCHIAT INST & CLIN, PITTSBURGH, PA USA. HARVARD UNIV, SCH PUBL HLTH, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK42314, DK36836, DK27845] NR 50 TC 80 Z9 80 U1 1 U2 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0002-9343 EI 1555-7162 J9 AM J MED JI Am. J. Med. PD FEB PY 1995 VL 98 IS 2 BP 135 EP 144 DI 10.1016/S0002-9343(99)80397-0 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA QF552 UT WOS:A1995QF55200006 PM 7847430 ER PT J AU GRAGOUDAS, ES EGAN, KM WALSH, SM REGAN, S MUNZENRIDER, JE TARATUTA, V AF GRAGOUDAS, ES EGAN, KM WALSH, SM REGAN, S MUNZENRIDER, JE TARATUTA, V TI LENS CHANGES AFTER PROTON-BEAM IRRADIATION FOR UVEAL MELANOMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID MALIGNANT-MELANOMA; CATARACT-EXTRACTION; PLAQUE RADIOTHERAPY; RADIATION; EYE AB PURPOSE: Because limited data exist on the incidence of lens changes after therapeutic intraocular irradiation, we studied a group of patients who underwent proton irradiation for uveal melanoma, in order to estimate cumulative rates of radiation-induced posterior subcapsular opacities and age related lens changes at specific time points after irradiation. METHODS: Cumulative rates for each type of opacity were estimated from among the 383 patients, treated between 1987 and 1989, who had clear lenses or minimal lens changes before irradiation. Cox's proportional hazards model was used to evaluate the independent effects of tumor and treatment-related characteristics on the development of posterior subcapsular opacities in these patients. Risk factors for posterior subcapsular opacities were evaluated. RESULTS: By three years after irradiation, posterior subcapsular opacities had developed in 42% of the patients, and rates increased significantly with lens dose and with tumor height. The risk of posterior subcapsular opacities was over three times higher when the lens received a substantial dose of irradiation (adjusted relative risk, 3.25;95% confidence interval, 1.60-6.59), as compared with minimal dose, and was three times higher when the tumor was highly elevated (adjusted relative risk, 3.05; 95% confidence interval, 1,45-6.40) as compared with minimally elevated lesions. Opacities in the other segments of the lens were age related. CONCLUSIONS: These data show that patients receiving therapeutic intraocular irradiation have a high risk of developing posterior subcapsular opacities. As expected, the leading risk determinant of posterior subcapsular change is the amount of irradiation received by the lens. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA. OCULON CORP,CAMBRIDGE,MA. RP GRAGOUDAS, ES (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 26 TC 42 Z9 42 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 FEB PY 1995 VL 119 IS 2 BP 157 EP 164 PG 8 WC Ophthalmology SC Ophthalmology GA QE782 UT WOS:A1995QE78200005 PM 7832221 ER EF