FN Thomson Reuters Web of Science™ VR 1.0 PT J AU GROVES, JE LAVORI, PW ROSENBAUM, JF AF GROVES, JE LAVORI, PW ROSENBAUM, JF TI IN-HOSPITAL INJURIES OF MEDICAL AND SURGICAL PATIENTS - THE PREDICTIVE EFFECT OF A PRIOR INJURY SO PSYCHOSOMATIC MEDICINE LA English DT Article ID RISK AB Four hundred three consecutive injury victims admitted via emergency ward over a 3-month period were tracked with 403 contemporaneous controls with medical illness and blindly assessed for in-hospital accidents. There was a high frequency of "incidents" (n = 161 in 107 patients, mainly falls and medication errors), but injury victim admissions resembled medically ill controls when compared by the Kaplan-Meier method for cumulative probability of occurrence of an in-hospital incident. Accelerated failure/time models using the Weibull method to compute average times from admission to incident showed little difference between groups. Admission type (injury victim vs. control) did not predict psychiatric consultation, incident type, or multiple incidents in hospital. Although the injury group had a larger proportion of males and lower mean age, stratification to control for age and sex did not significantly discriminate injury victims from controls in production of incidents: Over all risk of incidents was random. By studying patients during a hospital stay, the effects of differences in individual environment and drug and alcohol intoxication are largely factored out; under these conditions the predictive effect of a prior injury becomes insignificant. In-hospital injury is associated with host factors long known to promote falls: increasing age, debility-cum-mobility, and central nervous system depressant medication. C1 MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. RP GROVES, JE (reprint author), HARVARD UNIV,SCH MED,FRUIT ST,BOSTON,MA 02114, USA. NR 46 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0033-3174 J9 PSYCHOSOM MED JI Psychosom. Med. PD MAY-JUN PY 1992 VL 54 IS 3 BP 264 EP 274 PG 11 WC Psychiatry; Psychology; Psychology, Multidisciplinary SC Psychiatry; Psychology GA HW895 UT WOS:A1992HW89500001 PM 1620803 ER PT J AU MCLOUD, TC NAIDICH, DP AF MCLOUD, TC NAIDICH, DP TI THORACIC DISEASE IN THE IMMUNOCOMPROMISED PATIENT SO RADIOLOGIC CLINICS OF NORTH AMERICA LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; PNEUMOCYSTIS-CARINII PNEUMONIA; IMMUNE-DEFICIENCY SYNDROME; COMPLICATING NEOPLASTIC DISEASE; NONSPECIFIC INTERSTITIAL PNEUMONITIS; OPEN LUNG-BIOPSY; KAPOSIS SARCOMA; PULMONARY COMPLICATIONS; SYNDROME AIDS; PATHOLOGIC CORRELATION C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. NYU MED CTR,BELLEVUE HOSP,DEPT RADIOL,NEW YORK,NY 10016. RP MCLOUD, TC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 113 TC 37 Z9 41 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 MAY PY 1992 VL 30 IS 3 BP 525 EP 554 PG 30 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HR682 UT WOS:A1992HR68200003 PM 1570394 ER PT J AU MARK, EJ SHIN, DH AF MARK, EJ SHIN, DH TI ASBESTOS AND THE HISTOGENESIS OF LUNG-CARCINOMA SO SEMINARS IN DIAGNOSTIC PATHOLOGY LA English DT Article DE ASBESTOS; LUNG CARCINOMA RP MARK, EJ (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 0 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 0740-2570 J9 SEMIN DIAGN PATHOL JI Semin. Diagn. Pathol. PD MAY PY 1992 VL 9 IS 2 BP 110 EP 116 PG 7 WC Medical Laboratory Technology; Pathology SC Medical Laboratory Technology; Pathology GA JA076 UT WOS:A1992JA07600004 PM 1609153 ER PT J AU BULLER, R WINTER, P AMERING, M KATSCHNIG, H LAVORI, PW DELTITO, JA KLERMAN, GL AF BULLER, R WINTER, P AMERING, M KATSCHNIG, H LAVORI, PW DELTITO, JA KLERMAN, GL TI CENTER DIFFERENCES AND CROSS-NATIONAL INVARIANCE IN HELP-SEEKING FOR PANIC DISORDER - A REPORT FROM THE CROSS-NATIONAL COLLABORATIVE PANIC STUDY SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY LA English DT Article ID MENTAL-HEALTH-SERVICES; PSYCHIATRIC-DISORDERS; DEPRESSION; ANXIETY; ILLNESS; PREVALENCE; MORTALITY; SITES AB Help-seeking behaviour for treatment of panic disorder was investigated in the sample of the Cross-National Collaborative Panic Study Second Phase. A total of 1168 patients were entered into this trial in 14 countries. Although there were significant center differences in prior treatment and utilization of health services there were also similarities. Treatment had been provided mainly by general practitioners. Drug treatment consisted mostly of prescription of classical tranquilizers and had a longer duration than treatment by psychotherapy. Patients with agoraphobic avoidance, past major depression and longer duration of illness used medical and psychiatric treatment facilities more intensely. Older and more severely disabled subjects were more frequently treated by medical health care providers and were more likely to receive psychotropic drugs. The results indicate that general practitioners carry an important load in the treatment of panic disorders but may need more information about recent developments in pharmacotherapy for this condition. C1 UNIV VIENNA,DEPT PSYCHIAT,A-1010 VIENNA,AUSTRIA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BIOSTAT UNIT,BOSTON,MA 02114. CORNELL UNIV,NEW YORK HOSP,MED CTR,ANXIETY & DEPRESS CLIN,WHITE PLAINS,NY 10605. CORNELL UNIV,MED CTR,PAYNE WHITNEY CLIN,DEPT PSYCHIAT,NEW YORK,NY 10021. RP BULLER, R (reprint author), UNIV MAINZ,DEPT PSYCHIAT,UNTERE ZAHLBACHER STR 8,W-6500 MAINZ,GERMANY. NR 29 TC 18 Z9 18 U1 5 U2 6 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0933-7954 J9 SOC PSYCH PSYCH EPID JI Soc. Psychiatry Psychiatr. Epidemiol. PD MAY PY 1992 VL 27 IS 3 BP 135 EP 141 PG 7 WC Psychiatry SC Psychiatry GA HY633 UT WOS:A1992HY63300005 PM 1621138 ER PT J AU BARSKY, AJ CLEARY, PD KLERMAN, GL AF BARSKY, AJ CLEARY, PD KLERMAN, GL TI DETERMINANTS OF PERCEIVED HEALTH-STATUS OF MEDICAL OUTPATIENTS SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE HEALTH PERCEPTION; HEALTH STATUS; ILLNESS; SOMATIZATION; HYPOCHONDRIASIS ID SELF-RATED HEALTH; NEGATIVE AFFECTIVITY; ARTHRITIC SEVERITY; PREDICTING PAIN; FOLLOW-UP; MORTALITY; PERSONALITY; VALIDITY; OLD; HYPOCHONDRIASIS AB The aim of this study was to examine the relative contributions made by medical morbidity, psychiatric disorder, functional status, and hypochondriacal attitudes to medical patients' opinions of their overall health status. The study was conducted in the general medical clinic of a large academic teaching hospital. Consecutive clinic visitors on randomly selected days were screened with a hypochondriasis self-report questionnaire, since the overall project was designed as a study of hypochondriasis. A random sample of the patients below a pre-established cutoff (n = 100), along with all those exceeding the cutoff (n = 88), returned to undergo a research battery. For this analysis, a representative sample of the entire clinic was reconstituted by weighting the data from patients above and below the screening cutoff in proportion to their prevalence in the clinic. Measures of psychiatric disorder (the Diagnostic Interview Schedule), personality disorder, functional status and disability, medical morbidity (from physician ratings and medical record audit), and hypochondriacal attitudes were obtained. Patient self-ratings of global health status were significantly correlated with aggregate medical morbidity (r = 0.36; P < 0.001); psychiatric morbidity (r = 0.48; P < 0.001); functional disability (for intermediate activities of daily living, r = 0.62; P < 0.001); hypochondriacal attitudes (r = 0.79; P < 0.001); and with the tendency to somatize (r = 0.77; P < 0.001). Using multiple regression analysis, the most powerful correlates of perceived global health were hypochondriasis, somatization and disability (model R2 = 0.762). Once these factors entered the regression model, objective measures of medical morbidity did not explain any additional variance in perceived health status. These findings suggest that how healthy patients feel is more closely related to their fears and beliefs about disease, and their tendency to somatize distress, than it is to clinical assessments of medical status. In addition, the findings confirm prior work indicating that functional impairment is also a key factor that patients take into account when judging how healthy they are. C1 HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SOCIAL MED,BOSTON,MA 02115. CORNELL UNIV,MED CTR,COLL MED,DEPT PSYCHIAT,NEW YORK,NY 10021. RP BARSKY, AJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,PSYCHIAT SERV & PRIMARY CARE PROGRAM,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH 40487] NR 66 TC 84 Z9 85 U1 4 U2 7 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 MAY PY 1992 VL 34 IS 10 BP 1147 EP 1154 DI 10.1016/0277-9536(92)90288-2 PG 8 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA HZ044 UT WOS:A1992HZ04400009 PM 1641676 ER PT J AU KATTAPURAM, SV KHURANA, JS ROSENTHAL, DI AF KATTAPURAM, SV KHURANA, JS ROSENTHAL, DI TI PERCUTANEOUS NEEDLE-BIOPSY OF THE SPINE SO SPINE LA English DT Article DE PERCUTANEOUS; BIOPSY; SPINE; METASTASES; TUMORS AB The results of 75 percutaneous needle biopsies of the spine were analyzed. There were 8 cervical, 25 thoracic, 27 lumbar, and 15 sacral biopsies. An accurate diagnosis was made in 92% of all cases. Metastatic disease yielded the best accuracy rate (96%). The lowest accuracy rate (82%) was noted with benign primary tumors and fractures. The results were better in female patients than male (97% vs. 86%). Larger needles gave slightly better accuracy (97%). No relationship between accuracy and spine level was found. There were two complications: one pneumothorax and an episode of self-limited hemorrhage. Percutaneous needle biopsy is a safe and reliable method of obtaining a diagnosis in many different spine lesions. RP KATTAPURAM, SV (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 57 Z9 62 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0362-2436 J9 SPINE JI SPINE PD MAY PY 1992 VL 17 IS 5 BP 561 EP 564 DI 10.1097/00007632-199205000-00014 PG 4 WC Clinical Neurology; Orthopedics SC Neurosciences & Neurology; Orthopedics GA HU682 UT WOS:A1992HU68200014 PM 1621156 ER PT J AU TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S MORTEL, KF AF TERAYAMA, Y MEYER, JS KAWAMURA, J WEATHERS, S MORTEL, KF TI PATTERNS OF CEREBRAL HYPOPERFUSION COMPARED AMONG DEMENTED AND NONDEMENTED PATIENTS WITH STROKE SO STROKE LA English DT Article DE DEMENTIA; WHITE MATTER; CEREBRAL INFARCTION ID MULTI-INFARCT DEMENTIA; WHITE-MATTER LESIONS; BLOOD-FLOW MEASUREMENTS; SCAN LEUKO-ARAIOSIS; VASCULAR DEMENTIA; RISK-FACTORS; COMPUTED-TOMOGRAPHY; NEUROLOGIC FINDINGS; NORMAL INDIVIDUALS; ELDERLY SUBJECTS AB Background and Purpose: No reports are available that compare local cerebral perfusion among groups of patients suffering from multiple cerebral infarctions with and without cognitive impairments. The present study was designed to correlate changes in regional cerebral perfusion that may lead to dementia among patients with multiple cerebral infarctions by comparing measurements of local cerebral blood flow. Methods: local perfusion was measured using xenon-contrasted computed tomographic scanning among two groups of patients who had suffered from multiple cerebral infarctions: Group D (n = 12) were demented and had severe cognitive impairments, and group I (n = 11) were cognitively intact. Results were compared with similar measurements among neurologically and cognitively normal, age-matched volunteers (group N, n = 16). Results: Mean local perfusion values were reduced among both groups with cerebral infarctions but to a more marked degree in group D (p < 0.05). Perfusion of cerebral white matter was diffusely and severely reduced in group D (p < 0.05) but was mildly reduced only in frontal and capsular white matter in group I (p < 0.05). Perfusion of cerebral cortex was reduced in frontal (p < 0.01) and temporal (p < 0.01) regions among both groups but to a significantly greater degree in group D subjects (frontal, p < 0.05; temporal, p < 0.01), who also showed hypoperfusion of the occipital cortex (p < 0.05), apparently because of underlying leukoaraiosis and cortical disconnections. Perfusion ot the basal ganglia was reduced to the same degree among both groups of stroke patients (p < 0.01). Conclusions: Leukoaraiosis with white matter hypoperfusion appears to be an important determinant for cognitive impairments among patients with multiple cerebral infarctions. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,BLDG 7,ROOM 209,2002 HOLCOMBE BLVD 151A,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR,RES SERV,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT RADIOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. NR 47 TC 23 Z9 23 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD MAY PY 1992 VL 23 IS 5 BP 686 EP 692 PG 7 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HT395 UT WOS:A1992HT39500011 PM 1579967 ER PT J AU ALBERT, DM NIFFENEGGER, AS WILLSON, JKV AF ALBERT, DM NIFFENEGGER, AS WILLSON, JKV TI TREATMENT OF METASTATIC UVEAL MELANOMA - REVIEW AND RECOMMENDATIONS SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE CHEMOTHERAPY; CUTANEOUS MELANOMA; IMMUNOTHERAPY; MALIGNANT MELANOMA; UVEAL MELANOMA ID ACTIVATED KILLER CELLS; PHASE-I TRIAL; MALIGNANT-MELANOMA; CHOROIDAL MELANOMA; OCULAR MELANOMA; ADJUVANT CHEMOTHERAPY; HEPATIC METASTASES; POLYVINYL SPONGE; CILIARY BODY; CISPLATIN AB This article reviews the published clinical responses of metastatic uveal melanoma and metastatic cutaneous melanoma with visceral involvement to current therapeutic protocols. Despite isolated patient responses to systemic treatment, no effective treatment currently exists for metastatic uveal melanoma. However, several new approaches involving interferons and interleukin and combination chemotherapy have shown some activity against metastatic cutaneous melanoma. The effectiveness against metastatic uveal melanomas has not been determined. A new approach to intrahepatic administration of chemotherapy also warrants further evaluation because of the high incidence of hepatic involvement with metastatic uveal melanoma. When an effective systemic treatment is found, early administration as an adjuvant to primary treatment may provide the best strategy for control of systemic spread. C1 UNIV HOSP CLEVELAND,IRELAND CANC CTR,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,CLEVELAND,OH 44106. RP ALBERT, DM (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DAVID G COGAN EYE PATHOL LAB,BOSTON,MA 02114, USA. NR 56 TC 97 Z9 98 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD MAY-JUN PY 1992 VL 36 IS 6 BP 429 EP 438 DI 10.1016/S0039-6257(05)80024-4 PG 10 WC Ophthalmology SC Ophthalmology GA HT496 UT WOS:A1992HT49600005 PM 1589858 ER PT J AU KERK, D GEE, A DEWHIRST, FE DRUM, AS ELSTON, RA AF KERK, D GEE, A DEWHIRST, FE DRUM, AS ELSTON, RA TI PHYLOGENETIC PLACEMENT OF NUCLEAR INCLUSION-X (NIX) INTO THE GAMMA-SUBCLASS OF PROTEOBACTERIA ON THE BASIS OF 16S RIBOSOMAL-RNA SEQUENCE COMPARISONS SO SYSTEMATIC AND APPLIED MICROBIOLOGY LA English DT Article DE NUCLEAR INCLUSION-X (NIX); 16S RIBOSOMAL-RNA SEQUENCE; INTRANUCLEAR PATHOGEN; PHYLOGENY; SILIQUA-PATULA ID NUCLEOTIDE-SEQUENCE; SECONDARY STRUCTURE; ESCHERICHIA-COLI; GEN-NOV; DIVERSITY; NEISSERIA; KINGELLA AB "Nuclear Inclusion X (NIX)" is an obligate intranuclear pathogen which has been associated with severe mortality of the Pacific razor clam, Siliqua patula. We have developed procedures to isolate the organism, and purify its RNA. A partial sequence (692 bases) was determined by directly sequencing the 16S rRNA using a modified Sanger dideoxy chain termination method. Analysis of the sequence data indicated that the NIX organism is a member of the gamma subclass of the eubacterial class Proteobacteria. Comparison of the NIX sequence with those of over 100 gamma proteobacteria revealed no closely related organisms. NIX sequence is most similar to that of Pseudomonas aeruginosa and Cardiobacterium hominis, at a level of about 89 percent. This relatively distant relationship suggests that NIX represents a novel genus. C1 FORSYTH DENT CTR,BOSTON,MA 02115. BATTELLE MEM INST,MARINE RES LAB,SEQUIM,WA 98382. RP KERK, D (reprint author), PACIFIC LUTHERAN UNIV,DEPT BIOL,TACOMA,WA 98447, USA. NR 29 TC 7 Z9 7 U1 2 U2 3 PU GUSTAV FISCHER VERLAG PI JENA PA VILLENGANG 2, D-07745 JENA, GERMANY SN 0723-2020 J9 SYST APPL MICROBIOL JI Syst. Appl. Microbiol. PD MAY PY 1992 VL 15 IS 2 BP 191 EP 196 PG 6 WC Biotechnology & Applied Microbiology; Microbiology SC Biotechnology & Applied Microbiology; Microbiology GA HW364 UT WOS:A1992HW36400005 ER PT J AU SYKES, M ABRAHAM, VS AF SYKES, M ABRAHAM, VS TI THE MECHANISM OF IL-2-MEDIATED PROTECTION AGAINST GVHD IN MICE .2. PROTECTION OCCURS INDEPENDENTLY OF NK/LAK CELLS SO TRANSPLANTATION LA English DT Article ID VERSUS-HOST DISEASE; ACTIVATED KILLER-CELLS; MARROW GRAFT-REJECTION; MURINE BONE-MARROW; T-CELL; IFN-GAMMA; INTERLEUKIN-2; ANTIBODY; MOUSE; PHENOTYPE AB We have recently demonstrated that high-dose IL-2, when begun on the day of bone marrow transplantation, has a potent protective effect against graft-vs.-host disease mortality, especially when coadministered with T cell-depleted syngeneic bone marrow cells. Because several groups of investigators have demonstrated that lymphokine-activated killer cells can mediate GVHD protection, we hypothesized that the mechanism of protection by IL-2 administration might involve the in vivo activation of natural killer and/or LAK cells. In order to test this hypothesis, we evaluated the effect of IL-2 administration on the number of NK1+ cells and on NK-mediated cytotoxic activity in recipients of GVHD-producing inocula. Furthermore, we evaluated the effects on IL-2-induced GVHD protection of depleting NK cells and LAK precursor cells in vivo with mAb against NK1.1 or antiserum against asialo GM1. The results demonstrate that: (1) The number of NK1+ cells is not increased in spleens of IL-2-treated compared with control recipients of GVHD-producing inocula; (2) NK activity is not increased in IL-2-treated compared with control recipients of GVHD-producing inocula during or immediately following the period of IL-2 administration; (3) depletion of NK cells and LAK precursors from the donor and host influenced the time course of GVHD-related mortality in a complex fashion; and (4) IL-2-induced GVHD protection is largely independent of the activity of an NK or LAK cell population of donor or host origin. IL-2-induced GVHD protection therefore reflects primarily the activity of non-LAK protective cell populations, or it may be a direct inhibitory effect on responding donor cell populations as they encounter host antigen. C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BLDG 149,13TH ST,BOSTON,MA 02129, USA. FU NIAID NIH HHS [AI 31158-01, R01AI31158] NR 36 TC 17 Z9 17 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 MAY PY 1992 VL 53 IS 5 BP 1063 EP 1070 DI 10.1097/00007890-199205000-00018 PG 8 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HU814 UT WOS:A1992HU81400018 PM 1533968 ER PT J AU AKSENTIJEVICH, I SACHS, DH SYKES, M AF AKSENTIJEVICH, I SACHS, DH SYKES, M TI HUMORAL TOLERANCE IN XENOGENEIC BMT RECIPIENTS CONDITIONED BY A NONMYELOABLATIVE REGIMEN SO TRANSPLANTATION LA English DT Article ID MONOCLONAL-ANTIBODIES; MICE; RESISTANCE; ANTIGENS; BARRIER; GRAFTS; CELLS; L3T4 AB We have recently demonstrated that mixed xenogeneic chimerism and donor-specific tolerance can be produced across a species barrier using a nonmyeloablative conditioning regimen (1). This regimen involves pretreatment of B10 mice with mAbs against CD4+, CD8+, Thy1+, and NK1+ cells, followed by a low dose (3 Gy) of whole-body irradiation and a higher dose (7 Gy) of local irradiation to the thymus and administration of T cell-depleted (TCD) F344 strain rat BMC. Although initial mixed chimerism and de novo maturation of donor rat T cells can be demonstrated in such animals, chimerism is gradually lost, and is no longer detectable by 6 months following BMT (1). When rat skin was grafted onto such animals 4 months following BMT, however, donor-specific skin graft survival was markedly prolonged, while non-donor type rat skin grafts were rapidly rejected (1). These results suggested that a state of donor-specific T cell tolerance existed, and that loss of chimerism was not due to a T cell-mediated immune mechanism. In order to evaluate the possibility that a humoral mechanism might mediate delayed loss of xenogeneic bone marrow grafts, we have now examined sera at various times for the presence of antibody against donor cells. Groups of animals not receiving the complete tolerizing mAb pretreatment regimen produced antidonor lymphocytotoxic antibody in response to BMT and skin grafting. Flow cytometric studies demonstrated high levels of IgM and of IgG of all subclasses against rat BMC and spleen cells in these control mice immunized by BMT. In contrast, such antibodies were not detectable in sera from animals receiving BMT following pretreatment with the tolerance-inducing mAb regimen. Furthermore, the tolerant animals did not develop cytotoxic antibodies or high levels of IgM or IgG against donor BMC after loss of hematopoietic chimerism. Donor-type skin grafts were eventually rejected, but rejection of these and repeat skin grafts did not lead to a cytotoxic antibody response. Low levels of rat BMC-binding IgM antibody were also detected in sera of tolerant mice, but the intensity of staining of rat BMC was lower than that of control animals receiving conditioning without BMT. These results suggest that a state of tolerance exists among cells responsible for T cell-dependent IgG antibody subclasses and natural IgM antibodies in animals receiving BMT following this nonmyeloablative conditioning regimen. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,SURG SERV,BLDG 149,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X NR 20 TC 54 Z9 54 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 MAY PY 1992 VL 53 IS 5 BP 1108 EP 1114 DI 10.1097/00007890-199205000-00025 PG 7 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HU814 UT WOS:A1992HU81400025 PM 1585475 ER PT J AU GARNICK, MB AF GARNICK, MB TI TUMORS OF THE URINARY-TRACT SO WESTERN JOURNAL OF MEDICINE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP GARNICK, MB (reprint author), INST CLIN DEV GENET,CAMBRIDGE,MA, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0093-0415 J9 WESTERN J MED JI West. J. Med. PD MAY PY 1992 VL 156 IS 5 BP 556 EP 556 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HU809 UT WOS:A1992HU80900019 PM 18750877 ER PT J AU GUDAS, JM AF GUDAS, JM TI TRANSCRIPTION INITIATION AND TEMPORAL EXPRESSION OF THYMIDINE KINASE MESSENGER-RNA IN CHINESE-HAMSTER CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID SERUM-STIMULATED CELLS; DNA-SYNTHESIS; S-PHASE; GENE-EXPRESSION; PROMOTER; CYCLE; INDUCTION; SEQUENCES C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. FU NCI NIH HHS [CA08317-03]; NIGMS NIH HHS [GM 24571] NR 32 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 30 PY 1992 VL 184 IS 2 BP 908 EP 914 DI 10.1016/0006-291X(92)90677-D PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HR526 UT WOS:A1992HR52600053 PM 1575759 ER PT J AU JAIN, J MCCAFFREY, PG VALGEARCHER, VE RAO, A AF JAIN, J MCCAFFREY, PG VALGEARCHER, VE RAO, A TI NUCLEAR FACTOR OF ACTIVATED T-CELLS CONTAINS FOS AND JUN SO NATURE LA English DT Article ID LYMPHOCYTE-SPECIFIC FACTORS; INTERLEUKIN-2 GENE; DNA-BINDING; PROTEIN; ENHANCER; ELEMENT; AP-1 AB THE nuclear factor NF-AT (ref. 1) is induced in T cells stimulated through the T-cell receptor/CD3 complex, and is required for interleukin-2 (IL-2) gene induction. Although NF-AT has not been cloned or purified, there is evidence that it is a major target for immunosuppression by cyclosporin A (CsA) and FK506 (refs 2-7). NF-AT induction may require two activation-dependent events: the CsA-sensitive translocation of a pre-existing component and the CsA-resistant synthesis of a nuclear component 8. Here we report that the newly synthesized nuclear component of NF-AT is the transcription factor AP-1. We show that the inducible nuclear form of NF-AT contains Fos and Jun proteins. Furthermore, we identify a pre-existing NF-AT-binding factor that is present in hypotonic extracts of unstimulated T cells. On the basis of binding, reconstitution and cotransfection experiments, we propose that activation of NF-AT occurs in at least two stages: a CsA-sensitive stage involving modification and/or translocation of the pre-existing NF-AT complex, and a CsA-insensitive stage involving the addition of newly synthesized Fos or Fos/Jun proteins to the pre-existing complex. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. NR 26 TC 473 Z9 476 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD APR 30 PY 1992 VL 356 IS 6372 BP 801 EP 804 DI 10.1038/356801a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR186 UT WOS:A1992HR18600053 PM 1533441 ER PT J AU ROELKE, M YURCHAK, PM AF ROELKE, M YURCHAK, PM TI ADENOSINE AND SUPRAVENTRICULAR TACHYCARDIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID DIPYRIDAMOLE RP ROELKE, M (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 TC 3 Z9 3 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 30 PY 1992 VL 326 IS 18 BP 1221 EP 1221 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HR008 UT WOS:A1992HR00800016 PM 1557100 ER PT J AU VINIEGRA, S CRAGOE, EJ RABITO, CA AF VINIEGRA, S CRAGOE, EJ RABITO, CA TI HETEROGENEITY OF THE NA+-H+ ANTIPORT SYSTEMS IN RENAL-CELLS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Article DE SODIUM ION PROTON ANTIPORT SYSTEM; URINE ACIDIFICATION; AMILORIDE; CELL PROLIFERATION; INTRACELLULAR PH REGULATION; PH REGULATION; SODIUM ION TRANSPORT ID MICROVILLUS MEMBRANE-VESICLES; PROXIMAL TUBULAR CELLS; GROWTH-FACTOR; INTRACELLULAR PH; EPITHELIAL-CELL; PHORBOL ESTERS; LINE LLC-PK1; QUIESCENT FIBROBLASTS; OCCLUDING JUNCTIONS; VOLUME REGULATION AB This study analyzes the differential characteristics of the Na+-H+ antiport systems observed in several epithelial and non-epithelial renal cell lines. Confluent monolayers of LLC-PK1A cells have a Na+-H+ antiport system located in the apical membrane of the cell. This system, however, is not expressed during cell proliferation or after incubation in the presence of different mitogenic agents. In contrast, confluent monolayers of MDCK4 express minimal Na+-H+ antiport activity in the confluent monolayer state but reach maximal antiport activity during cell proliferation or after activation of the cells by different mitogenic agents. Similar results were obtained with the renal fibroblastic cell line BHK. The system present in MDCK4 cells is localized in the basolateral membrane of the epithelial cell. In LLC-PK1A cells, an increase in the extracellular Na+ concentration produces a hyperbolic increase in the activity of the Na+-H+ antiporter. In MDCK, and BHK cells, however, an increase in external Na+ produces a sigmoid activation of the system. Maximal activation of the system occur at a pH(o) 7.5 in LLC-PK1A cells and pH(o) 7.0 in MDCK4 cells. The Na+-H+ antiporter of LLC-PK1A cells is more sensitive to the inhibitory effect of amiloride (K(i) 1.8 . 10(-7) M) than is the antiporter of MDCK4 cells (K(i) 7.0 . 10(-6) M). Moreover, 5-(N-methyl-N-isobutyl)amiloride is the most effective inhibitor of Na+-H+ exchange in LLC-PK1A cells, but the least effective inhibitor in MDCK4 cells. Conversely, the analog, 5-(N,N-dimethyl)amiloride, is the most effective inhibitor of Na+-H+ exchange in MDCK4 cells, but is the least effective inhibitor in LLC-PK1A cells. These results support the hypothesis that Na+-H+ exchange observed in LLC-PK1A and other cell lines may represent the activity of different Na+-H+ antiporters. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Viniegra, Salvador/K-5063-2014 OI Viniegra, Salvador/0000-0002-3892-8563 FU NIDDK NIH HHS [DK 27401] NR 52 TC 4 Z9 4 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-3002 J9 BIOCHIM BIOPHYS ACTA PD APR 29 PY 1992 VL 1106 IS 1 BP 99 EP 109 DI 10.1016/0005-2736(92)90227-D PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HT697 UT WOS:A1992HT69700014 PM 1316166 ER PT J AU CHANG, YH TEICHERT, U SMITH, JA AF CHANG, YH TEICHERT, U SMITH, JA TI MOLECULAR-CLONING, SEQUENCING, DELETION, AND OVEREXPRESSION OF A METHIONINE AMINOPEPTIDASE GENE FROM SACCHAROMYCES-CEREVISIAE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ESCHERICHIA-COLI; SALMONELLA-TYPHIMURIUM; BINDING DOMAINS; ZINC-FINGER; PROTEINS; YEAST; ACETYLTRANSFERASE; SPECIFICITIES; PURIFICATION; INVIVO AB A yeast gene for a methionine aminopeptidase, one of the central enzymes in protein synthesis, was cloned and sequenced. The DNA sequence encodes a precursor protein containing 387 amino acid residues. The mature protein, whose NH2-terminal sequence, was confirmed by Edman degradation, consists of 377 amino acids. The function of the 10-residue sequence at the NH2 terminus, containing 1 serine and 6 threonine residues, remains to be established. In contrast to the structure of the prokaryotic enzyme, the yeast methionine aminopeptidase consists of two functional domains: a unique NH2-terminal domain containing two motifs resembling zine fingers, which may allow the protein to interact with ribosomes, and a catalytic COOH-terminal domain resembling other prokaryotic methionine aminopeptidases. Furthermore, unlike the case for the prokaryotic gene, the deletion of the yeast MAP1 gene is not lethal, suggesting for the first time that alternative NH2-terminal processing pathway(s) exist for cleaving methionine from nascent polypeptide chains in eukaryotic cells. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP CHANG, YH (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 33 TC 101 Z9 103 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 APR 25 PY 1992 VL 267 IS 12 BP 8007 EP 8011 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HQ185 UT WOS:A1992HQ18500011 PM 1569059 ER PT J AU CHAN, BMC ELICES, MJ MURPHY, E HEMLER, ME AF CHAN, BMC ELICES, MJ MURPHY, E HEMLER, ME TI ADHESION TO VASCULAR CELL-ADHESION MOLECULE-1 AND FIBRONECTIN - COMPARISON OF ALPHA-4-BETA-1 (VLA-4) AND ALPHA-4-BETA-7 ON THE HUMAN B-CELL LINE JY SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MONOCLONAL-ANTIBODY; INTESTINAL LYMPHOCYTES; PLASMA FIBRONECTIN; INTEGRIN VLA-4; BINDING-SITE; BETA-SUBUNIT; T-CELLS; RECEPTOR; ATTACHMENT; IDENTIFICATION AB Most mononuclear leukocytes and cell lines express the integrin alpha-4-beta-1 (VLA-4) heterodimer. In this study we have used Northern blotting and immunoprecipitation experiments to demonstrate that a B lymphoblastoid cell line (JY) expressed the integrin beta-7 subunit in association with alpha-4. These alpha-4-beta-7-positive JY cells bound poorly or not at all to VLA-4 ligands (soluble form of vascular cell adhesion molecule 1 (sVCAM-1) and the CS1 region of fibronectin). In contrast, a beta-1-positive variant of JY cells (selected to express a mixture of alpha-4-beta-1 and alpha-4-beta-7) bound avidly to VLA-4 ligands, and this binding was completely inhibitable by anti-alpha-4 and anti-beta-1 monoclonal antibodies. Thus, beta-1 expression appears to be a critically important component of VLA-4-mediated binding to its ligands. After either JY or JY-beta-1 cells were stimulated for 15 min with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate, the majority of adhesion to VCAM or fibronectin remained alpha-4- and beta-1-dependent, but a low amount of adhesion to sVCAM-1 or fibronectin became alpha-4-dependent, beta-1-independent, thus suggesting a role for alpha-4-beta-7. In summary, we have found (i) that alpha-4-beta-7 makes little or no contribution to fibronectin or VCAM-1 binding on unstimulated JY cells, (ii) that alpha-4-beta-7 perhaps makes a minor contribution to ligand binding on 12-O-tetradecanoylphorbol-13-acetate-stimulated cells, and (iii) that alpha-4-beta-1 is the functionally dominant VCAM-1 and fibronectin receptor even when expressed in relatively low amounts compared to alpha-4-beta-7. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCI NIH HHS [CA-42368]; NIGMS NIH HHS [GM-38903] NR 59 TC 234 Z9 234 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 25 PY 1992 VL 267 IS 12 BP 8366 EP 8370 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HQ185 UT WOS:A1992HQ18500064 PM 1373725 ER PT J AU MOORE, SEH SPIRO, RG AF MOORE, SEH SPIRO, RG TI CHARACTERIZATION OF THE ENDOMANNOSIDASE PATHWAY FOR THE PROCESSING OF N-LINKED OLIGOSACCHARIDES IN GLUCOSIDASE-II-DEFICIENT AND PARENT MOUSE LYMPHOMA-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LIVER MICROSOMAL GLUCOSIDASES; ROUGH ENDOPLASMIC-RETICULUM; ALPHA-D-MANNOSIDASE; RAT-LIVER; GLYCOPROTEIN-BIOSYNTHESIS; SECRETORY GLYCOPROTEINS; CARBOHYDRATE UNITS; GOLGI-COMPLEX; INHIBITORS; TRANSPORT AB Studies on N-linked oligosaccharide processing in the mouse lymphoma glucosidase II-deficient mutant cell line (PHA(R)2.7) as well as the parent BW5147 cells indicated that the former maintain their capacity to synthesize complex carbohydrate units through the use of the deglucosylation mechanism provided by endomannosidase. The in vivo activity of this enzyme was evident in the mutant cells from their production of substantial amounts of glucosylated mannose saccharides, predominantly Glc2Man; moreover, in the presence of 1-deoxymannojirimycin or kifunensine to prevent processing by mannosidase I, N-linked Man8GlcNAc2 was observed entirely in the form of the characteristic isomer in which the terminal mannose of the alpha-1,3-linked branch is missing (isomer A). In contrast, parent lymphoma cells, as well as HepG2 cells in the presence of 1-deoxymannojirimycin accumulated Man9GlcNAc2 as the primary deglucosylated N-linked oligosaccharide and contained only about 16% of their Man8GlcNAc2 as isomer A. In the presence of the glucosidase inhibitor castanospermine the mutant released Glc3Man instead of Glc2Man, and the parent cells converted their deglucosylation machinery to the endomannosidase route. Despite the mutant's capacity to accommodate a large traffic through this pathway no increase in the in vitro determined endomannosidase activity was evident. The exclusive utilization of endomannosidase by the mutant for the deglucosylation of its predominant N-linked Glc2Man9GlcNAc2 permitted an exploration of the in vivo site of this enzyme's action. Pulse-chase studies utilizing sucrose-D2O density gradient centrifugation indicated that the Glc2Man9GlcNAc2 to Man8GlcNAc2 conversion is a relatively late event that is temporally separated from the endoplasmic reticulum-situated processing of Glc3Man9GlcNAc2 to Glc2Man9GlcNAc2 and in contrast to the latter takes place in the Golgi compartment. C1 JOSLIN DIABET CTR, ELLIOTT P JOSLIN RES LAB, 1 JOSLIN PL, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MED, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK17477] NR 30 TC 44 Z9 44 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA SN 0021-9258 EI 1083-351X J9 J BIOL CHEM JI J. Biol. Chem. PD APR 25 PY 1992 VL 267 IS 12 BP 8443 EP 8451 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HQ185 UT WOS:A1992HQ18500075 PM 1533222 ER PT J AU WATKINS, H ROSENZWEIG, A HWANG, DS LEVI, T MCKENNA, W SEIDMAN, CE SEIDMAN, JG AF WATKINS, H ROSENZWEIG, A HWANG, DS LEVI, T MCKENNA, W SEIDMAN, CE SEIDMAN, JG TI CHARACTERISTICS AND PROGNOSTIC IMPLICATIONS OF MYOSIN MISSENSE MUTATIONS IN FAMILIAL HYPERTROPHIC CARDIOMYOPATHY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID HEAVY-CHAIN GENE; SUDDEN-DEATH; CLINICAL MANIFESTATIONS; PATHO-PHYSIOLOGY; MOLECULAR-BASIS; INTERRELATIONS; SEQUENCE; THERAPY; DNA AB Background. Familial hypertrophic cardiomyopathy is characterized by a variable degree of myocardial hypertrophy and a wide range of symptoms. Different mutations in the beta-cardiac myosin heavy-chain gene have been identified in three affected families. However, neither the proportion of cases attributable to myosin mutations nor the effects of different mutations on clinical outcome are known. Methods. Using a ribonuclease protection assay, we screened the beta-cardiac myosin heavy-chain genes of probands from 25 unrelated families with familial hypertrophic cardiomyopathy; this assay is a sensitive method for detecting the presence and location of mutations. We further defined the mutations by analyzing their nucleotide sequences. The clinical features of the disease were compared in families with various myosin mutations. Results. Seven mutations in the beta-cardiac myosin heavy-chain gene were identified in 12 of the 25 families. All were missense mutations (i.e., causing the substitution of a single amino acid) clustered in the head and head-rod junction regions of the molecule. Six mutations resulted in a change in the charge of the amino acid. Patients with mutations that changed the charge of the altered amino acid (such as that from arginine to glutamine at nucleotide 403 or from arginine to cysteine at nucleotide 453) had a significantly shorter life expectancy (mean age at death, 33 years), whereas patients with the one mutation that did not produce a change in charge (Val606Met) had nearly normal survival. However, patients with different mutations did not differ appreciably in their clinical manifestations of familial hypertrophic cardiomyopathy. Conclusions. Different missense mutations in the beta-cardiac myosin heavy-chain gene can be identified in approximately 50 percent of families with hypertrophic cardiomyopathy. In those families, a definite genetic diagnosis can be made in all members. Since the location of a mutation or its DNA-sequence alteration (or both) appears to influence survival, we suggest that the precise definition of the disease-causing mutation can provide important prognostic information about affected members. C1 ST GEORGE HOSP,SCH MED,DEPT CARDIOL SCI,LONDON,ENGLAND. TAICHUNG VET GEN HOSP,DIV CARDIOL,TAICHUNG,TAIWAN. HOWARD HUGHES MED INST,BOSTON,MA. BRIGHAM & WOMENS HOSP,DIV CARDIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP WATKINS, H (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,25 SHATTUCK ST,BOSTON,MA 02115, USA. RI McKenna, William/C-3243-2008 OI McKenna, William/0000-0001-7994-2460 FU NHLBI NIH HHS [HL-41474, HL-02228, HL-46320] NR 36 TC 521 Z9 540 U1 0 U2 6 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 23 PY 1992 VL 326 IS 17 BP 1108 EP 1114 DI 10.1056/NEJM199204233261703 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HP800 UT WOS:A1992HP80000003 PM 1552912 ER PT J AU STONE, RM HAHN, PF MARK, EJ KADISON, P QUINTANILLA, L AF STONE, RM HAHN, PF MARK, EJ KADISON, P QUINTANILLA, L TI REPEATED BOUTS OF HEMATOCHEZIA IN AN 80-YEAR-OLD HYPERTENSIVE MAN - REFRACTORY-ANEMIA WITH RING SIDEROBLASTS WITH THROMBOCYTHEMIA (ESSENTIAL THROMBOCYTHEMIA, MYELODYSPLASTIC TYPE) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHRONIC MYELOPROLIFERATIVE DISEASES; ABNORMAL PLATELET COUNTS; POLYCYTHEMIA-VERA; CIRCULATING MEGAKARYOCYTES; STIMULATING HEMATOPOIESIS; SECONDARY THROMBOCYTOSIS; CLINICAL CHARACTERISTICS; PHILADELPHIA-CHROMOSOME; DYSPLASTIC PLATELETS RP STONE, RM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 94 TC 4 Z9 4 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 23 PY 1992 VL 326 IS 17 BP 1137 EP 1146 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA HP800 UT WOS:A1992HP80000007 ER PT J AU WARREN, HS DANNER, RL MUNFORD, RS AF WARREN, HS DANNER, RL MUNFORD, RS TI ANTIENDOTOXIN MONOCLONAL-ANTIBODIES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID GRAM-NEGATIVE BACTEREMIA; SEPTIC SHOCK; ESCHERICHIA-COLI C1 NIH,BETHESDA,MD 20205. UNIV TEXAS,SW MED CTR,DALLAS,TX 75235. RP WARREN, HS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 27 TC 176 Z9 177 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 23 PY 1992 VL 326 IS 17 BP 1153 EP 1157 DI 10.1056/NEJM199204233261711 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HP800 UT WOS:A1992HP80000011 PM 1552919 ER PT J AU GRIBBEN, JG NADLER, LM AF GRIBBEN, JG NADLER, LM TI IMMUNOLOGICAL PURGING OF MARROW ASSESSED BY POLYMERASE CHAIN-REACTION - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP GRIBBEN, JG (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 4 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 APR 23 PY 1992 VL 326 IS 17 BP 1163 EP 1164 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HP800 UT WOS:A1992HP80000027 ER PT J AU EMANUEL, EJ EMANUEL, LL AF EMANUEL, EJ EMANUEL, LL TI 4 MODELS OF THE PHYSICIAN-PATIENT RELATIONSHIP SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID PATERNALISM C1 HARVARD UNIV,JOHN F KENNEDY SCH GOVT,PROGRAM ETH & PROFESS,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DIV MED ETH,BOSTON,MA 02115. AMER COLL PHYSICIANS,PHILADELPHIA,PA. RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 33 TC 832 Z9 847 U1 2 U2 47 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 APR 22 PY 1992 VL 267 IS 16 BP 2221 EP 2226 DI 10.1001/jama.267.16.2221 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HN841 UT WOS:A1992HN84100033 PM 1556799 ER PT J AU BARNHILL, RL MIHM, MC CEBALLOS, PI AF BARNHILL, RL MIHM, MC CEBALLOS, PI TI ANGIOGENESIS AND REGRESSING CUTANEOUS MALIGNANT-MELANOMA SO LANCET LA English DT Letter ID THICKNESS; PROGNOSIS RP BARNHILL, RL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV DERMATOPATHOL,BOSTON,MA 02114, USA. NR 8 TC 15 Z9 15 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD APR 18 PY 1992 VL 339 IS 8799 BP 991 EP 992 DI 10.1016/0140-6736(92)91569-T PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HP036 UT WOS:A1992HP03600033 PM 1373461 ER PT J AU ELGHORR, A AF ELGHORR, A TI IN SEARCH OF A STRUCTURED CAREER SO NEW SCIENTIST LA English DT Editorial Material RP ELGHORR, A (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 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 APR 18 PY 1992 VL 134 IS 1817 BP 46 EP 47 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HQ558 UT WOS:A1992HQ55800041 ER PT J AU NEUMEYER, JL KULA, NS BALDESSARINI, RJ BAINDUR, N AF NEUMEYER, JL KULA, NS BALDESSARINI, RJ BAINDUR, N TI STEREOISOMERIC PROBES FOR THE D(1)-DOPAMINE RECEPTOR - SYNTHESIS AND CHARACTERIZATION OF R-(+)-ENANTIOMERS AND S-(-)-ENANTIOMERS OF 3-ALLYL-7,8-DIHYDROXY-1-PHENYL-2,3,4,5-TETRAHYDRO-1H-3-BENZAZEPINE AND ITS 6-BROMO ANALOG SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID D-1 DOPAMINE RECEPTOR; ANTAGONIST; SCH-23390; AGONIST; BRAIN; CLASSIFICATION; SUBTYPES; BINDING; LIGAND AB Substituted 1-phenyl-3-benzazepines (e.g., SKF 38393 and fenoldopam) exhibit stereoselectivity in moderately high-affinity binding to and partial agonist activation of D1 dopamine receptors. The 3-allyl (APB) and the 3-allyl-6-chloro (6-Cl-APB) analogues of SKF 38393 are reported to have higher affinity and selectivity for the D1 DA receptor and higher in vivo central neuropharmacologic activity than SYF 38393. We recently reported the corresponding 3-allyl-6-bromo analogue (6-Br-APB) also to be a high-affinity D1 agonist We now describe the synthesis and characterization of the R-(+) and S-(-) enantiomers of both APB and 6-Br-APB and their comparison with corresponding enantiomers of SKF 38393 with respect to D1 receptor binding affinity and D1 and D2 selectivity. The R-(+) enantiomers of both novel substituted 1-Phenyl-3-benzazepines bound to the D1 receptor sites in rat forebrain tissue with much higher affinity and selectivity than their S-(-) antipodes. R-(+)-3-Allyl-6-bromo-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine [(R)-(+)-6-Br-APB, 18] exhibits the highest affinity of the reported 1-phenyl-3-benzazepine D1 agonists. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,SCH MED,BELMONT,MA 02178. HARVARD UNIV,MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,NEUROSCI PROGRAM,BELMONT,MA 02178. NORTHEASTERN UNIV,COLL PHARM & ALLIED HLTH PROFESS,MED CHEM SECT,BOSTON,MA 02115. RP NEUMEYER, JL (reprint author), RES BIOCHEM INC,NATICK,MA 01760, USA. NR 37 TC 36 Z9 37 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD APR 17 PY 1992 VL 35 IS 8 BP 1466 EP 1471 DI 10.1021/jm00086a016 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HQ011 UT WOS:A1992HQ01100016 PM 1533424 ER PT J AU SINGER, DE NATHAN, DM FOGEL, HA SCHACHAT, AP AF SINGER, DE NATHAN, DM FOGEL, HA SCHACHAT, AP TI SCREENING FOR DIABETIC-RETINOPATHY SO ANNALS OF INTERNAL MEDICINE LA English DT Review DE DIABETIC RETINOPATHY; LIGHT COAGULATION; OPHTHALMOSCOPY; PHOTOGRAMMETRY; COST SAVINGS ID MYDRIATIC FUNDUS PHOTOGRAPHY; NON-HISPANIC WHITES; RISK-FACTORS; MACULAR EDEMA; BLOOD-PRESSURE; PIMA-INDIANS; PROLIFERATIVE RETINOPATHY; 4-YEAR INCIDENCE; PROGRESSION; DIAGNOSIS AB Purpose: To determine the appropriate patients, methods, and timing for screening for diabetic retinopathy. Data Sources: Relevant articles were identified through prominent review articles, the authors' files, recommendations from experts, and a MEDLINE search (1 986 to the present); additional references were selected from the bibliographies of identified articles. Study Selection: Selection of articles on the natural history of retinopathy was limited to large clinical series and formal epidemiologic studies of defined populations. Selection of articles on the therapeutic effect of photocoagulation and of glycemic control was limited to randomized trials. Sources bearing on the accuracy of screening modalities were necessarily more varied. Data Extraction: For important variables, individual estimates from multiple studies are presented rather than a single meta-analytic summary estimate. Results: Screening for retinopathy is justifiable if early detection leads to less vision loss at an acceptable cost. The evidence shows that 1) laser therapy reduces the rate of vision loss by 50% among patients with proliferative retinopathy and macular edema, conditions that are often asymptomatic; 2) duration of diabetes is the main risk factor for retinopathy; and 3) standard ophthalmoscopic examination has only moderate sensitivity (about 80% in research settings) and specificity (> 90% for proliferative retinopathy but lower for macular edema), making seven-field stereo-photography a more accurate method. Estimates of cost effectiveness indicate that screening for retinopathy not only saves years of vision but may be cost saving from a societal perspective. Conclusions: Screening for retinopathy in patients with diabetes, and subsequent photocoagulation therapy for those who have high risk macular edema or proliferative retinopathy, is clearly beneficial. C1 HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. JOHNS HOPKINS UNIV, BALTIMORE, MD 21218 USA. JOHNS HOPKINS UNIV HOSP, BALTIMORE, MD 21205 USA. RP SINGER, DE (reprint author), MASSACHUSETTS GEN HOSP, GEN INTERNAL MED UNIT, BULLFINCH 1, BOSTON, MA 02114 USA. FU AHRQ HHS [1 RO1 HS06665] NR 74 TC 143 Z9 143 U1 0 U2 4 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 EI 1539-3704 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 15 PY 1992 VL 116 IS 8 BP 660 EP 671 PG 12 WC Medicine, General & Internal SC General & Internal Medicine GA HN844 UT WOS:A1992HN84400010 PM 1546868 ER PT J AU LAM, KT CALDERWOOD, SK AF LAM, KT CALDERWOOD, SK TI HSP70 BINDS SPECIFICALLY TO A PEPTIDE DERIVED FROM THE HIGHLY CONSERVED DOMAIN (I) REGION OF P53 SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID HEAT-SHOCK PROTEINS; CELL-LINES; MUTATIONS; GENE; CANCER; HSC70 C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP LAM, KT (reprint author), HARVARD UNIV,SCH MED,MGH CANC CTR,BLDG 149,BOSTON,MA 02129, USA. FU NCI NIH HHS [CA47407, CA09078, CA44940] NR 16 TC 38 Z9 38 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 15 PY 1992 VL 184 IS 1 BP 167 EP 174 DI 10.1016/0006-291X(92)91174-O PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HP168 UT WOS:A1992HP16800026 PM 1567424 ER PT J AU CASSILETH, PA LYNCH, E HINES, JD OKEN, MM MAZZA, JJ BENNETT, JM MCGLAVE, PB EDELSTEIN, M HARRINGTON, DP OCONNELL, MJ AF CASSILETH, PA LYNCH, E HINES, JD OKEN, MM MAZZA, JJ BENNETT, JM MCGLAVE, PB EDELSTEIN, M HARRINGTON, DP OCONNELL, MJ TI VARYING INTENSITY OF POSTREMISSION THERAPY IN ACUTE MYELOID-LEUKEMIA SO BLOOD LA English DT Article ID ACUTE NONLYMPHOCYTIC LEUKEMIA; BONE-MARROW TRANSPLANTATION; ACUTE MYELOGENOUS LEUKEMIA; ACUTE NONLYMPHOBLASTIC LEUKEMIA; HIGH-DOSE CYTARABINE; 1ST REMISSION; MAINTENANCE CHEMOTHERAPY; CONSOLIDATION THERAPY; FOLLOW-UP; SURVIVAL C1 HOSP UNIV PENN,PHILADELPHIA,PA 19104. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. HARVARD UNIV,SCH PUBL HLTH,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. MARSHFIELD CLIN FDN MED RES & EDUC,MARSHFIELD,WI 54449. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. FU NCI NIH HHS [CA 14548, CA 15488, CA 23318] NR 28 TC 225 Z9 229 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1992 VL 79 IS 8 BP 1924 EP 1930 PG 7 WC Hematology SC Hematology GA HW416 UT WOS:A1992HW41600005 PM 1562720 ER PT J AU MILLENSON, MM BAUER, KA KISTLER, JP BARZEGAR, S TULIN, L ROSENBERG, RD AF MILLENSON, MM BAUER, KA KISTLER, JP BARZEGAR, S TULIN, L ROSENBERG, RD TI MONITORING MINI-INTENSITY ANTICOAGULATION WITH WARFARIN - COMPARISON OF THE PROTHROMBIN TIME USING A SENSITIVE THROMBOPLASTIN WITH PROTHROMBIN FRAGMENT F1+2 LEVELS SO BLOOD LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; PROTEIN-C ACTIVATION; ANTITHROMBOTIC THERAPY; VENOUS THROMBOSIS; LONG-TERM; PREVENTION; GENERATION; ASPIRIN; HUMANS; TRIAL C1 BETH ISRAEL HOSP,DEPT MED,330 BROOKLINE AVE,BOSTON,MA 02215. BROCKTON W ROXBURY DEPT VET AFFAIRS MED CTR,BROCKTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE SERV,BOSTON,MA 02114. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. FU NHLBI NIH HHS [HL33233, HL33014, HL07516] NR 28 TC 70 Z9 70 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 15 PY 1992 VL 79 IS 8 BP 2034 EP 2038 PG 5 WC Hematology SC Hematology GA HW416 UT WOS:A1992HW41600019 PM 1562730 ER PT J AU ROSOWSKY, A GALIVAN, J BEARDSLEY, GP BADER, H OCONNOR, BM RUSSELLO, O MOROSON, BA DEYARMAN, MT KERWAR, SS FREISHEIM, JH AF ROSOWSKY, A GALIVAN, J BEARDSLEY, GP BADER, H OCONNOR, BM RUSSELLO, O MOROSON, BA DEYARMAN, MT KERWAR, SS FREISHEIM, JH TI BIOCHEMICAL AND BIOLOGICAL STUDIES ON 2-DESAMINO-2-METHYLAMINOPTERIN, AN ANTIFOLATE THE POLYGLUTAMATES OF WHICH ARE MORE POTENT THAN THE MONOGLUTAMATE AGAINST 3 KEY ENZYMES OF FOLATE METABOLISM SO CANCER RESEARCH LA English DT Article ID MAMMALIAN FOLYLPOLYGLUTAMATE SYNTHETASE; HUMAN DIHYDROFOLATE-REDUCTASE; DENOVO PURINE SYNTHESIS; BREAST-CANCER-CELLS; METHOTREXATE POLYGLUTAMATES; THYMIDYLATE SYNTHASE; HEPATOMA-CELLS; LEUCOVORIN RESCUE; DIRECT INHIBITION; CHICKEN LIVER AB Biochemical and biological studies have been carried out with 2-desamino-2-methylaminopterin (dmAMT), which inhibits tumor cell growth in culture but is only a weak inhibitor of dihydrofolate reductase (DHFR). Since it was possible that the species responsible for growth inhibition are polyglutamylated metabolites, the di-, tri-, and tetraglutamates of dmAMT were synthesized and tested as inhibitors of purified recombinant human DHFR, murine L1210 leukemia thymidylate synthase (TS), chicken liver glycinamide ribonucleotide formyltransferase (GARFT), and murine L1210 leukemia aminoimidazolecarboxamide ribonucleotide formyltransferase (AICARFT). The compounds with three and four gamma-glutamyl residues were found to bind two orders of magnitude better than dmAMT itself to DHFR, TS, and AICARFT, with 50% inhibitory concentration values in the 200 to 300 nM range against all three enzymes. In contrast, at a concentration of 10-mu-M, dmAMT polyglutamates had no appreciable effect on GARFT activity. These findings support the hypothesis that dmAMT requires intracellular polyglutamylation for activity and indicate that replacement of the 2-amino group by 2-methyl is as acceptable a structural modification in antifolates targeted against DHFR as it is in antifolates targeted against TS. In growth assays against methotrexate (MTX)-sensitive H35 rat hepatoma cells and MTX-resistant H35 sublines with a transport defect, dmAMT was highly cross-resistant with MTX, but not with the TS inhibitors N10-propargyl-5,8-dideazafolic acid and N-{5-[N-(3,4-dihydro-2-methyl-4-oxoquinazolin-6-yl)-N-methylamino]thenoyl}-L-glutamic acid, implicating DHFR rather than TS as the principal target for dmAMT polyglutamates in intact cells. On the other hand, an H35 subline resistant to 2'-deoxy-5-fluorouridine by virtue of increased TS activity was highly cross-resistant to N10-propargyl-5,8-dideazafolic acid and not cross-resistant to MTX, but showed partial cross-resistance to dmAMT. Both thymidine and hypoxanthine were required to protect H35 cells treated with concentrations of dmAMT and MTX that inhibited growth by > 90% relative to unprotected controls. In contrast, N10-propargyl-5,8-dideazafolic acid and N-{5-[N-3,4-dihydro-2-methyl-4-oxoquinazolin-6-yl)-N-methylamino]thenoyl}L-glutamic acid required only thymidine for protection. Like MTX, therefore, dmAMT appears to inhibit purine as well as pyrimidine de novo synthesis, and its effect on cell growth probably reflects the ability of dmAMT polyglutamates to not only block dihydrofolate reduction but also interfere with other steps of folate metabolism, either directly or indirectly via alteration of reduced folate pools. A similar protection pattern was obtained with mouse L1210 leukemia cells as with H35 cells, in that both thymidine and hypoxanthine were required for normal growth in the presence of dmAMT. Although folinic acid alone afforded full protection, 5-aminoimidazole-4-carboxamide could not be used instead of hypoxanthine, suggesting that de novo purine synthesis inhibition by dmAMT probably occurs at the level of AIRCARFT rather than GARFT. In antitumor assays against L1210 leukemia in mice, comparable lifespan increases were achieved with dmAMT and MTX, but more dmAMT than MTX had to be used to produce the same therapeutic effect. The results of this study suggest that dmAMT may be a promising lead for the development of other, more potent, 2-desamino analogues of classical 2,4-diamino antifolates. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NEW YORK STATE DEPT HLTH,WADSWORTH CTR LABS & RES,ALBANY,NY 12201. YALE UNIV,SCH MED,DEPT PEDIAT,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06510. AMER CYANAMID CO,LEDERLE LABS,DIV MED RES,PEARL RIVER,NY 10965. MED COLL OHIO,DEPT BIOCHEM & MOLEC BIOL,TOLEDO,OH 43699. RP ROSOWSKY, A (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA19589, CA25394, CA25933] NR 60 TC 23 Z9 23 U1 1 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 15 PY 1992 VL 52 IS 8 BP 2148 EP 2155 PG 8 WC Oncology SC Oncology GA HN842 UT WOS:A1992HN84200004 PM 1313737 ER PT J AU HARLOW, E AF HARLOW, E TI 11TH ANNUAL SAPPORO CANCER SEMINAR - CONNECTING THE DOTS - ASSEMBLING THE PATHWAYS THAT CONTROL CELL-DIVISION SO CANCER RESEARCH LA English DT Editorial Material RP HARLOW, E (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129, USA. NR 0 TC 1 Z9 1 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 APR 15 PY 1992 VL 52 IS 8 BP 2362 EP 2366 PG 5 WC Oncology SC Oncology GA HN842 UT WOS:A1992HN84200040 PM 1559240 ER PT J AU EMANUEL, EJ EMANUEL, LL AF EMANUEL, EJ EMANUEL, LL TI PROXY DECISION-MAKING FOR INCOMPETENT PATIENTS - AN ETHICAL AND EMPIRICAL-ANALYSIS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID CARE; LIFE; PREFERENCES; CONSENT C1 HARVARD UNIV,SCH MED,DIV MED ETH,BOSTON,MA 02115. RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 46 TC 115 Z9 115 U1 1 U2 9 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 APR 15 PY 1992 VL 267 IS 15 BP 2067 EP 2071 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HM650 UT WOS:A1992HM65000033 PM 1552642 ER PT J AU SUNDSETH, R HANSEN, U AF SUNDSETH, R HANSEN, U TI ACTIVATION OF RNA POLYMERASE-II TRANSCRIPTION BY THE SPECIFIC DNA-BINDING PROTEIN LSF - INCREASED RATE OF BINDING OF THE BASAL PROMOTER FACTOR TFIIB SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MAJOR LATE PROMOTER; FUNCTIONAL PREINITIATION COMPLEX; TATA-BOX FACTOR; ACCURATE TRANSCRIPTION; INVITRO TRANSCRIPTION; ESSENTIAL COMPONENT; INITIATION SITE; FACTOR ATF; GENE; PURIFICATION AB While the components of the initiation complex at an RNA polymerase II basal promoter have been well characterized, few mechanistic studies have focused on how upstream DNA-binding, transcriptional activators influence protein assembly at the initiation site. Our analysis of basal transcription on both the simian virus 40 and adenovirus major late promoters demonstrates that two slow steps in initiation of transcription are the assembly of the general transcription factors TFIID and TFIIB onto the template DNA. On the simian virus 40 major late promoter, the rate of initiation complex formation is dramatically increased in the presence of the cellular transcriptional activator LSF. Direct analysis by band mobility shift assays demonstrates that LSF has no effect on the rate of binding, or the stability of TFIID on the promoter, predicting that LSF would not affect the template commitment step. Rather, kinetic analyses demonstrate that LSF reduces the lag in the rate of initiation complex formation attributable to the slow addition of TFIIB and suggest that LSF increases the rate of association of TFIIB with the committed template. In addition, LSF increases the total number of transcription complexes in long term assays, which is also consistent with LSF increasing the rate of association of TFIIB, where TFIIB is not saturating. These results indicate a mechanism for the activation of the initiation of RNA polymerase II transcription by one upstream activating protein, LSF. This mechanism may also be applicable to other activators that function in cases where limiting concentrations of TFIIB in the cell dictate slow binding of TFIIB. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,EUKARYOT TRANSCRIPT LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [CA38038] NR 65 TC 40 Z9 40 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 15 PY 1992 VL 267 IS 11 BP 7845 EP 7855 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HN485 UT WOS:A1992HN48500091 PM 1313810 ER PT J AU ERON, JJ GORCZYCA, P KAPLAN, JC DAQUILA, RT AF ERON, JJ GORCZYCA, P KAPLAN, JC DAQUILA, RT TI SUSCEPTIBILITY TESTING BY POLYMERASE CHAIN-REACTION DNA QUANTITATION - A METHOD TO MEASURE DRUG-RESISTANCE OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ISOLATES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ZIDOVUDINE; DIDANOSINE; ANTIVIRAL DRUGS; REVERSE TRANSCRIPTASE; CLINICAL TRIALS ID ASSAY; HIV AB Polymerase chain reaction (PCR) DNA quantitation (PDQ) susceptibility testing rapidly and directly measures nucleoside sensitivity of human immunodeficiency virus type 1 (HIV-1) isolates. PCR is used to quantitate the amount of HIV-1 DNA synthesized after in vitro infection of peripheral blood mononuclear cells. The relative amounts of HIV-1 DNA in cell lysates from cultures maintained at different drug concentrations reflect drug inhibition of virus replication. The results of PDQ susceptibility testing of 2- or 3-day cultures are supported by assays measuring HIV-1 p24 antigen production in supernatants of 7- or 10-day cultures. DNA sequence analyses to identify mutations in the reverse transcriptase gene that cause resistance to 3'-azido-3'-deoxythymidine also support the PDQ results. With the PDQ method, both infectivity titration and susceptibility testing can be performed on supernatants from primary cultures of peripheral blood mononuclear cells. PDQ susceptibility testing should facilitate epidemiologic studies of the clinical significance of drug-resistant HIV-1 isolates. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,149 13TH ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NIAID NIH HHS [AI29193, AI07061] NR 17 TC 31 Z9 31 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1992 VL 89 IS 8 BP 3241 EP 3245 DI 10.1073/pnas.89.8.3241 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HP043 UT WOS:A1992HP04300017 PM 1565615 ER PT J AU DOU, QP MARKELL, PJ PARDEE, AB AF DOU, QP MARKELL, PJ PARDEE, AB TI THYMIDINE KINASE TRANSCRIPTION IS REGULATED AT G1/S PHASE BY A COMPLEX THAT CONTAINS RETINOBLASTOMA-LIKE PROTEIN AND A CDC2 KINASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL CYCLE; DNA-BINDING PROTEINS; INDUCIBLE DNA-BINDING ACTIVITY YI ID CELL-CYCLE; GENE-PRODUCT; PROMOTER; PHOSPHORYLATION; IDENTIFICATION; ACTIVATION; RNA; RB AB Transcription of the murine thymidine kinase gene, which is coregulated with the G1/S phase transition, is activated by changing the binding of protein complexes Yi1 and Yi2 to three upstream DNA motifs. Yi1 is replaced by Yi2 shortly before S phase. Yi1 contains a protein of 110 kDa that binds to the DNA motif sites and may be an underphosphorylated murine retinoblastoma protein, shown by its molecular mass, timing of its activity, and antibody recognition. An H1 kinase related to cdc2 cofractionates with both complexes. We propose that this kinase phosphorylates the murine retinoblastoma protein, releasing transcriptional inhibitions by Yi1 and Permitting cell cycle progression. These results provide a cycle-related molecular target for such complexes. They are based on investigations of cycle control in uninfected cells. The Yi complexes are similar but not identical to complexes that include a cellular protein, E2F, that was originally found to bind to adenovirus DNA. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP DOU, QP (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA22427]; NCRR NIH HHS [2 S07 RR05526-28] NR 33 TC 99 Z9 99 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1992 VL 89 IS 8 BP 3256 EP 3260 DI 10.1073/pnas.89.8.3256 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HP043 UT WOS:A1992HP04300020 PM 1565617 ER PT J AU NELSON, RD GUO, XL MASOOD, K BROWN, D KALKBRENNER, M GLUCK, S AF NELSON, RD GUO, XL MASOOD, K BROWN, D KALKBRENNER, M GLUCK, S TI SELECTIVELY AMPLIFIED EXPRESSION OF AN ISOFORM OF THE VACUOLAR H+-ATPASE 56-KILODALTON SUBUNIT IN RENAL INTERCALATED CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID BOVINE KIDNEY; PROTON PUMP; CDNA CLONE; H+ATPASE; SEQUENCE; DNA; HOMOLOGY; RNA AB The intercalated cells of the kidney collecting duct are specialized for physiologically regulated proton transport. In these cells, a vacuolar H+-ATPase is expressed at enormous levels in a polarized distribution on the plasma membrane, enabling it to serve in transepithelial H+ transport. In contrast, in most eukaryotic cells, vacuolar H+-ATPases reside principally in intracellular compartments to effect vacuolar acidification. To investigate the basis for the selective amplification of the proton pump in intercalated cells, we isolated and sequenced cDNA clones for two isoforms of the almost-equal-to 56-kDa subunit of the H+-ATPase and examined their expression in various tissues. The predicted amino acid sequence of the isoforms was highly conserved in the internal region but diverged in the amino and carboxyl termini. mRNA hybridization to a cDNA probe for one isoform (the "kidney" isoform) was detected only in kidney cortex and medulla, whereas mRNA hybridization to the other isoform of the almost-equal-to 56-kDa subunit and to the H+-ATPase 31-kDa subunit was found in the kidney and other tissues. Immunocytochemistry of rat kidney with an antibody specific to the kidney isoform revealed intense staining only in the intercalated cells. Staining was absent from proximal tubule and thick ascending limb, where H+-ATPase was detected with a monoclonal antibody to the 31-kDa subunit of the H+-ATPase. This example of specific amplification of an isoform of one subunit of the vacuolar H+-ATPase being limited to a specific cell type suggests that the selective expression of the kidney isoform of the almost-equal-to 56-kDa subunit may confer the capacity for amplification and other specialized functions of the vacuolar H+-ATPase in the renal intercalated cell. C1 JEWISH HOSP ST LOUIS,DIV RENAL,ST LOUIS,MO 63110. ST LOUIS CHILDRENS HOSP,DIV NEPHROL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. WASHINGTON UNIV,SCH MED,DEPT MED,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,ST LOUIS,MO 63110. RP NELSON, RD (reprint author), WASHINGTON UNIV,SCH MED,DEPT PEDIAT,ST LOUIS,MO 63110, USA. FU NIDDK NIH HHS [DK09976, DK38848, DK40535] NR 25 TC 194 Z9 197 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1992 VL 89 IS 8 BP 3541 EP 3545 DI 10.1073/pnas.89.8.3541 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HP043 UT WOS:A1992HP04300079 PM 1373501 ER PT J AU KOPIN, AS LEE, YM MCBRIDE, EW MILLER, LJ LU, M LIN, HY KOLAKOWSKI, LF BEINBORN, M AF KOPIN, AS LEE, YM MCBRIDE, EW MILLER, LJ LU, M LIN, HY KOLAKOWSKI, LF BEINBORN, M TI EXPRESSION CLONING AND CHARACTERIZATION OF THE CANINE PARIETAL-CELL GASTRIN RECEPTOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE G-PROTEIN-COUPLED RECEPTOR; CHOLECYSTOKININ; GASTRIC MUCOSA ID CHOLECYSTOKININ RECEPTOR; MOLECULAR-CLONING; SEQUENCE-ANALYSIS; CROSS-LINKING; CA-2+; SECRETAGOGUES; ANTAGONIST; PROGRAMS; PROTEIN; PEPTIDE AB Gastrin is an important stimulant of acid secretion by gastric parietal cells and is structurally related to the peptide hormone cholecystokinin (CCK). The pharmacologic properties of the parietal cell gastrin receptor are very similar to the predominant CCK receptor in the brain, CCK-B. Neither the gastrin nor the CCK-B receptor have been cloned thus far, making it difficult to resolve whether these two receptors are distinct. We have isolated a clone encoding the canine gastrin receptor by screening a parietal cell cDNA expression library using a radioligand-binding strategy. Nucleotide sequence analysis revealed an open reading frame encoding a 453-amino acid protein with seven putative hydrophobic transmembrane domains and significant homology with members of the beta-adrenergic family of G protein-coupled receptors. The expressed recombinant receptor shows the same binding specificity for gastrin/CCK agonists and antagonists as the canine parietal cell receptor. Gastrin-stimulated phosphatidylinositol hydrolysis and intracellular Ca2+ mobilization in COS-7 cells expressing the cloned receptor suggest second-messenger signaling through phospholipase C. Affinity labeling of the expressed receptor in COS-7 cells revealed a protein identical in size to the native parietal cell receptor. Gastrin receptor transcripts were identified by high-stringency RNA blot analysis in both parietal cells and cerebral cortex, suggesting that the gastrin and CCK-B receptors are either highly homologous or identical. C1 TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,GRASP DIGEST DIS CTR,BOSTON,MA 02111. MAYO CLIN & MAYO GRAD SCH MED,GASTROENTEROL RES UNIT,ROCHESTER,MN 55901. BAYLOR COLL MED,DEPT CELL BIOL,HOUSTON,TX 77030. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HANOVER MED SCH,DEPT GEN PHARMACOL,W-3000 HANNOVER 61,GERMANY. RP KOPIN, AS (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,DIV GASTROENTEROL,BOSTON,MA 02111, USA. FU NIDDK NIH HHS [DK01934, P30 DK39428, DK32878] NR 34 TC 460 Z9 462 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 15 PY 1992 VL 89 IS 8 BP 3605 EP 3609 DI 10.1073/pnas.89.8.3605 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HP043 UT WOS:A1992HP04300092 PM 1373504 ER PT J AU ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA AF ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA TI EFFECTS OF ANTIANGINAL THERAPY ON LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC PERFORMANCE - COMPARISON OF THE RESPONSE TO BEPRIDIL, PROPRANOLOL, AND DILTIAZEM SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article AB Abnormalities of left ventricular (LV) systolic performance develop during exercise in patients with coronary artery disease (CAD) as a result of ischemia-induced regional wall motion abnormalities. Like patients with hypertension and those with hypertrophic cardiomyopathy, patients with CAD display abnormalities of LV diastolic performance under basal conditions in the absence of ischemia. The purpose of these studies was to compare the effects of bepridil versus those of propranolol or diltiazem in patients with exertional angina pectoris. LV systolic and diastolic performance were assessed at rest and during peak upright bicycle exercise by first-pass radionuclide ventriculography. Compared with propranolol, bepridil increased exercise capacity, cardiac output, and stroke volume and decreased systemic vascular resistance. Compared with diltiazem, bepridil increased exercise capacity, peak filling rate, and early diastolic filling fraction and decreased systemic vascular resistance, heart rate, time to peak filling rate, and atrial filling volume. Bepridil therapy is associated with improved exercise capacity and decreased anginal frequency and nitroglycerin consumption. In addition, its use is accompanied by favorable changes in LV systolic and diastolic function at rest and during exercise. These changes are consistent with benefits resulting from resolution of myocardial ischemia as well as from positive lusitropic effects of bepridil on the ventricular myocardium. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CARDIAC UNIT,DIV HYPERTENS & VASC MED,15 PARKMAN ST,SUITE 482,BOSTON,MA 02114, USA. NR 13 TC 4 Z9 4 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD APR 9 PY 1992 VL 69 IS 11 BP D25 EP D30 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HM449 UT WOS:A1992HM44900005 PM 1553888 ER PT J AU BERGSAGEL, DJ FINEGOLD, MJ BUTEL, JS KUPSKY, WJ GARCEA, RL AF BERGSAGEL, DJ FINEGOLD, MJ BUTEL, JS KUPSKY, WJ GARCEA, RL TI DNA-SEQUENCES SIMILAR TO THOSE OF SIMIAN VIRUS-40 IN EPENDYMOMAS AND CHOROID-PLEXUS TUMORS OF CHILDHOOD SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID HUMAN-BRAIN-TUMORS; B-LYMPHOTROPIC PAPOVAVIRUS; TRANSGENIC MICE; JC-VIRUS; PANCREATIC-ISLETS; POLYOMAVIRUS-JC; T-ANTIGEN; SV40; HAMSTERS; TISSUE AB Background. Ependymomas and papillomas of the choroid plexus occur in early childhood. The ubiquitous human polyomaviruses, BK virus and JC virus, have been associated with the induction of these neoplasms in animal models. A related monkey polyomavirus, simian virus 40 (SV40), is highly tumorigenic in rodents and also induces choroid plexus papillomas. Methods. We tested the possibility that polyomaviruses were associated with these tumors in humans. Tumors from 31 children - 20 with choroid plexus neoplasms and 11 with ependymomas - were evaluated for the presence of polyomavirus T-antigen gene sequences by means of amplification with the polymerase chain reaction. Results. Ten of the 2O choroid plexus tumors and 10 of the 11 ependymomas contained amplification products that preferentially hybridized to probes specific for SV40 viral DNA rather than BK or JC viral DNA. In two specimens, DNA sequencing demonstrated that the amplified sequence was identical to the sequence of that region of the SV40 gene. In three other specimens, amplification with SV40-specific primers revealed a 574-bp segment of the SV40 viral gene. In 7 of 11 tumors examined by immunohistochemical staining, viral T antigen was expressed in the nuclei of the neoplastic cells. Conclusions. Half of the choroid plexus tumors and most of the ependymomas that we studied contained and expressed a segment of T-antigen gene related to SV40. These results suggest that SV40 or a closely related virus may have an etiologic role in the development of these neoplasms during childhood, as in animal models. C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DIV PEDIAT ONCOL,D1620,44 BINNEY ST,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. BAYLOR COLL MED,DEPT PATHOL,HOUSTON,TX 77030. BAYLOR COLL MED,DIV MOLEC VIROL,HOUSTON,TX 77030. FU NCI NIH HHS [CA-22555] NR 59 TC 347 Z9 352 U1 0 U2 1 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 9 PY 1992 VL 326 IS 15 BP 988 EP 993 DI 10.1056/NEJM199204093261504 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HM285 UT WOS:A1992HM28500004 PM 1312224 ER PT J AU SACHS, DH AF SACHS, DH TI T-CELL IMMUNOINCOMPETENCE IN ALLOGENEIC CHIMERISM - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID VERSUS-HOST DISEASE; LEUKEMIA RP SACHS, DH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 5 TC 2 Z9 2 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 9 PY 1992 VL 326 IS 15 BP 1029 EP 1029 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HM285 UT WOS:A1992HM28500024 ER PT J AU FORSCH, RA REICH, VE ROSOWSKY, A MORAN, RG AF FORSCH, RA REICH, VE ROSOWSKY, A MORAN, RG TI 5-DEAZA-5,6,7,8-TETRAHYDROFOLATE AND (6R,6S)-5-DEAZA-5,6,7,8-TETRAHYDROFOLATE ANALOGS WITH MODIFIED AMINO-ACID SIDE-CHAINS SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV SO CALIF,NORRIS COMPREHENS CANC CTR,LOS ANGELES,CA 90033. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 5 PY 1992 VL 203 BP 26 EP MEDI PN 2 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA HK162 UT WOS:A1992HK16200228 ER PT J AU GARRIDO, L AF GARRIDO, L TI NMR IMAGING OF MATERIALS - MICROSCOPY OR NOT SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 5 PY 1992 VL 203 BP 539 EP POLY PN 3 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA HK163 UT WOS:A1992HK16300526 ER PT J AU PFLEIDERER, B MOORE, J ACKERMAN, JL GARRIDO, L AF PFLEIDERER, B MOORE, J ACKERMAN, JL GARRIDO, L TI STUDY OF THE AGING PROCESS OF PDMS-IMPLANTS INVIVO AND EXVIVO BY NUCLEAR-MAGNETIC-RESONANCE SPECTROSCOPY AND IMAGING SO ABSTRACTS OF PAPERS OF THE AMERICAN CHEMICAL SOCIETY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0065-7727 J9 ABSTR PAP AM CHEM S JI Abstr. Pap. Am. Chem. Soc. PD APR 5 PY 1992 VL 203 BP 542 EP POLY PN 3 PG 0 WC Chemistry, Multidisciplinary SC Chemistry GA HK163 UT WOS:A1992HK16300529 ER PT J AU URAKAZE, M KAMITANI, T DEGASPERI, R SUGIYAMA, E CHANG, HM WARREN, CD YEH, ETH AF URAKAZE, M KAMITANI, T DEGASPERI, R SUGIYAMA, E CHANG, HM WARREN, CD YEH, ETH TI IDENTIFICATION OF A MISSING LINK IN GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR BIOSYNTHESIS IN MAMMALIAN-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID VARIANT SURFACE GLYCOPROTEINS; PHOSPHOLIPID MEMBRANE ANCHOR; GLYCOSYL-PHOSPHATIDYLINOSITOL; GLYCOLIPID PRECURSORS; RESISTANT GLYCOLIPIDS; PROTEIN; ACTIVATION; HYDROLYSIS; MOLECULES AB A large number of mammalian proteins are anchored to the cell membrane by a glycosylphosphatidylinositol (GPI) anchor. Biosynthetic intermediates of the GPI anchor have been identified in mammalian cells. The early GPI precursors are sensitive to phosphatidylinositol (PI)-specific phospholipase C (PLC). However, all of the later GPI precursors, which contain 1 or more mannose residues, are PI-PLC-resistant, suggesting that there is another unidentified precursor. Here, we report the identification of this missing link. This GPI precursor can only be labeled with glucosamine and inositol, and is resistant to PI-PLC but sensitive to GPI-phospholipase D. It accumulates in large quantity only in mutants which are defective in the addition of the first mannose residue to the elongating GPI core. Thus, fatty acylation of glucosaminylphosphatidylinositol, to render it PI-PLC-resistant, is an obligatory step in the biosynthesis of mammalian GPI anchor precursors. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ARTHRIT UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-45851]; NIAMS NIH HHS [AR-03564]; NIDDK NIH HHS [DK-40930] NR 24 TC 71 Z9 71 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1992 VL 267 IS 10 BP 6459 EP 6462 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HM053 UT WOS:A1992HM05300003 PM 1313004 ER PT J AU CHEATHAM, B KAHN, CR AF CHEATHAM, B KAHN, CR TI CYSTEINE-647 IN THE INSULIN-RECEPTOR IS REQUIRED FOR NORMAL COVALENT INTERACTION BETWEEN ALPHA-SUBUNIT AND BETA-SUBUNIT AND SIGNAL TRANSDUCTION SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID POLYACRYLAMIDE GEL-ELECTROPHORESIS; LIVER PLASMA-MEMBRANES; RAT HEPATOMA-CELLS; TYROSINE KINASE; DISULFIDE BONDS; PHOSPHORYLATION; DITHIOTHREITOL; REDUCTION; AFFINITY; PROTEIN AB We have investigated the structural and functional properties of two mutant insulin receptors in which Cys647 and Cys682,683,685 have been replaced with Ser (IR(S647) and IR(S682,683,685), respectively). Compared with the wild-type receptor (IR(WT)), both mutant receptors displayed altered sensitivities to dithiothreitol with respect to insulin binding and reduction of oligomeric forms. Subunit composition of the oligomeric forms of the receptors as determined by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis of I-125-labeled receptors indicated that Cys682,683,685 are required for normal heterotetrameric structure and that Cys647 plays a major role in the normal covalent association of the alpha- and beta-subunits. Under nonreducing conditions, the affinity-labeled IR(S647) migrated, almost exclusively, as a 230-kDa species which appeared to represent an alpha(2) form of the receptor. Furthermore, Chinese hamster ovary cells expressing IR(S647) did not exhibit basal or insulin-stimulated autophosphorylation, suggesting that Cys647 is also required for signal transduction. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,DEPT MED,RES DIV,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-31036, DK-36836] NR 37 TC 33 Z9 34 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1992 VL 267 IS 10 BP 7108 EP 7115 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HM053 UT WOS:A1992HM05300100 PM 1551916 ER PT J AU ROTHSTEIN, DM SAITO, H STREULI, M SCHLOSSMAN, SF MORIMOTO, C AF ROTHSTEIN, DM SAITO, H STREULI, M SCHLOSSMAN, SF MORIMOTO, C TI THE ALTERNATIVE SPLICING OF THE CD45 TYROSINE PHOSPHATASE IS CONTROLLED BY NEGATIVE REGULATORY TRANS-ACTING SPLICING FACTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; PRE-MESSENGER-RNA; BRANCH POINT LOCATION; T-CELLS; SITE SELECTION; MONOCLONAL-ANTIBODY; GENE-EXPRESSION; HELPER-INDUCER; 2H4 MOLECULE; DIFFERENTIATION AB CD45, a receptor-type protein tyrosine phosphatase involved in lymphocyte activation, consists of five isoforms generated by alternative mRNA splicing. The pattern of CD45 splicing depends upon cell type, state of activation, and thymic development. We previously showed that mouse B and thymocyte cell lines transfected with a human CD45 minigene construct appropriately splice the alternative exons, demonstrating the presence of trans-acting tissue-specific splicing factors. To study the regulation of CD45 alternative splicing, cells having different splicing patterns were transiently fused, and mRNA was analyzed using reverse transcription-polymerase chain reaction. Human B cells, normally producing only the largest CD45 mRNAs, could splice out the alternative exons after fusion with mouse thymocytes. In contrast, the splicing pattern of human T cell lines (smaller CD45 isoforms) was unaltered by fusion with mouse B cells. This suggests that cells expressing the smallest CD45 isoform contain negatively acting trans-factor(s) that allow the alternative exons to be skipped, and that the full length isoform containing all three alternative exons is the default pattern of splicing. In agreement, incubation of thymocytes or T cell subsets with cycloheximide increased mRNA corresponding to the larger isoforms. CD45 isoform expression can now be interpreted in terms of the presence or absence of negative regulatory trans-acting splicing factors. C1 BRIGHAM & WOMENS HOSP,DIV NEPHROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROTHSTEIN, DM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-26598]; NIAMS NIH HHS [AR33713]; NIDDK NIH HHS [1KO8DK02011-01A1] NR 69 TC 48 Z9 48 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD APR 5 PY 1992 VL 267 IS 10 BP 7139 EP 7147 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HM053 UT WOS:A1992HM05300105 PM 1532394 ER PT J AU MILLER, JB AF MILLER, JB TI MYOBLAST DIVERSITY IN SKELETAL MYOGENESIS - HOW MUCH AND TO WHAT END SO CELL LA English DT Review ID FIBER TYPES; EXPRESSION; CELLS; GENE; DIFFERENTIATION; MUSCLES; LINEAGE; EMBRYO C1 HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. RP MILLER, JB (reprint author), MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,BOSTON,MA 02129, USA. OI Miller, Jeffrey/0000-0001-5273-2201 NR 20 TC 72 Z9 72 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 3 PY 1992 VL 69 IS 1 BP 1 EP 3 DI 10.1016/0092-8674(92)90111-O PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM445 UT WOS:A1992HM44500001 PM 1555234 ER PT J AU RODEWALD, HR MOINGEON, P LUCICH, JL DOSIOU, C LOPEZ, P REINHERZ, EL AF RODEWALD, HR MOINGEON, P LUCICH, JL DOSIOU, C LOPEZ, P REINHERZ, EL TI A POPULATION OF EARLY FETAL THYMOCYTES EXPRESSING FC-GAMMA-RII/III CONTAINS PRECURSORS OF LYMPHOCYTES-T AND NATURAL-KILLER-CELLS SO CELL LA English DT Article ID AFFINITY IGE RECEPTOR; MONOCLONAL-ANTIBODY; ANTIGEN RECEPTOR; BONE-MARROW; ZETA-CHAIN; NK CELLS; DEVELOPMENTAL BIOLOGY; ACTIVATION PATHWAYS; TRANSFECTED CELLS; B-CELLS AB We have identified a dominant fetal thymocyte population at day 14.5 of gestation in the mouse that lacks CD4 and CD8 but expresses Fc-gamma-RII/III+ several days prior to acquisition of the T cell receptor (TCR) in vivo. If maintained in a thymic microenvironment, this population of CD4-CD8-TCR-Fc-gamma-RII/III+ thymocytes differentiates first into CD4+CD8+TCR(low)Fc-gamma-RII/III- thymocytes and subsequently CD4+CD8-TCR(high)Fc-gamma-RII/III- and CD4-CD8+TCR(high)Fc-gamma-RII/III mature Ti alpha-beta lineage T cells. However, if removed from the thymus, the CD4-CD8-TCR-Fc-gamma-RII/III+ thymocyte population selectively generates functional natural killer (NK) cells in vivo as well as in vitro. These findings show that a cellular pool of Fc-gamma-RII/III+ precursors gives rise to T and NK lineages in a microenvironment-dependent manner. Moreover, they suggest a hitherto unrecognized role for Fc receptors on primitive T cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,FLOW CYTOMETRY FACIL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP RODEWALD, HR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI21226, AI 19807] NR 97 TC 265 Z9 267 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD APR 3 PY 1992 VL 69 IS 1 BP 139 EP 150 DI 10.1016/0092-8674(92)90125-V PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM445 UT WOS:A1992HM44500013 PM 1532536 ER PT J AU KATKOV, WN COMPTON, CC FERRUCCI, JT SCULLY, RE PODOLSKY, DK SHELLITO, PC SCHAPIRO, RH AF KATKOV, WN COMPTON, CC FERRUCCI, JT SCULLY, RE PODOLSKY, DK SHELLITO, PC SCHAPIRO, RH TI A 37-YEAR-OLD MAN WITH A 3RD BOUT OF MAJOR HEMATOCHEZIA - ARTERIOVENOUS MALFORMATION OF LARGE AND SMALL-INTESTINE, WITH FOCAL RUPTURE AND HEMORRHAGE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID NODULAR LYMPHOID HYPERPLASIA; GASTROINTESTINAL-TRACT; COLONOSCOPIC DIAGNOSIS; VASCULAR ECTASIAS; UNCOMMON CAUSE; RIGHT COLON; ANGIODYSPLASIA; TELANGIECTASIA; DISEASE; BOWEL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KATKOV, WN (reprint author), MASSACHUSETTS GEN HOSP,MED,BOSTON,MA 02114, USA. NR 52 TC 5 Z9 5 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 2 PY 1992 VL 326 IS 14 BP 936 EP 944 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HL261 UT WOS:A1992HL26100007 ER PT J AU FERRUCCI, JT AF FERRUCCI, JT TI GASTROINTESTINAL ENDOSCOPY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP FERRUCCI, JT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 2 PY 1992 VL 326 IS 14 BP 955 EP 956 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HL261 UT WOS:A1992HL26100021 PM 1542353 ER PT J AU CARROLL, PB HERSKOWITZ, RD GOODMAN, AD BUSCH, RS BEASER, RS AF CARROLL, PB HERSKOWITZ, RD GOODMAN, AD BUSCH, RS BEASER, RS TI RAPID ONSET OF SEVERE RETINOPATHY, CATARACTS AND NEUROPATHY IN YOUNG-PATIENTS WITH DIABETES-MELLITUS SO ACTA PAEDIATRICA LA English DT Article DE CATARACTS; DIABETES-MELLITUS; EARLY COMPLICATIONS; NEUROPATHY; RETINOPATHY ID GLYCEMIC CONTROL; CHILDREN; PROGRESSION; COMPLICATIONS; ADOLESCENTS; NEPHROPATHY; PREVALENCE; DIAGNOSIS; DISEASE AB It is rare for young diabetic patients to develop severe complications in the first years of their disease. We describe three patients, aged 14-23 years who developed cataracts and severe retinopathy within one to five years of diagnosis of diabetes. During the same period, one patient developed peripheral neuropathy and a second severe autonomic neuropathy. Rapid development of chronic complications in these patients raises the possibility that there may be a subset of patients with unusual susceptibility to complications. We re-emphasize the need for vigilant monitoring for complications in young diabetic patients, even in the first few years of their discase. In particular, young patients with visual complaints should be evaluated carefully for evidence of treatable eye disease. C1 JOSLIN DIABET CTR,DEPT MED,BOSTON,MA. UNION UNIV,DEPT MED,ALBANY,NY 12208. NR 34 TC 4 Z9 4 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0803-5253 J9 ACTA PAEDIATR JI Acta Paediatr. PD APR PY 1992 VL 81 IS 4 BP 355 EP 358 DI 10.1111/j.1651-2227.1992.tb12243.x PG 4 WC Pediatrics SC Pediatrics GA HT820 UT WOS:A1992HT82000017 PM 1606400 ER PT J AU BROWN, JH DELUCA, SA AF BROWN, JH DELUCA, SA TI IMAGING OF SINONASAL TUMORS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Imaging of the paranasal sinuses and the nasal cavity provides important anatomic information in the evaluation of suspected neoplasia. The primary modalities employed are conventional films, computed tomography (CT) and magnetic resonance imaging (MRI). Although plain sinus films remain the screening procedure of choice, CT is the preferred modality for more detailed assessment of the paranasal sinuses and the nasal cavity. When soft tissue discrimination is required, MRI is indicated. Imaging studies are used to define the limits of disease, not to diagnose malignancy. RP BROWN, JH (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 4 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 APR PY 1992 VL 45 IS 4 BP 1653 EP 1656 PG 4 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HP040 UT WOS:A1992HP04000016 PM 1558041 ER PT J AU LI, B LLOYD, ML GUDJONSSON, H SHUG, AL OLSEN, WA AF LI, B LLOYD, ML GUDJONSSON, H SHUG, AL OLSEN, WA TI THE EFFECT OF ENTERAL CARNITINE ADMINISTRATION IN HUMANS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE CARNITINE; HUMAN; INTESTINAL ABSORPTION; JEJUNUM; RENAL REABSORPTION; TRIPLE-LUMEN PERFUSIONS ID ABSORPTION; DEFICIENCY; TRANSPORT; EXCRETION; CARDIOMYOPATHY; METABOLISM; INTESTINE; JEJUNUM; SERUM; RAT AB We previously determined that the L-carnitine uptake by human duodenal tissue occurs by both active (K(T) 558-mu-mol/L) and passive mechanisms. The effects of enteral carnitine was studied in humans. A hamburger meal (345-mu-mol total carnitine) induced peak jejunal fluid free (unesterified) and short-chain acylcarnitine concentrations (SCAC) of 209 and 130-mu-mol/L, respectively. Plasma carnitine concentrations and the percent renal reabsorption remained unchanged. By contrast, a pharmacologic dose of free carnitine (25 298-mu-mol) raised peak intraluminal free and SCAC to 20 660 and 4204-mu-mol/L. Plasma total carnitine concentrations doubled to 93-mu-mol/L, and the percent renal reabsorption of free and SCAC declined to 76% and 52%, respectively. In triple-lumen perfusions, 200-mu-mol carnitine/L was absorbed at 484 nmol.min-1.30cm-1 jejunum, a rate sufficient for prandial but not pharmacologic assimilation. Our findings indicate that absorption of physiologic and pharmacologic amounts of carnitive occurs predominantly by active transport and passive diffusion, respectively. C1 OHIO STATE UNIV,DEPT PEDIAT,COLUMBUS,OH 43210. MIDDLETON VET ADM HOSP,METABOL RES LABS,MADISON,WI. FU NIADDK NIH HHS [5P30 AM-26659, R01 AM-32667, R0 AM-13927] NR 30 TC 26 Z9 26 U1 0 U2 4 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD APR PY 1992 VL 55 IS 4 BP 838 EP 845 PG 8 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HM118 UT WOS:A1992HM11800012 PM 1550066 ER PT J AU ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA AF ZUSMAN, RM CHRISTENSEN, DM HIGGINS, J BOUCHER, CA TI EFFECTS OF FOSINOPRIL ON CARDIAC-FUNCTION IN PATIENTS WITH HYPERTENSION - RADIONUCLIDE ASSESSMENT OF LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC PERFORMANCE SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Article DE ANGIOTENSIN CONVERTING ENZYME INHIBITION; CINEANGIOGRAPHY; EXERCISE; LUSITROPY; DIASTOLE; RENIN-ANGIOTENSIN SYSTEM AB Numerous pharmacologic agents are capable of lowering the blood pressure of hypertensive patients; however, each drug has a characteristic side effect profile and effect on cardiac performance. In this study, the hemodynamic effects of the angiotensin converting enzyme inhibitor fosinopril were assessed at rest and at peak upright bicycle exercise by first-pass radionuclide cineangiography in 12 patients with essential hypertension. Fosinopril reduced blood pressure at rest in the seated position from 152/101 to 131/85 mm Hg (P < .01) and at peak exercise from 206/103 to 184/91 mm Hg (P < .01). Fosinopril therapy was associated with an increase in stroke volume and cardiac output and a decrease in systemic vascular resistance at rest and during peak exercise. Both peak ejection rate and peak filling rate increased significantly at rest during fosinopril therapy. The unique cardiotropic response to fosinopril may reflect its effects on the myocardial renin-angiotensin system, and suggests that this agent may offer a therapeutic advantage compared with other angiotensin converting enzyme inhibitors. RP ZUSMAN, RM (reprint author), MASSACHUSETTS GEN HOSP,DIV HYPERTENS & VASC MED,MED SERV,CARDIAC UNIT,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 13 Z9 13 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD APR PY 1992 VL 5 IS 4 BP 219 EP 223 PN 1 PG 5 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HP876 UT WOS:A1992HP87600003 PM 1534664 ER PT J AU ZHOU, WG MCCOLLUM, MO LEVINE, BA OLSON, MS AF ZHOU, WG MCCOLLUM, MO LEVINE, BA OLSON, MS TI ROLE OF PLATELET-ACTIVATING-FACTOR IN PANCREATITIS-ASSOCIATED ACUTE LUNG INJURY IN THE RAT SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GUINEA-PIG; RABBIT; CELL; PAF; PHOSPHOLIPASE-A2; NEUTROPHILS; ANTAGONIST; PULMONARY AB Acute necrotizing pancreatitis induced by infusion of bile salt into the pancreatic duct in rats is consistently associated with acute lung injury similar to the adult respiratory distress syndrome. The role of platelet-activating factor (PAF) in this pancreatitis-associated remote organ failure (lung injury) was investigated. Pulmonary tissue levels of PAF were increased gradually and reached a level of 1345 +/- 455 pg/g (6 times the control level) at 12 hours after induction of pancreatitis, whereas pancreatic PAF levels were undetectable and blood PAF remained unchanged. This local pulmonary PAF accumulation occurred at approximately the same time as the progression of lung injury. Pulmonary responses detected (i.e., eicosanoid production, leukocytic infiltration, Evan's blue extravasation, beta-glucuronidase release) were attenuated to varying degrees by treatment of rats in which pancreatitis was initiated with the PAF receptor antagonists (WEB2170 and BN52021). Rat lung lavages were examined after a 12-hour course of pancreatitis and no changes in PAF concentration, surfactant content, and phospholipase A2 (PLA2) activity were noted. Intravenous administration of PLA2 promoted pulmonary PAF production in experimental rats with pancreatitis but not in normal rats. This observation indicates that PLA2, which was determined to be elevated in plasma during pancreatitis, may be responsible for the accumulation of PAF in the lung. In conclusion, pancreatitis-associated lung injury appears to result from an endogenous inflammatory response in which PAF may play an important role. C1 UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. FU NIADDK NIH HHS [AM 19473] NR 35 TC 60 Z9 70 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD APR PY 1992 VL 140 IS 4 BP 971 EP 979 PG 9 WC Pathology SC Pathology GA HM481 UT WOS:A1992HM48100024 PM 1562055 ER PT J AU PINZANI, M ABBOUD, HE GESUALDO, L ABBOUD, SL AF PINZANI, M ABBOUD, HE GESUALDO, L ABBOUD, SL TI REGULATION OF MACROPHAGE COLONY-STIMULATING FACTOR IN LIVER FAT-STORING CELLS BY PEPTIDE GROWTH-FACTORS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE PLATELET-DERIVED GROWTH FACTOR; BASIC FIBROBLAST GROWTH FACTOR ID TUMOR NECROSIS FACTOR; ENDOTHELIAL-CELLS; TRANSITIONAL CELLS; HEPATIC LIPOCYTES; MOLECULAR-CLONING; KUPFFER CELLS; MESSENGER-RNA; FACTOR-ALPHA; FACTOR CSF-1; RAT-LIVER AB Macrophage colony-stimulating factor (M-CSF) selectively promotes mononuclear phagocyte survival, proliferation, and differentiation. The production of this factor within the liver may be necessary to support the relatively long-term survival of circulating monocytes as they migrate into tissues and differentiate into macrophages. We studied the constitutive expression and the effects of platelet-derived growth factor (PDGF), basic fibroblast growth factor (bFGF), and epidermal growth factor (EGF) on M-CSF mRNA levels and secretion of M-CSF in murine liver fat-storing cells (FSC), vascular pericytes likely involved in the development of liver fibrosis. By Northern analysis, using a murine M-CSF cDNA, FSC constitutively express two major transcripts of 4.4 and 2.2 kb, similar to those detected in mouse L cells, used as a control. Exposure to 10 ng/ml PDGF or bFGF increased M-CSF mRNA levels. Peak effects were observed at 3 and 6 h for PDGF and bFGF, respectively, returning to baseline levels by 12 h. Under basal conditions, detectable amounts of M-CSF, measured by radioimmunoassay, were found in cell supernatants conditioned for 8 and 24 h. PDGF and bFGF markedly stimulated the release of M-CSF as early as 8 h, an effect persisting for at least 24 h. These findings suggest that liver FSC release M-CSF upon stimulation by PDGF and bFGF and may contribute to the activation of resident or infiltrating cells in inflammatory liver diseases. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. CASE WESTERN RESERVE UNIV,DEPT MED,CLEVELAND,OH 44106. CASE WESTERN RESERVE UNIV,DEPT PATHOL,CLEVELAND,OH 44106. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV FLORENCE,IST CLIN MED 2,I-50134 FLORENCE,ITALY. FU NIDDK NIH HHS [DK-33655] NR 33 TC 41 Z9 42 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1992 VL 262 IS 4 BP C876 EP C881 PN 1 PG 6 WC Physiology SC Physiology GA HQ053 UT WOS:A1992HQ05300009 PM 1566815 ER PT J AU PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH YOUNG, AJ SAWKA, MN AF PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH YOUNG, AJ SAWKA, MN TI HUMAN THERMOREGULATORY RESPONSES DURING COLD WATER IMMERSION AFTER ARTIFICIALLY INDUCED SUNBURN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE BLOOD RESPONSES; EXERCISE-COLD STRESS; PERCEPTUAL RESPONSES; PHYSIOLOGICAL RESPONSES; TEMPERATURE REGULATION; ULTRAVIOLET ERYTHEMA; ULTRAVIOLET RADIATION ID ULTRAVIOLET-RADIATION; TEMPERATURE-CHANGES; HUMAN-SKIN; IRRADIATION; EXERCISE; BLOOD AB Thermoregulatory responses during cold-water immersion (water temperature 22-degrees-C) were compared in 10 young men before as well as 24 h and 1 wk after twice the minimal erythemal dose of ultraviolet-B radiation that covered approximately 85% of the body surface area. After 10 min of seated rest in cold water, the men exercised for 50 min on a cycle ergometer (approximately 51% of maximal aerobic power). Rectal temperature, regional and mean heat flow (h(c)-), mean skin temperature from five sites, and heart rate were measured continuously for all volunteers while esophageal temperature was measured for six subjects. Venous blood samples were collected before and after cold water immersion. The mean skin temperature was higher (P < 0.05) throughout the 60-min cold water exposure both 24 h and 1 wk after sunburn compared with before sunburn. Mean h(c) was higher (P < 0.05) after 10 min resting immersion and during the first 10 min of exercise when 24 h postsunburn was compared with presunburn, with the difference attributed primarily to higher h(c) from the back and chest. While rectal temperature and heart rate did not differ between conditions, esophageal temperature before immersion and throughout the 60 min of cold water immersion was higher (P < 0.05) when 24 h postsunburn was compared with presunburn. Plasma volume increased (P < 0.05) after 1 wk postsunburn compared with presunburn, whereas plasma protein concentration was reduced (P < 0.05). After exercise cortisol was greater (P < 0.05) 24 h postsunburn compared with either presunburn or 1 wk postsunburn. Rated perceived exertion and thermal sensation during the 60 min of cold water immersion did not differ between conditions. In conclusion, artificially induced sunburn impaired the ability of these men to vasoconstrict during cold water immersion, resulting in greater heat loss. These adverse thermoregulatory effects were still present 1 wk after sunburn when the associated erythema had disappeared. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP PANDOLF, KB (reprint author), USA,ENVIRONM MED RES INST,NATICK,MA 01760, USA. NR 32 TC 9 Z9 9 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1992 VL 262 IS 4 BP R617 EP R623 PN 2 PG 7 WC Physiology SC Physiology GA HQ056 UT WOS:A1992HQ05600065 PM 1566926 ER PT J AU PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH KRANING, KK GONZALEZ, RR AF PANDOLF, KB GANGE, RW LATZKA, WA BLANK, IH KRANING, KK GONZALEZ, RR TI HUMAN THERMOREGULATORY RESPONSES DURING HEAT EXPOSURE AFTER ARTIFICIALLY INDUCED SUNBURN SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE BLOOD RESPONSES; EXERCISE-HEAT STRESS; PERCEPTUAL RESPONSES; PHYSIOLOGICAL RESPONSES; SWEATING RESPONSES; TEMPERATURE REGULATION; ULTRAVIOLET ERYTHEMA; ULTRAVIOLET RADIATION ID ECCRINE SWEAT GLAND; EXERCISE; ERYTHEMA; BLOOD; SKIN AB Thermoregulatory responses in the heat (ambient temperature 49-degrees-C, 20% relative humidity, 1 m/s wind) were investigated in 10 unacclimated men during 50 min of cycle ergometer exercise (approximately 53% of maximal aerobic power) after a 10-min rest before as well as 24 h and 1 wk after twice the minimal erythemal dose of UV-B radiation that covered approximately 85% of the body surface area. In 7 subjects esophageal temperature (T(es)) was recorded while in all 10 subjects five-site skin and rectal temperatures, heart rate, and back, left forearm, and shielded (12 cm2 area) right forearm sweating rates (m(sw)) were recorded at 15-s intervals. Venous blood was collected before and after exercise-heat stress. Mean skin temperature, T(es), rectal temperature, heart rate, and total body sweating rate were not significantly (P > 0.05) affected by sunburn. Pre- and postexercise values of hematocrit, hemoglobin, plasma protein, plasma volume, and plasma osmolality were also not affected (P > 0.05) by sunburn. Analysis of presunburn and post-sunburn data showed that the T(es) intercept for sweating (degrees-C) was unaffected (P > 0.05), but m(sw)/T(es) and final m(sw) from the left forearm (m(sw)/T(es)) 0.24 +/- 0.02 vs. 0.17 +/- 0.01 mg.cm-2.min-1.degrees-C-1, P < 0.05; m(sw) 0.60 +/- 0.05 vs. 0.37 +/- 0.02, mg.cm-2.min-1, P < 0.05) and back (m(sw)/T(es) 0.43 +/- 0.03 vs. 0.36 +/- 0.01 mg.cm-2.min-1.degrees-C-1, P = 0.052; m(sw) 1.08 +/- 0.09 vs. 0.74 +/- 0.05 mg.cm-2.min-1, P < 0.05) were significantly reduced 24 h postsunburn. Because the protected right forearm m(sw)/T(es) (0.26 +/- 0.01 vs. 0.26 +/- 0.01 mg.cm-2.min-1.degrees-C-1) and final m(sw) (0.63 +/- 0.06 vs. 0.54 +/- 0.03 mg.cm-2.min-1) were not impeded (P > 0.05) by sunburn, decrements in sudomotor drive and level of hydration were not factors in the response. In addition, rated perceived exertion at 45 min and thermal sensation at 30 min of exercise in the heat were significantly greater (P < 0.05) 24 h and 1 wk postsunburn compared with presunburn. These data suggested that after sunburn there was an effect, locally mediated, on both the responsiveness and capacity of the sweat gland. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RP PANDOLF, KB (reprint author), USA,ENVIRONM MED RES INST,NATICK,MA 01760, USA. NR 32 TC 13 Z9 14 U1 1 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD APR PY 1992 VL 262 IS 4 BP R610 EP R616 PN 2 PG 7 WC Physiology SC Physiology GA HQ056 UT WOS:A1992HQ05600064 PM 1566925 ER PT J AU ROSENBAUM, JF BIEDERMAN, J BOLDUC, EA HIRSHFELD, DR FARAONE, SV KAGAN, J AF ROSENBAUM, JF BIEDERMAN, J BOLDUC, EA HIRSHFELD, DR FARAONE, SV KAGAN, J TI COMORBIDITY OF PARENTAL ANXIETY DISORDERS AS RISK FOR CHILDHOOD-ONSET ANXIETY IN INHIBITED CHILDREN SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BEHAVIORAL-INHIBITION; PSYCHIATRIC-DISORDERS; MULTIPLE THRESHOLDS; YOUNG-CHILDREN; PANIC DISORDER; FAMILY; INTERVIEW; ADOLESCENTS; UNFAMILIAR; MORBIDITY AB Objective: Previous work suggested that children of parents with panic disorder and agoraphobia were likely to be classified as behaviorally inhibited and that behaviorally inhibited children were likely to develop anxiety disorders. However, the factors determining which inhibited children were at risk for childhood onset of anxiety disorders remained unknown. The authors of this study hypothesized that greater anxiety loading in parents would increase the risk for anxiety disorders in children with behavioral inhibition. Method: Using DSM-III structured interviews, the authors examined patterns of aggregation of anxiety disorders in parents of two existing cohorts of children, one cross-sectional and clinically derived (31 children, 60 parents) and the other epidemiologically derived and longitudinal (40 children, 75 parents). Within each cohort, parents were stratified into three groups based on the presence (behavioral inhibition and anxiety) or absence (behavioral inhibition only, no behavioral inhibition and no anxiety) of behavioral inhibition and two or more anxiety disorders in their child. Results: Parents of children with behavioral inhibition and anxiety, from both the clinical and nonclinical cohorts, had significantly higher rates of two or more anxiety disorders than did parents of children with behavioral inhibition only and parents of children with no behavioral inhibition and no anxiety. Conclusions: These results indicate that the presence of parental loading for anxiety disorders may help to identify the subgroup of inhibited children at very high risk for developing childhood-onset anxiety disorders. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BEHAV THERAPY UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,DEPT PSYCHOL & SOCIAL RELAT,CAMBRIDGE,MA 02138. RP ROSENBAUM, JF (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Faraone, Stephen/0000-0002-9217-3982 NR 33 TC 83 Z9 83 U1 3 U2 6 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 APR PY 1992 VL 149 IS 4 BP 475 EP 481 PG 7 WC Psychiatry SC Psychiatry GA HL732 UT WOS:A1992HL73200005 PM 1554032 ER PT J AU TORRY, DS AF TORRY, DS TI PROTOONCOGENES AND GERM-CELL DIFFERENTIATION SO AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY LA English DT Review DE PROTOONCOGENE; SPERMATOGENESIS; OOCYTE MATURATION ID MEIOTIC MATURATION; TRANSFORMING GENE; SARCOMA-VIRUSES; MESSENGER-RNA; MOUSE OOCYTES; HUMAN BLADDER; GROWTH-FACTOR; CYCLIN-B; EXPRESSION; PROTOONCOGENES AB Oncogenes are identified functionally by their ability to induce neoplastic transformation of susceptible cells. The first oncogenes to be characterized were isolated from acutely transforming retroviruses. Subsequently, it was determined that the retroviral oncogenes were formed from normal, progenitor genes. These cellular homologs of the viral oncogenes are termed proto-oncogenes: The derivation of oncogenes from proto-oncogenes is the consequence of mutations that remove regulatory constraints from the proto-oncogene. The ability of oncogenes to induce transformation implies that proto-oncogenes may function in growth and differentiation pathways in normal cells. Although many proto-oncogenes have been defined, the normal physiological function of most is not known. Studies of proto-oncogene expression during normal gametogenesis have determined that some genes are expressed in a stage-specific manner. The use of germ cells to provide homogeneous and defined normal cell populations facilitates identifying the roles proto-oncogenes have in regulating cell growth and differentiation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP TORRY, DS (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MOLEC GENET,BOSTON,MA 02115, USA. NR 38 TC 3 Z9 3 U1 0 U2 2 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 8755-8920 J9 AM J REPROD IMMUNOL JI Am. J. Reprod. Immunol. PD APR-MAY PY 1992 VL 27 IS 3-4 BP 167 EP 170 PG 4 WC Immunology; Reproductive Biology SC Immunology; Reproductive Biology GA JK800 UT WOS:A1992JK80000014 PM 1418409 ER PT J AU WARREN, RL AKINS, CW CONN, AKT HILGENBERG, AD MCCABE, CJ AF WARREN, RL AKINS, CW CONN, AKT HILGENBERG, AD MCCABE, CJ TI ACUTE TRAUMATIC DISRUPTION OF THE THORACIC AORTA - EMERGENCY DEPARTMENT MANAGEMENT SO ANNALS OF EMERGENCY MEDICINE LA English DT Article AB Study objective: To evaluate the safety and effectiveness of temporary IV antihypertensive therapy in patients with acute traumatic thoracic aortic disruption. Design: Retrospective chart review of all patients treated for proven traumatic aortic disruption during the ten-year period of 1980 through 1989. Setting: Emergency department of a large, urban, Level l trauma center. Interventions: Preoperative IV-beta-blockade and nitroprusside after initial resuscitation in hemodynamically stable patients. Results: Thirty-seven patients with angiographically proven aortic disruption were separated retrospectively into one of three groups. Group 1 (15 patients without preoperative antihypertensive therapy) had two deaths. Group 2 (15 patients treated for two to seven hours [mean, 3.8 hours] before surgery with antihypertensives) had one death. Group 3 (seven patients treated with antihypertensives for 24 hours to four months before surgery to allow recovery from associated severe injuries) had one death. There were no complications resulting from antihypertensive therapy. Conclusion: Temporary antihypertensive therapy appears to be safe and effective in patients with aortic disruption. RP WARREN, RL (reprint author), MASSACHUSETTS GEN HOSP,DEPT EMERGENCY SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 17 Z9 17 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0196-0644 J9 ANN EMERG MED JI Ann. Emerg. Med. PD APR PY 1992 VL 21 IS 4 BP 391 EP 396 DI 10.1016/S0196-0644(05)82657-5 PG 6 WC Emergency Medicine SC Emergency Medicine GA HL853 UT WOS:A1992HL85300009 PM 1554176 ER PT J AU BARZILAY, J WARRAM, JH RAND, LI PFEIFER, MA KROLEWSKI, AS AF BARZILAY, J WARRAM, JH RAND, LI PFEIFER, MA KROLEWSKI, AS TI RISK FOR CARDIOVASCULAR AUTONOMIC NEUROPATHY IS ASSOCIATED WITH THE HLA-DR3/4 PHENOTYPE IN TYPE-I DIABETES-MELLITUS SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE DIABETES-MELLITUS, INSULIN-DEPENDENT; DIABETIC NEUROPATHIES; CARDIOVASCULAR DISEASES; HLA-DR ANTIGENS ID SUBCUTANEOUS INSULIN INFUSION; HEART-RATE-VARIABILITY; METABOLIC CONTROL; NERVE FUNCTION; TRANSPLANTATION; RETINOPATHY; NEPHROPATHY; PREVALENCE; EXPERIENCE; TESTS AB Objective: To identify risk factors for the development of cardiovascular autonomic neuropathy in patients with juvenile-onset type I diabetes mellitus. Design: Cross-sectional examination of an inception cohort 15 to 21 years after the onset of diabetes. Setting: Outpatient diabetes clinic. Patients: Seventy-nine patients with type I diabetes who experienced onset of disease before 21 years of age and who were followed for 15 to 21 years. Measurements: Autonomic nerve function was evaluated in all patients using deep breathing and tilt tests. On the basis of these tests, an index of cardiovascular autonomic neuropathy was derived and patients were classified as having intact, mildly impaired, or significantly impaired autonomic function. Results: The group with significantly impaired function had a higher mean hemoglobin A1 at the time of examination than the group without impairment, yet the groups did not differ regarding glycemic control during the first decade of diabetes. The HLA-DR3/4 phenotype was present in more than 50% of the patients with significant autonomic dysfunction and conferred relative odds of 6.2 (95% CI, 1.7 to 23.3) for the development of autonomic neuropathy when compared with other HLA-DR phenotypes. Sex, percent ideal body weight, and smoking did not have a statistically significant effect on the development of autonomic neuropathy. Conclusions: The development of cardiovascular autonomic neuropathy in type I diabetes mellitus is strongly associated with the HLA-DR3/4 phenotype. Thus, genetic predisposition may play an important role in the development of this complication. C1 JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215. HUMANA HOSP,LEXINGTON,KY. FU NEI NIH HHS [EY-02636]; NIDDK NIH HHS [DK-41526] NR 42 TC 18 Z9 18 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD APR 1 PY 1992 VL 116 IS 7 BP 544 EP 549 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HL258 UT WOS:A1992HL25800004 PM 1543308 ER PT J AU DEVEBER, GA SCHWARTING, GA KOLODNY, EH KOWALL, NW AF DEVEBER, GA SCHWARTING, GA KOLODNY, EH KOWALL, NW TI FABRY DISEASE - IMMUNOCYTOCHEMICAL CHARACTERIZATION OF NEURONAL INVOLVEMENT SO ANNALS OF NEUROLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; GLYCOSPHINGOLIPIDS; STORAGE; BRAIN AB Fabry disease is an X-linked glycosphingolipid storage disease caused by deficiency of alpha-galactosidase. Storage of globotriaosylceramide, also known as ceramide trihexoside, is maximal in blood vessels but also occurs in neurons. We performed neuropathological histochemical studies on the brains and spinal cords of 2 patients with confirmed Fabry disease. Luxol fast blue-positive deposits were found in blood vessels throughout the central and peripheral nervous system and within selected neurons in spinal cord and ganglia, brainstem, amygdala, hypothalamus, and entorhinal cortex. Regions adjacent to involved neuronal groups, including nucleus basalis, striatum, globus pallidus, and thalamus, were spared. Electron microscopy showed lamellar cytoplasmic neuronal inclusion bodies. Using a monoclonal antibody reactive with ceramide trihexoside, we found more extensive neuronal deposition than evident by Luxol-fast blue staining and new areas of neuronal storage in the spinal cord and cerebral cortex. Blood vessels throughout the nervous system were strongly immunoreactive. The highly selective pattern of neuronal involvement we found suggests that glycosphingolipid exposure, uptake, or catabolism varies greatly with respect to neuronal morphology and distribution. The degree of toxicity to neurons and the clinical significance of this neuronal storage remains to be defined. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. EK SHRIVER CTR,DEPT BIOCHEM,WALTHAM,MA. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 FU NIA NIH HHS [AG05134]; NICHD NIH HHS [HD005515]; NINDS NIH HHS [NS10828] NR 33 TC 62 Z9 62 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1992 VL 31 IS 4 BP 409 EP 415 DI 10.1002/ana.410310410 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA HM460 UT WOS:A1992HM46000009 PM 1375013 ER PT J AU RISKIND, PN AF RISKIND, PN TI THE THERAPEUTIC EFFECT OF BROMOCRIPTINE ON ACUTE AND CHRONIC EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS - REPLY SO ANNALS OF NEUROLOGY LA English DT Letter RP RISKIND, PN (reprint author), MASSACHUSETTS GEN HOSP,NEUROENDOCRINOL LAB,BOSTON,MA 02129, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD APR PY 1992 VL 31 IS 4 BP 451 EP 451 DI 10.1002/ana.410310421 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA HM460 UT WOS:A1992HM46000020 ER PT J AU STEIN, EH CUNNINGHAM, MJ WEBER, AL AF STEIN, EH CUNNINGHAM, MJ WEBER, AL TI NONINVASIVE RADIOLOGIC OPTIONS IN EVALUATING INTRACRANIAL COMPLICATIONS OF OTITIS-MEDIA SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article ID LATERAL SINUS THROMBOSIS; JUGULAR VEIN-THROMBOSIS; DURAL SINUS; DIAGNOSIS C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT RADIOL,BOSTON,MA 02114. NR 14 TC 4 Z9 4 U1 0 U2 1 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD APR PY 1992 VL 101 IS 4 BP 363 EP 366 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA HM679 UT WOS:A1992HM67900014 PM 1562143 ER PT J AU CAPPELLER, WA BLOCH, KJ HATZ, RA CARTER, EA FAGUNDES, J SULLIVAN, DA HARMATZ, PR AF CAPPELLER, WA BLOCH, KJ HATZ, RA CARTER, EA FAGUNDES, J SULLIVAN, DA HARMATZ, PR TI REDUCTION IN BILIARY IGA AFTER BURN INJURY - ROLE OF DIMINISHED DELIVERY VIA THE THORACIC-DUCT AND OF ENHANCED LOSS FROM THE SYSTEMIC CIRCULATION SO ANNALS OF SURGERY LA English DT Article ID GASTROINTESTINAL-TRACT; THERMAL-INJURY; RATS; TRANSLOCATION; MICE; OBSTRUCTION; PROTEIN; LIVER; SERUM; FLUID AB The concentration of biliary IgA is greatly reduced after scald burn injury in the rat, thereby contributing to a deficiency in upper intestinal immune defense. This reduction in biliary IgA might have several explanations, including failure of the transhepatic transport of polymeric IgA (pIgA) from the circulation, decreased delivery of pIgA to the hepatocyte, or decreased local synthesis of IgA in the liver. The authors examined whether burn injury reduces circulating pIgA available for delivery to the hepatocyte. In initial studies, they demonstrated that burn injury induces a decrease in circulating pIgA in bile-duct-ligated rats. They then sought to determine whether this decrease in pIgA was due to increased loss from the circulation or to a decreased supply of pIgA to the circulation through the thoracic duct. After injection of purified I-125-pIgA into bile duct-ligated rats, radioactivity was removed more rapidly from the circulation of burn-injured compared with control rats. The radioactivity localized in the skin and muscle at the site of burn injury. In another group of rats with patent bile ducts, the thoracic duct was cannulated and lymph collected for 12 hours. The total amount of IgA protein in lymph was found to be reduced in burn-injured compared with control animals. Thus, burn injury is accompanied by reduced circulating pIgA, which may be attributed to its enhanced loss from the circulation and to decreased delivery of pIgA from the intestinal mucosa to the systemic circulation via the thoracic duct. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,COMPINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. SHRINERS HOSP CRIPPLED CHILDREN,BOSTON,MA. MASSACHUSETTS GEN HOSP,CLIN IMMUNOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,ALLERGY UNIT,BOSTON,MA 02114. EYE RES INST,IMMUNOL UNIT,BOSTON,MA. UNIV MUNICH,KLINIKUM GROSSHADERN,CHIRURG KLIN & POLIKLIN,W-8000 MUNICH 70,GERMANY. FU NEI NIH HHS [EY05612]; NIADDK NIH HHS [AM33506]; NIDDK NIH HHS [DK34854] NR 24 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-4932 J9 ANN SURG JI Ann. Surg. PD APR PY 1992 VL 215 IS 4 BP 338 EP 343 DI 10.1097/00000658-199204000-00006 PG 6 WC Surgery SC Surgery GA HM324 UT WOS:A1992HM32400006 PM 1558414 ER PT J AU KANSAS, GS AF KANSAS, GS TI STRUCTURE AND FUNCTION OF L-SELECTIN SO APMIS LA English DT Review DE SELECTIN; ADHESION; LEUKOCYTE; ENDOTHELIUM; LECTIN ID NODE HOMING RECEPTOR; LEUKOCYTE ADHESION MOLECULE-1; HIGH-ENDOTHELIAL VENULES; CELL-SURFACE MOLECULE; ACTIVATED PLATELETS; INTERACTION DOMAINS; MEMBRANE-PROTEIN; ANTIGEN INVIVO; MEL-14 ANTIGEN; HUMAN HOMOLOG AB The selectins are a newly described family of carbohydrate-binding adhesion molecules involved in the regulation of leukocyte traffic. Selectins are composed of an N-terminal C-type lectin domain, a single EGF domain, a variable number of short concensus repeat (SCR) domains, a transmembrane region and a cytoplasmic tail. L-selectin (LAM-1/LECAM-1/LECCAM-1) is the only selectin expressed on leukocytes, and mediates a number of leukocyte-endothelial interactions, including the binding of lymphocytes to HEV of peripheral lymph node high endothelial venules (HEV), neutrophil rolling, and leukocyte attachment to cytokine-treated endothelium in vitro. Stable transfectants expressing a series of chimeric selectins and deletion mutants were functionally analyzed in order to determine the molecular basis of adhesion mediated by L-selectin. The specificity of adhesion was found to reside entirely within the lectin domain, suggesting that this domain is the only domain of the protein to interact with the carbohydrate ligand. These results make previous observations that certain mAbs which block function map to each of the extracellular domains difficult to interpret. In addition, deletion of the cytoplasmic tail of L-selectin abolished adhesion, without affecting ligand recognition. Thus, each domain of the selectins has an important, but distinct, role in cell adhesion. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP KANSAS, GS (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. NR 43 TC 38 Z9 40 U1 0 U2 3 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0903-4641 J9 APMIS JI APMIS PD APR PY 1992 VL 100 IS 4 BP 287 EP 293 PG 7 WC Immunology; Microbiology; Pathology SC Immunology; Microbiology; Pathology GA HT832 UT WOS:A1992HT83200001 PM 1374617 ER PT J AU SANDOR, T JOLESZ, F TIEMAN, J KIKINIS, R JONES, K ALBERT, M AF SANDOR, T JOLESZ, F TIEMAN, J KIKINIS, R JONES, K ALBERT, M TI COMPARATIVE-ANALYSIS OF COMPUTED TOMOGRAPHIC AND MAGNETIC-RESONANCE-IMAGING SCANS IN ALZHEIMER PATIENTS AND CONTROLS SO ARCHIVES OF NEUROLOGY LA English DT Article ID DEMENTIA; DISEASE AB Ten patients with Alzheimer's disease underwent computed tomography and magnetic resonance imaging at the same point in time. The mean Mini-Mental State examination score of the patients was 23, indicating that they were mildly impaired. Ten age-equivalent controls also obtained computed tomographic and magnetic resonance imaging scans. A semiautomated computer program analyzed nine comparable regions of interest on each set of scans. When regions of interest from both types of scans were combined in the same discriminant function analysis, the first two variables selected were from the magnetic resonance imaging data set, and they significantly differentiated 95% of the patients and controls. C1 BRANDEIS UNIV,HELLER SCH,WALTHAM,MA 02254. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SANDOR, T (reprint author), BRIGHAM & WOMENS HOSP,DEPT RADIOL,BOSTON,MA 02115, USA. FU NIA NIH HHS [P01-AG04953] NR 19 TC 34 Z9 34 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9942 J9 ARCH NEUROL-CHICAGO JI Arch. Neurol. PD APR PY 1992 VL 49 IS 4 BP 381 EP 384 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA HM463 UT WOS:A1992HM46300017 PM 1558519 ER PT J AU GRAGOUDAS, ES EGAN, KM ARRIGG, PG SEDDON, JM GLYNN, RJ MUNZENRIDER, JE AF GRAGOUDAS, ES EGAN, KM ARRIGG, PG SEDDON, JM GLYNN, RJ MUNZENRIDER, JE TI CATARACT-EXTRACTION AFTER PROTON-BEAM IRRADIATION FOR MALIGNANT-MELANOMA OF THE EYE SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID UVEAL MELANOMAS AB We evaluated visual outcome and risk of metastases in patients who underwent cataract extraction after proton-beam irradiation of a uveal melanoma. A total of 84 patients underwent cataract extraction between 2 months and 11 years after irradiation. One year after cataract extraction, approximately half of the patients had visual acuity of 20/100 or better, and approximatel one third had an acuity of 20/40 or better. Larger tumor size was highly correlated with poor visual outcome 1 year after extraction. Six patients underwent enucleation after cataract removal, five due to blind, painful eyes and one due to continued growth of a previously undiagnosed ring melanoma. The rate of metastases was not higher among patients who underwent cataract extraction (adjusted rate ratio, 0.83). Results suggests that cataract extraction offers improvement of vision in selected eyes previously irradiated for a uveal melanoma, without adding to the risk of metastases among patients undergoing the procedure. C1 MASSACHUSETTS EYE & EAR HOSP,EPIDEMIOL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHANNING LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,JOSELIN DIABET CTR,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. RP GRAGOUDAS, ES (reprint author), MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 17 TC 23 Z9 23 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1992 VL 110 IS 4 BP 475 EP 479 PG 5 WC Ophthalmology SC Ophthalmology GA HN279 UT WOS:A1992HN27900020 PM 1562251 ER PT J AU BERDY, GJ ABELSON, MB SMITH, LM GEORGE, MA AF BERDY, GJ ABELSON, MB SMITH, LM GEORGE, MA TI PRESERVATIVE-FREE ARTIFICIAL TEAR PREPARATIONS - ASSESSMENT OF CORNEAL EPITHELIAL TOXIC EFFECTS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID DRY-EYE; OPHTHALMIC PRESERVATIVES; DRUGS; MANAGEMENT; VEHICLES AB Scanning electron microscopy was used to evaluate the corneal epithelium of rabbit eyes after administration of two preservative-free ocular lubricants, preservative-free artificial tear-1 (Hypotears PF) and preservative-free artificial tear-2 (Refresh), and 0.02% benzalkonium chloride. Animals were randomly assigned to either mild or exaggerated use regimens. A quantitative rating system was used to assess epithelial damage. With mild use, scanning electron micrscopy revealed normal epithelial morphologic characteristics for both preservative-free artificial tear solutions (mean relative damage score, solution 1,075 +/- 0.16; solution 2, 1.02 +/- 0.23), which were not significantly different from eyes treated with phosphate-buffered saline (1.38 +/- 0.38) or a mild dosage regimen of 0.02% benzalkonium chloride (1.20 +/- 0.12). Exaggerated use with preservative-free artificial tear solutions (solution 1, 1.31 +/- 0.21; solution 2, 1.35 +/- 0.08) induced minimal damage that was not different from control eyes treated with phosphate-buffered saline (1.26 +/- 0.13). Compared with an exaggerated use of 0.02% benzalkonium chloride (4.0 +/- 0.16), both preservative-free artificial tear solutions induced significantly less epithelial damage (P = .0001). These results suggests that with frequent-dosage regimens, preservation-free artificial tear solutions-1 and -2 are free of the toxic effects associated with preserved solutions. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,20 STANIFORD ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 17 TC 60 Z9 63 U1 1 U2 8 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1992 VL 110 IS 4 BP 528 EP 532 PG 5 WC Ophthalmology SC Ophthalmology GA HN279 UT WOS:A1992HN27900034 PM 1562263 ER PT J AU AZAR, DT SPURRMICHAUD, SJ TISDALE, AS GIPSON, IK AF AZAR, DT SPURRMICHAUD, SJ TISDALE, AS GIPSON, IK TI ALTERED EPITHELIAL BASEMENT-MEMBRANE INTERACTIONS IN DIABETIC CORNEAS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID COLLAGEN PRODUCTION; ANCHORING FIBRILS; CLOSED VITRECTOMY; IV COLLAGEN; COMPLICATIONS; HEMIDESMOSOME; MELLITUS; SURFACE AB Morphologic alterations of the extracellular matrix in diabetes include thickening of the basement membrane and, as evidenced in the corneal epithelium, a decrease in the area of the basal cell membrane occupied by hemidesmosomes. To determine if the abnormal basement membrane in diabetes has altered epithelial recognition of sites for hemidesmosome formation and if diabetic epithelium can recognize sites for hemidesmosome formation on normal basement membrane, we recombined epithelial sheets and corneal stromas with denuded basement membranes in vitro using diabetic and control corneas. In recombinations of diabetic epithelium on normal stromas, the area of the basal cell membrane occupied by hemidesmosomes was 10.7%, significantly less than control recombinations (19.5%). Similarly, in diabetic stromas, the value (8.6%) was significantly decreased from control. These data may indicate altered cell-extracellular matrix interactions in diabetes. C1 HARVARD UNIV,SCH MED,EYE RES INST,20 STANIFORD ST,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. FU FIC NIH HHS [TW03814]; PHS HHS [R3703306] NR 34 TC 78 Z9 79 U1 0 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD APR PY 1992 VL 110 IS 4 BP 537 EP 540 PG 4 WC Ophthalmology SC Ophthalmology GA HN279 UT WOS:A1992HN27900036 PM 1532888 ER PT J AU AOBA, T SHIMODA, S AKITA, H HOLMBERG, C TAUBMAN, MA AF AOBA, T SHIMODA, S AKITA, H HOLMBERG, C TAUBMAN, MA TI ANTIPEPTIDE ANTIBODIES REACTIVE WITH EPITOPIC DOMAINS OF PORCINE AMELOGENINS AT THE C-TERMINUS SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE AMELOGENESIS; AMELOGENINS; ANTIPEPTIDE ANTIBODIES; EPITOPES AT THE C-TERMINUS ID MONOCLONAL-ANTIBODY; MINERAL INTERACTION; ENAMEL; PROTEIN; COMPONENTS; KERATINS; MATRIX AB This was an immunological investigation of the processing of porcine amelogenins in situ. Rabbit and rat anti-peptide sera reacted specifically with the hydrophilic segment of the intact amelogenins at the C-terminus. The immunogens used were the synthetic peptides: (a) C13 composed of PATDKTKREEVDC and (b) C25 composed of MQSLLPDLPLEAWPATDKTKREEVD. These peptides correspond to the C-terminal 12- and 25-residue segments of porcine amelogenin, respectively. Cystine was introduced at the C-terminus of C12 for KLH-binding (C13). Western blot analysis disclosed that: (i) both rabbit and rat anti-C13 sera reacted selectively with the 25-kDa porcine amelogenin and three other minor components (27, 22 and 18 kDa); (ii) anti-C25 peptide sera, additionally, reacted with the 23-kDa amelogenins (a degradation derivative of the 25-kDa protein, lacking the 12-residue segment at the C-ter-minus) and as trace components, 20-, 16- and 14-kDa moieties. Importantly, all the proteins reactive with the anti-C[3 serum were concentrated in the outer secretory enamel adjacent to the ameloblasts, decreasing significantly in the underlying inner secretory enamel. Immunohistochemical studies applying the anti-peptide sera to the developing tooth germs of a minipig also confirmed the localization of reactivity in the outer secretory region. Neither anti-peptide serum reacted with porcine non-amelogenins, serum proteins nor dentine matrix proteins at the dilutions tested. However, it was found that both the anti-C 1 3 and C25 sera reacted with human keratin. The overall results indicate that: (a) the last 25-amino acid residue segment of porcine amelogenin contains at least two epitopes at the C-terminus; (b) porcine amelogenesis may include the secretion of multiple amelogenins; and (c) the cleavage of the epitope(s) in the last 12-residue segment occurs shortly after secretion of the intact amelogenins. C1 TSURUMI UNIV,SCH PHYS EDUC,YOKOHAMA,KANAGAWA,JAPAN. RP AOBA, T (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE04733, DE07623] NR 31 TC 12 Z9 12 U1 0 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PD APR PY 1992 VL 37 IS 4 BP 249 EP 255 DI 10.1016/0003-9969(92)90046-B PG 7 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HM446 UT WOS:A1992HM44600002 PM 1381576 ER PT J AU LEIFER, D CROS, D HALPERIN, JJ GALLICO, GG PIERCE, DS SHAHANI, BT AF LEIFER, D CROS, D HALPERIN, JJ GALLICO, GG PIERCE, DS SHAHANI, BT TI FAMILIAL BILATERAL CARPAL-TUNNEL SYNDROME - REPORT OF 2 FAMILIES SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE CARPAL TUNNEL SYNDROME; ELECTROPHYSIOLOGY; GENETICS ID THROMBOCYTOPENIC PURPURA; THRESHOLDS; CHILDHOOD AB Cases of familial carpal tunnel syndrome without other associated conditions are rare. We report two families in which multiple members had bilateral carpal tunnel syndromes. The pattern was consistent with autosomal dominant inheritance. Electrophysiologic studies were performed on nine of the 15 patients, and they demonstrated bilateral pathology of the median nerves at the wrist in all but one patient, without evidence for subclinical, generalized peripheral neuropathy. Quantitative sensory testing was performed in two cases, and it corroborated the absence of peripheral neuropathy. Five of the six patients who underwent carpal tunnel release improved after surgery. C1 MASSACHUSETTS GEN HOSP,DEPT PLAST SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPED SURG,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. SUNY STONY BROOK,DEPT NEUROL,STONY BROOK,NY 11794. RP LEIFER, D (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,ACC 835,BOSTON,MA 02114, USA. NR 37 TC 10 Z9 12 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD APR PY 1992 VL 73 IS 4 BP 393 EP 397 DI 10.1016/0003-9993(92)90017-Q PG 5 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA HM910 UT WOS:A1992HM91000017 PM 1554316 ER PT J AU UENO, N CHAKRABARTI, B GARG, HG AF UENO, N CHAKRABARTI, B GARG, HG TI HYALURONIC-ACID OF HUMAN SKIN AND POSTBURN SCAR - HETEROGENEITY IN PRIMARY STRUCTURE AND MOLECULAR-WEIGHT SO BIOCHEMISTRY INTERNATIONAL LA English DT Article ID PERIODATE-OXIDATION; CIRCULAR-DICHROISM; GLYCOSAMINOGLYCANS; CARTILAGE; COLLAGEN C1 HARVARD UNIV,SHRINERS BURNS INST,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP UENO, N (reprint author), HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,EYE RES INST,BOSTON,MA 02114, USA. FU NEI NIH HHS [5R01 EY05301] NR 31 TC 4 Z9 4 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 0158-5231 J9 BIOCHEM INT PD APR PY 1992 VL 26 IS 5 BP 787 EP 796 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT563 UT WOS:A1992HT56300002 PM 1610381 ER PT J AU BLAZERYOST, BL FESSEHA, Y COX, M AF BLAZERYOST, BL FESSEHA, Y COX, M TI ALDOSTERONE-MEDIATED NA+ TRANSPORT IN RENAL EPITHELIA - TIME-COURSE OF INDUCTION OF A POTENTIAL REGULATORY COMPONENT OF THE CONDUCTIVE NA+ CHANNEL SO BIOCHEMISTRY INTERNATIONAL LA English DT Article ID INDUCED PROTEINS; HORMONAL-REGULATION; URINARY BLADDERS; SODIUM-CHANNELS; TOAD BLADDER; ELECTROPHORESIS; LOCALIZATION; SUBUNIT C1 UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. RP BLAZERYOST, BL (reprint author), VET AFFAIRS MED CTR,DEPT MED,DIV RENAL ELECTROLYTE,PHILADELPHIA,PA 19104, USA. NR 22 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS AUST PI MARRICKVILLE PA LOCKED BAG 16, MARRICKVILLE NSW 2204, AUSTRALIA SN 0158-5231 J9 BIOCHEM INT PD APR PY 1992 VL 26 IS 5 BP 887 EP 897 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT563 UT WOS:A1992HT56300012 PM 1319156 ER PT J AU BAENZIGER, JE MILLER, KW MCCARTHY, MP ROTHSCHILD, KJ AF BAENZIGER, JE MILLER, KW MCCARTHY, MP ROTHSCHILD, KJ TI PROBING CONFORMATIONAL-CHANGES IN THE NICOTINIC ACETYLCHOLINE-RECEPTOR BY FOURIER-TRANSFORM INFRARED DIFFERENCE SPECTROSCOPY SO BIOPHYSICAL JOURNAL LA English DT Article; Proceedings Paper CT CONF ON BIOPHYSICS AND RECOMBINANT DNA : PROBLEMS, STRATEGIES, AND NEW QUESTIONS CY JAN 19-22, 1992 CL AIRLIE, VA SP NIH, NATL SCI FDN, USN, OFF NAVAL RES ID BINDING AB We have developed a Fourier transform infrared (FTIR) difference method tor probing conformational changes that occur upon the binding of ligands to the nicotinic acetylcholine receptor (nAChR), Our approach is to deposit reconstituted nAChR membranes in a thin film on the surface of a germanium internal reflection element, acquire FTIR spectra in the presence of bulk aqueous solution using attenuated total reflection, and then trigger conformational changes by sequentially flowing a buffer either with or without an agonist past the film surface. Using the fluorescent probe, ethidium bromide, it is demonstrated that the method of nAChR film deposition does not affect the ability of the receptor to undergo the resting-to-desensitized state transition. The difference of FTIR spectra of nAChR films recorded in the presence and absence of agonists reveal highly reproducible infrared bands that are not observed in the difference of spectra recorded with only buffer flowing past the film surface. Some of the bands are assigned to changes in protein secondary structure and to changes in the structure of individual amino acid residues. Bands arising from the vibrations of the agonist bound to the receptor are also observed. The results demonstrate that FTIR difference spectroscopy can detect structural changes in the nAChR that occur upon the binding of ligands. The technique will be an effective method for investigating nAChR structure and function as well as receptor-drug interactions. C1 BOSTON UNIV,DEPT PHYS,BOSTON,MA 02215. BOSTON UNIV,DEPT PHYSIOL,BOSTON,MA 02215. BOSTON UNIV,PROGRAM CELLULAR BIOPHYS,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,CTR ADV BIOTECHNOL & MED,PISCATAWAY,NJ 08854. FU NEI NIH HHS [EYO5499]; NIGMS NIH HHS [GM 15904] NR 8 TC 26 Z9 26 U1 0 U2 1 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1992 VL 62 IS 1 BP 64 EP 66 DI 10.1016/S0006-3495(92)81780-0 PG 3 WC Biophysics SC Biophysics GA HT995 UT WOS:A1992HT99500023 PM 1600101 ER PT J AU BAENZIGER, JE MILLER, KW ROTHSCHILD, KJ AF BAENZIGER, JE MILLER, KW ROTHSCHILD, KJ TI INCORPORATION OF THE NICOTINIC ACETYLCHOLINE-RECEPTOR INTO PLANAR MULTILAMELLAR FILMS - CHARACTERIZATION BY FLUORESCENCE AND FOURIER-TRANSFORM INFRARED DIFFERENCE SPECTROSCOPY SO BIOPHYSICAL JOURNAL LA English DT Article ID X-RAY-DIFFRACTION; PURPLE MEMBRANE; POSTSYNAPTIC MEMBRANES; CONFORMATIONAL-CHANGES; TORPEDO-CALIFORNICA; PROTONATION CHANGES; BACTERIORHODOPSIN; PROTEIN; BINDING; SPECTRA AB A method for preparing thin, planar films of nicotinic acetylcholine receptor (nAChR) membranes that retain the ability to undergo the resting to desensitized state transition and that are suitable for spectroscopic studies has been developed. Native, alkaline-extracted nAChR membranes from Torpedo are dried under nitrogen on either a plastic microscope coverslip or a germanium internal reflection element (IRE) and then equilibrated with buffer. The drying procedure has no effect on the functional state of the nAChR as judged by a fluorescence assay using the probe ethidium bromide. The times required for an acetylcholine analogue (carbamylcholine), a local anesthetic (dibucaine), and a fluorescent probe (ethidium bromide) to penetrate films of varying degrees of thickness, interact with the receptor, and then to be washed from the films have been established. Under these conditions, the nAChR films can be repetitively cycled between the resting and desensitized states. Both fluorescence and infrared spectroscopy show that the films adhere strongly to either support even with buffer flowing continuously past the film surface. Fourier transform infrared difference spectra calculated from spectra recorded in the presence and absence of carbamylcholine show small, reproducible bands which reflect changes in nAChR structure upon desensitization. C1 BOSTON UNIV,DEPT PHYS,BOSTON,MA 02215. BOSTON UNIV,DEPT PHYSIOL,BOSTON,MA 02215. BOSTON UNIV,PROGRAM CELLULAR BIOL,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NEI NIH HHS [EY05499]; NIGMS NIH HHS [GM-15904] NR 39 TC 50 Z9 50 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD APR PY 1992 VL 61 IS 4 BP 983 EP 992 PG 10 WC Biophysics SC Biophysics GA HM259 UT WOS:A1992HM25900015 PM 1581507 ER PT J AU REMOLDODONNELL, E VANBROCKLYN, J KENNEY, DM AF REMOLDODONNELL, E VANBROCKLYN, J KENNEY, DM TI EFFECT OF PLATELET CALPAIN ON NORMAL LYMPHOCYTE-T CD43 - HYPOTHESIS OF EVENTS IN THE WISKOTT-ALDRICH SYNDROME SO BLOOD LA English DT Article ID CALCIUM-DEPENDENT PROTEASE; SURFACE SIALOGLYCOPROTEIN; MONOCLONAL-ANTIBODY; SIALOPHORIN CD43; PERIPHERAL-BLOOD; GLYCOPROTEIN-IB; CELL-SURFACE; ACTIVATION; MEMBRANE; EXPRESSION C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV IMMUNOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DIV PEDIAT,BOSTON,MA 02115. RP REMOLDODONNELL, E (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. RI Van Brocklyn, Jim/A-9733-2010 FU NHLBI NIH HHS [HL29583]; NIAID NIH HHS [AI21163]; NIGMS NIH HHS [GM37298] NR 73 TC 26 Z9 26 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD APR 1 PY 1992 VL 79 IS 7 BP 1754 EP 1762 PG 9 WC Hematology SC Hematology GA HL673 UT WOS:A1992HL67300017 PM 1558970 ER PT J AU LEES, S HUKINS, DWL AF LEES, S HUKINS, DWL TI X-RAY-DIFFRACTION BY COLLAGEN IN THE FULLY MINERALIZED CORTICAL BONE OF COW TIBIA SO BONE AND MINERAL LA English DT Article DE COLLAGEN; CORTICAL BONE; MINERALIZATION ID TURKEY LEG TENDON; NEUTRON-DIFFRACTION; WATER; TISSUES AB X-ray diffraction patterns were recorded from fully mineralized and demineralized sections of the cortical bone from cow tibia. The results were used to obtain a measure, d, of the mean side-to-side spacing (equatorial diffraction spacing) of the molecules in the type I collagen fibrils of bone. Mineralized bone yielded a d value of 1.23 nm; for the demineralized tissue this value increased to 1.52 nm. Thus it appears that mineralization of bone compacts its collagen molecules within the fibrils. C1 UNIV MANCHESTER,DEPT MED BIOPHYS,MANCHESTER M13 9PL,LANCS,ENGLAND. RP LEES, S (reprint author), FORSYTH DENT CTR,DEPT BIOENGN,140 FENWAY,BOSTON,MA 02115, USA. FU PHS HHS [2325] NR 16 TC 19 Z9 20 U1 0 U2 3 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-6009 J9 BONE MINER JI Bone Miner. PD APR PY 1992 VL 17 IS 1 BP 59 EP 63 DI 10.1016/0169-6009(92)90710-U PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL774 UT WOS:A1992HL77400005 PM 1581706 ER PT J AU ABBOUD, SL AF ABBOUD, SL TI EPIDERMAL GROWTH-FACTOR STIMULATES MACROPHAGE COLONY-STIMULATING FACTOR (M-CSF) MESSENGER-RNA EXPRESSION AND M-CSF RELEASE IN CULTURED MURINE STROMAL CELLS SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article ID TUMOR NECROSIS FACTOR; HUMAN-MONOCYTES; GENE-EXPRESSION; GRANULOCYTE; INTERLEUKIN-1; UROGASTRONE; PLATELETS; CLONING; MARROW; BLOOD AB Macrophage colony-stimulating factor (M-CSF) released by stromal cells of the bone marrow microenvironment plays a crucial role in the growth and proliferation of mononuclear cells. Several peptide mitogens including interleukin-1, tumour necrosis factor, platelet-derived growth factor and fibroblast growth factor stimulate the release of M-CSF and may be important in mediating the haematopoietic response to inflammation. Epidermal growth factor (EGF), released from platelets during aggregation, is mitogenic for a variety of cell types and may cause the release of certain cytokines. In this study we used the TC-1 murine stromal cells which constitutively secrete M-CSF as a model to study the regulation of M-CSF in response to EGF. EGF markedly stimulated the steady state expression of M-CSF mRNA with a peak effect observed at 3 h. This was associated with the release of M-CSF protein as determined by radioimmunoassay. EGF also stimulated DNA synthesis in a concentration dependent manner. Although TC-1 cells express GM-CSF mRNA, this was not induced by EGF. These findings suggest that EGF is a key regulatory molecule for M-CSF and may indirectly effect haematopoiesis via the release of M-CSF from stromal cells. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ABBOUD, SL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 40 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD APR PY 1992 VL 80 IS 4 BP 452 EP 457 DI 10.1111/j.1365-2141.1992.tb04557.x PG 6 WC Hematology SC Hematology GA HM876 UT WOS:A1992HM87600006 PM 1581229 ER PT J AU HABERMANN, TM ANDERSEN, JW CASSILETH, PA BENNETT, JM OKEN, MM AF HABERMANN, TM ANDERSEN, JW CASSILETH, PA BENNETT, JM OKEN, MM TI SEQUENTIAL ADMINISTRATION OF RECOMBINANT INTERFERON ALPHA AND DEOXYCOFORMYCIN IN THE TREATMENT OF HAIRY-CELL LEUKEMIA SO BRITISH JOURNAL OF HAEMATOLOGY LA English DT Article ID LEUKEMIC-RETICULOENDOTHELIOSIS; PENTOSTATIN 2'-DEOXYCOFORMYCIN; FOLLOW-UP; SPLENECTOMY; REMISSIONS; INFECTIONS; RESISTANT; INDUCTION; THERAPY AB Both recombinant interferon alpha and deoxycoformycin (dCF) are effective in the treatment of hairy cell leukaemia. In an attempt to reduce the complications from dCF therapy, a pilot study of the Eastern Cooperative Oncology Group (ECOG) first treated patients with interferon to improve peripheral blood cell counts before dCF treatment began. Thirty-four patients were treated for 3 months with recombinant interferon alpha-2a (rIFN alpha-2a), 3 x 10(6) IU subcutaneously three times a week for 3 months, and then by dCF, 4 mg/m2 intravenously every 2 weeks for a maximum of 12 months. The overall response rate was 94% (32/34); 76% of patients (26/34) had complete response (CR) (90% confidence interval, 62-88%) and 18% (6/34) partial response. One patient was found to have a Mycobacterium avium infection while receiving rIFN alpha-2a. Without specific antimycobacterial therapy and with continued administration of rIFN alpha-2a and dCF, the infection resolved and he achieved CR. Three patients had culture-negative febrile episodes during the dCF phase of treatment. Non-disseminated herpes zoster developed in four patients, but three of the episodes occurred only after treatment was discontinued. Sequential administration of rIFN alpha-2a and dCF resulted in fewer infections (P = 0.027) than in ECOG's previous study of dCF used alone. Two patients died, one of combined hairy cell leukaemia and non-Hodgkin's lymphoma of intermediate histologic type 17 months after entry into the study and the other of cardiac arrest 20 months after entry. Thirty-two patients were alive with a median follow-up of 21 months (range 13-31 months). This combination produces durable CRs with a low incidence of infection. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HOSP UNIV PENN,PHILADELPHIA,PA 19104. UNIV ROCHESTER,CTR CANC,ROCHESTER,NY 14627. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. RP HABERMANN, TM (reprint author), MAYO CLIN & MAYO FDN,200 1ST ST SW,ROCHESTER,MN 55905, USA. NR 41 TC 37 Z9 38 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1048 J9 BRIT J HAEMATOL JI Br. J. Haematol. PD APR PY 1992 VL 80 IS 4 BP 466 EP 471 DI 10.1111/j.1365-2141.1992.tb04559.x PG 6 WC Hematology SC Hematology GA HM876 UT WOS:A1992HM87600008 PM 1581231 ER PT J AU TROP, M SCHIFFRIN, EJ CARTER, EA AF TROP, M SCHIFFRIN, EJ CARTER, EA TI EFFECT OF ACUTE AND CHRONIC LIPOPOLYSACCHARIDE (LPS) ADMINISTRATION ON RETICULOENDOTHELIAL SYSTEM (RES) PHAGOCYTIC-ACTIVITY INVIVO SO BURNS LA English DT Article AB The effect of injection or chronic infusion of lipopolysaccharide (LPS) into unanaesthetized rats on the distribution of [Tc-99m]SC has been determined. At a dose of 2.5 mg/kg, LPS injection caused a marked alteration in the distribution of the radiolabelled material, with more uptake being achieved in the lung while less was taken up by the spleen. Kidney and liver uptake were also changed. Chronic infusion of LPS at a similar dose (3 mg/kg in 24 h) caused a marked increase in the uptake of the radioactive material by the lung only. These data are consistent with a working hypothesis that the alterations in RES phagocytic activity of the lung observed in rats subjected to burn trauma could be related in part to LPS, either coming as a bolus, or being continuously presented. C1 MASSACHUSETTS GEN HOSP,DEPT PEDIAT,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0305-4179 J9 BURNS JI Burns PD APR PY 1992 VL 18 IS 2 BP 107 EP 108 DI 10.1016/0305-4179(92)90004-E PG 2 WC Critical Care Medicine; Dermatology; Surgery SC General & Internal Medicine; Dermatology; Surgery GA HJ747 UT WOS:A1992HJ74700004 PM 1590922 ER PT J AU CARTER, EA GONNELLA, A TOMPKINS, RG AF CARTER, EA GONNELLA, A TOMPKINS, RG TI INCREASED TRANSCELLULAR PERMEABILITY OF RAT SMALL-INTESTINE AFTER THERMAL-INJURY SO BURNS LA English DT Article AB The pathway which results in a loss of intestinal barrier function and transepithelial transfer of macromolecules after cutaneous thermal injury is unknown. To determine the enhanced absorption pathway, transepithelial transport of horseradish peroxidase (HRP) was examined ultrastructurally after a thermal injury. Within 6 h after the injury, increased HRP uptake was seen in the portal and systemic blood with the maximal increase in uptake measured at 18 h postinjury; permeability returned to normal by 72 h postinjury. Morphologically, the increased uptake was found to be transcellular through ultrastructurally normal intestinal absorptive cells. Occasional focal regions of enhanced HRP uptake were found and this enhanced uptake was attributed to focal intestinal epithelial disruptions. This increase in intestinal permeability represents a transient loss of intestinal barrier function and potentially allows absorption of macromolecules such as endotoxin from the intestinal lumen into the portal circulation early after thermal injury. RP CARTER, EA (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT GASTROINTESTINAL & NUTR LAB,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM 21700] NR 0 TC 24 Z9 24 U1 0 U2 1 PU BUTTERWORTH-HEINEMANN LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0305-4179 J9 BURNS JI Burns PD APR PY 1992 VL 18 IS 2 BP 117 EP 120 DI 10.1016/0305-4179(92)90007-H PG 4 WC Critical Care Medicine; Dermatology; Surgery SC General & Internal Medicine; Dermatology; Surgery GA HJ747 UT WOS:A1992HJ74700007 PM 1590925 ER PT J AU WILLETT, CG LEWANDROWSKI, K DONNELLY, S SHELLITO, PC CONVERY, K ELISEO, R COMPTON, CC AF WILLETT, CG LEWANDROWSKI, K DONNELLY, S SHELLITO, PC CONVERY, K ELISEO, R COMPTON, CC TI ARE THERE PATIENTS WITH STAGE-I RECTAL-CARCINOMA AT RISK FOR FAILURE AFTER ABDOMINOPERINEAL RESECTION SO CANCER LA English DT Article ID CURATIVE SURGERY; ADENOCARCINOMA; PATTERNS; THERAPY; CANCER AB The clinical courses of 64 patients undergoing abdominoperineal resection for Stage I lower rectal carcinoma (tumors confined to the muscularis propria without lymph node involvement) were reviewed to identify subsets at risk for failure. Twelve of 12 patients with tumors limited to the submucosa remained disease free without evidence of recurrence. Of the 52 patients with muscularis propria involvement, there have been eight failures with three patients having local failure only, three patients with local failure and distant metastases, and two patients with distant metastases only. The 6-year actuarial disease-free survival, local control, and freedom from distant metastases rates for patients with tumors invasive of the muscularis propria were 80%, 84%, and 88%, respectively. Patients with tumors exhibiting vascular/lymph vessel involvement were at even higher risk for failure. Although adjuvant treatment is infrequently advised for these patients, the use of radiation therapy and chemotherapy should be reconsidered for patients with Stage I lower rectal carcinoma, specifically for patients with tumors invasive of the muscularis propria with vascular/lymph vessel involvement. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. RP WILLETT, CG (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 12 TC 28 Z9 28 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 APR 1 PY 1992 VL 69 IS 7 BP 1651 EP 1655 DI 10.1002/1097-0142(19920401)69:7<1651::AID-CNCR2820690703>3.0.CO;2-4 PG 5 WC Oncology SC Oncology GA HK770 UT WOS:A1992HK77000002 PM 1551050 ER PT J AU COOLEY, ME AF COOLEY, ME TI BEREAVEMENT CARE - A ROLE FOR NURSES SO CANCER NURSING LA English DT Article DE BEREAVEMENT CARE; GRIEF; NURSING ASSESSMENT; NURSING MANAGEMENT; HIGH-RISK INDIVIDUALS ID INTERVENTION; ADJUSTMENT AB Bereavement care is an important, yet often forgotten, area of care. Evidence suggests that early and prompt interventions for high-risk individuals can facilitate grief and can minimize the adverse consequences of grief. Nurses can play a pivotal role in providing care to bereaved individuals. However, it is essential to have a thorough knowledge of the normal grief response, and a framework for assessment and management. This article provides fundamental information about the manifestations of grief and offers information about appropriate nursing assessment and management for bereaved individuals. C1 PHILADELPHIA VET AFFAIRS MED CTR,LUNG TUMOR CLIN,PHILADELPHIA,PA. NR 27 TC 7 Z9 7 U1 2 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0162-220X J9 CANCER NURS JI Cancer Nurs. PD APR PY 1992 VL 15 IS 2 BP 125 EP 129 PG 5 WC Oncology; Nursing SC Oncology; Nursing GA HT413 UT WOS:A1992HT41300004 PM 1617618 ER PT J AU GUTMANN, R LEUNIG, M FEYH, J GOETZ, AE MESSMER, K KASTENBAUER, E JAIN, RK AF GUTMANN, R LEUNIG, M FEYH, J GOETZ, AE MESSMER, K KASTENBAUER, E JAIN, RK TI INTERSTITIAL HYPERTENSION IN HEAD AND NECK TUMORS IN PATIENTS - CORRELATION WITH TUMOR SIZE SO CANCER RESEARCH LA English DT Note ID FLUID PRESSURE; MACROMOLECULES; TRANSPORT; GROWTH AB Elevated interstitial fluid pressure (IFP) is associated with poor blood supply and inadequate delivery of drugs to solid tumors. IFP was measure in squamous cell carcinomas of the head and neck region in humans using the wick-in-needle technique. In all lesions (n = 19), the IFP was elevated (4-33 mm Hg). Furthermore, the IFP increased with tumor size. The highest IFP was 33 mm Hg in a 24-ml tumor. In one tumor, the IFP was found to be negative (-2.6 mm Hg), which is comparable to that in human skin or subcutaneous tissue. The histopathology of this tumor was benign. If this pressure difference between malignant and benign lesions can be confirmed in a large number of tumors, then the IFP could be used to aid tumor detection during needle biopsy. The value of IFP as a predictor of response to radiotherapy, photodynamic therapy, hyperthermia, and chemotherapy should be assessed prospectively. C1 UNIV MUNICH,KLINIKUM GROSSHADERN,INST SURG RES,W-8000 MUNICH 70,GERMANY. UNIV MUNICH,KLINIKUM GROSSHADERN,INST ANESTHESIOL,W-8000 MUNICH 70,GERMANY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. RP GUTMANN, R (reprint author), UNIV MUNICH,KLINIKUM GROSSHADERN,EAR NOSE & THROAT CLIN,MARCHIONINISTR 15,W-8000 MUNICH 70,GERMANY. RI Leunig, Michael/E-7951-2017 OI Leunig, Michael/0000-0002-2036-5416 FU NCI NIH HHS [CA37239, CA49792] NR 15 TC 164 Z9 164 U1 0 U2 2 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD APR 1 PY 1992 VL 52 IS 7 BP 1993 EP 1995 PG 3 WC Oncology SC Oncology GA HL505 UT WOS:A1992HL50500057 PM 1551128 ER PT J AU SCHROEDER, SA SHANNON, DC MARK, EJ AF SCHROEDER, SA SHANNON, DC MARK, EJ TI CELLULAR INTERSTITIAL PNEUMONITIS IN INFANTS - A CLINICOPATHOLOGICAL STUDY SO CHEST LA English DT Article ID CHILDREN; DISEASE AB Five infants had interstitial pneumonitis with constant histologic findings, which was different from that previously described in children. All the infants presented with tachypnea at birth and persistent disease, both clinically and radiographically, despite treatment. Open-lung biopsy in each case showed a diffuse interstitial thickening due to pale oval and spindle-shaped histiocytes without scarring. This neonatal cellular interstitial pneumonitis differs both clinically and histologically from the usual interstitial pneumonitis, lymphocytic interstitial pneumonitis and desquamative interstitial pneumonitis observed in adults and children. The etiology of this cellular interstitial pneumonitis in neonates is unknown. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SCHROEDER, SA (reprint author), NEW YORK MED COLL,RM 106,MUNGER PAVIL,VALHALLA,NY 10591, USA. NR 16 TC 46 Z9 51 U1 0 U2 0 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD APR PY 1992 VL 101 IS 4 BP 1065 EP 1069 DI 10.1378/chest.101.4.1065 PG 5 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HN511 UT WOS:A1992HN51100038 PM 1555422 ER PT J AU FERRELL, M FUSTER, V GOLD, HK CHESEBRO, JH AF FERRELL, M FUSTER, V GOLD, HK CHESEBRO, JH TI A DILEMMA FOR THE 1990S - CHOOSING APPROPRIATE EXPERIMENTAL ANIMAL-MODEL FOR THE PREVENTION OF RESTENOSIS SO CIRCULATION LA English DT Editorial Material DE ANGIOTENSIN CONVERTING ENZYMES; PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY; CLINICAL TRIALS; RESTENOSIS; EDITORIAL COMMENTS C1 MAYO CLIN & MAYO FDN,DIV CARDIOVASC DIS,ROCHESTER,MN 55905. RP FUSTER, V (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULFINCH 1,32 FRUIT ST,BOSTON,MA 02114, USA. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 10 TC 94 Z9 94 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD APR PY 1992 VL 85 IS 4 BP 1630 EP 1631 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HN049 UT WOS:A1992HN04900050 PM 1532546 ER PT J AU HERIAN, AM BUSH, RK TAYLOR, SL AF HERIAN, AM BUSH, RK TAYLOR, SL TI PROTEIN AND ALLERGEN CONTENT OF COMMERCIAL SKIN-TEST EXTRACTS FOR SOYBEANS SO CLINICAL AND EXPERIMENTAL ALLERGY LA English DT Article ID FOOD HYPERSENSITIVITY; ATOPIC-DERMATITIS; CHILDREN; RAST AB The protein and allergen contents of four commercial soybean skin test extracts were tested by SDS-PAGE and immunoblotting using sera from soy-allergic adults. Polyacrylamide gels stained with Coomassie Blue showed an absence of several major soybean proteins, particularly those at higher molecular weights. The acidic subunits of glycinin and beta-conglycinin. major soybean storage proteins. appear to be absent or present in much reduced amounts. Immunoblots with soy-allergic sera indicate alteration, reduction, or loss of IgE-binding in the commercial extracts as compared to extracts of soy flour. In one soy-allergic patient, skin tests revealed a negative response to three of the commercial soybean extracts and a mild response to one extract. Defatted soy flour obtained from two of the four extract manufacturers was extracted in the laboratory using a standard procedure for the isolation of soybean proteins. In one case, the extract still had an abnormal protein profile on gel electrophoresis while in the other case, the new extraction procedure gave significantly improved extraction of soy protein. Preparation methods appear to be partially responsible for the variable allergen content in commercial soybean skin test extracts. C1 UNIV NEBRASKA,DEPT FOOD SCI & TECHNOL,LINCOLN,NE 68583. UNIV NEBRASKA,CTR FOOD PROC,LINCOLN,NE 68583. UNIV WISCONSIN,INST FOOD RES,MADISON,WI 53706. UNIV WISCONSIN,CTR CLIN SCI,DEPT MED,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. NR 15 TC 13 Z9 13 U1 0 U2 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0954-7894 J9 CLIN EXP ALLERGY JI Clin. Exp. Allergy PD APR PY 1992 VL 22 IS 4 BP 461 EP 468 DI 10.1111/j.1365-2222.1992.tb00148.x PG 8 WC Allergy; Immunology SC Allergy; Immunology GA HT084 UT WOS:A1992HT08400008 PM 1611546 ER PT J AU PRENCE, EM NATOWICZ, MR AF PRENCE, EM NATOWICZ, MR TI DIAGNOSIS OF ALPHA-MANNOSIDOSIS BY MEASURING ALPHA-MANNOSIDASE IN PLASMA SO CLINICAL CHEMISTRY LA English DT Article DE LYSOSOMES; HERITABLE DISORDERS AB Alpha-mannosidosis is a lysosomal storage disease resulting from a deficiency of lysosomal alpha-mannosidase activity. Diagnosis of alpha-mannosidosis has traditionally been accomplished by demonstrating reduced alpha-mannosidase activity in leukocytes. We describe a new assay of alpha-mannosidase in serum or plasma that allows specific detection of the enzyme deficiency in alpha-mannosidosis with small, easily obtained sample volumes. The assay utilizes 40-mu-L of serum or plasma and a fluorescent substrate, 4-methylumbelliferyl-alpha-D-mannopyranoside in sodium acetate buffer, pH 4.0. The mean activity of a control population was 194 (SD 67) mU/L, whereas the activities obtained for four alpha-mannosidosis patients were 0, 17, 17, and 33 mU/L. Comparison with the standard leukocyte alpha-mannosidase assay showed this serum or plasma assay to be equally effective in diagnosing alpha-mannosidosis. C1 EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV BIOCHEM,WALTHAM,MA 02254. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP PRENCE, EM (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,DIV MED GENET,LYSOSOMAL STORAGE DIS LAB,WALTHAM,MA 02254, USA. NR 13 TC 13 Z9 14 U1 0 U2 2 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD APR PY 1992 VL 38 IS 4 BP 501 EP 503 PG 3 WC Medical Laboratory Technology SC Medical Laboratory Technology GA HN921 UT WOS:A1992HN92100007 PM 1568314 ER PT J AU WAJNER, M SANSEVERINO, MT GIUGLIANI, R SWEETMAN, L YAMAGUCHI, S FUKAO, T SHIH, VE AF WAJNER, M SANSEVERINO, MT GIUGLIANI, R SWEETMAN, L YAMAGUCHI, S FUKAO, T SHIH, VE TI BIOCHEMICAL INVESTIGATION OF A BRAZILIAN PATIENT WITH A DEFECT IN MITOCHONDRIAL ACETOACETYL-COENZYME-A THIOLASE SO CLINICAL GENETICS LA English DT Article DE INBORN ERRORS OF METABOLISM; 3-KETOTHIOLASE DEFICIENCY; METABOLIC ACIDOSIS; ORGANIC ACIDURIA ID 3-KETOTHIOLASE DEFICIENCY; CULTURED FIBROBLASTS; 2-METHYL-3-HYDROXYBUTYRIC ACIDURIA; ISOLEUCINE CATABOLISM; IDENTIFICATION; BIOSYNTHESIS; DISORDER AB A case report of 3-ketothiolase deficiency due to a defect of mitochondrial acetoacetyl-CoA thiolase protein in a Brazilian boy and its biochemical investigation is presented. The child had moderate generalized hypotonia, EEG alterations and crises of metabolic acidosis following infections. Hypotonia and EEG abnormalities disappeared with a low protein diet, and physical and mental development are normal. Urinary organic acid excretion was typical of 3-ketothiolase deficiency, showing consistently high levels of 2-methyl-3-hydroxybutyric acid and tiglylglycine. Activation of acetoacetyl-CoA thiolase activity by potassium (K) ion in cultured fibroblasts was not observed, demonstrating the lack of activity of mitochondrial acetoacetyl-CoA thiolase. In addition, the signal for the mitochondrial acetoacetyl-CoA thiolase protein was undetectable in the immunoblot analysis. In the pulse-chase experiments, the signal for mitochondrial acetoacetyl-CoA thiolase was detected after a 1-h pulse but not after a 24-h chase. These results indicate that the deficiency was caused by an unstable mitochondrial acetoacetyl-CoA thiolase protein. C1 HOSP CLIN PORTO ALEGRE,UNIDADE GENET MED,PORTO ALEGRE,RS,BRAZIL. GIFU UNIV,SCH MED,DEPT PEDIAT,GIFU 500,JAPAN. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP WAJNER, M (reprint author), UNIV FED RIO GRANDE SUL,INST BIOCIENCIAS,DEPT BIOQUIM,RUA SARMENTO LEITE 500,BR-90050 PORTO ALEGRE,RS,BRAZIL. RI Giugliani, Roberto/G-4790-2015 OI Giugliani, Roberto/0000-0001-9655-3686 FU NINDS NIH HHS [NS05096] NR 18 TC 6 Z9 6 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD APR PY 1992 VL 41 IS 4 BP 202 EP 205 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA HM520 UT WOS:A1992HM52000007 PM 1349518 ER PT J AU CONWAY, B TOMFORD, WW AF CONWAY, B TOMFORD, WW TI RADIOSENSITIVITY OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 SO CLINICAL INFECTIOUS DISEASES LA English DT Letter C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPED,BOSTON,MA 02114. RP CONWAY, B (reprint author), OTTAWA GEN HOSP,DIV INFECT DIS,501 SMYTH,ROOM LM-15,OTTAWA K1H 8L6,ONTARIO,CANADA. NR 9 TC 9 Z9 9 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD APR PY 1992 VL 14 IS 4 BP 978 EP 979 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HL304 UT WOS:A1992HL30400035 PM 1576300 ER PT J AU CUNNINGHAM, MJ EAVEY, RD AF CUNNINGHAM, MJ EAVEY, RD TI THE TAN TONSIL SIGN - A CLINICAL MARKER OF LYMPHOPROLIFERATIVE DISEASE SO CLINICAL PEDIATRICS LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; RENAL-TRANSPLANTATION; THERAPY; CHILD C1 HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02115. RP CUNNINGHAM, MJ (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 10 TC 2 Z9 2 U1 0 U2 1 PU WESTMINSTER PUBL INC PI GLEN HEAD PA 708 GLEN COVE AVE, GLEN HEAD, NY 11545 SN 0009-9228 J9 CLIN PEDIATR JI Clin. Pediatr. PD APR PY 1992 VL 31 IS 4 BP 237 EP 240 DI 10.1177/000992289203100410 PG 4 WC Pediatrics SC Pediatrics GA HP625 UT WOS:A1992HP62500010 PM 1563199 ER PT J AU MARTYN, JAJ BISHOP, AL OLIVERI, MF AF MARTYN, JAJ BISHOP, AL OLIVERI, MF TI PHARMACOKINETICS AND PHARMACODYNAMICS OF RANITIDINE AFTER BURN INJURY SO CLINICAL PHARMACOLOGY & THERAPEUTICS LA English DT Article ID CRITICALLY ILL PATIENTS; DRUG-THERAPY; CIMETIDINE; CHILDREN; KINETICS; VOLUME AB The pharmacokinetics and pharmacodynamics of ranitidine were studied in 10 hypermetabolic burned patients with normal creatinine clearance and compared with healthy volunteers. Ranitidine was administered as a single 50 mg intravenous bolus and multiple blood samples were obtained up to 10 hours after the dose for determination of plasma ranitidine concentrations. Gastric pH in burned patients was monitored by way of a nasogastric tube. Burned patients exhibited significantly higher (p < 0.01) ranitidine clearance (mean +/- SD; 10.80 +/- 2.38 versus 7.53 +/- 1.71 ml/min/kg) and steady-state distribution volume (1.63 +/- 0.13 versus 1.16 +/- 0.33 L/kg). Within an hour of administration of drug the gastric pH was greater-than-or-equal-to 4.0 in all but one patient. This pH was maintained for at least 6 hours. In five patients the pH was greater-than-or-equal-to 4.0 throughout the 10-hour study. Thus, despite increased ranitidine clearance, the recommended dose of ranitidine maintained gastric pH greater-than-or-equal-to 4.0 throughout the normal dosing interval in the majority of patients. Dosage adjustment reported for many other drugs after burn injury may not be necessary for ranitidine. C1 HARVARD UNIV,SCH MED,DEPT ANESTHESIA,CLIN PHARMACOL LAB,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA. GLAXO INC,CLIN DEV,RES TRIANGLE PK,NC. RP MARTYN, JAJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,CLIN PHARMACOL LAB,ANESTHESIA SERV,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM31569] NR 30 TC 13 Z9 13 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0009-9236 J9 CLIN PHARMACOL THER JI Clin. Pharmacol. Ther. PD APR PY 1992 VL 51 IS 4 BP 408 EP 414 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HQ702 UT WOS:A1992HQ70200007 PM 1563210 ER PT J AU AHMED, AR MOHIMEN, A MIRZA, NM YUNIS, EJ ALPER, CA AF AHMED, AR MOHIMEN, A MIRZA, NM YUNIS, EJ ALPER, CA TI LINKAGE OF PEMPHIGUS-VULGARIS ANTIBODY TO MHC IN HEALTHY RELATIVES OF PATIENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,SCH DENT MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A447 EP A447 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101768 ER PT J AU ANDREWS, NC ORKIN, SH AF ANDREWS, NC ORKIN, SH TI PURIFIED NUCLEAR FACTOR-ERYTHROID-2 (NF-E2) SELECTIVELY RECOGNIZES ERYTHROID AP-1 SITES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,HOWARD HUGHES MED INST,DEPT PEDIAT,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A300 EP A300 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100944 ER PT J AU ATLAS, SJ SINGER, DE AF ATLAS, SJ SINGER, DE TI CHANGING BLOOD USE IN THE AIDS ERA - THE CASE OF ELECTIVE HIP-SURGERY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A551 EP A551 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102389 ER PT J AU BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B AF BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B TI ANGIOGENESIS AND TUMOR PROGRESSION OF MELANOMA - QUANTIFICATION OF VASCULARITY IN MELANOCYTIC NEVI AND MELANOMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL & NEUROL,DIV DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A476 EP A476 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101945 ER PT J AU BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G AF BAUER, RL VENKATACHALAM, H FORRESTER, R HARRIS, G TI A RANDOMIZED TRIAL OF AMBULATORY CARE IN THE 3RD YEAR CLERKSHIP SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A596 EP A596 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102656 ER PT J AU BAUER, RL HAFFNER, SM AF BAUER, RL HAFFNER, SM TI INCREASED ANDROGENICITY OF OBESE PREMENOPAUSAL WOMEN DOES NOT ACCOUNT FOR INCREASED BONE-DENSITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A413 EP A413 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101581 ER PT J AU BELZER, MB PARENTI, C LENZ, S LURIE, N AF BELZER, MB PARENTI, C LENZ, S LURIE, N TI WHAT KIND OF TEACHING IS THERE ON ATTENDING ROUNDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HENNEPIN CTY MED CTR,MINNEAPOLIS,MN 55415. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A596 EP A596 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102658 ER PT J AU BERGELSON, JM CHAN, BMC HEMLER, ME FINBERG, RW AF BERGELSON, JM CHAN, BMC HEMLER, ME FINBERG, RW TI VLA-2, THE ECHOVIRUS 1 RECEPTOR, INTERACTS WITH VIRUS AND EXTRACELLULAR-MATRIX LIGANDS BY DISTINCT MECHANISMS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A334 EP A334 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101131 ER PT J AU BICKEL, PE FREEMAN, MW AF BICKEL, PE FREEMAN, MW TI STRUCTURE OF RABBIT SCAVENGER RECEPTORS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A291 EP A291 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100895 ER PT J AU BIERER, MF SLAVIN, PL HERMANN, PA ILES, SS AF BIERER, MF SLAVIN, PL HERMANN, PA ILES, SS TI THE FINANCIAL IMPACT OF A CLINIC FOR HOMELESS PEOPLE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BOSTON HLTH CARE HOMELESS PROGRAM,GEN INTERNAL MED UNIT,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A577 EP A577 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102540 ER PT J AU BILDEN, PF PHILLIPS, SB KOLLIAS, N MUCCINI, JA DRAKE, LA AF BILDEN, PF PHILLIPS, SB KOLLIAS, N MUCCINI, JA DRAKE, LA TI POLARIZED-LIGHT PHOTOGRAPHY OF ACNE-VULGARIS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A454 EP A454 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101810 ER PT J AU BLEICHER, PA DUNN, DA SIMHA, S GADENNE, AS BIGBY, M AF BLEICHER, PA DUNN, DA SIMHA, S GADENNE, AS BIGBY, M TI LIMITED T-CELL RECEPTOR-V-BETA EXPRESSION IN NORMAL HUMAN SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A496 EP A496 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102063 ER PT J AU CARTER, ME RAISHER, BD GULICK, T MOORE, DD CAIRA, T STRAUSS, AW KELLY, DP AF CARTER, ME RAISHER, BD GULICK, T MOORE, DD CAIRA, T STRAUSS, AW KELLY, DP TI REGULATION OF THE MEDIUM-CHAIN ACYL-COA DEHYDROGENASE (MCAD) GENE BY MEMBERS OF THE RETINOIC ACID RECEPTOR FAMILY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WASHINGTON UNIV,DEPT MED,ST LOUIS,MO 63130. WASHINGTON UNIV,DEPT PEDIAT,ST LOUIS,MO 63130. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A149 EP A149 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100072 ER PT J AU CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C WARYAS, P AF CROW, SE LICHTENSTEIN, MJ TULEY, MR MASCARENHAS, C WARYAS, P TI OBSERVER VARIABILITY IN SCREENING FOR HEARING-LOSS IN THE ELDERLY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A569 EP A569 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102497 ER PT J AU DOYLE, K HALLAQ, Y THOR, AM CLUETTEBROWN, J HOJNACKI, JL LAPOSATA, M AF DOYLE, K HALLAQ, Y THOR, AM CLUETTEBROWN, J HOJNACKI, JL LAPOSATA, M TI FATTY-ACID ETHYL-ESTERS ARE PRESENT IN HUMAN SERUM AFTER ETHANOL-CONSUMPTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. UNIV MASSACHUSETTS,LOWELL,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A236 EP A236 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100570 ER PT J AU DRABICK, J BHATTACHARJEE, A WILLIAMS, W SIBER, G CROSS, A AF DRABICK, J BHATTACHARJEE, A WILLIAMS, W SIBER, G CROSS, A TI COVALENT POLYMYXIN B-STARCH AND POLYMYXIN B-IMMUNOGLOBULIN G CONJUGATES AS NOVEL ANTIENDOTOXIN REAGENTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 WALTER REED ARMY MED CTR,DEPT BACTERIAL DIS,WASHINGTON,DC 20307. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 5 Z9 5 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A287 EP A287 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100871 ER PT J AU DRAKE, L BRENEMAN, D GREENE, S RAIMER, S SCHUPBACH, CW HALPERIN, M AF DRAKE, L BRENEMAN, D GREENE, S RAIMER, S SCHUPBACH, CW HALPERIN, M TI EFFECTS OF TOPICAL DOXEPIN 5-PERCENT CREAM ON PRURITIC ECZEMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 COOPERAT HLTH,SEATTLE,WA. GENDERM CORP,LINCOLNSHIRE,IL. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. UNIV CINCINNATI,DEPT DERMATOL,CINCINNATI,OH 45221. UNIV TEXAS,MED BRANCH,GALVESTON,TX 77550. UNIV N CAROLINA,CHARLOTTE,NC 28223. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A455 EP A455 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101818 ER PT J AU DUKE, D CASTRESANA, J LUCCHINA, L LEE, TH MIHM, MC SOBER, AJ BARNHILL, RL AF DUKE, D CASTRESANA, J LUCCHINA, L LEE, TH MIHM, MC SOBER, AJ BARNHILL, RL TI FAMILIAL MELANOMA AND 2-MUTATIONAL-EVENT MODELING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A164 EP A164 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100160 ER PT J AU EMANUEL, EJ WEINBERG, DS HUMMEL, L GONIN, R EMANUEL, LL AF EMANUEL, EJ WEINBERG, DS HUMMEL, L GONIN, R EMANUEL, LL TI DOES PROXY APPOINTMENT IMPROVE ADVANCE CARE PLANNING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02215. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A612 EP A612 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102751 ER PT J AU EMANUEL, LL BARRY, MJ STOECKLE, JD EMANUEL, EJ AF EMANUEL, LL BARRY, MJ STOECKLE, JD EMANUEL, EJ TI ADVANCE DIRECTIVES - HOW DO SCENARIO BASED TREATMENT CHOICES CHANGE WITH TIME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A612 EP A612 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102750 ER PT J AU EMANUEL, LL BARRY, MJ STOECKLE, JD EMANUEL, EJ AF EMANUEL, LL BARRY, MJ STOECKLE, JD EMANUEL, EJ TI ADVANCE DIRECTIVES - DO SCENARIO BASED TREATMENT CHOICES EXTRAPOLATE TO DIFFERENT DECISIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 3 Z9 3 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A611 EP A611 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102749 ER PT J AU ERON, JJ CHOW, YK COOLEY, TP LIEBMAN, HA HIRSCH, MS DAQUILA, RT AF ERON, JJ CHOW, YK COOLEY, TP LIEBMAN, HA HIRSCH, MS DAQUILA, RT TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 DIDANOSINE RESISTANCE - EFFECTS OF PRIOR ZIDOVUDINE EXPOSURE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BOSTON CITY HOSP,DEPT MED,BOSTON,MA 02118. BOSTON UNIV,SCH MED,BOSTON,MA 02118. UNIV SO CALIF,SCH MED,DIV HEMATOL,LOS ANGELES,CA 90033. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A246 EP A246 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100632 ER PT J AU FOLLI, F SAAD, MJA BACKER, JM KAHN, CR AF FOLLI, F SAAD, MJA BACKER, JM KAHN, CR TI INSULIN STIMULATES THE PI-3 KINASE ASSOCIATED WITH IRS-1 IN LIVER AND MUSCLE OF THE INTACT RAT SO CLINICAL RESEARCH 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A320 EP A320 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101057 ER PT J AU FRASER, PA YUNIS, EJ ALPER, CA AF FRASER, PA YUNIS, EJ ALPER, CA TI EXCESS ADMIXTURE PROPORTION OF NON-HLA-DR4 EXTENDED MHC HAPLOTYPES OF CAUCASIAN ORIGIN AMONG RA-ASSOCIATED HAPLOTYPES IN AFRICAN-AMERICANS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RHEUMATOL IMMUNOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A268 EP A268 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100762 ER PT J AU GADENNE, ASJ BLEICHER, PA DUNN, DA BIGBY, M AF GADENNE, ASJ BLEICHER, PA DUNN, DA BIGBY, M TI INFILTRATING LYMPHOCYTES IN LICHEN-PLANUS CONTAIN A SIGNIFICANT POPULATION OF T-CELL RECEPTOR GAMMA-DELTA-BEARING CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CBRC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A500 EP A500 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102086 ER PT J AU GALLO, RL BERNFIELD, M AF GALLO, RL BERNFIELD, M TI SYNDECAN EXPRESSION IS INDUCED DURING FOLLICULAR DEVELOPMENT IN DERMAL MESENCHYME AND FOLLOWING CYTOKINE STIMULATION OF NIH 3T3 CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. NR 3 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A442 EP A442 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101739 ER PT J AU GIANANI, R JACKSON, R EISENBARTH, GS AF GIANANI, R JACKSON, R EISENBARTH, GS TI LOSS OF HUMORAL TOLERANCE TO SINGLE AUTOANTIGENS IN RELATIVES OF PATIENTS WITH TYPE-I DIABETES SO CLINICAL RESEARCH 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 SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A239 EP A239 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100590 ER PT J AU GORN, AH FLANNERY, MS MANNING, CA GOLDRING, SR AF GORN, AH FLANNERY, MS MANNING, CA GOLDRING, SR TI EXPRESSION OF A CLONED HIGH-AFFINITY CALCITONIN (CT) RECEPTOR CDNA CONFERS BINDING AND CAMP RESPONSIVENESS FOR AMYLIN (AMY) AND CALCITONIN GENE RELATED PEPTIDE (CGRP) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NE DEACONESS HOSP,BOSTON,MA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A209 EP A209 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100417 ER PT J AU GRABBE, S KNISELY, TL GRANSTEIN, RD AF GRABBE, S KNISELY, TL GRANSTEIN, RD TI DECREASED PRODUCTION OF GRANULOCYE-MACROPHAGE COLONY STIMULATING FACTOR (GM-CSF) BY EPIDERMAL-CELLS FROM ATHYMIC NUDE-MICE INVITRO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A467 EP A467 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101891 ER PT J AU GRANSTEIN, RD BRUVERS, S GRABBE, S AF GRANSTEIN, RD BRUVERS, S GRABBE, S TI EFFECTS OF TGF-BETA AND IFN-GAMMA ON THE PRESENTATION OF TUMOR-ASSOCIATED ANTIGEN BY MURINE EPIDERMAL ANTIGEN PRESENTING CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A501 EP A501 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102092 ER PT J AU GRECO, MA LADAS, D RUDOLPH, S BADEN, H AF GRECO, MA LADAS, D RUDOLPH, S BADEN, H TI MODULATION OF PANCORNULIN EXPRESSION BY CALCIUM AND RELATIVE CONFLUENCE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CBRC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A513 EP A513 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102164 ER PT J AU GREVELINK, SA VIBBARD, DE OSBORNE, JA LOSCALZO, J LERNER, EA AF GREVELINK, SA VIBBARD, DE OSBORNE, JA LOSCALZO, J LERNER, EA TI CHRYSOPTIN, A NOVEL INHIBITOR OF PLATELET-AGGREGATION ISOLATED FROM SALIVARY-GLANDS OF THE DEERFLY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A202 EP A202 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100379 ER PT J AU HALL, JE MARTIN, KA WHITNEY, HA ADAMS, JM LANDY, H CROWLEY, WF AF HALL, JE MARTIN, KA WHITNEY, HA ADAMS, JM LANDY, H CROWLEY, WF TI ACQUIRED HYPOGONADOTROPIC HYPOGONADISM - A PREDOMINANTLY HYPOTHALAMIC DEFECT CORRECTABLE WITH PULSATILE GONADOTROPIN-RELEASING-HORMONE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINOL UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A281 EP A281 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100836 ER PT J AU HOLZ, GG KUHTREIBER, WM HABENER, JF AF HOLZ, GG KUHTREIBER, WM HABENER, JF TI INDUCTION OF GLUCOSE-COMPETENCE IN PANCREATIC BETA-CELLS BY GLUCAGON-LIKE PEPTIDE-1(7-37) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. RI Holz, George/A-3386-2012 NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A320 EP A320 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101056 ER PT J AU HOSOI, J GRABBE, S LERNER, E GRANSTEIN, RD AF HOSOI, J GRABBE, S LERNER, E GRANSTEIN, RD TI CALCITONIN GENE RELATED PEPTIDE (CGRP) INHIBITS LANGERHANS CELL (LC) ANTIGEN PRESENTATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A502 EP A502 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102098 ER PT J AU HUSAIN, Z RATLIFF, J WICK, MM AF HUSAIN, Z RATLIFF, J WICK, MM TI MEDIATION OF GROWTH AND DIFFERENTIATION IN HUMAN MELANOCYTE CELL-LINES BY PHORBOL ESTERS INVOLVES DIFFERENTIAL EXPRESSION OF CELLULAR GENES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A527 EP A527 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102249 ER PT J AU INGELFINGER, JR BOUYOUNES, B CARTER, EA AF INGELFINGER, JR BOUYOUNES, B CARTER, EA TI BOTH INTRARENAL AND CIRCULATING RENIN-ANGIOTENSIN SYSTEMS (RAS) ARE STIMULATED IN A STANDARD BURN MODEL SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. SHRINERS BURN INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A389 EP A389 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101445 ER PT J AU INOGUCHI, T BATTAN, R HANDLER, E KING, GL AF INOGUCHI, T BATTAN, R HANDLER, E KING, GL TI PERSISTENT ACTIVATION OF PROTEIN-KINASE-C ISOFORM BETA-II BY DIABETES IN HEART AND AORTA, AND ITS DIFFERENTIAL REVERSIBILITY BY ISLET CELL TRANSPLANTATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV MASSACHUSETTS,AMHERST,MA 01003. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A141 EP A141 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100026 ER PT J AU JAHROUDI, N LYNCH, DC AF JAHROUDI, N LYNCH, DC TI ENDOTHELIAL-CELL SPECIFIC REGULATION OF VONWILLEBRAND-FACTOR GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A210 EP A210 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100423 ER PT J AU JUNG, FF ANDERSON, S INGELFINGER, JR AF JUNG, FF ANDERSON, S INGELFINGER, JR TI PREVENTION OF INCREASED INTRARENAL ANGIOTENSIN CONVERTING ENZYME DISTRIBUTION IN STREPTOZOTOCIN DIABETES BY INTERRUPTION OF RENIN-ANGIOTENSIN SYSTEM (RAS) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. OREGON HLTH SCI UNIV,DIV RENAL,PORTLAND,OR 97201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A389 EP A389 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101446 ER PT J AU KLICKSTEIN, LB ETEMAD, JK SPRINGER, TA AF KLICKSTEIN, LB ETEMAD, JK SPRINGER, TA TI EFFICIENT EXPRESSION OF A SOLUBLE FORM OF COMPLEMENT RECEPTOR TYPE-1 REQUIRES A SEQUENCE IN THE COOH-TERMINAL REGION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CTR BLOOD RES,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A361 EP A361 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101279 ER PT J AU KOLACZYNSKI, JW CARTER, R SOPRANO, J MOSCICKI, R BODEN, G AF KOLACZYNSKI, JW CARTER, R SOPRANO, J MOSCICKI, R BODEN, G TI INSULIN BINDING AND DEGRADATION BY RAT-LIVER KUPFFER AND ENDOTHELIAL-CELLS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 TEMPLE UNIV,HLTH SCI CTR,SCH MED,PHILADELPHIA,PA 19140. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A238 EP A238 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100586 ER PT J AU KOLLIAS, N GILLIES, R MORAN, M KOCHEVAR, I ANDERSON, RR AF KOLLIAS, N GILLIES, R MORAN, M KOCHEVAR, I ANDERSON, RR TI FLUORESCENCE SPECTROSCOPY OF AGED AND PHOTOAGED HAIRLESS MOUSE SKIN SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A539 EP A539 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102323 ER PT J AU KOLLIAS, N MUCCINI, JA PHILLIPS, SB ANDERSON, RR DRAKE, LA AF KOLLIAS, N MUCCINI, JA PHILLIPS, SB ANDERSON, RR DRAKE, LA TI REFLECTANCE SPECTROSCOPY - A RAPID, SENSITIVE, AND REPRODUCIBLE MEANS OF CLINICALLY ASSESSING ERYTHEMA AND PIGMENTATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A458 EP A458 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101833 ER PT J AU LAWRENCE, VA HILSENBECK, SG PAGE, CP AF LAWRENCE, VA HILSENBECK, SG PAGE, CP TI POSTOPERATIVE PULMONARY COMPLICATIONS - FORGOTTEN RISK SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A559 EP A559 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102437 ER PT J AU LAWRENCE, VA PAGE, CP HILSENBECK, SG TULEY, MR AF LAWRENCE, VA PAGE, CP HILSENBECK, SG TULEY, MR TI PREDICTING POSTOPERATIVE PULMONARY COMPLICATIONS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A560 EP A560 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102438 ER PT J AU LERNER, EA VIBBARD, DE GREVELINK, SA AF LERNER, EA VIBBARD, DE GREVELINK, SA TI MAXADILAN, A POTENT VASODILATOR FROM SAND FLY SALIVARY-GLANDS SO CLINICAL RESEARCH 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 1 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A346 EP A346 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101191 ER PT J AU LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA CORNELL, JE AF LICHTENSTEIN, MJ GRIFFIN, MR RAY, WA CORNELL, JE TI IN-HOSPITAL HIP-FRACTURES - A CASE-CONTROL STUDY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,GERONTOL RES EDUC & CLIN CTR,SAN ANTONIO,TX 78284. VANDERBILT UNIV,DEPT PREVENT MED,NASHVILLE,TN 37240. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A268 EP A268 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100758 ER PT J AU MA, J SY, MS HAUSER, C BIGBY, M AF MA, J SY, MS HAUSER, C BIGBY, M TI TRINITROPHENOL REACTIVE T-CELL HYBRIDOMAS RECOGNIZE ANTIGENS THAT REQUIRE ANTIGEN PROCESSING SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CBRC,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV GENEVA,HOP CANTONAL,CH-1211 GENEVA 4,SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A503 EP A503 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102108 ER PT J AU MANGIONE, CM PHILLIPS, RS GILBERT, MM SEDDON, JM ORAV, EJ GOLDMAN, L AF MANGIONE, CM PHILLIPS, RS GILBERT, MM SEDDON, JM ORAV, EJ GOLDMAN, L TI CORRELATES OF CHANGE IN VISUAL FUNCTIONAL STATUS FOLLOWING CATARACT-EXTRACTION AND INTRAOCULAR-LENS IMPLANTATION IN ELDERLY ADULTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A560 EP A560 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102442 ER PT J AU MAYTIN, EV LAMBERTI, LA AF MAYTIN, EV LAMBERTI, LA TI HEAT-SHOCK REDUCES UVB-INDUCED SUNBURN CELL-FORMATION IN MURINE EPIDERMIS INVIVO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A541 EP A541 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102332 ER PT J AU MILANI, RV LAVIE, CJ LITTMAN, AB AF MILANI, RV LAVIE, CJ LITTMAN, AB TI HOSTILITY AND DEPRESSION INDEXES PREDICT FUNCTIONAL IMPROVEMENT FOLLOWING CARDIAC REHABILITATION AND EXERCISE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. ALTON OCHSNER MED FDN & OCHSNER CLIN,NEW ORLEANS,LA 70121. RI Milani, Richard/A-6045-2011 NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A348 EP A348 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101202 ER PT J AU MUCCINI, JA KOLLIAS, N SOBER, AJ PHILLIPS, SB DRAKE, LA AF MUCCINI, JA KOLLIAS, N SOBER, AJ PHILLIPS, SB DRAKE, LA TI EVALUATION OF TRETINOIN 0.025-PERCENT CREAM IN THE TREATMENT OF PHOTOAGED SKIN USING SPECIALIZED PHOTOGRAPHIC TECHNIQUES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A459 EP A459 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101844 ER PT J AU MULROW, CD GERETY, MB KANTEN, D CORNELL, J DENINO, L AF MULROW, CD GERETY, MB KANTEN, D CORNELL, J DENINO, L TI PHYSICAL REHABILITATION FOR FRAIL ELDERS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DIV GERIATR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A573 EP A573 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102517 ER PT J AU PHILLIPS, S MUCCINI, J KOLLIAS, N DRAKE, L AF PHILLIPS, S MUCCINI, J KOLLIAS, N DRAKE, L TI POLARIZED-LIGHT PHOTOGRAPHY PROVIDES AN ENHANCED PHOTOGRAPHIC RECORD OF PSORIATIC PLAQUES AND THEIR RESPONSE TO TREATMENT SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A460 EP A460 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101848 ER PT J AU PUGLIESE, A GIANANI, R ALPER, CA AWDEH, Z JACKSON, RA GORDON, MF KAUFMAN, M PFEIFFER, F EISENBARTH, GS AF PUGLIESE, A GIANANI, R ALPER, CA AWDEH, Z JACKSON, RA GORDON, MF KAUFMAN, M PFEIFFER, F EISENBARTH, GS TI CLASS-II DETERMINANTS OF RESTRICTED ISLET CELL ANTIBODIES (STIFF-MAN SYNDROME LIKE ANTI-GAD ICA) AND PROTECTION FROM TYPE-I DIABETES SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 4 Z9 4 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A299 EP A299 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100940 ER PT J AU RABINOWE, SL MYEROV, A AF RABINOWE, SL MYEROV, A TI CHROMOGRANIN-A IGG AUTOANTIBODIES IN TYPE-I DIABETES - ASSOCIATION WITH ADRENAL-MEDULLARY AUTOIMMUNITY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABET CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A147 EP A147 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100060 ER PT J AU REDDY, SV SCARCEZ, T CHIRGWIN, J LEACH, R WENDLE, J ROBERTS, MR ROODMAN, CD AF REDDY, SV SCARCEZ, T CHIRGWIN, J LEACH, R WENDLE, J ROBERTS, MR ROODMAN, CD TI CLONING AND CHARACTERIZATION OF THE 5' FLANKING REGION OF THE MOUSE TARTRATE RESISTANT ACID-PHOSPHATASE (TRAP) GENE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 UNIV TEXAS,DEPT MED,SAN ANTONIO,TX 78285. UNIV TEXAS,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78285. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV MISSOURI,DEPT ANIM SCI,COLUMBIA,MO 65201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A166 EP A166 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100175 ER PT J AU RIGOTTI, NA STOTO, MA SCHELLING, TC AF RIGOTTI, NA STOTO, MA SCHELLING, TC TI DO BUSINESSES COMPLY WITH NO-SMOKING LAWS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GEN INTERNAL MED UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A610 EP A610 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102739 ER PT J AU RIVKEES, SA STEHLE, JS WEAVER, DR REPPERT, SM AF RIVKEES, SA STEHLE, JS WEAVER, DR REPPERT, SM TI MOLECULAR-CLONING AND EXPRESSION OF A NOVEL ADENOSINE-A2 RECEPTOR SUBTYPE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEV CHRONOBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A331 EP A331 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101116 ER PT J AU ROSENBERG, CL MOTOKURA, T KRONENBERG, HM ARNOLD, A AF ROSENBERG, CL MOTOKURA, T KRONENBERG, HM ARNOLD, A TI SEQUENCE OF THE OVEREXPRESSED PRAD1 ONCOGENE TRANSCRIPT FROM A PARATHYROID ADENOMA SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 2 TC 0 Z9 0 U1 0 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A297 EP A297 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100928 ER PT J AU SELINGER, R SHORT, R BREWSTER, R LEONARD, J SELINGER, S BERG, R DEWOOD, MA AF SELINGER, R SHORT, R BREWSTER, R LEONARD, J SELINGER, S BERG, R DEWOOD, MA TI SURVIVAL FOLLOWING AORTIC-VALVE REPLACEMENT - MULTIVARIATE-ANALYSIS ON 407 PATIENTS OVER 10 YEARS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 SACRED HEART MED CTR,HEART INST SPOKANE,SPOKANE,WA 99204. DEACONESS MED CTR,SPOKANE,WA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A324 EP A324 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101074 ER PT J AU SHARMA, CP MAGIL, S ARNAOUT, MA AF SHARMA, CP MAGIL, S ARNAOUT, MA TI MICRODOMAINS IN THE CYTOPLASMIC TAIL OF CD18 INVOLVED IN BINDING TO CYTOSKELETON SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A343 EP A343 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101174 ER PT J AU SIMON, M COMPTON, CC SOROFF, HS AF SIMON, M COMPTON, CC SOROFF, HS TI THE DIFFERENTIATION OF NEWLY FORMED EPIDERMIS ON ULCERS TREATED WITH CULTURED EPITHELIAL ALLOGRAFTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 SUNY STONY BROOK,SCH MED,DEPT SURG,STONY BROOK,NY 11794. SUNY STONY BROOK,SCH MED,DEPT DERMATOL,STONY BROOK,NY 11794. SUNY STONY BROOK,SCH DENT MED,DEPT ORAL BIOL & PATHOL,STONY BROOK,NY 11794. SUNY STONY BROOK HOSP,LIVING SKIN BANK,STONY BROOK,NY. MASSACHUSETTS GEN HOSP,SHRINERS BURN INST,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A462 EP A462 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101858 ER PT J AU SINGER, DE AF SINGER, DE TI THE EFFECT OF ASPIRIN ON THE RISK OF STROKE IN NONRHEUMATIC ATRIAL-FIBRILLATION - THE BAATAF STUDY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A563 EP A563 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102461 ER PT J AU STAINIER, DYR FISHMAN, MC AF STAINIER, DYR FISHMAN, MC TI CARDIOVASCULAR FORM AND FUNCTION - A GENETIC APPROACH USING THE ZEBRAFISH EMBRYO SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIOVASC RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 1 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A293 EP A293 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100905 ER PT J AU SUNDAY, ME REYES, B SHIPP, MA AF SUNDAY, ME REYES, B SHIPP, MA TI CD10 NEUTRAL ENDOPEPTIDASE-24.11 IN HUMAN FETAL LUNG - TEMPORAL AND CELL-SPECIFIC PATTERNS OF GENE-EXPRESSION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A305 EP A305 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100971 ER PT J AU SUNDAY, ME WILLETT, CG PATIDAR, K SMITH, DI AF SUNDAY, ME WILLETT, CG PATIDAR, K SMITH, DI TI DIFFERENTIAL EXPRESSION OF 7 DISTINCT HUMAN CHROMOSOME-3 CLONES IN HAMSTER LUNG DURING PRENEOPLASTIC LUNG INJURY SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. WAYNE STATE UNIV,SCH MED,DEPT GENET,DETROIT,MI 48201. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A169 EP A169 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100190 ER PT J AU TAYLOR, AE MARTIN, KA ADAMS, JM CROWLEY, WF AF TAYLOR, AE MARTIN, KA ADAMS, JM CROWLEY, WF TI MOST WOMEN WITH PREMATURE OVARIAN FAILURE HAVE OVARIAN CYSTS ON ULTRASOUND SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPRO ENDO UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A375 EP A375 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101359 ER PT J AU THOMAS, LJ YEH, ETH AF THOMAS, LJ YEH, ETH TI DEFINITION OF SIGNAL TRANSDUCTION DEFICITS IN T-CELL GLYCOSYLATION MUTANTS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,BOSTON,MA 02114. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A264 EP A264 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100738 ER PT J AU UYEYAMA, R MUCCINI, JA DAVIS, M KOLLIAS, N PHILLIPS, SB DRAKE, LA AF UYEYAMA, R MUCCINI, JA DAVIS, M KOLLIAS, N PHILLIPS, SB DRAKE, LA TI ASSESSMENT OF IRRITANCY USING FIBEROPTIC REFLECTANCE SPECTROPHOTOMETRY AND PHOTOGRAPHIC RECORDS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A463 EP A463 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101866 ER PT J AU VALLEJO, M MILLER, CP PENCHUK, L HABENER, JF AF VALLEJO, M MILLER, CP PENCHUK, L HABENER, JF TI REGULATION OF THE PANCREATIC CELL-SPECIFIC EXPRESSION OF THE SOMATOSTATIN GENE BY SMS-UE, AN UPSTREAM ENHANCER ELEMENT THAT BINDS ALPHA-CBF-LIKE, ISL-1-LIKE AND CREB PROTEINS SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A300 EP A300 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100947 ER PT J AU WILLIAMS, JW SIMEL, DL AF WILLIAMS, JW SIMEL, DL TI FUNCTIONAL OUTCOMES IN AMBULATORY MEDICAL PATIENTS WITH SHOULDER PAIN - 3 MONTH PROSPECTIVE OBSERVATION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DIV GEN INTERNAL MED,DURHAM,NC 27705. VET ADM MED CTR,DEPT GEN INTERNAL MED,SAN ANTONIO,TX. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A595 EP A595 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102648 ER PT J AU WILLIAMS, JW SIMEL, DL AF WILLIAMS, JW SIMEL, DL TI SHOULDER PAIN AND DISABILITY INDEX - CLINICALLY IMPORTANT CHANGE OVER TIME SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 VET ADM MED CTR,DIV GEN INTERNAL MED,DURHAM,NC 27705. VET ADM MED CTR,DEPT GEN INTERNAL MED,SAN ANTONIO,TX. RI Williams, Jr., John/A-3696-2008 OI Williams, Jr., John/0000-0002-5267-5558 NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A595 EP A595 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74102650 ER PT J AU YAMATO, E HIROKAWA, KJ MINOSHIMA, T KATOH, H MAKINO, S HATTORI, M AF YAMATO, E HIROKAWA, KJ MINOSHIMA, T KATOH, H MAKINO, S HATTORI, M TI BOTH ISLET BETA-CELLS AND THE IMMUNE-SYSTEM ARE RESPONSIBLE FOR THE DEVELOPMENT OF DIABETES IN NOD MICE SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A210 EP A210 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100422 ER PT J AU YOKOYAMA, CT WEISS, M SIEFF, CA AF YOKOYAMA, CT WEISS, M SIEFF, CA TI THE PROXIMAL CYTOPLASMIC REGION OF THE ALPHA-SUBUNIT AND THE BETA-SUBUNIT OF THE HUMAN GM-CSF RECEPTOR ARE ESSENTIAL FOR SIGNAL TRANSDUCTION SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 CHILDRENS HOSP MED CTR,DIV PEDIAT HEMATOL & ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NR 2 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A185 EP A185 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74100283 ER PT J AU ZHENG, QG RHOADS, DB MINK, K LEVITSKY, LL AF ZHENG, QG RHOADS, DB MINK, K LEVITSKY, LL TI GLUT-1 MESSENGER-RNA AND GLUT-1 TRANSPORTER ACTIVITY IS PRESENT IN ISOLATED FETAL-RAT HEPATOCYTES (FH) SO CLINICAL RESEARCH LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0009-9279 J9 CLIN RES JI Clin. Res. PD APR PY 1992 VL 40 IS 2 BP A369 EP A369 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HN741 UT WOS:A1992HN74101324 ER PT J AU FOX, SH OGILVY, CS DUBOIS, AB AF FOX, SH OGILVY, CS DUBOIS, AB TI CARDIOVASCULAR-RESPONSES OF BLUEFISH (POMATOMUS-SALTATRIX) TO EPINEPHRINE, PHENTOLAMINE AND ATROPINE SO COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-PHARMACOLOGY TOXICOLOGY & ENDOCRINOLOGY LA English DT Article ID BLOOD-PRESSURE; ATLANTIC COD; GADUS-MORHUA; RAINBOW-TROUT; EXERCISE AB 1. Ventral aortic blood pressure and heart rate were recorded in bluefish (Pomatomus saltatrix) that were either unanesthetized or anesthetized with tricaine methanesulfonate. 2. Epinephrine caused a dose-related increase of blood pressure. The competitive inhibitor phentolamine inhibited the epinephrine response. 3. Phentolamine lowered the resting blood pressure indicating a tonic adrenergic influence on baseline vasomotor tone. Phentolamine had no significant effect on heart rate. 4. Atropine increased heart rate, as in other teleosts, indicating there had been vagal inhibition of the heart rate at rest. 5. These pharmacological studies demonstrate that bluefish have parasympathetic influence on heart rate and can respond to adrenergically mediated vasomotor tone as do other teleosts. C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP FOX, SH (reprint author), JOHN B PIERCE FDN LAB,NEW HAVEN,CT 06519, USA. NR 21 TC 2 Z9 2 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0742-8413 J9 COMP BIOCHEM PHYS C JI Comp. Biochem. Physiol. C-Pharmacol. Toxicol. Endocrinol. PD APR PY 1992 VL 101 IS 3 BP 493 EP 497 DI 10.1016/0742-8413(92)90076-J PG 5 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Toxicology; Zoology SC Biochemistry & Molecular Biology; Endocrinology & Metabolism; Toxicology; Zoology GA HV174 UT WOS:A1992HV17400010 ER PT J AU BURSELL, SE CLERMONT, AC SHIBA, T KING, GL AF BURSELL, SE CLERMONT, AC SHIBA, T KING, GL TI EVALUATING RETINAL CIRCULATION USING VIDEO FLUORESCEIN ANGIOGRAPHY IN CONTROL AND DIABETIC RATS SO CURRENT EYE RESEARCH LA English DT Article ID BLOOD-FLOW; ENDOTHELIAL-CELLS; AUTO-REGULATION; MELLITUS; GLUCOSE; HEMODYNAMICS; RETINOPATHY; DECREASE; VELOCITY; VESSELS AB Video fluorescein angiography has been used to evaluate retinal circulatory parameters in diabetic and non-diabetic Sprague-Dawley rats. Video fluorescein angiograms were recorded from the retina using a modified retinal fundus camera following a 5 ul bolus injection of sodium fluorescein dye into the jugular vein. Retinal circulatory parameters were measured using computer assisted image analysis. These analyses were performed on 25 diabetic rats with 1 week duration of diabetes and 26 matched, non-diabetic, rats. There was a significant (p = .0001) increase in retinal Mean Circulation Time (MCT) in the diabetic group (1.83 +/- 0.40 s) compared to the control group (1.09 +/- 0.27 s). There were no significant differences in arterial or venous diameters comparing diabetic and control groups. In a separate paired experiment, measurements were made from the same animals both before and after one week duration of diabetes. A paired t-test analysis demonstrated significantly increased MCT times in the 6 diabetic animals (p = .001) while there was no significant differences detected in the 4 corresponding control animals. These results indicate that significant increases in retinal circulation times can be measured as early as 1 week after streptozotocin induced diabetes in this animal model. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. RP BURSELL, SE (reprint author), BEETHAM EYE INST,JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY05110]; NIDDK NIH HHS [DK36836] NR 41 TC 66 Z9 67 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD APR PY 1992 VL 11 IS 4 BP 287 EP 295 DI 10.3109/02713689209001782 PG 9 WC Ophthalmology SC Ophthalmology GA HT219 UT WOS:A1992HT21900001 PM 1388117 ER PT J AU MINER, JH MILLER, JB WOLD, BJ AF MINER, JH MILLER, JB WOLD, BJ TI SKELETAL-MUSCLE PHENOTYPES INITIATED BY ECTOPIC MYOD IN TRANSGENIC MOUSE HEART SO DEVELOPMENT LA English DT Article DE MYOD; MYOGENIN; TRANSGENIC MICE; MYOGENESIS; SKELETAL MUSCLE DEVELOPMENT; HEART ID MYOSIN HEAVY-CHAIN; MYOGENIC DETERMINATION FACTORS; MYC HOMOLOGY; GENE FAMILY; CELL-LINES; EXPRESSION; FIBROBLASTS; ENHANCER; ACTIVATION; MYOBLASTS AB Forced expression of the myogenic regulatory gene MyoD in many types of cultured cells initiates their conversion into skeletal muscle. It is not known, however, if MyoD expression serves to activate all or part of the skeletal muscle program in vivo during animal development, nor is it known how limiting the influences of cellular environment may be on the regulatory effects of MyoD. To begin to address these issues, we have produced transgenic mice which express MyoD in developing heart, where neither MyoD nor its three close relatives - myogenin, Myf-5, and MRF4/herculin/Myf-6 - are normally expressed. The resulting gross phenotype in offspring from multiple, independent transgenic founders includes abnormal heart morphology and ultimately leads to death. At the molecular level, affected hearts exhibit activation of skeletal muscle-specific regulatory as well as structural genes. We conclude that MyoD is able to initiate the program that leads to skeletal muscle differentiation during mouse development, even in the presence of the ongoing cardiac differentiation program. Thus, targeted misexpression of this tissue-specific regulator during mammalian embryogenesis can activate, either directly or indirectly, a diverse set of genes normally restricted to a different cell lineage and a different cellular environment. C1 CALTECH,DIV BIOL 15629,PASADENA,CA 91125. MASSACHUSETTS GEN HOSP,CECIL B DAY LAB NEUROMUSCULAR RES,BOSTON,MA 02129. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. NR 50 TC 77 Z9 77 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0950-1991 J9 DEVELOPMENT JI Development PD APR PY 1992 VL 114 IS 4 BP 853 EP 860 PG 8 WC Developmental Biology SC Developmental Biology GA HR732 UT WOS:A1992HR73200006 PM 1618148 ER PT J AU CATLIN, EA EZZELL, RM DONAHOE, PK MANGANARO, TF EBB, RG MACLAUGHLIN, DT AF CATLIN, EA EZZELL, RM DONAHOE, PK MANGANARO, TF EBB, RG MACLAUGHLIN, DT TI MULLERIAN INHIBITING SUBSTANCE BINDING AND UPTAKE SO DEVELOPMENTAL DYNAMICS LA English DT Article DE RECEPTOR; BINDING PROTEIN; GLYCOPROTEIN ID FETAL-RAT LUNG; INSULIN-RECEPTOR; INTERNALIZATION; HEPATOCYTES; MEMBRANES; GENE AB Mullerian inhibiting substance (MIS) is a 140,000 M(r) Sertoli cell derived glycoprotein with a critical regulatory role in the male fetus initiated presumably by ligand binding with receptor. To localize this binding species we performed time course incubations of cultured fetal rat lungs or control tissues with MIS, applied rabbit anti-MIS IgG, and fluorescein conjugated anti-rabbit IgG, and examined specimens with laser confocal microscopy. Punctate surface fluorescence followed by cytosolic and nuclear localization in lung consistent with specific adsorptive endocytosis was seen. Confocal imaging also detected MIS binding to the Mullerian duct in the urogenital ridge. Crosslinking of I-125-MIS with plasma membranes revealed a high molecular mass binder with signal displaceable by excess unlabeled ligand. These data support the hypothesis that a specific plasma membrane binding protein for MIS exists. C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NEONATAL & PEDIAT INTENS CARE,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. FU NCI NIH HHS [CA17393]; NHLBI NIH HHS [1 R29HLHD46198-01] NR 16 TC 8 Z9 8 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 APR PY 1992 VL 193 IS 4 BP 295 EP 299 PG 5 WC Anatomy & Morphology; Developmental Biology SC Anatomy & Morphology; Developmental Biology GA JF758 UT WOS:A1992JF75800001 PM 1511169 ER PT J AU KROLEWSKI, AS BARZILAY, J WARRAM, JH MARTIN, BC PFEIFER, M RAND, LI AF KROLEWSKI, AS BARZILAY, J WARRAM, JH MARTIN, BC PFEIFER, M RAND, LI TI RISK OF EARLY-ONSET PROLIFERATIVE RETINOPATHY IN IDDM IS CLOSELY RELATED TO CARDIOVASCULAR AUTONOMIC NEUROPATHY SO DIABETES LA English DT Article ID DIABETIC-RETINOPATHY; VASCULAR REACTIVITY; ALDOSE REDUCTASE; COMPLICATIONS; NEPHROPATHY; MELLITUS; NOREPINEPHRINE AB Determinants of proliferative diabetic retinopathy (PDR) that occur during the 2nd decade of insulin-dependent diabetes mellitus (IDDM) (early-onset PDR) were investigated in a nested case-control study. From an inception cohort of patients with juvenile-onset IDDM that now has 15-21 yr diabetes duration, the patients with PDR (cases, n = 74) were selected for study along with a random sample of the patients in the cohort without PDR (control subjects, n = 88). The risk of PDR was associated with poor glycemic control during the first 12 yr of diabetes. Relative to patients in the first quartile of the index of hyperglycemia, those in higher quartiles and nonattenders had a four- to fivefold risk of developing PDR. A striking relationship with cardiovascular autonomic neuropathy (CAN) was found. Relative to patients without CAN, patients with significant and mild CAN had odds ratios of 77.5 and 34.6, respectively. Patients with albumin excretion rates > 30-mu-g/min had moderately increased risk of PDR (ranging from 4-fold for microalbuminuria to 7-fold for proteinuria). In contrast, patients with impaired renal function had an extremely high risk of PDR. All 20 of these patients were cases, therefore the odds ratio was infinite. All three factors (poor glycemic control, CAN, and various stages of nephropathy) were associated with PDR in multiple logistic regression analysis. However, in models including glycemic control, the association between microalbuminuria or proteinuria and PDR was weakened. In conclusion, our findings are consistent with a hypothesis that the level of glycemia is a primary determinant of early-onset PDR. Autonomic neuropathy, almost universal among cases, may be a strong risk factor for or a risk indicator of an etiologic process underlying the development of PDR. Conditions associated with advanced diabetic nephropathy, on the other hand, may accelerate the progression of nonproliferative retinopathy to PDR. C1 JOSLIN DIABET CTR,EYE RES SECT,BOSTON,MA 02215. HUMANA HOSP,DIABET CTR EXCELLENCE,DIABET RES & ANAL ASSOC,LEXINGTON,KY. RP KROLEWSKI, AS (reprint author), JOSLIN DIABET CTR,EPIDEMIOL & GENET SECT,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY-02636]; NIDDK NIH HHS [DK-41526] NR 35 TC 61 Z9 66 U1 0 U2 1 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0012-1797 J9 DIABETES JI Diabetes PD APR PY 1992 VL 41 IS 4 BP 430 EP 437 DI 10.2337/diabetes.41.4.430 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HK692 UT WOS:A1992HK69200005 PM 1607070 ER PT J AU DEFRONZO, RA AF DEFRONZO, RA TI PATHOGENESIS OF TYPE-2 (NON-INSULIN-DEPENDENT) DIABETES-MELLITUS - A BALANCED OVERVIEW SO DIABETOLOGIA LA English DT Discussion ID HEPATIC GLUCOSE-PRODUCTION; ORAL GLUCOSE; POSTPRANDIAL HYPERGLYCEMIA; RELATIVE IMPAIRMENT; NATURAL-HISTORY; FOREARM GLUCOSE; PLASMA-GLUCOSE; PIMA-INDIANS; BETA-CELL; METABOLISM AB Following an overnight fast the majority of glucose disposal occurs in insulin-independent tissues, the brain (approximately 50%) and splanchnic organs (approximately 25%), while only 25% occurs in insulin-dependent tissues, primarily muscle [1-4]. Basal glucose utilization (approximately 2 mg.kg-1.min-1) is precisely matched by glucose production by the liver [1-4]. Following glucose ingestion, the balance between uptake and output is disrupted and maintenance of glucose homeostasis depends upon three processes that must occur in a co-ordinated fashion: (1) insulin secretion; (2) stimulation of glucose uptake by splanchnic (liver and gut) and peripheral (primarily muscle) tissues in response to hyperinsulinaemia plus hyperglycaemia; (3) suppression of hepatic glucose production. It logically follows that abnormalities at the level of the Beta cell, muscle, and/or liver can lead to the development of glucose intolerance. The full blown syndrome of Type 2 (non-insulin-dependent) diabetes mellitus requires the simultaneous presence of two defects, insulin resistance and impaired Beta-cell function. In Type 2 diabetes the primary or inherited defect most likely represents impaired tissue (muscle and/or liver) sensitivity to insulin. Eventually, however, the Beta cell fails to maintain a sufficiently high rate of insulin secretion to compensate for the insulin resistance, and overt diabetes mellitus ensues. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DEFRONZO, RA (reprint author), UNIV TEXAS,HLTH SCI CTR,DIV DIABET,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCRR NIH HHS [M01-RR-01346]; NIDDK NIH HHS [DK 24092] NR 71 TC 303 Z9 312 U1 4 U2 15 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0012-186X J9 DIABETOLOGIA JI Diabetologia PD APR PY 1992 VL 35 IS 4 BP 389 EP 397 DI 10.1007/BF00401208 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HL175 UT WOS:A1992HL17500014 PM 1516769 ER PT J AU KVEDAR, JC MANABE, M PHILLIPS, SB ROSS, BS BADEN, HP AF KVEDAR, JC MANABE, M PHILLIPS, SB ROSS, BS BADEN, HP TI CHARACTERIZATION OF SCIELLIN, A PRECURSOR TO THE CORNIFIED ENVELOPE OF HUMAN KERATINOCYTES SO DIFFERENTIATION LA English DT Article ID HUMAN EPIDERMAL-KERATINOCYTES; CROSS-LINKED ENVELOPE; INVOLUCRIN GENE; CULTURED KERATINOCYTES; MAMMALIAN EPIDERMIS; BASIC-PROTEIN; REGION; HOMINOIDS; EVOLUTION; CELLS AB The cornified envelope, located beneath the plasma membrane of terminally differentiated keratinocytes, is formed as protein precursors are cross-linked by a membrane associated transglutaminase. This report characterizes a new precursor to the cornified envelope. A monoclonal antibody derived from mice immunized with cornified envelopes of human cultured keratinocytes stained the periphery of more differentiated cells in epidermis and other stratified squamous epithelia including hair and nails. The epitope was widely conserved among mammals as determined by immunohistochemical and Western analysis. Immunoelectron microscopy localized the epitope to the cell periphery in the upper stratum spinosum and granulosum of epidermis. In the hair follicle, the epitope was present in the internal root sheath and in the infundibulum, the innermost aspect of the external root sheath. The antibody recognized a protein of relative mobility (M(r)) 82,000, pl 7.8. The protein was a transglutaminase substrate as shown by a dansylcadaverine incorporation assay. Purified cornified envelopes absorbed the reactivity of the antibody to the partially purified protein and cleavage of envelopes by cyanogen bromide resulted in release of immunoreactive fragments. The protein was soluble only in denaturing buffers such as 8 M urea or 2% sodium dodecyl-sulfate (SDS). Partial solubility could be achieved in 50 mM TRIS pH 8.3 plus 0.3 M NaCl (high salt buffer); the presence of a reducing agent did not affect solubility. Extraction of cultured keratinocytes in 8 M urea and subsequent dialysis against 50 mM TRIS pH 8.3 buffer resulted in precipitation of the protein with the keratin filaments. Dialysis against high salt buffer prevented precipitation of the protein. The unique solubility properties of this protein suggest that it aggregates with itself and/or with keratin filaments. The possible role of the protein in cornified envelope assembly is discussed. We have named this protein Sciellin (from the old english "sciell" for shell). C1 NYU,SCH MED,DEPT DERMATOL,EPITHELIAL BIOL UNIT,NEW YORK,NY 10003. RP KVEDAR, JC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,13TH ST,BOSTON,MA 02129, USA. FU NIADDK NIH HHS [AM 34511]; NIAMS NIH HHS [AR 06838-27, AR 01804-02] NR 39 TC 43 Z9 45 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-4681 J9 DIFFERENTIATION JI Differentiation PD APR PY 1992 VL 49 IS 3 BP 195 EP 204 DI 10.1111/j.1432-0436.1992.tb00667.x PG 10 WC Cell Biology; Developmental Biology SC Cell Biology; Developmental Biology GA HT362 UT WOS:A1992HT36200008 PM 1377656 ER PT J AU RAHMAN, MU CANTWELL, R JOHNSON, CC HODINKA, RL SCHUMACHER, HR HUDSON, AP AF RAHMAN, MU CANTWELL, R JOHNSON, CC HODINKA, RL SCHUMACHER, HR HUDSON, AP TI INAPPARENT GENITAL-INFECTION WITH CHLAMYDIA-TRACHOMATIS AND ITS POTENTIAL ROLE IN THE GENESIS OF REITERS-SYNDROME SO DNA AND CELL BIOLOGY LA English DT Article ID REACTIVE ARTHRITIS AB An infectious etiology has been suggested for Reiter's syndrome (RS) because the disease has often been observed to follow episodes of urethritis or dysentery. Despite demonstrations of bacterial antigens in the synovial tissues of RS patients, it is not dear whether viable organisms are present in the synovium in any particular stage of this disease. Furthermore, it is not clear how either viable organisms or their product(s) might reach the joints. Infection with the bacterium Chlamydia trachomatis is the most common sexually transmitted disease in the United States, and as such this organism has emerged as a primary pathogen associated with RS. Previous work from our group has shown that synovial biopsy tissues from a majority of RS patients studied show significant levels of apparently intact chlamydial RNA, even when synovial or urethral cultures from the same patients are unequivocally negative for the organism. We show here that inapparent urethral infection with chlamydia occurs with high prevalence in men, and that inapparent cervical infection with the organism occurs at high prevalence in women. These data provide an important link in the relationship between initial chlamydial infection and possible subsequent genesis of RS, and they may give useful insight into mechanisms by which chlamydial infection can lead to development of this disease. Our data argue further that inapparent infection may be a significant factor in pathogenesis for all chlamydia-related diseases, and they suggest that, contrary to current ideas, C. trachomatis can generate disseminated infection. C1 DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. UNIV PENN,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,CLIN VIROL LAB,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,PATHOL,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,CTR ARTHRITIS IMMUNOL,PHILADELPHIA,PA 19104. NR 18 TC 11 Z9 11 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1044-5498 J9 DNA CELL BIOL JI DNA Cell Biol. PD APR PY 1992 VL 11 IS 3 BP 215 EP 219 DI 10.1089/dna.1992.11.215 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Cell Biology; Genetics & Heredity GA JG734 UT WOS:A1992JG73400007 PM 1567554 ER PT J AU MULROW, CD TULEY, MR AGUILAR, C AF MULROW, CD TULEY, MR AGUILAR, C TI CORRELATES OF SUCCESSFUL HEARING-AID USE IN OLDER ADULTS SO EAR AND HEARING LA English DT Article ID VALIDATION; BENEFIT AB Objective: To evaluate whether age, education, functional handicap, degree of hearing loss, amount of hearing and speech recognition gain achieved with hearing aid, locus of control, visual acuity, manual dexterity, number of comorbid diseases, and number of medications predict which elderly individuals with hearing loss are likely to benefit from hearing aids. Design: A logistic regression prediction model for hearing aid benefit was developed on a training set of 89 individuals and verified in a test set of 87 individuals. Hearing aid success was assessed 4 mo after hearing aid administration. It was defined by assessing hearing aid satisfaction, functional handicap change post-hearing aid, and number of hours of weekly hearing aid use. Setting: All patients were elderly male veterans from the Audie L. Murphy Memorial Veterans Hospital. There were no differences in demographic or clinical characteristics in training versus test set individuals. Results: Several variables, including baseline perceived functional handicap, education, number of medications, and age correlated with individual success measures. However, no variables consistently correlated with all success measures. The accuracy of prediction rules for success utilizing the variables ranged from 75 to 88% in the training set, and 54 to 84% in the test set. Conclusion: Although certain baseline factors were statistically significantly related to individual measures of successful hearing aid use, no factors were good enough to consistently differentiate successful from unsuccessful hearing aid candidates. C1 UNIV TEXAS,HLTH SCI CTR,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DIV GERIATR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT GERONTOL,SAN ANTONIO,TX 78284. RP MULROW, CD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,CTR GERIATR RES EDUC & CLIN,11C,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 33 TC 33 Z9 34 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0196-0202 J9 EAR HEARING JI Ear Hear. PD APR PY 1992 VL 13 IS 2 BP 108 EP 113 DI 10.1097/00003446-199204000-00007 PG 6 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA HQ094 UT WOS:A1992HQ09400007 PM 1601191 ER PT J AU BRACH, MA HERRMANN, F YAMADA, H BAUERLE, PA KUFE, DW AF BRACH, MA HERRMANN, F YAMADA, H BAUERLE, PA KUFE, DW TI IDENTIFICATION OF NF-JUN, A NOVEL INDUCIBLE TRANSCRIPTION FACTOR THAT REGULATES C-JUN GENE-TRANSCRIPTION SO EMBO JOURNAL LA English DT Article DE BINDING SPECIFICITY; C-JUN GENE; NF-JUN; TRANSCRIPTION FACTORS ID NECROSIS-FACTOR-ALPHA; EXPRESSION; CELLS; ACTIVATION; PROTOONCOGENE; FIBROBLASTS; INDUCTION; TRANSIENT AB In this study we report the identification of a novel transcription factor, termed Nuclear Factor-jun (NF-jun). This factor contributes to inducible transcription of the c-jun gene in human myeloid leukemia cells. NF-jun was, however, undetectable in nuclear proteins from human monocytes, granulocytes, resting T lymphocytes and lung fibroblasts. NF-jun shares several features with the well characterized NF-kappa-B in that binding activity can be generated in cytosolic extracts by treatment with dissociating agents. In addition, binding of NF-jun to its recognition site is enhanced by treatment of cells with 12-O-tetradecanoylphorbol-13-acetate, tumor necrosis factor alpha or the protein synthesis inhibitor cycloheximide (CHX). However, as revealed by competition assays and electrophoretic mobility shift assays, purified NF-kappa-B fails to bind to the c-jun fragment which contains the NF-jun site, and this fragment fails to compete with NF-kappa-B for binding. UV crosslinking showed that NF-jun contains a 55 and a 125 kDa protein species. These findings demonstrate that the c-jun gene can be regulated by a transcription factor distinct from AP-1. Our findings also indicate that while NF-jun has several features in common with the NF-kappa-B binding protein including its subcellular localization and its ability to translocate from the cytoplasm to the nucleus, this factor recognizes a unique DNA sequence. Moreover, the activity of this protein is differentially regulated in various cell types. NF-jun might function as a signal transducing molecule in order to mediate rapid induction of the early response gene c-jun in a cell type- and stimulus-specific manner. C1 UNIV MUNICH,CTR GENE,MOLEC BIOL LAB,W-8000 MUNICH 2,GERMANY. UNIV FREIBURG,MED CTR,DEPT HEMATOL & ONCOL,MOLEC HEMATOPOIESIS LAB,W-7800 FREIBURG,GERMANY. RP BRACH, MA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA34183, CA42802] NR 38 TC 29 Z9 29 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD APR PY 1992 VL 11 IS 4 BP 1479 EP 1486 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HM836 UT WOS:A1992HM83600026 PM 1339344 ER PT J AU EVANS, DG GRAHAM, DY AF EVANS, DG GRAHAM, DY TI INTERNALIZATION OF HELICOBACTER-PYLORI BY EPITHELIAL-CELLS - THE KEY TO THE INFLAMMATORY RESPONSE TO HELICOBACTER-PYLORI INFECTION SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL SYMP ON HELICOBACTER-PYLORI AND ITS DISEASE CY MAY 09, 1991 CL TOKYO, JAPAN SP TAISHO PHARM, UEHARA MEM FDN DE HELICOBACTER-PYLORI; HEP-2 CELLS; Y-1 ADRENAL CELLS; INTERNALIZATION; ENDOCYTOSIS; RECEPTOR-MEDIATED ENDOCYTOSIS; IMMUNE RESPONSE AB Objective. To better understand the pathogenesis of the intense humoral and cellular response to Helicobacter pylori infection. Design. The mechanism of the uptake of H. pylori into epithelial cells was studied in vitro, using four strains of H. pylori and two different cultured cells. Methods. H. pylori were grown on blood agar. They were counted visually after staining and by colony-forming units of viable bacteria grown with and without gentamicin. Adherence assays were performed with Y-1 mouse adrenal cells and HEp-2 cells grown in 24-cell tissue-culture plates under 12-mm coverslips. To assay viable bacteria, the tissue-culture cells were washed, lysed, and the lysate cultured. The location (attached extracellular versus intracellular) was determined by gentamicin sensitivity and electron microscopy. Results. Isolates of H. pylori enter into the cytoplasm of tissue-culture epithelial cell lines such as HEp-2 cells. The intracellular uptake of H. pylori by HEp-2 cells is rapid and appears to require both the N-acetylneuraminyllactose-binding adhesin and another factor present only in living bacteria. Internalization of H. pylori was inhibited by ammonium chloride and chloroquine at concentrations which did not affect either adherence or bacterial viability. The internalization was completely inhibited when H. pylori and HEp-2 cells were incubated at 4-degrees-C under conditions which did not affect bacterial adherence. Conclusion. Internalization of H. pylori may be the key event that provokes a sustained immune response. RP EVANS, DG (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-691X J9 EUR J GASTROEN HEPAT JI Eur. J. Gastroenterol. Hepatol. PD APR PY 1992 VL 4 SU 1 BP S45 EP S47 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HV997 UT WOS:A1992HV99700010 ER PT J AU GRAHAM, DY KLEIN, PD EVANS, DG FIEDOREK, SC EVANS, DJ ADAM, E MALATY, HM AF GRAHAM, DY KLEIN, PD EVANS, DG FIEDOREK, SC EVANS, DJ ADAM, E MALATY, HM TI HELICOBACTER-PYLORI - EPIDEMIOLOGY, RELATIONSHIP TO GASTRIC-CANCER AND THE ROLE OF INFANTS IN TRANSMISSION SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY LA English DT Article; Proceedings Paper CT 4TH INTERNATIONAL SYMP ON HELICOBACTER-PYLORI AND ITS DISEASE CY MAY 09, 1991 CL TOKYO, JAPAN SP TAISHO PHARM, UEHARA MEM FDN DE HELICOBACTER-PYLORI; EPIDEMIOLOGY; GASTRIC CANCER; PEPTIC ULCER; DUODENAL ULCER; TRANSMISSION; GASTRITIS AB Objective. To further understand the epidemiology of Helicobacter pylori infection in man, including the pattern of transmission and the relationship to gastric cancer. Design. This paper reviews the known data on H. pylori epidemiology and provides new data and insights obtained from cross-sectional studies of asymptomatic subjects, including infants and children. Results. The pattern of clinical H. pylori disease found within a population is determined by the age of acquisition of the infection; infection in childhood leads to a predominance of gastric ulcer and gastric cancer, whereas infection in adulthood allows duodenal ulcer to predominate and gastric cancer is rare. H. pylori spreads rapidly among families with children but not in those without, suggesting that children might be involved in the transmission of the infection. infants may be more susceptible than adults to H. pylori, and close contact among the young child segment of the population, which is usually less hygienic, may be a dominant mechanism of transmission. Differences in the prevalence of H. pylori infection in whites, blacks and Hispanics may be a reflection of the distance (expressed in number of generations or generation cohorts) from ancestors of very low socio-economic status; this factor may better define the H. pylori prevalence in a population. Conclusions. Recent insights into the epidemiology of H. pylori infection may allow the identification of critical areas where transmission may be prevented. RP GRAHAM, DY (reprint author), VET AFFAIRS MED CTR 111D,DEPT MED,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 0 TC 37 Z9 37 U1 2 U2 2 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-691X J9 EUR J GASTROEN HEPAT JI Eur. J. Gastroenterol. Hepatol. PD APR PY 1992 VL 4 SU 1 BP S1 EP S6 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HV997 UT WOS:A1992HV99700003 ER PT J AU GRAHAM, DY AF GRAHAM, DY TI PATHOGENIC MECHANISMS LEADING TO HELICOBACTER-PYLORI-INDUCED INFLAMMATION SO EUROPEAN JOURNAL OF GASTROENTEROLOGY & HEPATOLOGY LA English DT Article; Proceedings Paper CT WORKSHOP AND DISCUSSION ON SHORT-TERM AND LONG-TERM CONSEQUENCES OF GASTRITIS / DUODENITIS CY OCT 26, 1991 CL AMSTERDAM, NETHERLANDS SP ROHM PHARMA DE HELICOBACTER-PYLORI; INFLAMMATION; HUMORAL IMMUNITY; PHAGOCYTOSIS; MECHANISMS AB Purpose: Although there is ample literature concerning the interaction of bacteria and the cellular and humoral immune systems, there are scant data about the gastric mucosal immune response to Helicobacter infection. This paper reviews H. pylori immune system interactions from the perspective of phases of disease while posing questions and approaches for future studies. Conclusion: There is no reason to believe that mucosal interactions are unique and that most lessons previously learned will not apply. H. pylori gastritis is most consistent with response to an invasive pathogen with limited virulence. Recent studies have confirmed internalization of H. pylori by epithelial cells and have provided a possible explanatioin of how H. pylori elicits a systemic immune response. RP GRAHAM, DY (reprint author), VET ADM MED CTR 111D,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 0 TC 11 Z9 11 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-691X J9 EUR J GASTROEN HEPAT JI Eur. J. Gastroenterol. Hepatol. PD APR PY 1992 VL 4 SU 2 BP S9 EP S16 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HV998 UT WOS:A1992HV99800003 ER PT J AU MACKAY, CR MARSTON, WL DUDLER, L SPERTINI, O TEDDER, TF HEIN, WR AF MACKAY, CR MARSTON, WL DUDLER, L SPERTINI, O TEDDER, TF HEIN, WR TI TISSUE-SPECIFIC MIGRATION PATHWAYS BY PHENOTYPICALLY DISTINCT SUBPOPULATIONS OF MEMORY T-CELLS SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Article ID VASCULAR ENDOTHELIAL-CELLS; PERIPHERAL LYMPH-NODES; DIFFERENTIATION ANTIGENS; ADHESION MOLECULES; HOMING RECEPTOR; HELPER-INDUCER; LYMPHOCYTES; EXPRESSION; SUBSETS; SHEEP AB A proportion of T cells recirculate in a tissue-selective manner. Recent studies which showed that the skin-tropic subset of T cells was of memory/activated type, led us to examine whether the preferential homing of T cells to the gut also involved memory T cells, and if so whether these memory T cells were phenotypically distinct from other memory T cells. Lymphocytes migrating through the gut and the skin of sheep was collected by cannulating the lymphatic ducts draining these tissues. Both naive and memory T cells were found to recirculate through the gut, although only memory T cells migrated through the skin. However, when T cells from the gut were labeled with fluorescein isothiocyanate and assessed for their migration back to the gut., it was the memory population which showed a tropism for the gut. Gut-tropic memory T cells migrated poorly through the skin, indicating that these cells were distinct from skin-tropic memory T cells. This was confirmed by phenotypic analysis. Gut memory T cells expressed very low levels of the alpha-6 and beta-1 integrins, in contrast to skin memory T cells which expressed high levels. There was no evidence for heterogeneity within the naive T cell population, which migrated preferentially to lymph nodes. This migration pattern could be explained in part by the high expression of the L-selectin (lymph node homing receptor, LAM - 1) on naive T cells, in contrast to memory T cells from gut or skin which were mostly L-selectin negative. These results in sheep indicate that subsets of alpha/beta memory T cells show tissue-selective migration patterns, which probably develop in a particular environment following encounter with antigen. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP MACKAY, CR (reprint author), BASEL INST IMMUNOL,GRENZACHERSTR 487,CH-4005 BASEL,SWITZERLAND. RI Mackay, Charles/A-9673-2008; Hein, Wayne/E-9090-2013 OI Mackay, Charles/0000-0002-6338-7340; Hein, Wayne/0000-0003-0769-6525 NR 51 TC 221 Z9 222 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 APR PY 1992 VL 22 IS 4 BP 887 EP 895 DI 10.1002/eji.1830220402 PG 9 WC Immunology SC Immunology GA HQ494 UT WOS:A1992HQ49400001 PM 1372559 ER PT J AU SCHOMACKER, KT FRISOLI, JK COMPTON, CC FLOTTE, TJ RICHTER, JM DEUTSCH, TF NISHIOKA, NS AF SCHOMACKER, KT FRISOLI, JK COMPTON, CC FLOTTE, TJ RICHTER, JM DEUTSCH, TF NISHIOKA, NS TI ULTRAVIOLET-LASER INDUCED FLUORESCENCE OF COLONIC POLYPS SO GASTROENTEROLOGY LA English DT Article ID COLORECTAL POLYPS; BRAIN; PHOTOCOAGULATION; SPECTROSCOPY; SPECTRA; INVIVO C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN MED UNIT,MED SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 34 TC 129 Z9 132 U1 0 U2 3 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD APR PY 1992 VL 102 IS 4 BP 1155 EP 1160 PN 1 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HK976 UT WOS:A1992HK97600009 PM 1551525 ER PT J AU FLETCHER, JA HENKLE, C ATKINS, L ROSENBERG, AE MORTON, CC AF FLETCHER, JA HENKLE, C ATKINS, L ROSENBERG, AE MORTON, CC TI TRISOMY-5 AND TRISOMY-7 ARE NONRANDOM ABERRATIONS IN PIGMENTED VILLONODULAR SYNOVITIS - CONFIRMATION OF TRISOMY-7 IN UNCULTURED CELLS SO GENES CHROMOSOMES & CANCER LA English DT Note ID NORMAL KIDNEY TISSUE; CHROMOSOME-ABERRATIONS; CARCINOMA AB Pigmented villonodular synovitis (PVNS) is a proliferative lesion of disputed genesis. Recently, we reported trisomy 7 in short-term cultures of I PVNS. In the present report, we describe another specimen of PVNS in which 9 of 26 (35 percent) metaphase cells demonstrated trisomy 7 when analyzed after 3-15 days of tissue culture. In situ hybridization analysis, with a biotinylated probe to chromosome 7 alpha-satellite DNA, revealed trisomy 7 in 53 of 200 uncultured cells from this PVNS sample. Our findings indicate that trisomy 7 is a nonrandom aberration that arises in vivo in PVNS. C1 CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FLETCHER, JA (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1K11CA01498-01]; NCRR NIH HHS [507 RR05950-06] NR 11 TC 71 Z9 72 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 APR PY 1992 VL 4 IS 3 BP 264 EP 266 DI 10.1002/gcc.2870040312 PG 3 WC Oncology; Genetics & Heredity SC Oncology; Genetics & Heredity GA HT014 UT WOS:A1992HT01400011 PM 1382569 ER PT J AU HAQQ, C LEE, MM TIZARD, R WYSK, M DEMARINIS, J DONAHOE, PK CATE, RL AF HAQQ, C LEE, MM TIZARD, R WYSK, M DEMARINIS, J DONAHOE, PK CATE, RL TI ISOLATION OF THE RAT GENE FOR MULLERIAN INHIBITING SUBSTANCE SO GENOMICS LA English DT Article ID HORMONE; BOVINE; FETAL; CELLS; EXPRESSION; SERTOLI; INVITRO; ACID C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD MIT DIV HLTH SCI & TECHNOL,BOSTON,MA 02115. BIOGEN INC,DEPT MOLEC BIOL,CAMBRIDGE,MA 02142. RP HAQQ, C (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LABS,BOSTON,MA 02114, USA. OI Lee, Mary/0000-0002-7204-4884 FU NCI NIH HHS [CA17393] NR 27 TC 54 Z9 56 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1992 VL 12 IS 4 BP 665 EP 669 DI 10.1016/0888-7543(92)90291-Y PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400007 PM 1572639 ER PT J AU KROLEWSKI, AS KROLEWSKI, B GRAY, M STANTON, V WARRAM, JH HOUSMAN, D AF KROLEWSKI, AS KROLEWSKI, B GRAY, M STANTON, V WARRAM, JH HOUSMAN, D TI HIGH-FREQUENCY DNA-SEQUENCE POLYMORPHISMS IN THE INSULIN-RECEPTOR GENE DETECTED BY DENATURING GRADIENT GEL BLOTS SO GENOMICS LA English DT Article ID FRAGMENT LENGTH POLYMORPHISMS; SINGLE BASE SUBSTITUTIONS; LINKAGE ANALYSIS; GENOMIC DNA; GC-CLAMP; ELECTROPHORESIS; MARKER; FAMILY C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. TUFTS UNIV,SCH MED,DEPT OBSTET & GYNECOL,DIV REPROD ENDOCRINOL,BOSTON,MA 02111. RP KROLEWSKI, AS (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,EPIDEMIOL & GENET SECT,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL43203]; NIDDK NIH HHS [DK08033] NR 20 TC 19 Z9 19 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD APR PY 1992 VL 12 IS 4 BP 705 EP 709 DI 10.1016/0888-7543(92)90298-7 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HJ574 UT WOS:A1992HJ57400014 PM 1572644 ER PT J AU JACOBS, HE WISSUSIK, D COLLIER, R STACKMAN, D BURKEMAN, D AF JACOBS, HE WISSUSIK, D COLLIER, R STACKMAN, D BURKEMAN, D TI CORRELATIONS BETWEEN PSYCHIATRIC DISABILITIES AND VOCATIONAL OUTCOME SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID REHABILITATION; SCHIZOPHRENIA; PREDICTION AB Eighty-nine subjects were recruited from inpatient and community psychiatric treatment programs in the Los Angeles area to participate in the Brentwood Job Finding Club. They were trained in job-seeking skills and were given logistical support during their job search. Thirty-six percent either obtained a job or entered a job training program. Persons with good work histories, good job interviewing skills, and nonpsychotic diagnoses were more likely to find employment. Persons with psychotic diagnoses and poor work histories and those receiving Supplemental Security Income were the least successful. C1 SPRINGBROOK INST,NEWBERG,OR. W LOS ANGELES VET AFFAIRS MED CTR,BRENTWOOD DIV,REHABIL MED SERV,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,MED CTR,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. RP JACOBS, HE (reprint author), MOSS REHABIL HOSP,DRUCKER BRAIN INJURY CTR,1200 W TABOR RD,PHILADELPHIA,PA 19141, USA. NR 19 TC 58 Z9 59 U1 0 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD APR PY 1992 VL 43 IS 4 BP 365 EP 369 PG 5 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA HL362 UT WOS:A1992HL36200009 PM 1577428 ER PT J AU FASSLER, D COTTON, N AF FASSLER, D COTTON, N TI A NATIONAL SURVEY ON THE USE OF SECLUSION IN THE PSYCHIATRIC-TREATMENT OF CHILDREN SO HOSPITAL AND COMMUNITY PSYCHIATRY LA English DT Article ID RESTRAINT; INPATIENT AB Officials in 36 states responded to a survey of state policies, procedures, and regulations for the use of seclusion in the psychiatric treatment of children. Thirty-five of the states permit its use in emergencies, and 18 allow its use as part of a therapeutic treatment program. Only six states responding have regulations specifically addressing the use of seclusion with children. The authors summarize state regulations, including duration and frequency of seclusion episodes; orders required to implement seclusion and who may authorize it; rules about observation, documentation, and termination of episodes and breaks during episodes; design of seclusion rooms; and staff training. The authors present a model policy and procedure statement based on clinical and developmental considerations. C1 CHOATE HLTH SYST,CHILD & ADOLESCENT PSYCHIAT,WOBURN,MA. MASSACHUSETTS DEPT MENTAL HLTH,BROCKTON,MA. UNIV VERMONT,DEPT PSYCHIAT,BURLINGTON,VT 05405. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02114. NR 27 TC 28 Z9 28 U1 0 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0022-1597 J9 HOSP COMMUNITY PSYCH PD APR PY 1992 VL 43 IS 4 BP 370 EP 374 PG 5 WC Public, Environmental & Occupational Health; Psychiatry SC Public, Environmental & Occupational Health; Psychiatry GA HL362 UT WOS:A1992HL36200011 PM 1577429 ER PT J AU YOUNG, RH EICHHORN, JH DICKERSIN, GR SCULLY, RE AF YOUNG, RH EICHHORN, JH DICKERSIN, GR SCULLY, RE TI OVARIAN INVOLVEMENT BY THE INTRAABDOMINAL DESMOPLASTIC SMALL ROUND CELL TUMOR WITH DIVERGENT DIFFERENTIATION - A REPORT OF 3 CASES SO HUMAN PATHOLOGY LA English DT Article DE OVARY; DESMOPLASTIC SMALL CELL TUMOR ID CARCINOMA; CHILDHOOD C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP YOUNG, RH (reprint author), MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,DEPT PATHOL,BOSTON,MA 02114, USA. NR 21 TC 95 Z9 101 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD APR PY 1992 VL 23 IS 4 BP 454 EP 464 DI 10.1016/0046-8177(92)90094-J PG 11 WC Pathology SC Pathology GA HR055 UT WOS:A1992HR05500016 PM 1563748 ER PT J AU YOUNG, RH HART, WR AF YOUNG, RH HART, WR TI RENAL-CELL CARCINOMA METASTATIC TO THE OVARY - A REPORT OF 3 CASES EMPHASIZING POSSIBLE CONFUSION WITH OVARIAN CLEAR CELL ADENOCARCINOMA SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE OVARY; METASTASIS; RENAL CELL CARCINOMA ID MONOCLONAL-ANTIBODIES; VAGINAL METASTASIS; SURGICAL PATHOLOGY; TUMORS AB The clinical and pathological features of three personally observed and six previously reported cases of renal cell carcinoma metastatic to the ovary are reviewed. The patients' ages ranged from 39 to 64 (average, 52) years. In five patients the ovarian tumor was discovered first. In four of these patients renal tumors were detected during the initial clinical studies or in the early postoperative period, but in the fifth the renal primary tumor was not detected until 8 years later. The ovarian tumor in two cases was initially misdiagnosed as a primary ovarian clear cell carcinoma. In the remaining four patients the ovarian metastasis was detected 5 months, 12 months, 19 months, and 11 years after a renal tumor had been removed. In two patients the initial clinical manifestations were due to a metastasis of the renal tumor, to the thyroid gland in one and to the vagina in the other. The renal tumors in these nine patients typically were well-differentiated renal cell adenocarcinomas of clear cell type. The ovarian tumors measured from 7 to 18 (average, 12.5) cm in greatest dimension; two of them were bilateral. Grossly they were usually solid or solid and cystic; one was a unilocular cyst with a predominantly smooth lining and a 2.5-cm solid nodule in one area. The solid component of the tumors was typically either uniformly yellow or had focal yellow areas with hemorrhagic foci. Microscopic examination showed a relatively uniform picture in most cases: solid or alveolar nests of epithelial cells with abundant clear cytoplasm or tubules lined by clear cells and containing intraluminal eosinophilic material and extravasated blood. A prominent sinusoidal vascular pattern was characteristically present. Special stains for mucin were negative. The major features of metastatic renal cell carcinoma that distinguish it from primary ovarian clear cell adenocarcinoma are the presence of a striking sinusoidal vascular pattern, a homogeneous clear cell pattern with an absence of hobnail cells, the absence of hyaline basement membrane-like material, negative intraluminal mucin, and a lack of the mixtures of solid, papillary, and tubulocystic or glandular histologic patterns usually found in primary ovarian clear cell adenocarcinoma. C1 CLEVELAND CLIN EDUC FDN,DEPT PATHOL,CLEVELAND,OH 44106. RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LAB,BOSTON,MA 02114, USA. NR 43 TC 46 Z9 51 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1992 VL 11 IS 2 BP 96 EP 104 DI 10.1097/00004347-199204000-00003 PG 9 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA HL203 UT WOS:A1992HL20300003 PM 1582751 ER PT J AU DAYA, D YOUNG, RH SCULLY, RE AF DAYA, D YOUNG, RH SCULLY, RE TI ENDOMETRIOID CARCINOMA OF THE FALLOPIAN-TUBE RESEMBLING AN ADNEXAL TUMOR OF PROBABLE WOLFFIAN ORIGIN - A REPORT OF 6 CASES SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL PATHOLOGY LA English DT Article DE FALLOPIAN TUBE; ADENOCARCINOMA; WOLFFIAN DUCT-LIKE TUMOR ID ULTRASTRUCTURAL FINDINGS; CELL-CARCINOMA; UTERINE CERVIX; OVARIAN-TUMORS; ADENOCARCINOMA; LIGHT AB Six adenocarcinomas of the fallopian tube that resembled the female adnexal tumor of probable wolffian origin are described. The tumors, which occurred in patients from 38 to 66 (average 55) years of age, typically formed intraluminal masses. One was an incidental finding on microscopic examination. On microscopic examination, the tumors were characterized by a predominant pattern of small, closely packed cells punctured by numerous glandular spaces, which were typically small but occasionally were cystically dilated. Many of the glands contained a dense colloid-like secretion that was positive with the periodic acid-Schiff stain. Small amounts of intracellular mucin were present in all cases. In the solid areas of three cases, spindle cells that focally formed concentric whorls were present. In all cases, small numbers of tubular glands typical of endometrioid adenocarcinoma were identified. The cytologic atypia and mitotic activity of the tumors were variable, but they exceeded that usually seen in wolffian duct tumors. The evidence indicates that this neoplasm represents an unusual form of endometrioid adenocarcinoma. It is important that it is distinguished from a tumor of wolffian duct origin. C1 HAMILTON CIV HOSP,HENDERSON GEN DIV,DEPT OBSTET & GYNECOL,HAMILTON L8V 1C3,ONTARIO,CANADA. MCMASTER UNIV,HAMILTON L8S 4L8,ONTARIO,CANADA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP DAYA, D (reprint author), HAMILTON CIV HOSP,HENDERSON GEN DIV,DEPT PATHOL,711 CONCESS ST,HAMILTON L8V 1C3,ONTARIO,CANADA. NR 33 TC 35 Z9 37 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-1691 J9 INT J GYNECOL PATHOL JI Int. J. Gynecol. Pathol. PD APR PY 1992 VL 11 IS 2 BP 122 EP 130 DI 10.1097/00004347-199204000-00006 PG 9 WC Obstetrics & Gynecology; Pathology SC Obstetrics & Gynecology; Pathology GA HL203 UT WOS:A1992HL20300006 PM 1582746 ER PT J AU RUHNKE, HL MADOFF, S AF RUHNKE, HL MADOFF, S TI MYCOPLASMA-PHOCIDAE SP-NOV, ISOLATED FROM HARBOR SEALS (PHOCA-VITULINA L) SO INTERNATIONAL JOURNAL OF SYSTEMATIC BACTERIOLOGY LA English DT Article ID UREAPLASMA; PNEUMONIA; VIRUS AB In 1979 and 1980, more than 400 harbor seals (Phoca vitulina) along the New England coast of the United States died of epizootic pneumonia that was attributed to an influenza virus. Six mycoplasma isolates that were recovered from the respiratory tracts of affected seals were investigated and were found to be serologically identical and distinct from previously described species. These isolates required serum for growth, did not possess a cell wall, and did not hydrolyze urea. Arginine was hydrolyzed, glucose was not fermented, film and spots were observed on horse serum agar, phosphatase was produced, tetrazolium was not reduced, and serum and casein were not digested. The guanine-plus-cytosine content of the DNA was 27.8 mol%. We propose the name Mycoplasma phocidae for these isolates. The type strain of M. phocidae is strain 105 (= ATCC 33657). C1 MASSACHUSETTS GEN HOSP,DEPT BACTERIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP RUHNKE, HL (reprint author), ONTARIO MINIST AGR & FOOD,VET LAB SERV,BOX 3612,GUELPH N1H 6R8,ONTARIO,CANADA. NR 18 TC 11 Z9 11 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0020-7713 J9 INT J SYST BACTERIOL JI Int. J. Syst. Bacteriol. PD APR PY 1992 VL 42 IS 2 BP 211 EP 214 PG 4 WC Microbiology SC Microbiology GA HN405 UT WOS:A1992HN40500002 PM 1581181 ER PT J AU WITTE, RS ELSON, P BRYAN, GT TRUMP, DL AF WITTE, RS ELSON, P BRYAN, GT TRUMP, DL TI TRIMETREXATE IN ADVANCED RENAL-CELL CARCINOMA - AN ECOG PHASE-II TRIAL SO INVESTIGATIONAL NEW DRUGS LA English DT Note DE TRIMETREXATE; RENAL CELL CARCINOMA ID CANCER; CYCLOPHOSPHAMIDE; METHOTREXATE; VINBLASTINE; RECURRENT; SCHEDULE; TMQ AB Thirty-four chemotherapy-naive, ambulatory patients with advanced renal cell cancer were treated with the non-classical antifol trimetrexate at the intravenous dose of 12 mg/m2 daily x 5 every three weeks (8 mg/m2 qd x 5 for > 30% bone marrow previously irradiated). One patient experienced a partial response lasting 24 weeks for a response rate of 3% (exact 95% CI, 0.1 to 15.3%). Toxicity was manageable and primarily myelosuppression, gastrointestinal, and mucosal. Trimetrexate has little activity in advanced renal cell carcinoma at this dose and schedule. C1 UNIV WISCONSIN,CTR CLIN CANC,MADISON,WI 53706. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WISCONSIN,CTR CLIN,MADISON,WI 53706. FU NCI NIH HHS [CA 21076, CA 23318] NR 20 TC 10 Z9 10 U1 0 U2 0 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-6997 J9 INVEST NEW DRUG JI Invest. New Drugs PD APR PY 1992 VL 10 IS 1 BP 51 EP 54 DI 10.1007/BF01275483 PG 4 WC Oncology; Pharmacology & Pharmacy SC Oncology; Pharmacology & Pharmacy GA JA126 UT WOS:A1992JA12600013 PM 1535065 ER PT J AU HOWARD, E MARCUS, D OBRIEN, J ALBERT, D BERNARDS, R AF HOWARD, E MARCUS, D OBRIEN, J ALBERT, D BERNARDS, R TI 5 DNA TUMOR-VIRUSES UNDETECTABLE IN HUMAN RETINOBLASTOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE RETINOBLASTOMA; DNA TUMOR VIRUS; PCR; ANTIONCOGENE ID ADENOVIRUS E1A PROTEINS; GENE-PRODUCT; ASSOCIATION; BIND AB Retinoblastoma (RB) is a childhood eye cancer that arises when a retinal cell lacks a functional RB gene. Recent data indicate that the transforming proteins of adenovirus, papillomavirus, and the polyomaviruses BK and JC all can bind to the product of the RB gene. Furthermore, adenovirus 12, JC virus, and simian virus 40 are able to induce RB-like tumors in rodents. In view of these findings, 50 human RBs were tested for the presence of five human DNA tumor viruses: adenovirus 12, BK virus, JC virus, and human papillomaviruses 16 and 18. Using the polymerase chain reaction, no viral sequences were detected in 50 RB DNAs. These data provide no evidence that these viruses have an etiologic role in human RB. C1 MASSACHUSETTS GEN HOSP,CTR CANC,DIV MOLEC GENET,149 13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS EYE & EAR HOSP,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY01917] NR 19 TC 6 Z9 6 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD APR PY 1992 VL 33 IS 5 BP 1564 EP 1567 PG 4 WC Ophthalmology SC Ophthalmology GA HN775 UT WOS:A1992HN77500002 PM 1559753 ER PT J AU HOGUE, CW WARD, JM ITANI, MS MARTYN, JAJ AF HOGUE, CW WARD, JM ITANI, MS MARTYN, JAJ TI TOLERANCE AND UP-REGULATION OF ACETYLCHOLINE-RECEPTORS FOLLOW CHRONIC INFUSION OF D-TUBOCURARINE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE MUSCLE RELAXANTS; CHRONIC USE OF D-TUBOCURARINE; RESISTANCE TO D-TUBOCURARINE; ALPHA-BUNGAROTOXIN BINDING AFTER CHRONIC D-TUBOCURARINE ID NEUROMUSCULAR-JUNCTION; SKELETAL-MUSCLE; INJURY; RAT; RESISTANCE; PANCURONIUM; MECHANISMS AB The hypothesis that chronic competitive antagonism of nicotinic acetylcholine receptors (nAChR), even in the absence of immobilization or paralysis, induces proliferation of the receptor and tolerance to the competitive antagonist was tested. Chronic antagonism of the nAChR was achieved in rats by an infusion of d-tubocurarine (dTC) via subcutaneously placed osmotic pumps. After 2 wk of dTC or saline, the neuromuscular pharmacodynamics and nAChR number were examined. No differences in weight gain or mobility were observed between groups. Chronic dTC infusion at 2 wk resulted in a baseline concentration of 0.41 +/- 0.07 (SE) mu-g/ml, which, if achieved acutely, would cause a depression of the twitch tension to 60% of control twitch height. Moreover, the experimental group was able to develop a baseline twitch tension of 50 g, similar to that of controls. Despite the baseline dTC concentration in the experimental group, the effective doses of dTC for twitch depression were similar to those of controls. The plasma dTC concentration required for steady-state twitch inhibition was significantly (P < 0.05) higher in the experimental group (0.83 +/- 0.04 vs. 0.50 +/- 0.15-mu-g/ml) as were the extrajunctional nAChR (19.76 +/- 1.77 vs. 13.37 +/- 1.82 fmol/mg protein). The diaphragmatic nAChR were unaltered. This study confirms that chronic doses of dTC cause tolerance to its effects and proliferation of nAChR even in the absence of immobilization. The absence of nAChR changes in the diaphragm may be due to the higher margin of safety of the diaphragm for muscle relaxants than for peripheral muscles. Intensive Care Unit patients receiving chronic infusions of dTC to facilitate mechanical ventilation will require increased doses with time. C1 MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,CLIN PHARMACOL LAB,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANAESTHESIOL,BOSTON,MA 02115. SHRINERS BURN INST,BOSTON,MA 02114. NR 33 TC 46 Z9 47 U1 1 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1992 VL 72 IS 4 BP 1326 EP 1331 PG 6 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA HP086 UT WOS:A1992HP08600015 PM 1592722 ER PT J AU ANG, RC HOOP, B KAZEMI, H AF ANG, RC HOOP, B KAZEMI, H TI ROLE OF GLUTAMATE AS THE CENTRAL NEUROTRANSMITTER IN THE HYPOXIC VENTILATORY RESPONSE SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE CONTROL OF VENTILATION; HYPOXIA; MK-801 ID METHYL-D-ASPARTATE; RESPIRATORY DEPRESSION; ANTICONVULSANT MK-801; CO2 SENSITIVITY; BRAIN HYPOXIA; RAT-BRAIN; CAT; ANTAGONIST; CHEMOSENSITIVITY; MECHANISMS AB Recent data suggest that the increase in ventilation during hypoxia may be related to the release of the excitatory amino acid neurotransmitter glutamate centrally. To further investigate this, we studied the effects of MK-801, a selective noncompetitive N-methyl-D-aspartate receptor antagonist, on the hypoxic ventilatory response in lightly anesthetized spontaneously breathing intact dogs. The cardiopulmonary effects of sequential ventriculocisternal perfusion (VCP) at the rate of 1 ml/min with mock cerebrospinal fluid (CSF, control) and MK-801 (2 mM) were compared during normoxia and 8 min of hypoxic challenge with 12% O2. Minute ventilation ((V(E)), tidal volume (VT), and respiratory frequency (f) were recorded continuously, and hemodynamic parameters [heart rate (HR), blood pressure (MAP), cardiac output (CO), pulmonary arterial pressure, and pulmonary capillary wedge pressure] were measured periodically. Each dog served as its own baseline control before and after each period of sequential VCP under the two different O2 conditions. During 15 min of normoxia, there were no significant changes in the cardiopulmonary parameters with mock CSF VCP, whereas with MK-801 VCP for 15 min, VE decreased by approximately 27%, both by reductions in VT and f (17 and 9.5%, respectively). HR, MAP, and CO were unchanged. During 8 min of hypoxia with mock CSF VCP, VE increased by 171% associated with increased VT and f (25 and 125%, respectively). HR, MAP, and CO were likewise augmented. In contrast, the hypoxic response during MK-801 VCP was characterized by an increased VE of 84%, mainly by a rise in f by 83%, whereas the VT response was abolished. The cardiovascular excitation was also inhibited. In addition, we showed that these observations were not related to the effects of anesthesia in our VCP model using time control experiments in separate animals. We also demonstrated that these findings were not due to a generalized depression of central respiratory drive, because ventilation increased in response to central administration of acetylcholine in three other dogs. These findings support a major role for glutamate as the central excitatory neurotransmitter in the hyperventilatory response to hypoxia. C1 MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-29493] NR 31 TC 62 Z9 64 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD APR PY 1992 VL 72 IS 4 BP 1480 EP 1487 PG 8 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA HP086 UT WOS:A1992HP08600038 PM 1350580 ER PT J AU TALAL, N FLESCHER, E DANG, H AF TALAL, N FLESCHER, E DANG, H TI ARE ENDOGENOUS RETROVIRUSES INVOLVED IN HUMAN AUTOIMMUNE-DISEASE SO JOURNAL OF AUTOIMMUNITY LA English DT Article; Proceedings Paper CT 2ND CONGRESS OF IMMUNOINTERVENTION IN AUTOIMMUNE DISEASES CY MAY 13-16, 1991 CL PARIS, FRANCE ID PRIMARY SJOGRENS-SYNDROME; PROTEIN-KINASE-C; T-CELLS; EXPRESSION; CD5; ANTIBODIES; INHIBITION; SEQUENCES; IDIOTYPE; PEPTIDE C1 AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. RP TALAL, N (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [1R01 DE09311-01] NR 34 TC 43 Z9 43 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD APR PY 1992 VL 5 SU A BP 61 EP 66 DI 10.1016/0896-8411(92)90020-Q PG 6 WC Immunology SC Immunology GA HP721 UT WOS:A1992HP72100008 PM 1323968 ER PT J AU EISENBARTH, GS JACKSON, RA PUGLIESE, A AF EISENBARTH, GS JACKSON, RA PUGLIESE, A TI INSULIN AUTOIMMUNITY - THE RATE LIMITING FACTOR IN PRE-TYPE-I DIABETES SO JOURNAL OF AUTOIMMUNITY LA English DT Article; Proceedings Paper CT 2ND CONGRESS OF IMMUNOINTERVENTION IN AUTOIMMUNE DISEASES CY MAY 13-16, 1991 CL PARIS, FRANCE RP EISENBARTH, GS (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,IMMUNOL & IMMUNOGENET SECT,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [R01 DK 32083-08] NR 13 TC 22 Z9 23 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0896-8411 J9 J AUTOIMMUN JI J. Autoimmun. PD APR PY 1992 VL 5 SU A BP 241 EP 246 DI 10.1016/0896-8411(92)90039-S PG 6 WC Immunology SC Immunology GA HP721 UT WOS:A1992HP72100027 PM 1503616 ER PT J AU NARULA, N MCMORROW, I PLOPPER, G DOHERTY, J MATLIN, KS BURKE, B STOW, JL AF NARULA, N MCMORROW, I PLOPPER, G DOHERTY, J MATLIN, KS BURKE, B STOW, JL TI IDENTIFICATION OF A 200-KD, BREFELDIN-SENSITIVE PROTEIN ON GOLGI MEMBRANES SO JOURNAL OF CELL BIOLOGY LA English DT Article ID FUSION PROTEIN; ENDOPLASMIC-RETICULUM; MONOCLONAL-ANTIBODY; VESICULAR TRANSPORT; SECRETORY PROTEINS; COATED VESICLES; STACK; CLATHRIN; BINDING; YEAST AB A mAb AD7, raised against canine liver Golgi membranes, recognizes a novel, 200-kD protein (p200) which is found in a wide variety of cultured cell lines. Immunofluorescence staining of cultured cells with the AD7 antibody produced intense staining of p200 in the juxtanuclear Golgi complex and more diffuse staining of p200 in the cytoplasm. The p200 protein in the Golgi complex was colocalized with other Golgi proteins, including mannosidase II and beta-COP, a coatomer protein. Localization of p200 by immunoperoxidase staining at the electron microscopic level revealed concentrations of p200 at the dilated rims of Golgi cisternae. Biochemical studies showed that p200 is a peripheral membrane protein which partitions to the aqueous phase of Triton X-114 solutions and is phosphorylated. The p200 protein is located on the cytoplasmic face of membranes, since it was accessible to trypsin digestion in microsomal preparations. and is recovered in approximately equal amounts in membrane pellets and in the cytosol of homogenized cells. Immunofluorescence staining of normal rat kidney cells exposed to the toxin brefeldin A (BFA), showed that there was very rapid redistribution of p200, which was dissociated from Golgi membranes in the presence of this drug. The effect of BFA was reversible, since upon removal of the toxin, AD7 rapidly reassociated with the Golgi complex. In the BFA-resistant cell line PtK1, BFA failed to cause redistribution of p200 from Golgi membranes. Taken together, these results indicate that the p200 Golgi membrane-associated protein has many properties in common with the coatomer protein, beta-COP. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. RP NARULA, N (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114, USA. OI Stow, Jennifer/0000-0002-5409-9101 FU NIDDK NIH HHS [DK 42881]; NIGMS NIH HHS [GM 38556] NR 46 TC 113 Z9 114 U1 0 U2 1 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9525 J9 J CELL BIOL JI J. Cell Biol. PD APR PY 1992 VL 117 IS 1 BP 27 EP 38 DI 10.1083/jcb.117.1.27 PG 12 WC Cell Biology SC Cell Biology GA HL818 UT WOS:A1992HL81800003 PM 1556155 ER PT J AU BADER, SB PRICE, BD MANNHEIMRODMAN, LA CALDERWOOD, SK AF BADER, SB PRICE, BD MANNHEIMRODMAN, LA CALDERWOOD, SK TI INHIBITION OF HEAT-SHOCK GENE-EXPRESSION DOES NOT BLOCK THE DEVELOPMENT OF THERMOTOLERANCE SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID DNA TOPOISOMERASE-I; CHINESE-HAMSTER FIBROBLASTS; PROTEIN-SYNTHESIS; RIBOSOMAL-RNA; STRESS PROTEINS; MAMMALIAN-CELLS; SODIUM ARSENITE; HSP70 GENE; TRANSCRIPTION; TRANSLATION AB After cells have been exposed to a nonlethal heat shock, they develop an enhanced resistance to subsequent prolonged heat shock. This process, termed thermotolerance, correlates with the expression of a group of proteins called the heat shock proteins. When cells are exposed to heat, protein synthesis is rapidly turned off and takes 5-6 hr to recover. In thermotolerant cells, protein synthesis is not blocked by heat. The heat shock proteins are thought to be responsible for the development of thermotolerance and the protection of the protein synthesis machinery from heat inactivation. To test the hypothesis that the heat shock proteins are involved in the heat shock response, we used two inhibitors to block their transcription and expression during heating and then monitored the effect on the development of thermotolerance and on protein synthesis. Camptothecin inhibits DNA topoisomerase I and blocks transcription of all actively transcribed genes, whereas dichloro-D-ribofuranosylbenzimidazole (DRB) inhibits only those genes transcribed by RNA polymerase II. Both DRB and camptothecin blocked the heat-induced expression of the heat shock proteins, but the absence of these proteins did not block either the development of thermotolerance or the protection of protein synthesis after heating. The data indicate that thermotolerance can develop in the absence of new protein synthesis. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. FU NCI NIH HHS [R29CA44940]; PHS HHS [R0147407] NR 38 TC 27 Z9 27 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD APR PY 1992 VL 151 IS 1 BP 56 EP 62 DI 10.1002/jcp.1041510110 PG 7 WC Cell Biology; Physiology SC Cell Biology; Physiology GA HM960 UT WOS:A1992HM96000009 PM 1560048 ER PT J AU OLIVER, LC SPRINCE, NL GREENE, R AF OLIVER, LC SPRINCE, NL GREENE, R TI ASBESTOS-RELATED RADIOGRAPHIC ABNORMALITIES IN PUBLIC-SCHOOL CUSTODIANS SO JOURNAL OF CLEAN TECHNOLOGY AND ENVIRONMENTAL SCIENCES LA English DT Article DE ASBESTOS-CONTAINING MATERIAL (ACM); NO OUTSIDE EXPOSURE (NOE); PLEURAL PLAQUES; ANTERIOR OBLIQUE CHEST RADIOGRAPHS AB A cross-sectional prevalence study of 120 public school custodians was carried out to investigate the prevalence of asbestos-related disease and to determine the proportion with disease attributable to asbestos exposures in school buildings. Medical and occupational histories, flow-volume loops, and posterior-anterior, lateral, and anterior oblique (AO) chest radiographs were obtained. Single breath DLCO was measured and chest auscultation performed. The present report describes radiographic abnormalities and associations with exposure. Mean age of subjects was 57 years and mean duration of work as a custodian, 2 7 years. Fifty-seven (47.5%) had no known or likely exposure to asbestos outside of their work as a school custodian (NOE). Pleural plaques (PP) occurred in 40 (33%) of the total group and 12 (21%) of the group with NOE. Multivariate analysis revealed significant associations (p<0.05) between PP and duration of asbestos exposure. The proportion with PP increased with increasing years of latency. AO radiographs increased PP detection by a factor of 1.9. Our results reveal PP prevalence in excess of background in the study population and indicate that PP are attributable to asbestos exposure in schools in a subset with NOE. Prudent management of asbestos in buildings is indicated for the prevention of related disease. RP OLIVER, LC (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 1 U2 1 PU PRINCETON SCIENTIFIC PUBL INC PI PRINCETON PA PO BOX 2155, PRINCETON, NJ 08543 SN 1052-1062 J9 J CLEAN TECHNOL ENV JI J. Clean Technol. Environ. Sci. PD APR-JUN PY 1992 VL 2 IS 2 BP 93 EP 99 PG 7 WC Environmental Sciences SC Environmental Sciences & Ecology GA HX813 UT WOS:A1992HX81300002 ER PT J AU JAMESON, JL AF JAMESON, JL TI THYROID-HORMONE RESISTANCE - PATHOPHYSIOLOGY AT THE MOLECULAR-LEVEL SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID GENERALIZED RESISTANCE; BETA; TRIIODOTHYRONINE; KINDREDS; MUTATION; RECEPTOR; BINDING RP JAMESON, JL (reprint author), MASSACHUSETTS GEN HOSP, THYROID UNIT, JACKSON 1021, BOSTON, MA 02114 USA. OI Jameson, James/0000-0001-9538-4059 FU NIDDK NIH HHS [DK-42144] NR 13 TC 22 Z9 22 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1992 VL 74 IS 4 BP 708 EP 711 DI 10.1210/jc.74.4.708 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HK648 UT WOS:A1992HK64800002 PM 1548331 ER PT J AU KARGA, HJ ALEXANDER, JM HEDLEYWHYTE, ET KLIBANSKI, A JAMESON, JL AF KARGA, HJ ALEXANDER, JM HEDLEYWHYTE, ET KLIBANSKI, A JAMESON, JL TI RAS MUTATIONS IN HUMAN PITUITARY-TUMORS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID THYROID TUMORIGENESIS; ONCOGENES; ADENOMAS; CARCINOMA; ORIGIN; GLAND; GENES AB The cellular basis for pituitary neoplasia is poorly understood. Mutations that activate the ras protooncogenes have been identified in a number of different types of human cancers and potentially represent one of the genetic alterations that occur in pituitary tumors. In this study we examined 19 pituitary tumors for the occurrence of ras mutations. The tumor types included 11 nonfunctioning adenomas, 6 somatotroph adenomas, and 2 prolactinomas. Each of the three ras genes (K-ras, N-ras, and H-ras) was amplified from pituitary tumor DNA using the polymerase chain reaction. Oligonucleotide-specific hybridization was used to screen for mutations that inhibit GTPase activity and cause activation of the ras oncogene. No ras mutations were observed in 18 of the pituitary adenomas. However, a mutation was identified in codon 12 of the H-ras gene (Gly to Val) in a recurrent prolactinoma that was highly invasive and ultimately proved to be fatal. We conclude that ras mutations are uncommon in pituitary adenomas, but may provide a marker for highly invasive tumors. C1 MASSACHUSETTS GEN HOSP, THYROID UNIT, FRUIT ST, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROPATHOL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-23519]; NIDDK NIH HHS [DK-07028, DK-40947] NR 19 TC 190 Z9 195 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0021-972X J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD APR PY 1992 VL 74 IS 4 BP 914 EP 919 DI 10.1210/jc.74.4.914 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HK648 UT WOS:A1992HK64800035 PM 1312542 ER PT J AU SONNENBERG, LM POSNER, BM BELANGER, AJ CUPPLES, LA DAGOSTINO, RB AF SONNENBERG, LM POSNER, BM BELANGER, AJ CUPPLES, LA DAGOSTINO, RB TI DIETARY PREDICTORS OF SERUM-CHOLESTEROL IN MEN - THE FRAMINGHAM COHORT POPULATION SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE DIET; SERUM CHOLESTEROL; FRAMINGHAM COHORT ID CORONARY HEART-DISEASE; MONOUNSATURATED FATTY-ACIDS; PLASMA-LIPIDS; BLOOD CHOLESTEROL; FOLLOW-UP; LIPOPROTEINS; PREVALENCE; WEIGHT; RISK; ADULTS AB This study examines the cross-sectional relationships between diet and serum cholesterol in a sample of 413 Framingham cohort males, ages 37-70. Regression analyses controlling for age, calories, and coronary heart disease risk factors showed that the direct predictors of serum cholesterol included: fat (g) (p < 0.05), cholesterol (mg/1000 calories) (p < 0.05), protein (g and calorie density) (p < 0.05 and p < 0.001, respectively), Metropolitan relative weight (p < 0.05), and systolic blood pressure (p < 0.001). Fat (calorie density) and cholesterol (mg) were marginally significant direct positive predictors (0.05 less-than-or-equal-to p less-than-or-equal-to 0.10). Inverse correlates of serum cholesterol were total carbohydrate (g and calorie density) and simple carbohydrate (calorie density) (p < 0.001). A marginally inverse correlate of serum cholesterol was complex carbohydrate (calorie density) (0.05 less-than-or-equal-to p less-than-or-equal-to 0.10). These cross-sectional results show that dietary variables predict serum cholesterol levels in men independent of other coronary heart disease risk factors. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. BOSTON UNIV,SCH PUBL HLTH,DEPT SOCIAL & BEHAV SCI,OFF DIRECTOR,BOSTON,MA 02215. BOSTON UNIV,SCH PUBL HLTH,DIV EPIDEMIOL & BIOSTAT,BOSTON,MA 02215. BOSTON UNIV,DEPT MATH,BOSTON,MA 02215. RP SONNENBERG, LM (reprint author), MASSACHUSETTS GEN HOSP,DEPT DIETET,FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [R01-HL-40423-02, N01-HC-38038, N01-HV-38038] NR 40 TC 18 Z9 18 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD APR PY 1992 VL 45 IS 4 BP 413 EP 418 DI 10.1016/0895-4356(92)90042-L PG 6 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA HR886 UT WOS:A1992HR88600010 PM 1569437 ER PT J AU THOMAS, LJ URAKAZE, M DEGASPERI, R KAMITANI, T SUGIYAMA, E CHANG, HM WARREN, CD YEH, ETH AF THOMAS, LJ URAKAZE, M DEGASPERI, R KAMITANI, T SUGIYAMA, E CHANG, HM WARREN, CD YEH, ETH TI DIFFERENTIAL EXPRESSION OF GLYCOSYLPHOSPHATIDYLINOSITOL-ANCHORED PROTEINS IN A MURINE T-CELL HYBRIDOMA MUTANT PRODUCING LIMITING AMOUNTS OF THE GLYCOLIPID CORE - IMPLICATIONS FOR PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR; PAROXYSMAL NOCTURNAL HEMOGLOBINURIA ID DECAY-ACCELERATING FACTOR; VARIANT SURFACE GLYCOPROTEINS; PHOSPHATIDYLINOSITOL MEMBRANE ANCHOR; THY-1 GLYCOPROTEIN; RESISTANT GLYCOLIPIDS; RAPID DEGRADATION; LYMPHOMA MUTANTS; N-GLYCOSYLATION; BIOSYNTHESIS; DEFICIENT AB A T cell hybridoma mutant, which expressed a markedly reduced level of glycosylphosphatidylinositol (GPI)-anchored proteins on the cell surface, was characterized. The surface expression level of Thy-1 was approximately 17% of the wild-type level, whereas the surface expression of Ly-6A was approximately 2.4% of the wild-type level. We show here that these cells synthesized limiting amounts of the GPI core and that the underlying defect in these cells was an inability to synthesize dolichyl phosphate mannose (Dol-P-Man) at the normal level. The defect in Ly-6A expression could be partially corrected by tunicamycin, which blocked the biosynthesis of N-linked oligosaccharide precursors and shunted Dol-P-Man to the GPI pathway. Full restoration of Thy-1 and Ly-6A expression, however, required the stable transfection of a yeast Dol-P-Man synthase gene into the mutants. These results revealed that when the GPI core is limiting, there is a differential transfer of the available GPI core to proteins that contain GPI-anchor attachment sequences. Our findings also have implications for the elucidation of the defects in paroxysmal nocturnal hemoglobinuria. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ARTHRITIS UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,PAIN CONTROL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-45851]; NIAMS NIH HHS [AR-03564, T32AR07258-15] NR 39 TC 19 Z9 19 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1992 VL 89 IS 4 BP 1172 EP 1177 DI 10.1172/JCI115700 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HL840 UT WOS:A1992HL84000017 PM 1532587 ER PT J AU LARSSON, C SHEPHERD, J NAKAMURA, Y BLOMBERG, C WEBER, G WERELIUS, B HAYWARD, N TEH, B TOKINO, T SEIZINGER, B SKOGSEID, B OBERG, K NORDENSKJOLD, M AF LARSSON, C SHEPHERD, J NAKAMURA, Y BLOMBERG, C WEBER, G WERELIUS, B HAYWARD, N TEH, B TOKINO, T SEIZINGER, B SKOGSEID, B OBERG, K NORDENSKJOLD, M TI PREDICTIVE TESTING FOR MULTIPLE ENDOCRINE NEOPLASIA TYPE-1 USING DNA POLYMORPHISMS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE CANCER PREDISPOSITION; CHROMOSOME-11; GENETIC LINKAGE; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; TUMOR SUPPRESSOR GENE ID PARATHYROID TUMORS; SMALL REGION; CHROMOSOME-11; LOCALIZATION; ALLELES; GENE AB Mulitple endocrine neoplasia type 1 (MEN1) is an autosomal dominantly inherited predisposition to neoplastic lesions of the parathyroids, pancreas, and the pituitary. We have previously located the predisposing genetic defect to the long arm of chromosome 11 by genetic linkage. In this study, 124 members of six MEN1 families, including 59 affected individuals, were genotyped for restriction fragment length polymorphisms with different DNA probes, and the genetic linkage between these marker systems and MEN1 was determined. 13 marker systems (17 DNA probes) were found to be linked to MEN1. These markers are located within a region on chromosome 11 spanning 14% meiotic recombinations, with the MEN1 locus in the middle. Four of the marker systems are on the centromeric side of MEN1, and four on the telomeric side, based on meiotic crossovers. The remaining five DNA probes are closely linked to MEN1, with no crossovers in our set of families. The 13 marker systems can be used for an accurate and reliable premorbid test for MEN1. In most clinical situations it is possible to identify a haplotype of this part of chromosome 11 with the mutant MEN1 allele in the middle. The calculated predictive accuracy is > 99.5% if three such marker systems are informative. Therefore, genetic linkage testing can be used for informed genetic counseling in MEN1 families, and to avoid unnecessary biochemical screening programs. C1 UNIV TASMANIA,DEPT SURG,HOBART,TAS 7001,AUSTRALIA. JAPANESE FDN CANC RES,INST CANC,DIV BIOCHEM,TOKYO 170,JAPAN. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. QUEENSLAND INST MED RES,BRISBANE,QLD,AUSTRALIA. UNIV HOSP UPPSALA,DEPT INTERNAL MED,UPPSALA,SWEDEN. UNIV HOSP UPPSALA,LUDWIG INST CANC RES,UPPSALA,SWEDEN. RP LARSSON, C (reprint author), KAROLINSKA HOSP,DEPT CLIN GENET,S-10401 STOCKHOLM 60,SWEDEN. RI hayward, nicholas/C-1367-2015; Weber, Gunther/F-3410-2016 OI hayward, nicholas/0000-0003-4760-1033; NR 19 TC 71 Z9 72 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD APR PY 1992 VL 89 IS 4 BP 1344 EP 1349 DI 10.1172/JCI115720 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HL840 UT WOS:A1992HL84000037 PM 1348254 ER PT J AU JORGENSEN, JH DOERN, GV FERRARO, MJ KNAPP, CC SWENSON, JM WASHINGTON, JA AF JORGENSEN, JH DOERN, GV FERRARO, MJ KNAPP, CC SWENSON, JM WASHINGTON, JA TI MULTICENTER EVALUATION OF THE USE OF HAEMOPHILUS TEST MEDIUM FOR BROTH MICRODILUTION ANTIMICROBIAL SUSCEPTIBILITY TESTING OF STREPTOCOCCUS-PNEUMONIAE AND DEVELOPMENT OF QUALITY-CONTROL LIMITS SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID PENICILLIN RESISTANCE; HEMOPHILUS-INFLUENZAE; PNEUMOCOCCI; CHLORAMPHENICOL; PREVALENCE; INFECTIONS; ADULTS AB A five-laboratory collaborative study was undertaken to determine the precision and accuracy of broth microdilution susceptibility tests of Streptococcus pneumoniae isolates performed with Haemophilus test medium (HTM) compared with tests performed with lysed horse blood-supplemented Mueller-Hinton broth (LHB). The intra- and interlaboratory reproducibilities of MICs of 10 antimicrobial agents determined with the two media were found to be quite similar and highly reproducible in both media. On the basis of favorable performance in this study, S. pneumoniae ATCC 49619 is recommended as a quality control strain to assess the performance of HTM when this medium is used for testing of pneumococci. Testing of 293 unique clinical isolates of S. pneumoniae with both media in the respective participant laboratories allowed a direct comparison of MIC results and a calculation of interpretive error rates. Although there were some slight differences between MICs determined with HTM and MICs determined with LHB, few very major or major errors resulted from testing the clinical isolates against the 10 antimicrobial agents. However, MIC-interpretive criteria specific for S. pneumoniae should be developed and promulgated through a national consensus mechanism. C1 UNIV MASSACHUSETTS,MED CTR,DEPT CLIN MICROBIOL,WORCESTER,MA 01655. MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LAB,BOSTON,MA 02114. CLEVELAND CLIN FDN,DEPT CLIN MICROBIOL,CLEVELAND,OH 44195. CTR DIS CONTROL,DIV ANTIMICROB INVEST,ATLANTA,GA 30333. RP JORGENSEN, JH (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78184, USA. NR 22 TC 32 Z9 32 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD APR PY 1992 VL 30 IS 4 BP 961 EP 966 PG 6 WC Microbiology SC Microbiology GA HJ487 UT WOS:A1992HJ48700038 PM 1572984 ER PT J AU LERNER, A GONIN, R STEELE, GD MAYER, RJ AF LERNER, A GONIN, R STEELE, GD MAYER, RJ TI ETOPOSIDE, DOXORUBICIN, AND CISPLATIN CHEMOTHERAPY FOR ADVANCED GASTRIC ADENOCARCINOMA - RESULTS OF A PHASE-II TRIAL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID COMBINATION CHEMOTHERAPY; CANCER; 5-FLUOROURACIL; MITOMYCIN; DISEASE; FUTURE; TUMORS; BCNU; EAP C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. NR 32 TC 96 Z9 96 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1992 VL 10 IS 4 BP 536 EP 540 PG 5 WC Oncology SC Oncology GA HL575 UT WOS:A1992HL57500006 PM 1548518 ER PT J AU WOOLLEY, PV NAUTA, R SMITH, FP LINDBLAD, AS PETRELLI, N HERRERA, L DOUGLASS, HO MAYER, RJ BRUCKNER, HW DALTON, J BONADONNA, G GENNARI, L HALL, TC WEAVER, DW LEICHMAN, L KALSER, MH BENEDETTO, P MUGGIA, FM GREEN, M GREENWALD, E LEVIN, B GAYNOR, E HARRIS, J MARSH, JC BARWICK, K KNOWLTON, AH LIVSTONE, EM BUKOWSKI, RM LOUTFI, A RAMIREZ, G THOMAS, PRM AF WOOLLEY, PV NAUTA, R SMITH, FP LINDBLAD, AS PETRELLI, N HERRERA, L DOUGLASS, HO MAYER, RJ BRUCKNER, HW DALTON, J BONADONNA, G GENNARI, L HALL, TC WEAVER, DW LEICHMAN, L KALSER, MH BENEDETTO, P MUGGIA, FM GREEN, M GREENWALD, E LEVIN, B GAYNOR, E HARRIS, J MARSH, JC BARWICK, K KNOWLTON, AH LIVSTONE, EM BUKOWSKI, RM LOUTFI, A RAMIREZ, G THOMAS, PRM TI RADIATION-THERAPY AND FLUOROURACIL WITH OR WITHOUT SEMUSTINE FOR THE TREATMENT OF PATIENTS WITH SURGICAL ADJUVANT ADENOCARCINOMA OF THE RECTUM SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CANCER; CARCINOMA; 5-FLUOROURACIL; RADIOTHERAPY; SURVIVAL; LIFE C1 GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,BUFFALO,NY 14263. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MT SINAI MED CTR,NEW YORK,NY 10029. INST NAZL,MILAN,ITALY. HAWAII MED ASSOC,HONOLULU,HI. WAYNE STATE UNIV,DETROIT,MI 48202. UNIV MIAMI,MIAMI,FL 33152. NYU MED CTR,NEW YORK,NY 10016. UNIV CHICAGO,ILLINOIS CANC COUNCIL,CHICAGO,IL 60637. YALE UNIV,NEW HAVEN,CT 06520. CLEVELAND CLIN,CLEVELAND,OH 44106. MCGILL UNIV,CTR CANC,MONTREAL H3A 2T5,QUEBEC,CANADA. WISCONSIN CLIN CANC CTR,MADISON,WI. EDWARD MALLINCKRODT INST RADIOL,ST LOUIS,MO 63110. MONTEFIORE MED CTR,BRONX,NY 10467. RP WOOLLEY, PV (reprint author), EMMES CORP,GASTROINTESTINAL TUMOR STUDY GRP,CTR STAT,11325 7 LOCKS RD,SUITE 214,POTOMAC,MD 20854, USA. NR 19 TC 143 Z9 144 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1992 VL 10 IS 4 BP 549 EP 557 PG 9 WC Oncology SC Oncology GA HL575 UT WOS:A1992HL57500008 ER PT J AU NICHOLS, CR ANDERSEN, J LAZARUS, HM FISHER, H GREER, J STADTMAUER, EA LOEHRER, PJ TRUMP, DL AF NICHOLS, CR ANDERSEN, J LAZARUS, HM FISHER, H GREER, J STADTMAUER, EA LOEHRER, PJ TRUMP, DL TI HIGH-DOSE CARBOPLATIN AND ETOPOSIDE WITH AUTOLOGOUS BONE-MARROW TRANSPLANTATION IN REFRACTORY GERM-CELL CANCER - AN EASTERN COOPERATIVE ONCOLOGY GROUP PROTOCOL SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article C1 INDIANA UNIV,SCH MED,DIV HEMATOL ONCOL,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,CLEVELAND,OH 44106. UNIV HOSP CLEVELAND,IRELAND CANC CTR,CLEVELAND,OH 44106. VANDERBILT UNIV,MED CTR,SCH MED,DIV HEMATOL,NASHVILLE,TN 37232. ALBANY MED CTR,ALBANY,NY. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. DUKE UNIV,MED CTR,DURHAM,NC 27710. FU NCI NIH HHS [CA14548, CA45609, P30 CA43703] NR 13 TC 135 Z9 137 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1992 VL 10 IS 4 BP 558 EP 563 PG 6 WC Oncology SC Oncology GA HL575 UT WOS:A1992HL57500009 PM 1312584 ER PT J AU ALLRED, DC CLARK, GM TANDON, AK MOLINA, R TORMEY, DC OSBORNE, CK GILCHRIST, KW MANSOUR, EG ABELOFF, M EUDEY, L MCGUIRE, WL AF ALLRED, DC CLARK, GM TANDON, AK MOLINA, R TORMEY, DC OSBORNE, CK GILCHRIST, KW MANSOUR, EG ABELOFF, M EUDEY, L MCGUIRE, WL TI HER-2/NEU IN NODE-NEGATIVE BREAST-CANCER - PROGNOSTIC-SIGNIFICANCE OF OVEREXPRESSION INFLUENCED BY THE PRESENCE OF INSITU CARCINOMA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID LONG-TERM SURVIVAL; PROTO-ONCOGENE ABNORMALITIES; NEU ONCOGENE; EGF RECEPTOR; C-ERBB-2 AMPLIFICATION; ADJUVANT THERAPY; OVER-EXPRESSION; HIGH-RISK; C-MYC; GENE C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED ONCOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. HOSP CLIN BARCELONA,BIOQUIM LAB,BARCELONA,SPAIN. UNIV WISCONSIN,MADISON,WI 53706. CASE WESTERN RESERVE UNIV,METROHLTH MED CTR,CLEVELAND,OH 44106. JOHNS HOPKINS UNIV HOSP,CTR ONCOL,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 50 TC 414 Z9 416 U1 2 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD APR PY 1992 VL 10 IS 4 BP 599 EP 605 PG 7 WC Oncology SC Oncology GA HL575 UT WOS:A1992HL57500016 PM 1548522 ER PT J AU HURT, MA HARDARSON, S STADECKER, MJ CRUZ, DJS AF HURT, MA HARDARSON, S STADECKER, MJ CRUZ, DJS TI FIBROEPITHELIOMA-LIKE CHANGES ASSOCIATED WITH ANOGENITAL EPIDERMOTROPIC MUCINOUS CARCINOMA - FIBROEPITHELIOMATOUS PAGET PHENOMENON SO JOURNAL OF CUTANEOUS PATHOLOGY LA English DT Article ID HAIR FOLLICLE; DISEASE; ADENOCARCINOMA; TUMORS AB describe two patients with crusted perineal plaques that were biopsied and diagnosed as Paget's disease. Resection specimens of each contained a dermal mucinous carcinoma with extensive epidermotropism and coexistent epidermal basaloid proliferations closely resembling fibroepithelioma (Pinkus). The presence of the Paget phenomenon was supported by histochemical, immunohistochemical, and ultrastructural evidence. No other primary neoplasms were found in either patient. Followup at 2 1/2 and 3 1/2 years, respectively, has been negative. We conclude that either the fibroepitheliomatous changes may be induced by or may represent a collision (unlikely) with the epidermotropic mucinous carcinoma. It is proposed that the concept fibroepitheliomatous Paget phenomenon be used to stand for the histologic changes common to our cases as well as those previously reported. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. RP HURT, MA (reprint author), ST JOHNS MERCY MED CTR,DIV CUTANEOUS PATHOL,615 S NEW BALLAS RD,ST LOUIS,MO 63141, USA. NR 32 TC 10 Z9 10 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0303-6987 J9 J CUTAN PATHOL JI J. Cutan. Pathol. PD APR PY 1992 VL 19 IS 2 BP 134 EP 141 DI 10.1111/j.1600-0560.1992.tb01355.x PG 8 WC Dermatology; Pathology SC Dermatology; Pathology GA HQ660 UT WOS:A1992HQ66000010 PM 1375951 ER PT J AU KASHKET, S LOPEZ, LR AF KASHKET, S LOPEZ, LR TI REDUCTION OF INTRAORAL DEMINERALIZATION OF ENAMEL AFTER SINGLE EXPOSURES TO SODIUM-FLUORIDE SO JOURNAL OF DENTAL RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON TECHNOLOGICAL ADVANCES IN INTRA-ORAL MODEL SYSTEMS USED TO ASSESS CARIOGENICITY CY JUN 27-28, 1990 CL CHICAGO, IL SP AMER DENTAL ASSOC ID ARTIFICIAL CARIES; REMINERALIZATION; LESIONS; INVIVO; PLAQUE; MODEL AB Studies demonstrated the effects of single rinses with low concentrations of NaF on the intra-oral demineralization of enamel. Blocks of bovine enamel were covered with Streptococcus mutans IB1600, mounted in palatal appliances, and worn in the mouths of volunteers for specified times. Subjects rinsed with solutions of NaF, with or without sucrose. Demineralization was determined as changes in iodide penetrability (delta Ip) of the enamel, while the pH and F of the streptococcal plaque, and enamel F, were determined with ion-specific electrodes. Delta Ip was reduced by about 80% (from 14.5 +/- 2.7 to 2.8 +/- 2.3 units) when 250-mu-g F/mL was added to the sucrose rinse. Corresponding plaque pH's were 4.1 +/- 0.5 and 4.2 +/- 0.3, consistent with a lack of effect on bacterial acidogenesis. Protection against mineral loss was concentration-dependent. Administration of sucrose at different times after NaF revealed that the effect of F persisted for at least 60 min. Analyses of plaque F demonstrated an initial elevation and concentration within the cells, followed by a drop to stable, baseline values. Enamel F increased slowly to almost 500-mu-g/g enamel after 105 min. The protective effect of F appeared to be manifested in two stages, the first related to a high plaque F and the second to F that became incorporated into the enamel. Analysis of the data suggested that F was transferred from plaque to enamel during the experimental period. C1 FORSYTH DENT CTR,CTR RES ORAL BIOL EFFECTS FOODS,BOSTON,MA 02115. RP KASHKET, S (reprint author), FORSYTH DENT CTR,DEPT BIOCHEM,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-05253] NR 33 TC 4 Z9 4 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 APR PY 1992 VL 71 SI SI BP 867 EP 870 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HX273 UT WOS:A1992HX27300016 PM 1592977 ER PT J AU FRANK, W KURBAN, RS HOOVER, HC SOBER, AJ AF FRANK, W KURBAN, RS HOOVER, HC SOBER, AJ TI ANORECTAL MELANOMA - A CASE-REPORT AND BRIEF REVIEW OF THE LITERATURE SO JOURNAL OF DERMATOLOGIC SURGERY AND ONCOLOGY LA English DT Article ID MALIGNANT-MELANOMA AB Anorectal melanoma in an uncommon tumor that has a poor prognosis. We present a case of anorectal melanoma and review the literature pertaining to prognosis and treatment. Although no controlled trials of treatment of anorectal melanoma have been done, the evidence suggests that conservative excision confers comparable survival with less morbidity than radical surgery. C1 MASSACHUSETTS GEN HOSP,HARVARD SCH MED,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD SCH MED,DEPT DERMATOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,HARVARD SCH MED,DEPT DERMATOPATHOL,BOSTON,MA 02114. NR 12 TC 0 Z9 0 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0148-0812 J9 J DERMATOL SURG ONC PD APR PY 1992 VL 18 IS 4 BP 333 EP 336 PG 4 WC Oncology; Dermatology; Surgery SC Oncology; Dermatology; Surgery GA HM919 UT WOS:A1992HM91900011 PM 1560160 ER PT J AU ZIJLSTRA, M AUCHINCLOSS, H LORING, JM CHASE, CM RUSSELL, PS JAENISCH, R AF ZIJLSTRA, M AUCHINCLOSS, H LORING, JM CHASE, CM RUSSELL, PS JAENISCH, R TI SKIN-GRAFT REJECTION BY BETA-2-MICROGLOBULIN-DEFICIENT MICE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID T-CELL SUBSETS; MAJOR HISTOCOMPATIBILITY COMPLEX; EPIDERMAL LANGERHANS CELLS; CLASS-I MHC; ALLOGRAFT-REJECTION; DENDRITIC CELLS; H-Y; MOUSE; ANTIGENS; EXPRESSION AB Mice homozygous for a beta-2-microglobulin (beta-2-m) gene disruption lack beta-2-m protein and are deficient for functional major histocompatibility complex class I (MHC-I) molecules. The mutant mice have normal numbers of CD4+8- T helper cells, but lack MHC-I-directed CD4-8+ cytotoxic T lymphocytes (CTLs). In this study we used the beta-2-m mutant mice to study the importance of MHC-I-directed immunity in skin graft rejection. Our results indicate that MHC-I-directed CD8+ CTLs are not essential in the rejection of allografts with whole MHC or multiple minor H differences. However, the absence of MHC-I-guided immunity profoundly reduces the ability of mutant mice to reject H-Y disparate grafts. In addition, we show that natural killer cells which vigorously reject MHC-I-deficient bone marrow grafts, are not effective in the destruction of MHC-I-deficient skin grafts. C1 WHITEHEAD INST BIOMED RES,9 CAMBRIDGE CTR,CAMBRIDGE,MA 02142. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG & PATHOL,BOSTON,MA 02114. FU NCI NIH HHS [5R35 CA-44339] NR 50 TC 151 Z9 151 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1992 VL 175 IS 4 BP 885 EP 893 DI 10.1084/jem.175.4.885 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HL014 UT WOS:A1992HL01400002 PM 1552287 ER PT J AU VANDENBERGHE, P FREEMAN, GJ NADLER, LM FLETCHER, MC KAMOUN, M TURKA, LA LEDBETTER, JA THOMPSON, CB JUNE, CH AF VANDENBERGHE, P FREEMAN, GJ NADLER, LM FLETCHER, MC KAMOUN, M TURKA, LA LEDBETTER, JA THOMPSON, CB JUNE, CH TI ANTIBODY AND B7/BB1-MEDIATED LIGATION OF THE CD28 RECEPTOR INDUCES TYROSINE PHOSPHORYLATION IN HUMAN T-CELLS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HUMAN LYMPHOCYTES-T; CD3+ MATURE THYMOCYTES; ANTIGEN RECEPTOR; B-CELLS; SIGNAL TRANSDUCTION; ACTIVATION PATHWAY; PROLIFERATIVE SIGNAL; GENE-EXPRESSION; SURFACE-ANTIGEN; 9.3 ANTIGEN AB CD28 is an adhesion receptor expressed as a 44-kD dimer on the surface of a major subset of human T cells. The CD28 receptor regulates the production of multiple lymphokines, including interleukin 2 (IL-2), by activation of a signal transduction pathway that is poorly understood. Here we show that ligation of CD28 by a monoclonal antibody (mAb) or by a natural ligand, B7/BB1, induces protein tyrosine phosphorylation that is distinct from T cell receptor (TCR)-induced tyrosine phosphorylation. CD28-induced protein tyrosine phosphorylation was greatly enhanced in cells that had been preactivated by ligation of the TCR, or by pretreatment with phorbol esters. Rapid and prolonged tyrosine phosphorylation of a single substrate, pp100, was induced in T cells after interaction with B7/BB1 presented on transfected Chinese hamster ovary (CHO) cells. Anti-B7 mAb inhibited B7/BB1 receptor-induced tyrosine phosphorylation, indicating that B7-CD28 interaction was required. CD28-induced tyrosine phosphorylation was independent of the TCR because it occurred in a variant of the Jurkat T cell line that does not express the TCR. Herbimycin A, a protein tyrosine kinase inhibitor, could prevent CD28-induced tyrosine phosphorylation and CD28-induced IL-2 production in normal T cells. The simultaneous crosslinking of CD28 and CD45, a tyrosine phosphatase, could prevent tyrosine phosphorylation of pp100. These results suggest that specific tyrosine phosphorylation, particularly of pp100, occurs directly as a result of CD28 ligand binding and is involved in transducing the signal delivered through CD28 by accessory cells that express the B7/BB1 receptor. Thus, this particular form of signal transduction may be relevant to lymphokine production and, potentially may provide a means to study the induction of self-tolerance, given the putative role of the costimulatory signal in the induction of T cell activation or anergy. C1 USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,MAIL STOP 44,BETHESDA,MD 20814. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. UNIV PENN,SCH MED,DEPT PATHOL & LAB MED,PHILADELPHIA,PA 19104. UNIV MICHIGAN,DEPT INTERNAL MED,ANN ARBOR,MI 48109. ONCOGEN CORP,SEATTLE,WA 98121. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT MED,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT MICROBIOL IMMUNOL,ANN ARBOR,MI 48109. OI Vandenberghe, Peter/0000-0003-4719-1935 NR 40 TC 140 Z9 141 U1 1 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1992 VL 175 IS 4 BP 951 EP 960 DI 10.1084/jem.175.4.951 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HL014 UT WOS:A1992HL01400009 PM 1372649 ER PT J AU JOHNSON, RP TROCHA, A BUCHANAN, TM WALKER, BD AF JOHNSON, RP TROCHA, A BUCHANAN, TM WALKER, BD TI IDENTIFICATION OF OVERLAPPING HLA CLASS I-RESTRICTED CYTOTOXIC T-CELL EPITOPES IN A CONSERVED REGION OF THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN - DEFINITION OF MINIMUM EPITOPES AND ANALYSIS OF THE EFFECTS OF SEQUENCE VARIATION SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TOXIC LYMPHOCYTES-T; SEROPOSITIVE INDIVIDUALS; SYNTHETIC PEPTIDE; ANTIGENIC SITES; MATRIX PEPTIDE; AIDS VIRUS; HIV-1; RECOGNITION; PROTEIN; BINDING AB Although the immunologic basis of protective immunity in human immunodeficiency virus type 1 (HIV-1) infection has not yet been defined, virus-specific cytotoxic T lymphocytes (CTL) are likely to be an important host defense and may be a critical feature of an effective vaccine. These observations, along with the inclusion of the HIV-1 envelope in the majority of vaccine candidates presently in clinical trials, underscore the importance of the precise characterization of the cellular immune responses to this protein. Although humoral immune responses to the envelope protein have been extensively characterized, relatively little information is available regarding the envelope epitopes recognized by virus-specific CTL and the effects of sequence variation within these epitopes. Here we report the identification of two overlapping CTL epitopes in a highly conserved region of the HIV-1 transmembrane envelope protein, gp41, using CTL clones derived from two seropositive subjects. An eight-amino acid peptide was defined as the minimum epitope recognized by HLA-B8-restricted CTL derived from one subject, and in a second subject, an overlapping nine-amino acid peptide was identified as the minimal epitope for HLA-B14-restricted CTL clones. Selected single amino acid substitutions representing those found in naturally occurring HIV-1 isolates resulted in partial to complete loss of recognition of these epitopes. These data indicate the presence of a highly conserved region in the HIV-1 envelope glycoprotein that is immunogenic for CTL responses. In addition, they suggest that natural sequence variation may lead to escape from immune detection by HIV-1-specific CTL. Since the region containing these epitopes has been previously shown to contain an immunodominant B cell epitope and also overlaps with a major histocompatibility complex class II T cell epitope recognized by CD4+ CTL from HIV-1 rgp160 vaccine recipients, it may be particularly important for HIV-1 vaccine development. Finally, the identification of minimal CTL epitopes presented by class I HLA molecules should facilitate the definition of allele-specific motifs. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,GRAY 5,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV WASHINGTON,SEATTLE,WA 98144. FU NIAID NIH HHS [AI-28568, AI-08094, AI-26463] NR 64 TC 129 Z9 129 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1992 VL 175 IS 4 BP 961 EP 971 DI 10.1084/jem.175.4.961 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HL014 UT WOS:A1992HL01400010 PM 1372650 ER PT J AU NOJIMA, Y ROTHSTEIN, DM SUGITA, K SCHLOSSMAN, SF MORIMOTO, C AF NOJIMA, Y ROTHSTEIN, DM SUGITA, K SCHLOSSMAN, SF MORIMOTO, C TI LIGATION OF VLA-4 ON T-CELLS STIMULATES TYROSINE PHOSPHORYLATION OF A 105-KD PROTEIN SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID VIRUS-TRANSFORMED CELLS; HUMAN LYMPHOCYTES-T; ANTIGEN RECEPTOR; PLASMA FIBRONECTIN; ADHESION RECEPTOR; INTEGRIN FAMILY; ACTIVATION; IDENTIFICATION; CD4; DISTINCT AB The VLA/integrins are a family of heterodimeric adhesion receptors shown to be involved in cell-to-cell and cell-to-extracellular matrix (ECM) interactions. Given recent evidence that VLA molecules can synergize with the CD3/T cell receptor (TCR) pathway to activate T cells, it is important to identify biochemical event(s) generated by these molecules. Here, we report that the engagement of VLA-4 on T cells with specific antibodies or its ligand activates protein-tyrosine kinase (PTK) activity as detected by antiphosphotyrosine immunoblotting. The crosslinking of VLA-beta-1 (CD29) with a specific monoclonal antibody (mAb) (anti-4B4) plus anti-mouse immunoglobulin resulted in the rapid tyrosine phosphorylation of a 105-kD protein (pp105) in the human T cell line H9, as well as in peripheral resting T cells. The increase in tyrosine phosphorylation of pp105 was specifically mediated by VLA-4, since mAbs against alpha-4, but not against other VLA alpha-chains, could induce this phosphorylation. In addition, the binding of T cells with the CS1 alternatively spliced segment of fibronectin (the binding site recognized by VLA-4) induced pp105 tyrosine phosphorylation. Crosslinking the CD3 complex or VLA-4 molecules with mAbs demonstrated that each of these molecules stimulated the tyrosine phosphorylation of unique sets of proteins with different kinetics, suggesting that these two receptor systems are coupled to distinct PTKs. Since tyrosine phosphorylation of cellular proteins has been shown to be a crucial biochemical event in cell growth, our findings suggest that the induction of pp105 tyrosine phospborylation via VLA-4 may play a role in the transduction of activation signals through this molecule. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. FU NIAID NIH HHS [AI-12069]; NIAMS NIH HHS [AR-33713] NR 51 TC 167 Z9 168 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD APR 1 PY 1992 VL 175 IS 4 BP 1045 EP 1053 DI 10.1084/jem.175.4.1045 PG 9 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HL014 UT WOS:A1992HL01400018 PM 1372641 ER PT J AU COLLINS, TL UNIYAL, S SHIN, J STROMINGER, JL MITTLER, RS BURAKOFF, SJ AF COLLINS, TL UNIYAL, S SHIN, J STROMINGER, JL MITTLER, RS BURAKOFF, SJ TI P561CK ASSOCIATION WITH CD4 IS REQUIRED FOR THE INTERACTION BETWEEN CD4 AND THE TCR/CD3 COMPLEX AND FOR OPTIMAL ANTIGEN STIMULATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; TYROSINE-PROTEIN-KINASE; CROSS-LINKING; LYMPHOCYTES-T; PHYSICAL ASSOCIATION; CYTOPLASMIC DOMAINS; ACTIVATION; P56LCK; PHOSPHORYLATION; HYBRIDOMA AB By fluorescence resonance energy transfer, we have previously demonstrated that upon anti-CD3 mAb-mediated activation of a murine T cell hybridoma expressing human CD4, CD4 moves into close association with the TCR/CD3 complex. It was shown that this association between CD4 and the TCR/CD3 complex was dependent upon the presence of an intact CD4 cytoplasmic domain. We have now expressed, in a murine T cell hybridoma, mutated forms of CD4 containing cysteine to serine point mutations at positions 420, 422, or 430. The mutations at positions 420 and 422, but not 430, abolish association with p56lck. By using fluorescence resonance energy transfer, we demonstrate that mutations of CD4 which fail to interact with p56lck are unable to associate with the TCR/CD3 complex under conditions in which wild-type CD4 and the 430 mutant CD4 do associate with the TCR/CD3 complex. In addition, these mutants have a diminished response to CD4-dependent stimuli. We conclude that the association between CD4 and the TCR/CD3 complex during T cell activation plays an important role in CD4-dependent responsiveness and this association requires the interaction of CD4 with p56lck. These results also suggest that a substrate for p56lck may be expressed in the TCR/CD3 complex. C1 HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT IMMUNOL,WALLINGFORD,CT 06492. RP COLLINS, TL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA09141]; NIAID NIH HHS [AI17258] NR 23 TC 93 Z9 93 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 1992 VL 148 IS 7 BP 2159 EP 2162 PG 4 WC Immunology SC Immunology GA HJ596 UT WOS:A1992HJ59600029 PM 1532002 ER PT J AU NAKAJIMA, K SMITH, CV MIXON, A SYKES, M GUZZETTA, PC SPITZER, TR ECKHAUS, MA SACHS, DH AF NAKAJIMA, K SMITH, CV MIXON, A SYKES, M GUZZETTA, PC SPITZER, TR ECKHAUS, MA SACHS, DH TI INVITRO AND INVIVO EFFECTS OF RECOMBINANT HUMAN INTERLEUKIN-2 IN NAIVE MINIATURE SWINE SO JOURNAL OF IMMUNOTHERAPY LA English DT Article DE INTERLEUKIN-2; LYMPHOKINE-ACTIVATED KILLER CELLS; MINIATURE SWINE ID BONE-MARROW TRANSPLANTATION; MAJOR HISTOCOMPATIBILITY COMPLEX; PURIFIED HUMAN INTERLEUKIN-2; KILLER CELLS; HALF-LIFE; DISEASE; AUGMENTS; TOXICITY; CANCER AB Recent data in mice have shown that early administration of recombinant human interleukin-2 (rIL-2) provides significant protection from lethal graft-versus-host disease. Because of the potential clinical importance of these findings, it will be important to assess the effectiveness of this therapy in a large animal preclinical bone marrow transplantation model. We report here our initial studies of the in vitro and in vivo effects of rIL-2 in miniature swine. In vitro 4-day cultures of pig peripheral blood lymphocytes (PBL) in complete medium containing rIL-2 at 1,000 U/ml resulted in optimal proliferation and generation of lymphokine-activated killer (LAK) cells. A pig-mouse hybridoma cell line was found to be highly sensitive as a LAK cell target. Two naive pigs received 20,000 U/kg and 2 pigs received 100,000 U/kg of rIL-2 intravenously twice a day for 4 days. No clinical symptoms were seen during or after administration at the lower dose while both high dose-treated animals showed generalized erythema from days 2 to 4, and one showed mild diarrhea during this period. The disappearance of IL-2 activity from the serum showed two components: (1) an initial fast component with a half-time of approximately 10 min and (2) a slow component with a half-time of approximately 60 min. LAK cell precursors disappeared from the peripheral circulation by 6 min after rIL-2 administration and began to recover by 6 h in the low dose recipients and only after 12 h in the high dose recipients. These data indicate that the effects of rIL-2 in vivo in miniature swine are very similar to those previously demonstrated in humans, and suggest that these animals should provide an excellent preclinical model for studies of the effects of rIL-2 on graft-versus-host disease. C1 MASSACHUSETTS GEN HOSP,TRANSPLAT BIOL RES CTR,SURG SERV,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. CHILDRENS HOSP,NATL MED CTR,DEPT SURG,WASHINGTON,DC 20010. GEORGE WASHINGTON UNIV,DEPT CHILD HLTH & DEV,WASHINGTON,DC 20052. GEORGETOWN UNIV,MED CTR,VINCENT T LOMBARDI CANC RES CTR,WASHINGTON,DC 20007. NIH,DIV RES SERV,VET RESOURCES BRANCH,BETHESDA,MD 20892. NR 21 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1053-8550 J9 J IMMUNOTHER JI J. Immunother. PD APR PY 1992 VL 11 IS 3 BP 169 EP 175 DI 10.1097/00002371-199204000-00003 PG 7 WC Oncology; Immunology; Medicine, Research & Experimental SC Oncology; Immunology; Research & Experimental Medicine GA HK543 UT WOS:A1992HK54300003 PM 1515421 ER PT J AU ROSE, RM REYMARTINEZ, J CROTEAU, C SILVESTRI, RC HALEY, K DEPAMPHILIS, J SIBER, GR AF ROSE, RM REYMARTINEZ, J CROTEAU, C SILVESTRI, RC HALEY, K DEPAMPHILIS, J SIBER, GR TI FAILURE OF RECOMBINANT INTERLEUKIN-2 TO AUGMENT THE PRIMARY HUMORAL RESPONSE TO A RECOMBINANT HEPATITIS-B VACCINE IN HEALTHY-ADULTS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Letter ID IMMUNIZATION; ANTIBODY; ANTIGEN C1 HOFFMANN LA ROCHE INC,NUTLEY,NJ 07110. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02115. RP ROSE, RM (reprint author), NEW ENGLAND DEACONESS HOSP,DIV PULM & CRIT CARE MED,185 PILGRIM RD,BOSTON,MA 02215, USA. NR 9 TC 3 Z9 3 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD APR PY 1992 VL 165 IS 4 BP 775 EP 777 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HJ642 UT WOS:A1992HJ64200034 PM 1532407 ER PT J AU KOLLIAS, N GILLIES, R MORAN, M KOCHEVAR, I ANDERSON, RR AF KOLLIAS, N GILLIES, R MORAN, M KOCHEVAR, I ANDERSON, RR TI FLUORESCENCE SPECTROSCOPY OF AGED AND PHOTOAGED HAIRLESS MOUSE SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,PHOTOMED LABS,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 554 EP 554 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600285 ER PT J AU GRANSTEIN, RD BRUVERS, S GRABBE, S AF GRANSTEIN, RD BRUVERS, S GRABBE, S TI EFFECTS OF TGF-BETA AND IFN-GAMMA ON THE PRESENTATION OF TUMOR-ASSOCIATED ANTIGEN BY MURINE EPIDERMAL ANTIGEN PRESENTING CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HGH HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 557 EP 557 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600304 ER PT J AU GRABBE, S KNISELY, TL GRANSTEIN, RD AF GRABBE, S KNISELY, TL GRANSTEIN, RD TI DECREASED PRODUCTION OF GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR (GM-CSF) BY EPIDERMAL-CELLS FROM ATHYMIC NUDE-MICE INVITRO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 570 EP 570 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600381 ER PT J AU BLEICHER, PA DUNN, DA SIMHA, S GADENNE, AS BIGBY, M AF BLEICHER, PA DUNN, DA SIMHA, S GADENNE, AS BIGBY, M TI LIMITED T-CELL RECEPTOR-V-BETA EXPRESSION IN NORMAL HUMAN SKIN SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 577 EP 577 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600426 ER PT J AU GALLO, RL BERNFIELD, M AF GALLO, RL BERNFIELD, M TI SYNDECAN EXPRESSION IS INDUCED DURING FOLLICULAR DEVELOPMENT IN DERMAL MESENCHYME AND FOLLOWING CYTOKINE STIMULATION OF NIH 3T3 CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. NR 3 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 583 EP 583 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600459 ER PT J AU AHMED, AR MOHIMEN, A MIRZA, NM YUNIS, EJ ALPER, CA AF AHMED, AR MOHIMEN, A MIRZA, NM YUNIS, EJ ALPER, CA TI LINKAGE OF PEMPHIGUS-VULGARIS ANTIBODY TO MHC IN HEALTHY RELATIVES OF PATIENTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 590 EP 590 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600504 ER PT J AU GADENNE, ASJ BLEICHER, PA DUNN, DA BIGBY, M AF GADENNE, ASJ BLEICHER, PA DUNN, DA BIGBY, M TI INFILTRATING LYMPHOCYTES IN LICHEN-PLANUS CONTAIN A SIGNIFICANT POPULATION OF T-CELL RECEPTOR GAMMA-DELTA BEARING CELLS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CBRC,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 591 EP 591 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600506 ER PT J AU MA, J SY, MS HAUSER, C BIGBY, M AF MA, J SY, MS HAUSER, C BIGBY, M TI TRINITROPHENOL REACTIVE T-CELL HYBRIDOMAS RECOGNIZE ANTIGENS THAT REQUIRE ANTIGEN PROCESSING SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CBRC,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HOP CANTONAL GENEVA,DEPT DERMATOL,CH-1211 GENEVA 4,SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 594 EP 594 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600525 ER PT J AU HOSOI, J GRABBE, S LERNER, E GRANSTEIN, RD AF HOSOI, J GRABBE, S LERNER, E GRANSTEIN, RD TI CALCITONIN GENE RELATED PEPTIDE (CGRP) INHIBITS LANGERHANS CELL (LC) ANTIGEN PRESENTATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 596 EP 596 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600540 ER PT J AU SIMON, M COMPTON, CC SOROFF, HS AF SIMON, M COMPTON, CC SOROFF, HS TI THE DIFFERENTIATION OF NEWLY FORMED EPIDERMIS ON ULCERS TREATED WITH CULTURED EPITHELIAL ALLOGRAFTS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. SUNY STONY BROOK,SCH MED,DEPT DERMATOL,STONY BROOK,NY 11794. SUNY STONY BROOK,SCH DENT MED,DEPT ORAL BIOL & PATHOL,STONY BROOK,NY 11794. SUNY STONY BROOK,SCH MED,DEPT SURG,STONY BROOK,NY 11794. UNIV HOSP BOSTON,LIVING SKIN BANK,BOSTON,MA 02118. SUNY STONY BROOK,SCH DENT MED,DEPT DERMATOL,STONY BROOK,NY 11794. SHRINERS BURN INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 600 EP 600 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600560 ER PT J AU DRAKE, L BRENEMAN, D GREENE, S RAIMER, S SCHUPBACH, CW HALPERIN, M AF DRAKE, L BRENEMAN, D GREENE, S RAIMER, S SCHUPBACH, CW HALPERIN, M TI EFFECTS OF TOPICAL DOXEPIN 5-PERCENT CREAM ON PRURITIC ECZEMA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. UNIV CINCINNATI,DEPT DERMATOL,CINCINNATI,OH 45221. COOPERAT HLTH,DEPT DERMATOL,SEATTLE,WA. UNIV TEXAS,MED BRANCH,DEPT DERMATOL,GALVESTON,TX 77550. UNIV N CAROLINA,DEPT DERMATOL,CHARLOTTE,NC 28223. GENDERM CORP,DEPT DERMATOL,LINCOLNSHIRE,IL. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600589 ER PT J AU KOLLIAS, N MUCCINI, JA PHILLIPS, SB ANDERSON, RR DRAKE, LA AF KOLLIAS, N MUCCINI, JA PHILLIPS, SB ANDERSON, RR DRAKE, LA TI REFLECTANCE SPECTROSCOPY - A RAPID, SENSITIVE, AND REPRODUCIBLE MEANS OF CLINICALLY ASSESSING ERYTHEMA AND PIGMENTATION SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DERMATOL CLIN INVEST GRP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600591 ER PT J AU MUCCINI, JA KOLLIAS, N SOBER, AJ PHILLIPS, SB DRAKE, LA AF MUCCINI, JA KOLLIAS, N SOBER, AJ PHILLIPS, SB DRAKE, LA TI EVALUATION OF TRETINOIN 0.025-PERCENT CREAM IN THE TREATMENT OF PHOTOAGED SKIN USING SPECIALIZED PHOTOGRAPHIC TECHNIQUES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 605 EP 605 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600594 ER PT J AU BILDEN, PF PHILLIPS, SB KOLLIAS, N MUCCINI, JA DRAKE, LA AF BILDEN, PF PHILLIPS, SB KOLLIAS, N MUCCINI, JA DRAKE, LA TI POLARIZED-LIGHT PHOTOGRAPHY OF ACNE-VULGARIS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 5 Z9 6 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 606 EP 606 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600598 ER PT J AU PHILLIPS, S MUCCINI, J KOLLIAS, N DRAKE, L AF PHILLIPS, S MUCCINI, J KOLLIAS, N DRAKE, L TI POLARIZED-LIGHT PHOTOGRAPHY PROVIDES AN ENHANCED PHOTOGRAPHIC RECORD OF PSORIATIC PLAQUES AND THEIR RESPONSE TO TREATMENT SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 606 EP 606 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600595 ER PT J AU UYEYAMA, R MUCCINI, JA DAVIS, M KOLLIAS, N PHILLIPS, SB DRAKE, LA AF UYEYAMA, R MUCCINI, JA DAVIS, M KOLLIAS, N PHILLIPS, SB DRAKE, LA TI ASSESSMENT OF IRRITANCY USING FIBEROPTIC REFLECTANCE SPECTROPHOTOMETRY AND PHOTOGRAPHIC RECORDS SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 606 EP 606 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600596 ER PT J AU BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B AF BARNHILL, RL FANDREY, K LEVY, MA MIHM, MC HYMAN, B TI ANGIOGENESIS AND TUMOR PROGRESSION OF MELANOMA - QUANTIFICATION OF VASCULARITY IN MELANOCYTIC NEVI AND MELANOMA SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 618 EP 618 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600668 ER PT J AU GRECO, MA LADAS, D RUDOLPH, S BADEN, H AF GRECO, MA LADAS, D RUDOLPH, S BADEN, H TI MODULATION OF PANCORNULIN EXPRESSION BY CALCIUM AND RELATIVE CONFLUENCE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CBRC,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 640 EP 640 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600804 ER PT J AU HUSAIN, Z RATLIFF, J WICK, MM AF HUSAIN, Z RATLIFF, J WICK, MM TI MEDIATION OF GROWTH AND DIFFERENTIATION IN HUMAN MELANOCYTE CELL-LINES BY PHORBOL ESTERS INVOLVES DIFFERENTIAL EXPRESSION OF CELLULAR GENES SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC DERMATOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 645 EP 645 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600834 ER PT J AU MAYTIN, EV LAMBERTI, LA AF MAYTIN, EV LAMBERTI, LA TI HEAT-SHOCK REDUCES UVB-INDUCED SUNBURN CELL-FORMATION IN MURINE EPIDERMIS INVIVO SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD APR PY 1992 VL 98 IS 4 BP 654 EP 654 PG 1 WC Dermatology SC Dermatology GA HL846 UT WOS:A1992HL84600885 ER PT J AU HADDAD, FS AF HADDAD, FS TI RHAZES IS A PERSIAN - REPLY SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Letter RP HADDAD, FS (reprint author), US DEPT VET AFFAIRS,CARL T HAYDEN MED CTR,650 E INDIAN SCH RD,PHOENIX,AZ 85012, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0022-2143 J9 J LAB CLIN MED JI J. Lab. Clin. Med. PD APR PY 1992 VL 119 IS 4 BP 437 EP 437 PG 1 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA HM903 UT WOS:A1992HM90300020 ER PT J AU MOLEMAN, N VANDERHART, O VANDERKOLK, BA AF MOLEMAN, N VANDERHART, O VANDERKOLK, BA TI THE PARTUS STRESS REACTION - A NEGLECTED ETIOLOGIC FACTOR IN POSTPARTUM PSYCHIATRIC-DISORDERS SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Note C1 INST PSYCHOTRAUMA,UTRECHT,NETHERLANDS. MASSACHUSETTS GEN HOSP,ERICH LINDEMANN MENTAL HLTH CTR,TRAUMA CLIN,BOSTON,MA 02114. RP MOLEMAN, N (reprint author), FREE UNIV AMSTERDAM HOSP,DEPT PSYCHIAT,POB 7057,1007 MB AMSTERDAM,NETHERLANDS. NR 6 TC 56 Z9 57 U1 0 U2 3 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 APR PY 1992 VL 180 IS 4 BP 271 EP 272 DI 10.1097/00005053-199204000-00010 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HN906 UT WOS:A1992HN90600010 PM 1556567 ER PT J AU OJEMANN, RG AF OJEMANN, RG TI SKULL-BASE SURGERY - A PERSPECTIVE SO JOURNAL OF NEUROSURGERY LA English DT Editorial Material ID TEMPORAL BONE RP OJEMANN, RG (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 8 TC 57 Z9 57 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD APR PY 1992 VL 76 IS 4 BP 569 EP 570 DI 10.3171/jns.1992.76.4.0569 PG 2 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HK826 UT WOS:A1992HK82600001 PM 1545248 ER PT J AU POON, WS SCHOMACKER, KT DEUTSCH, TF MARTUZA, RL AF POON, WS SCHOMACKER, KT DEUTSCH, TF MARTUZA, RL TI LASER-INDUCED FLUORESCENCE - EXPERIMENTAL INTRAOPERATIVE DELINEATION OF TUMOR RESECTION MARGINS SO JOURNAL OF NEUROSURGERY LA English DT Article DE FLUORESCENCE DETECTION; GLIOMA; PHOTORADIATION THERAPY; PHTHALOCYANINE; TUMOR RESECTION; RAT ID PHOTODYNAMIC THERAPY; RAT-BRAIN; PHTHALOCYANINE SENSITIZATION; GLIOMA; TISSUE; CANCER; CELLS; GENE AB The ability of laser-induced fluorescence spectroscopy to delineate tumor margins intraoperatively was studied using a rat intracerebral glioma model. A fluorescent dye, chloro-aluminum phthalocyanine tetrasulfonate (ClAlPcS4), was injected intravenously 24 hours before tumor resection. The animals underwent tumor resection under the operating microscope, guided by laser-induced fluorescence measurement in one group (Group 1) and visual assessment in the other (Group 2). The Group 1 rats had a significantly reduced volume of residual tumor following resection (0.5 +/- 0.2 cu mm vs. 13.7 +/- 4.0 cu mm, mean +/- standard error of the mean, p < 0.02). Three of the nine animals in Group 1 were tumor-free at 2 weeks following resection, compared with none of the 10 rats in Group 2 (p < 0.05). Interference from brain autofluorescence was minimized using spectrally resolved detection and the ClAlPcS4 dye, which has a 680-nm fluorescence peak significantly higher than the 470-nm autofluorescence peak of normal brain. Contrast ratios of up to 40:1 were found for glioma:normal brain fluorescence signals. Spatially-resolved spectra were acquired in approximately 5 seconds using a fiberoptic probe. This study demonstrates the ability of an intraoperative laser-induced fluorescence system to detect tumor margins that could not be identified with the operating microscope. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG NEUROSURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. RI Poon, Wai Sang/F-1558-2011 NR 33 TC 54 Z9 57 U1 0 U2 3 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 APR PY 1992 VL 76 IS 4 BP 679 EP 686 DI 10.3171/jns.1992.76.4.0679 PG 8 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HK826 UT WOS:A1992HK82600017 PM 1545262 ER PT J AU DEC, GW AF DEC, GW TI PROGNOSIS IN CONGESTIVE-HEART-FAILURE - WHAT INFORMATION CAN BEST PREDICT THE FUTURE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID CARDIOMYOPATHY RP DEC, GW (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 14 TC 6 Z9 6 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD APR PY 1992 VL 33 IS 4 BP 477 EP 479 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HM082 UT WOS:A1992HM08200005 PM 1552327 ER PT J AU CORREIA, J AF CORREIA, J TI A BLOODY FUTURE FOR CLINICAL PET SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID VALIDATION; HUMANS RP CORREIA, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL SCI,EDWARDS RES BLDG,FRUIT ST,BOSTON,MA 02114, USA. NR 10 TC 15 Z9 16 U1 0 U2 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD APR PY 1992 VL 33 IS 4 BP 620 EP 622 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HM082 UT WOS:A1992HM08200033 PM 1552351 ER PT J AU MANDELL, RL DIRIENZO, J KENT, R JOSHIPURA, K HABER, J AF MANDELL, RL DIRIENZO, J KENT, R JOSHIPURA, K HABER, J TI MICROBIOLOGY OF HEALTHY AND DISEASED PERIODONTAL SITES IN POORLY CONTROLLED INSULIN-DEPENDENT DIABETICS SO JOURNAL OF PERIODONTOLOGY LA English DT Article DE DIABETES, INSULIN-DEPENDENT; PERIODONTITIS MICROBIOLOGY ID BLACK-PIGMENTED BACTEROIDES; ATTACHMENT LEVEL CHANGES; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; JUVENILE PERIODONTITIS; CLINICAL MEASUREMENTS; EIKENELLA-CORRODENS; YOUNG DIABETICS; MELLITUS; CHILDREN; GINGIVALIS AB A GROUP OF POORLY-CONTROLLED insulin dependent diabetes mellitus (IDDM) patients were examined in a cross-sectional design for total microbial levels, microbial incidence, and the percent levels of selected periodontal microorganisms. These organisms were selected on the basis of prior reports that associated them with either periodontal disease or health. One periodontally-healthy and one periodontally-diseased site were examined in each IDDM patient. Increased levels of the periodontal pathogens Prevotella intermedia, P. melaninogenica spp., Bacteroides gracilis, Eikenella corrodens, Fusobacterium nucleatum and Campylobacter rectus (formerly Wolinella recta) were found at the periodontal diseased sites. Increased prevalence of the organisms P. intermedia, P. melaninogenica spp., and C. rectus were found at the diseased sites. A significantly higher percentage of P. intermedia was found at the sites exhibiting deep pockets and attachment loss. C1 TUFTS UNIV,SCH DENT MED,BOSTON,MA 02111. RP MANDELL, RL (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE08463] NR 73 TC 33 Z9 34 U1 0 U2 0 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD APR PY 1992 VL 63 IS 4 BP 274 EP 279 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JA084 UT WOS:A1992JA08400006 PM 1315389 ER PT J AU SOCRANSKY, SS HAFFAJEE, AD AF SOCRANSKY, SS HAFFAJEE, AD TI THE BACTERIAL ETIOLOGY OF DESTRUCTIVE PERIODONTAL-DISEASE - CURRENT CONCEPTS SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON PERIODONTAL DIAGNOSIS : CURRENT STATUS, FUTURE DIRECTIONS CY MAY 09, 1991 CL BOSTON, MA SP HARVARD SCH DENTAL MED DE PERIODONTAL DISEASES, ETIOLOGY; PERIODONTAL DISEASES, MICROBIOLOGY; PERIODONTAL DISEASES, PATHOGENESIS ID LOCALIZED JUVENILE PERIODONTITIS; BLACK-PIGMENTED BACTEROIDES; INFECTED ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; SERUM ANTIBODY-RESPONSES; HUMAN IMMUNE-RESPONSES; GINGIVALIS W50; LEGIONNAIRES DISEASE; ORAL MICROORGANISMS; VIRULENCE; ASSOCIATION AB THE INTERPRETATION OF DIAGNOSTIC TESTS for the detection of subgingival bacterial species is dependent on knowledge of the microbial etiology of destructive periodontal diseases. Specific etiologic agents of these diseases have been sought for over 100 years; however, the complexity of the microbiota, an incomplete understanding of the biology of periodontal diseases, and technical problems have handicapped this search. Nonetheless, a number of possible pathogens have been suggested on the basis of their association with disease, animal pathogenicity, and virulence factors. The immunological response of the host to a species and the relation of successful therapy to the elimination of the species have also been used to support or refute suspected periodontal pathogens. Current data suggest that pathogens are necessary but not sufficient for disease activity to occur. Factors which influence activity include susceptibility of the individual host and the presence of interacting bacterial species which facilitate or impede disease progression. Recent studies have attempted to distinguish virulent and avirulent clonal types of suspected pathogenic species and seek transmission of genetic elements needed for pathogenic species to cause disease. Finally, the local environment of the periodontal pocket may be important in the regulation of expression of virulence factors by pathogenic species. Thus, in order that disease result from a pathogen, 1) it must be a virulent clonal type; 2) it must possess the chromosomal and extra-chromosomal genetic factors to initiate disease; 3) the host must be susceptible to this pathogen; 4) the pathogen must be in numbers sufficient to exceed the threshold for that host; 5) it must be located at the right place; 6) other bacterial species must foster, or at least not inhibit, the process; and 7) the local environment must be one which is conducive to the expression of the species' virulence properties. RP SOCRANSKY, SS (reprint author), FORSYTH DENT CTR,DEPT PERIODONT,140 FENWAY,BOSTON,MA 02115, USA. RI de la Flor, Maria/B-9212-2015 FU NIDCR NIH HHS [DE-02847, DE-04881] NR 58 TC 655 Z9 684 U1 4 U2 40 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD APR PY 1992 VL 63 IS 4 SU S BP 322 EP 331 DI 10.1902/jop.1992.63.4s.322 PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JA181 UT WOS:A1992JA18100004 PM 1573546 ER PT J AU GOODSON, JM AF GOODSON, JM TI DIAGNOSIS OF PERIODONTITIS BY PHYSICAL MEASUREMENT - INTERPRETATION FROM EPISODIC DISEASE HYPOTHESIS SO JOURNAL OF PERIODONTOLOGY LA English DT Article; Proceedings Paper CT SYMP ON PERIODONTAL DIAGNOSIS : CURRENT STATUS, FUTURE DIRECTIONS CY MAY 09, 1991 CL BOSTON, MA SP HARVARD SCH DENTAL MED DE PERIODONTAL DISEASES, DIAGNOSIS; PERIODONTAL ATTACHMENT; DISEASE ACTIVITY ID ATTACHMENT LEVEL MEASUREMENTS; CREVICULAR FLUID; PROBE; PROGRESSION; PREDICTOR; ABSENCE; THERAPY; SITES AB PHYSICAL MEASUREMENTS INCLUDING THE EVALUATION of probing depth, bleeding on probing, tooth mobility, and inflammation form the basis for most periodontal diagnostics in use today. The interpretation of these observations and the methods available for their measurement, however, have begun to change significantly. The episodic disease activity concept has done much to implement these changes. Observation of episodic attachment loss has been correlated with parallel radiographic changes, alteration in levels of probable pathogens, and changes in inflammatory mediator levels. The failure of pocket depth, suppuration, and bleeding on probing to predict episodic attachment loss has been given plausible explanations and enhanced meanings. Although attachment loss by a continuous process cannot be excluded in some disease conditions, the hypothesis of periodontal disease progression by episodic activity supplements and expands understanding of the disease process. Interest in periodontal diagnostics has accelerated in the last decade. As a parallel development, the technology of small computers has decreased in cost and increased in sophistication. The combination of these factors has created an environment for the development of intelligent diagnostic systems. Four commercially available systems and two systems under development are described. The systems, which measure pocket depth, pocket depth or attachment level, tooth mobility, and pocket temperature, all utilize computer processing of measurements. The result is to provide a simplified and more meaningful presentation of diagnostic information. As intelligent diagnostic systems prove themselves, some of these instruments are likely to become common to dental practice. The promise of more accurate identification of areas of the mouth that are diseased can increase both the efficiency and effectiveness of periodontal therapy. RP GOODSON, JM (reprint author), FORSYTH DENT CTR,DEPT PHARMACOL,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE04881] NR 45 TC 36 Z9 39 U1 0 U2 2 PU AMER ACAD PERIODONTOLOGY PI CHICAGO PA 737 NORTH MICHIGAN AVENUE, SUITE 800, CHICAGO, IL 60611-2690 SN 0022-3492 J9 J PERIODONTOL JI J. Periodont. PD APR PY 1992 VL 63 IS 4 SU S BP 373 EP 382 PG 10 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JA181 UT WOS:A1992JA18100009 PM 1573551 ER PT J AU RYAN, CM YARMUSH, ML TOMPKINS, RG AF RYAN, CM YARMUSH, ML TOMPKINS, RG TI SEPARATION AND QUANTITATION OF POLYETHYLENE GLYCOL-400 AND GLYCOL-3350 FROM HUMAN URINE BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY SO JOURNAL OF PHARMACEUTICAL SCIENCES LA English DT Article ID INTESTINAL PERMEABILITY; MOLECULAR-WEIGHT; EXPERIMENTAL COLITIS; CELIAC-DISEASE; ABSORPTION; PEG; MACROMOLECULES; LACTULOSE; RABBITS; PIG AB Polyethylene glycol 3350 (PEG 3350) is useful as an orally administered probe to measure in vivo intestinal permeability to macromolecules. Previous methods to detect polyethylene glycol (PEG) excreted in the urine have been hampered by inherent inaccuracies associated with liquid-liquid extraction and turbidimetric analysis. For accurate quantitation by previous methods, radioactive labels were required. This paper describes a method to separate and quantitate PEG 3350 and PEG 400 in human urine that is independent of radioactive labels and is accurate in clinical practice. The method uses sized regenerated cellulose membranes and mixed ion-exchange resin for sample preparation and high-performance liquid chromatography with refractive index detection for analysis. The 24-h excretion for normal individuals after an oral dose of 40 g of PEG 3350 and 5 g of PEG 400 was 0.12 +/- 0.04% of the original dose of PEG 3350 and 26.3 +/- 5.1% of the original dose of PEG 400. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,SURG SERV,BOSTON,MA 02114. FU NIDDK NIH HHS [DK 01746, DK 41709]; NIGMS NIH HHS [GM 21700] NR 22 TC 25 Z9 25 U1 3 U2 11 PU AMER PHARMACEUTICAL ASSN PI WASHINGTON PA 2215 CONSTITUTION AVE NW, WASHINGTON, DC 20037 SN 0022-3549 J9 J PHARM SCI JI J. Pharm. Sci. PD APR PY 1992 VL 81 IS 4 BP 350 EP 352 DI 10.1002/jps.2600810412 PG 3 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Pharmacology & Pharmacy SC Pharmacology & Pharmacy; Chemistry GA HL823 UT WOS:A1992HL82300011 PM 1501072 ER PT J AU DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC AF DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC TI GUIDELINES OF CARE FOR NEVI-I (NEVOCELLULAR NEVI AND SEBORRHEIC KERATOSES) SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID CUTANEOUS MALIGNANT-MELANOMA; POPULATION; PRECURSORS; MOLES RP DRAKE, LA (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN 2,BOSTON,MA 02114, USA. NR 19 TC 12 Z9 12 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD APR PY 1992 VL 26 IS 4 BP 629 EP 631 PG 3 WC Dermatology SC Dermatology GA HL541 UT WOS:A1992HL54100019 PM 1597550 ER PT J AU NIDORF, SM PICARD, MH TRIULZI, MO THOMAS, JD NEWELL, J KING, ME WEYMAN, AE AF NIDORF, SM PICARD, MH TRIULZI, MO THOMAS, JD NEWELL, J KING, ME WEYMAN, AE TI NEW PERSPECTIVES IN THE ASSESSMENT OF CARDIAC CHAMBER DIMENSIONS DURING DEVELOPMENT AND ADULTHOOD SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID GROWTH; LIMITS AB The use of body surface area to assess the normalcy of cardiac dimensions has several limitations. To determine whether cardiac dimensions can be assessed by other indexes of body size and growth, this study evaluated the relations between cardiac dimensions assessed by two-dimensional echocardiography and age, height, weight and body surface area. The study group included 268 normal persons aged 6 days to 76 years of age. The dimensions examined included the aortic anulus, left atrium and left ventricular end-diastolic diameter, each measured in the parasternal long-axis plane, and left ventricular length measured from the apical two-chamber view. The analysis confirmed that the heart and great vessels grow in unison and at a predictable rate after birth, reaching 50% of their adult dimensions at birth, 75% by 5 years and 90% by 12 years. Although each cardiac dimension related linearly with height (aortic anulus, r = 0.96; left atium, r = 0.91; left ventricular diameter, r = 0.94; left ventricular length, r = 0.93), the relations among age, weight and body surface area were best expressed by quadratic equations. Multiple regression confirmed that after adjustment for height, other indexes including age, gender, weight and body surface area had no independent effect on the prediction of each dimension. Therefore, because height is a nonderived variable that relates linearly with cardiac dimensions independent of age, it offers a simple yet accurate means of assessing the normalcy of cardiac dimensions in children and adults. RP NIDORF, SM (reprint author), MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,PHILLIPS 8,BOSTON,MA 02114, USA. OI Picard, Michael/0000-0002-9264-3243 NR 12 TC 128 Z9 140 U1 0 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 983 EP 988 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300018 PM 1552123 ER PT J AU FLACHSKAMPF, FA WEYMAN, AE GUERRERO, JL THOMAS, JD AF FLACHSKAMPF, FA WEYMAN, AE GUERRERO, JL THOMAS, JD TI CALCULATION OF ATRIOVENTRICULAR COMPLIANCE FROM THE MITRAL FLOW PROFILE - ANALYTIC AND INVITRO STUDY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID VENTRICULAR DIASTOLIC FUNCTION; PRESSURE HALF-TIME; DOPPLER ECHOCARDIOGRAPHY; VALVE AREA; CARDIOMYOPATHY; RELAXATION; INSIGHTS; DYNAMICS; INDEXES; MODEL AB The quantitative assessment of ventricular diastolic function is an important goal of Doppler echocardiography. Hydrodynamic analysis predicts that the net compliance (C(n)) of the left atrium and ventricle can be quantitatively predicted from the deceleration rate (dv/dt) of the mitral velocity profile by the simple expression: C(n) = - A/rho-dv/dt, where A is effective mitral valve area and rho is blood density. This formula was validated using an in vitro model of transmitral filling where mitral valve area ranged from 0.5 to 2.5 cm2 and net compliance from 0.012 to 0.023 cm3/(dynes/cm2) (15 to 30 cm3/mm Hg). In 34 experiments in which compliance was held constant throughout the filling period, net atrioventricular compliance was accurately calculated from the E wave downslope and mitral valve area (r = 0.95, p < 0.0001). In a second group of experiments, chamber compliance was allowed to vary as a function of chamber pressure. When net compliance decreased during diastole (as when the ventricle moved to a steeper portion of its pressure-volume curve), the transorifice velocity profile was concave downward, whereas when net compliance increased, the velocity profile was concave upward. Application of the preceding formula to these curved profiles allowed instantaneous compliance to be calculated throughout the filling period (r = 0.93, p < 0.001). Numeric application of a mathematic model of mitral filling demonstrated the accuracy of this approach in both restrictive and nonrestrictive orifices. It is concluded that 1) net compliance can be calculated noninvasively and quantitatively from mitral valve area and E wave downslope, and 2) the time course of net compliance determines the shape of the downslope: concave downward profiles indicate decreasing compliance whereas concave upward profiles indicate increasing compliance. C1 MASSACHUSETTS GEN HOSP,NONINVAS CARDIAC LAB,0 EMERSON PL,SUITE 2F,BOSTON,MA 02114. NR 25 TC 53 Z9 54 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD APR PY 1992 VL 19 IS 5 BP 998 EP 1004 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HL273 UT WOS:A1992HL27300020 PM 1552125 ER PT J AU OSTERWEIL, D SYNDULKO, K COHEN, SN PETTLERJENNINGS, PD HERSHMAN, JM CUMMINGS, JL TOURTELLOTTE, WW SOLOMON, DH AF OSTERWEIL, D SYNDULKO, K COHEN, SN PETTLERJENNINGS, PD HERSHMAN, JM CUMMINGS, JL TOURTELLOTTE, WW SOLOMON, DH TI COGNITIVE FUNCTION IN NONDEMENTED OLDER ADULTS WITH HYPOTHYROIDISM SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID EVENT-RELATED POTENTIALS; EVOKED-POTENTIALS; TRIIODOTHYRONINE; THYROTROPIN; PREVALENCE; DEPRESSION; THYROXINE AB Purpose: (1) to evaluate objectively changes in cognitive function and electrophysiologic characteristics associated with hypothyroidism of varying severity and duration in primarily older persons; (2) to determine whether these changes are reversible when a euthyroid state has been attained after treatment with thyroid hormone. Subjects and Methods: We enrolled 54 non-demented hypothyroid patients (31-99, mean 68.6 +/- 16.4 years) with biochemical evidence of hypothyroidism (38 had overt and 14 had minimal hypothyroidism) and 30 euthyroid controls (31-96, mean 63.7 +/- 18.4 years) screened for good general health. We evaluated attention, orientation, memory, learning, visual-spatial abilities, calculation, language, visual scanning, and motor speed using standardized neuropsychological tests. Electrophysiological measures of neurocognitive function included the P300 latency component of the auditory Event-Related Potentials (ERP) and conduction speed from eye to cortex, the P100 latency component of the Patterned Visual-Evoked Potential (PVEP). All patients were studied when hypothyroid. A subset of patients with minimal initial test abnormalities were available to be retested when euthyroid, 5 and 9 months after onset of thyroid replacement therapy. Results: Hypothyroid patients showed significantly lower scores on the Mini-Mental Status Test (MMS) and on five of 14 neuropsychological tests as compared to controls. The neuropsychological tests affected were copying a cube (visual-spatial function), the Inglis Paired Associates Learning Test-Low and Medium association items (memory and learning), Animal Naming (word fluency/production), and the Trail Making A test (attention, visual scanning and psychomotor function. Hypothyroidism also was associated with longer P100 latencies of PVEPs to 20' checks, but showed no significant differences in PVEP P100 latency to 50' checks, nor in the latency of the auditory ERP component P300. There was a statistically significant correlation between a laboratory index of the severity of hypothyroidism (serum T4) and the Inglis Medium Association items and Animal Naming. There was a statistically significant improvement after 5 months of treatment on three of the timed performance tests that previous studies have shown to be most sensitive to brain dysfunction. Conclusion: Hypothyroidism in non-demented older adults is associated with impairments in learning, word fluency, visual-spatial abilities, and some aspect of attention, visual scanning, and motor speed. The MMS by itself was sensitive in differentiating hypothyroid patients with cognitive deficits from controls, while electrophysiological measures did not generally differentiate the hypothyroid patients from normal controls. The MMS was not sensitive to treatment effects, but treatment was associated with significant improvements in three of the most sensitive measures of cognitive dysfunction. C1 UNIV CALIF LOS ANGELES,DEPT MED,DIV GERIATR,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. W LOS ANGELES VET ADM MED CTR NEUROL SERV,LOS ANGELES,CA. RP OSTERWEIL, D (reprint author), JEWISH HOMES AGING,7150 TAMPA AVE,RESEDA,CA 91335, USA. RI Ain, Kenneth/A-5179-2012 OI Ain, Kenneth/0000-0002-2668-934X FU NIA NIH HHS [1K08AG00259-01A1] NR 59 TC 128 Z9 132 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1992 VL 40 IS 4 BP 325 EP 335 PG 11 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HM369 UT WOS:A1992HM36900004 PM 1556359 ER PT J AU KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S AF KAWAMURA, J MEYER, JS TERAYAMA, Y WEATHERS, S TI LEUKOARAIOSIS AND CEREBRAL HYPOPERFUSION COMPARED IN ELDERLY NORMALS AND ALZHEIMERS DEMENTIA SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID WHITE MATTER LUCENCIES; BLOOD-FLOW; AMYLOID ANGIOPATHY; RISK-FACTORS; COMPUTED-TOMOGRAPHY; NORMAL INDIVIDUALS; VASCULAR DEMENTIA; BRAIN LUCENCIES; DISEASE; COGNITION AB Objective: To elucidate the pathogenesis of leuko-araiosis in patients with Alzheimer's disease by utilizing CT densitometry of the brain and measurements of local perfusion in order to quantify the extent of leuko-araiosis and local hypoperfusion compared with similar measurements made among age-matched normal volunteers. Design: Cross-sectional case-control study. Setting: Out-patient visits to a specialized laboratory located in a large hospital facility. Patients: Eighteen elderly patients with probable dementia of Alzheimer type (DAT, aged 71.8 +/- 5.1 years) and 17 neurologically and cognitively normal, age-matched volunteers (aged 68.2 +/- 9.6 years) were admitted to the study according to established criteria. Intervention: None Main Outcome Measures: Cerebral blood flow (mL/100 g brain/min estimated by the xenon inhalation CT-CBF method correlated with volume percentage ratio (%) measured by CT densitometry for leuko-araiosis, compared to normal white and gray matter. Results: Perfusion values for frontal and occipital white matter as well as frontal, parietal, temporal, and occipital cortex were all decreased in DAT patients. Ratios for leuko-araiosis to total brain tissue volumes were greater among patients with DAT compared with age-matched normal volunteers. White matter perfusion in zones of leuko-araiosis was decreased to a similar degree in both DAT and elderly normal volunteers. Conclusions: Perfusion is reduced to the same degree in regions of leuko-araiosis in elderly normals as in DAT patients, but the extent of leuko-araiosis is greater among DAT patients and presumably contributes to cognitive impairments. C1 DEPT VET AFFAIRS MED CTR,CEREBRAL BLOOD FLOW LAB,2002 HOLCOMBE BLVD 151A,HOUSTON,TX 77030. DEPT VET AFFAIRS MED CTR NEURORADIOL SERV,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT RADIOL,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. NR 46 TC 27 Z9 27 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-8614 J9 J AM GERIATR SOC JI J. Am. Geriatr. Soc. PD APR PY 1992 VL 40 IS 4 BP 375 EP 380 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HM369 UT WOS:A1992HM36900012 PM 1556365 ER PT J AU ABBOUD, HE AF ABBOUD, HE TI GROWTH-FACTORS AND THE MESANGIUM SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article; Proceedings Paper CT CONF ON THE GLOMERULAR MESANGIUM : FROM CELL BIOLOGY TO CLINICS CY SEP 27-28, 1991 CL FIUGGI TERME, ITALY SP INT SOC NEPHROL, ENTE FIUGGI, BAYER, MERCK SHARP & DOHME DE PLATELET-DERIVED GROWTH FACTOR; EPIDERMAL GROWTH FACTOR; INSULIN-LIKE GROWTH FACTOR; TRANSFORMING GROWTH FACTOR-BETA; PROLIFERATION; GLOMERULONEPHRITIS ID EXPERIMENTAL GLOMERULONEPHRITIS; FACTOR-BETA; FACTOR-I; CELLS; EXPRESSION; MITOGENS; CULTURE; MICE; RAT AB Growth factors are prime candidates to mediate and modulate the functions of the mesangium. Mesangial cells are effector cells producing a number of growth factors that act in an autocrine manner to regulate their own function. Mesangial cells are also targets for growth factors released from neighboring glomerular cells or infiltrating cells and platelets. Growth factors may promote hypertrophy, proliferation, matrix metabolism, and immune-inflammatory and vasoactive properties of mesangial cells. These peptides represent important mediators of mesangial cell responses to injury. Platelet-derived growth factor mediates predominantly cell proliferation, whereas transforming growth factor beta mediates mesangial cell matrix expansion. Mesangial cells may also modulate some of the hemodynamic effects of growth factors, such as the increased renal vascular resistance in response to platelet-derived growth factor and epidermal growth factor or the increased RBF and GFR in response to insulin-like growth factor-1. Changes in the expression of growth factors or their receptors during the course of glomerular injury point to a potential role in mediating some of the pathologic changes in vivo. Several agents appear to antagonize the mitogenic and perhaps other effects of growth factors in mesangial cells. Such agents include adenylate cyclase as well Os guanylate cyclase agonists. Recent studies also suggest that some traditional vasoactive agents may activate metabolic processes in mesangial cells similar to peptide growth factors. Collectively, these studies point to the interaction of both hemodynamic and metabolic factors in the response and contribution of glomerular and specifically mesangial cells to injury. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP ABBOUD, HE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK43988, DK 33665] NR 36 TC 32 Z9 32 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD APR PY 1992 VL 2 IS 10 SU S BP S185 EP S189 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA HR857 UT WOS:A1992HR85700019 PM 1600135 ER PT J AU BERGERON, L SULLIVAN, N SODROSKI, J AF BERGERON, L SULLIVAN, N SODROSKI, J TI TARGET CELL-SPECIFIC DETERMINANTS OF MEMBRANE-FUSION WITHIN THE HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GP120 3RD-VARIABLE REGION AND GP41 AMINO TERMINUS SO JOURNAL OF VIROLOGY LA English DT Article ID SITE-SPECIFIC MUTAGENESIS; HTLV-III/LAV ENVELOPE; INFLUENZA-VIRUS; T-CELLS; MONOCLONAL-ANTIBODY; CD4 RECEPTOR; GLYCOPROTEIN; RETROVIRUS; AIDS; HEMAGGLUTININ AB The entry of human immunodeficiency virus type 1 (HIV-1) into target cells involves binding to the viral receptor (CD4) and membrane fusion events, the latter influenced by target cell factors other than CD4. The third variable (V3) region of the HIV-1 gp120 exterior envelope glycoprotein and the amino terminus of the HIV-1 gp41 transmembrane envelope glycoprotein have been shown to be important for the membrane fusion process. Here we demonstrate that some HIV-1 envelope glycoproteins containing an altered V3 region or gp41 amino terminus exhibit qualitatively different abilities to mediate syncytium formation and virus entry when different target cells are used. These results demonstrate that the structure of these HIV-1 envelope glycoprotein regions determines the efficiency of membrane fusion in a target cell-specific manner and support a model in which the gp41 amino terminus interacts directly or indirectly with the target cell during virus entry. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI24755] NR 54 TC 108 Z9 108 U1 0 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD APR PY 1992 VL 66 IS 4 BP 2389 EP 2397 PG 9 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400066 PM 1548769 ER PT J AU LOEKEN, MR AF LOEKEN, MR TI SIMIAN VIRUS-40 SMALL T-ANTIGEN TRANS ACTIVATES THE ADENOVIRUS-E2A PROMOTER BY USING MECHANISMS DISTINCT FROM THOSE USED BY ADENOVIRUS-E1A SO JOURNAL OF VIROLOGY LA English DT Note ID E2F TRANSCRIPTION FACTOR; DNA-BINDING ACTIVITY; E1A GENE; PROTEIN PHOSPHATASE-2A; INDUCTION; ENHANCER; ELEMENTS; PRODUCT; TRANSACTIVATION; STIMULATION AB As reported previously for simian virus 40 small t antigen, polyomavirus small t antigen stimulates transcription directed by the adenovirus E2A and VA-I promoters during transient transfection assays. To determine whether papovaviral small t antigens might employ biochemical mechanisms during transcription activation that are either similar to or distinct from other viral trans activators, I compared the abilities of simian virus 40 small t antigen and adenovirus E1A to regulate the E2A promoter during transient transfection assays. I determined that, whereas activation of the E2A promoter by E1A involves the transcription factors ATF and EIIF, activation by small t antigen involves only EIIF. The effects of cotransfecting maximal concentrations of plasmids encoding small t antigen with E1A suggested that they activate the E2A promoter by different mechanisms. To determine whether small t antigen employs a mechanism different from that encoded in E1A domain II, domain III, or both, I compared the effects of transfecting plasmids expressing small t antigen, the 12S product of E1A, or the 13S product with a mutation in domain II on trans activation of the E2A promoter in two cellular backgrounds. On the basis of these comparisons, it appears that small t antigen does not activate transcription by a mechanism similar to either of the activities encoded in E1A. This suggests that papovavirus small t antigens belong to a distinct class of trans-acting proteins. RP LOEKEN, MR (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK36836] NR 34 TC 21 Z9 21 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 APR PY 1992 VL 66 IS 4 BP 2551 EP 2555 PG 5 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400089 PM 1532215 ER PT J AU SHARPLESS, NE OBRIEN, WA VERDIN, E KUFTA, CV CHEN, ISY DUBOISDALCQ, M AF SHARPLESS, NE OBRIEN, WA VERDIN, E KUFTA, CV CHEN, ISY DUBOISDALCQ, M TI HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 TROPISM FOR BRAIN MICROGLIAL CELLS IS DETERMINED BY A REGION OF THE ENV-GLYCOPROTEIN THAT ALSO CONTROLS MACROPHAGE TROPISM SO JOURNAL OF VIROLOGY LA English DT Note ID CENTRAL NERVOUS-SYSTEM; CD4 ANTIGEN; HIV-1; AIDS; INFECTION; GP120; SEQUENCE; RECEPTOR; TISSUE; DOMAIN AB Human immunodeficiency virus type 1 (HIV-1), the agent of AIDS, frequently infects the central nervous system. We inoculated adult human brain cultures with chimeric viruses containing parts of the env gene of a cloned primary isolate from brain tissue, HIV-1 JRFl, inserted into the cloned DNA of a T-cell-tropic strain. A chimeric virus containing the carboxy-terminal portion of HIV-1 JRFl env did not replicate in these brain tissue cultures, while a chimera expressing an env-encoded protein containing 158 amino acids of HIV-1 JRFl gp120, including the V3 loop, replicated well in brain microglial cells, as it does in blood macrophages. Infection of brain microglial cells with such a chimera was blocked by an antibody to the V3 loop of gp120. Thus, env determinants in the region of gp120, outside the CD4-binding site and comprising the V3 loop, are critical for efficient viral binding to and/or entry into human brain microglia. C1 NINCDS,VIRAL & MOLEC PATHOGENESIS LAB,BETHESDA,MD 20892. NINCDS,SURG NEUROL BRANCH,BETHESDA,MD 20892. NIH,HOWARD HUGHES MED INST,RES SCHOLARS PROGRAM,BETHESDA,MD 20814. UNIV CALIF LOS ANGELES,W LOS ANGELES VET ADM MED CTR,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,JONSSON COMPREHENS CANC CTR,DEPT MED,LOS ANGELES,CA 90024. OI Verdin, Eric/0000-0003-3703-3183 NR 37 TC 109 Z9 110 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 APR PY 1992 VL 66 IS 4 BP 2588 EP 2593 PG 6 WC Virology SC Virology GA HJ504 UT WOS:A1992HJ50400095 PM 1548785 ER PT J AU BARZILAY, J WARRAM, JH BAK, M LAFFEL, LMB CANESSA, M KROLEWSKI, AS AF BARZILAY, J WARRAM, JH BAK, M LAFFEL, LMB CANESSA, M KROLEWSKI, AS TI PREDISPOSITION TO HYPERTENSION - RISK FACTOR FOR NEPHROPATHY AND HYPERTENSION IN IDDM SO KIDNEY INTERNATIONAL LA English DT Article ID SODIUM-LITHIUM COUNTERTRANSPORT; DEPENDENT DIABETES-MELLITUS; BLOOD-PRESSURE; RED-CELLS; URINARY ALBUMIN; FAMILY HISTORY; JUVENILE-ONSET; DISEASE; EXCHANGE; PARENTS AB Less than a quarter of the patients with juvenile-onset IDDM develop diabetic nephropathy during the first 20 years of diabetes. To study the determinants of this complication, we selected patients who had come with newly diagnosed IDDM to the Joslin Clinic between 1967 to 1972, and we examined them in 1986 to 1988, that is, 15 to 21 years after onset of diabetes. Using a case control design we compared three groups of cases, that is, advanced nephropathy (N = 43), only microalbuminuria (N = 41), and hypertension alone (N = 17), with a group of controls who remained normoalbuminuric and normotensive despite the long duration of IDDM (N = 61). In comparison with controls, patients with advanced nephropathy had more parents with hypertension (odds ratio 3.8), higher V(max) values of Na/Li countertransport in red blood cells (odds ratio 10.0 for the highest tertile), and higher mean arterial pressure during adolescence and early adulthood (odds ratio 3.1 for those above the median). They also had significantly poorer glycemic control during their first 12 years of diabetes. Patients with hypertension alone were similar to those with advanced nephropathy with regard to markers of predisposition to hypertension but differed from them with regard to glycemic control, having the best glycemic control of all the study groups. Patients who developed only microalbuminuria during 15 to 21 years of IDDM (some of whom will progress to overt proteinuria later) did not differ significantly from controls with regard to predisposition to hypertension. In conclusion, predisposition to hypertension is a major risk factor for the development of advanced diabetic nephropathy and essential hypertension during the first 20 years of IDDM. C1 JOSLIN DIABET CTR, DIV RES, EPIDEMIOL & GENET SECT, 1 JOSLIN PL, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DIV ENDOCRINE HYPERTENS, BOSTON, MA 02115 USA. FU NHLBI NIH HHS [R01 HL35664]; NIDDK NIH HHS [R01 DK 41526] NR 34 TC 111 Z9 111 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0085-2538 EI 1523-1755 J9 KIDNEY INT JI Kidney Int. PD APR PY 1992 VL 41 IS 4 BP 723 EP 730 DI 10.1038/ki.1992.113 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA HM535 UT WOS:A1992HM53500003 PM 1513093 ER PT J AU SCHILLER, JH BITTNER, G SPRIGGS, DR AF SCHILLER, JH BITTNER, G SPRIGGS, DR TI TUMOR-NECROSIS-FACTOR, BUT NOT OTHER HEMATOPOIETIC GROWTH-FACTORS, PROLONGS THE SURVIVAL OF HAIRY-CELL LEUKEMIA-CELLS SO LEUKEMIA RESEARCH LA English DT Article DE HAIRY CELL LEUKEMIA; TUMOR NECROSIS FACTOR; CYTOKINES ID EPSTEIN-BARR VIRUS; HUMAN B-CELLS; FACTOR-ALPHA; PROLIFERATION; DIFFERENTIATION; INTERFERON; INTERLEUKIN-4; LYMPHOCYTES; MODULATION; ACTIVATION AB In order to determine the growth factor requirements of hairy cell leukemia (HCL) cells, we studied the in vitro effects of tumor necrosis factor (TNF), interleukin (IL) 1 alpha, IL-1 beta, IL-2, IL-3, IL-4, IL-5, IL-6, B-cell growth factor (BCGF), GM-CSF, PHA-stimulated lymphocyte-conditioned media (CM), and 5637 bladder carcinoma CM on HCL cells obtained from spleens of patients with HCL. Mononuclear cells from a normal donor, obtained at post-traumatic splenectomy, served as a control. TNF prolonged the survival of HCL cells obtained from five different HCL patients when compared to cells cultured in control media alone, although cell proliferation could be demonstrated in only two of the five. HCL cells stained negative for the Epstein-Barr nuclear antigen (EBNA) both before and after 4 weeks in culture. BCGF, 5637 CM, and PHA-stimulated lymphocyte CM also prolonged the survival of HC25 and HC56 cells, although not to the same degree as TNF. Cells cultured in BCGF, however, stained positive for EBNA. None of the other recombinantly produced or purified cytokines prolonged the survival of the leukemic cells. With the exception of IL-2, none of the growth factors studied prolonged the survival of purified normal spleen (NS) cells over a 4-week period of time when compared to NS cells incubated in media alone. TNF prolonged the survival of HC25 cells in a dose-dependent manner, and a highly purified antibody to TNF abrogated the effects of TNF. HC25 cells incubated in the presence of control media alone did not constitutively produce TNF mRNA; however, incubation of the cells in the presence of TNF for 48 h induced the cells to express TNF message. We conclude that TNF is important in prolonging the survival of HCL cells, and thus may be important in the pathogenesis of this disease. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP SCHILLER, JH (reprint author), UNIV WISCONSIN,CTR CLIN CANC,K4-666 CLIN SCI CTR,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NCI NIH HHS [CA047722] NR 29 TC 10 Z9 10 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0145-2126 J9 LEUKEMIA RES JI Leuk. Res. PD APR PY 1992 VL 16 IS 4 BP 337 EP & DI 10.1016/0145-2126(92)90135-T PG 0 WC Oncology; Hematology SC Oncology; Hematology GA HP443 UT WOS:A1992HP44300002 PM 1564938 ER PT J AU ROCHET, N ANDERSON, P VIVIER, E AF ROCHET, N ANDERSON, P VIVIER, E TI STRUCTURE AND FUNCTION OF THE CD16 - ZETA-GAMMA NK RECEPTOR COMPLEX SO M S-MEDECINE SCIENCES LA French DT Article AB Natural killer cells are large granular lymphocytes involved in host defence against tumor cells and virally-infected cells. Besides a natural non MHC-restricted cytotoxicity, NK cells can also effect an antibody-dependent cytoxicity (ADCC) mediated by Fc-gamma-RIIIA-alpha (CD16). It has been recently shown that CD16 is associated with disulfide-linked dimers composed of two homologous subunits, zeta and gamma. These transducing molecules are also associated with the T-cell antigen receptor (CD3:TCR) and the IgE receptor (Fc-epsilon-RI) expressed on basophils and mast cells. These results show that distinct cell surface receptors utilize common transducing subunits, and emphasize the homology between the CD16, Fc-epsilon-RI and CD3:TCR complexes. However, the gamma-gamma-homodimer is preferentially expressed in NK cells, suggesting that specific combinations of these transducing subunits might subserve distinct signal transducing functions, and contribute to the heterogeneity of these cellular populations. RP ROCHET, N (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115, USA. NR 0 TC 1 Z9 1 U1 1 U2 3 PU JOHN LIBBEY EUROTEXT LTD PI MONTROUGE PA 127 AVE DE LA REPUBLIQUE, 92120 MONTROUGE, FRANCE SN 0767-0974 J9 M S-MED SCI JI M S-Med. Sci. PD APR PY 1992 VL 8 IS 4 BP 359 EP 365 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HP403 UT WOS:A1992HP40300008 ER PT J AU WEISSKOFF, RM KIIHNE, S AF WEISSKOFF, RM KIIHNE, S TI MRI SUSCEPTOMETRY - IMAGE-BASED MEASUREMENT OF ABSOLUTE SUSCEPTIBILITY OF MR CONTRAST AGENTS AND HUMAN BLOOD SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note ID MAGNETIC-SUSCEPTIBILITY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WEISSKOFF, RM (reprint author), MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02129, USA. FU NCI NIH HHS [5PO1CA48729, CA54886] NR 18 TC 249 Z9 250 U1 0 U2 10 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 APR PY 1992 VL 24 IS 2 BP 375 EP 383 DI 10.1002/mrm.1910240219 PG 9 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HM149 UT WOS:A1992HM14900018 PM 1569876 ER PT J AU BATSON, SC SUNDSETH, R HEATH, CV SAMUELS, M HANSEN, U AF BATSON, SC SUNDSETH, R HEATH, CV SAMUELS, M HANSEN, U TI INVITRO INITIATION OF TRANSCRIPTION BY RNA POLYMERASE-II ON INVIVO-ASSEMBLED CHROMATIN TEMPLATES SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID SIMIAN VIRUS-40 CHROMOSOMES; ACTIVE SV40 MINICHROMOSOMES; DNA-BINDING-PROTEINS; NUCLEOPROTEIN COMPLEXES; LATE PROMOTER; PREINITIATION COMPLEXES; NUCLEOSOMES INHIBIT; FUNCTIONAL-ANALYSIS; REGULATORY REGION; MAJOR LATE AB We have studied the initiation of transcription in vitro by RNA polymerase II on simian virus 40 (SV40) minichromosomal templates isolated from infected cells. The efficiency and pattern of transcription from the chromatin templates were compared with those from viral DNA templates by using two in vitro transcription systems, either HeLa whole-cell extract or basal transcription factors, RNA polymerase II, and one of two SV40 promoter-binding transcription factors, LSF and Sp1. Dramatic increases in numbers of transcripts upon addition of transcription extract and different patterns of usage of the multiple SV40 initiation sites upon addition of Sp1 versus LSF strongly suggested that transcripts were being initiated from the minichromosomal templates in vitro. That the majority of transcripts from the minichromosomes were due to initiation de novo was demonstrated by the efficient transcription observed in the presence of alpha-amanitin, which inhibited minichromosome-associated RNA polymerase II, and an alpha-amanitin-resistant RNA polymerase II, which initiated transcription in vitro. The pattern of transcription from the SV40 late and early promoters on the minichromosomal templates was similar to the in vivo pattern of transcription during the late stages of viral infection and was distinct from the pattern of transcription generated from viral DNA in vitro. In particular, the late promoter of the minichromosomal templates was transcribed with high efficiency, similar to viral DNA templates, while the early-early promoter of the minichromosomal templates was inhibited 10- to 15-fold. Finally, the number of minichromosomes competent to initiate transcription in vitro exceeded the amount actively being transcribed in vivo. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,EUKARYOT TRANSCRIPT LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. MIT,CTR CANC RES,CAMBRIDGE,MA 02138. MIT,DEPT BIOL,CAMBRIDGE,MA 02138. FU NIGMS NIH HHS [GM 36667] NR 81 TC 7 Z9 7 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD APR PY 1992 VL 12 IS 4 BP 1639 EP 1651 PG 13 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK751 UT WOS:A1992HK75100027 PM 1312666 ER PT J AU BRENT, GA WILLIAMS, GR HARNEY, JW FORMAN, BM SAMUELS, HH MOORE, DD LARSEN, PR AF BRENT, GA WILLIAMS, GR HARNEY, JW FORMAN, BM SAMUELS, HH MOORE, DD LARSEN, PR TI CAPACITY FOR COOPERATIVE BINDING OF THYROID-HORMONE (T3) RECEPTOR DIMERS DEFINES WILD TYPE-T3 RESPONSE ELEMENTS SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID RAT OSTEOCALCIN GENE; HEAVY-CHAIN GENE; GROWTH-HORMONE; ALPHA-MYOSIN; PROMOTER; TRANSCRIPTION; SITE; 1,25-DIHYDROXYVITAMIN-D3; EXPRESSION; INDUCTION AB Thyroid hormone response elements (T3REs) have been identified in a variety of promoters including those directing expression of rat GH (rGH), alpha-myosin heavy chain (rMHC), and malic enzyme (rME). A detailed biochemical and genetic analysis of the rGH element has shown that it consists of three hexamers related to the consensus [(A/G)GGT(C/A)A]. We have extended this analysis to the rMHC and rME elements. Binding of highly purified thyroid hormone receptor (T3R) to T3REs was determined using the gel shift assay, and thyroid hormone (T3) induction was measured in transient transfections. We show that the wild type version of each of the three elements binds T3R dimers cooperatively. Mutational analysis of the rMHC and rME elements identified domains important for binding T3R dimers and allowed a direct determination of the relationship between T3R binding and function. In each element two hexamers are required for dimer binding, and mutations that interfere with dimer formation significantly reduce T3 induction. Similar to the rGH element, the rMHC T3RE contains three hexameric domains arranged as a direct repeat followed by an inverted copy, although the third domain is weaker than in rGH. All three are required for full function and T3R binding. The rME T3RE is a two-hexamer direct repeat T3RE, which also binds T3R monomer and dimer. Across a series of mutant elements, there was a strong correlation between dimer binding in vitro and function in vivo for rMHC (r = 0.99, P < 0.01) and rME (r = 0.67, P < 0.05) T3REs. Our results demonstrate a similar pattern of T3R dimer binding to a diverse array of hexameric sequences and arrangements in three wild type T3REs. Addition of nuclear protein enhanced T3R binding but did not alter the specificity of binding to wild type or mutant elements. Binding of purified T3R to T3REs was highly correlated with function, both with and without the addition of nuclear protein. T3R dimer formation is the common feature which defines the capacity of these elements to confer T3 induction. C1 BRIGHAM & WOMENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NYU MED CTR,DEPT PHARMACOL,DIV MOLEC ENDOCRINOL,NEW YORK,NY 10016. NYU MED CTR,DEPT MED,NEW YORK,NY 10016. RP BRENT, GA (reprint author), BRIGHAM & WOMENS HOSP,DIV THYROID,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIADDK NIH HHS [5-K12-AM01401]; NIDDK NIH HHS [DK-16636, DK-36256] NR 43 TC 79 Z9 79 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1992 VL 6 IS 4 BP 502 EP 514 DI 10.1210/me.6.4.502 PG 13 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HQ337 UT WOS:A1992HQ33700002 PM 1584220 ER PT J AU DEMAY, MB KIERNAN, MS DELUCA, HF KRONENBERG, HM AF DEMAY, MB KIERNAN, MS DELUCA, HF KRONENBERG, HM TI CHARACTERIZATION OF 1,25-DIHYDROXYVITAMIN-D(3) RECEPTOR INTERACTIONS WITH TARGET SEQUENCES IN THE RAT OSTEOCALCIN GENE SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID HORMONE RESPONSE ELEMENT; GROWTH-HORMONE; IDENTIFICATION; PROMOTER; EXPRESSION AB The sequences in the rat osteocalcin gene that bind the 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptor and mediate its effects on gene transcription contain three copies of a motif homologous to those found in other steroid response elements. To evaluate the relative importance of these motifs and their flanking sequences, functional properties and receptor binding of a series of mutant response elements were analyzed. Mutations in the third motif, including its deletion, have no effect on receptor binding and only modestly detrimental effects on the ability of the upstream motifs to confer 1,25-(OH)2D3 responsiveness in transfected cells. Mutations in the first two motifs have negative effects on both receptor binding and gene activation. Mutagenesis of bases upstream from each of the first two motifs alters receptor binding and gene activation; these bases are, therefore, an integral part of the rat osteocalcin 1,25-(OH)2D3 response element. Two direct hexameric repeats (GGGTGA ATG AGGACA) and not the palindromic motif thus characterize this 1,25-(OH)2D3 response element. C1 UNIV WISCONSIN, COLL AGR & LIFE SCI, DEPT BIOCHEM, MADISON, WI 53706 USA. RP DEMAY, MB (reprint author), HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. FU NIDDK NIH HHS [DK-36597] NR 18 TC 45 Z9 45 U1 0 U2 1 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0888-8809 J9 MOL ENDOCRINOL JI Mol. Endocrinol. PD APR PY 1992 VL 6 IS 4 BP 557 EP 562 DI 10.1210/me.6.4.557 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HQ337 UT WOS:A1992HQ33700008 PM 1316548 ER PT J AU SHAW, SY MARGOLIES, MN AF SHAW, SY MARGOLIES, MN TI A SPONTANEOUS VARIANT OF AN ANTIDIGOXIN HYBRIDOMA ANTIBODY WITH INCREASED AFFINITY ARISES FROM A HEAVY-CHAIN SIGNAL PEPTIDE MUTATION SO MOLECULAR IMMUNOLOGY LA English DT Article ID SEQUENCE CLEAVAGE SITES; SACCHAROMYCES-CEREVISIAE; DIGOXIN ANTIBODIES; HUMAN LYSOZYME; A-II; SECRETION; MUTAGENESIS; POLYMERASE; PROPEPTIDE; DIVERSITY AB The A/J murine hybridoma cell line 40-150 secretes antidigoxin antibodies with high affinity for digoxin. A first-order spontaneous mutant (40-150 A2.4) produces antibodies containing a mutation at heavy chain position 94 resulting in reduced affinity for digoxin. A second-order mutant (40-150 A2.4 P.10) derived from 40-150 A2.4 produces two species of antibody: one identical to 40-150 A2.4 and the other with a two amino acid truncation at the heavy chain amino-terminus [Panka et al., Proc. natn. Acad. Sci. U.S.A. 85, 3080-3084 (1988)]. The truncated antibody has increased affinity for digoxin relative to the nontruncated variant. Direct nucleotide sequence analysis of polymerase chain reaction amplified heavy chain variable region cDNA derived from 40-150 A2.4 P.10 reveals a point mutation at the -2 position of the signal peptide, resulting in a glutamine to proline change. Southern blots of genomic DNA from all three cell lines gave identical patterns and were consistent with a single heavy chain mRNA derived from a single rearranged gene. The presence of proline at the heavy chain -2 position of antibody 40-150 A2.4 P.10 partially shifts the cleavage site of the signal peptidase to the +2 position, resulting in the production of both full-length and truncated antibody heavy chains. Signal peptide mutation resulting in a change in antibody affinity for antigen is a hitherto unidentified possible mechanism for antibody diversification. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,JACKSON 14,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NHLBI NIH HHS [P01-HL19259] NR 34 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 0161-5890 J9 MOL IMMUNOL JI Mol. Immunol. PD APR PY 1992 VL 29 IS 4 BP 525 EP 529 DI 10.1016/0161-5890(92)90010-U PG 5 WC Biochemistry & Molecular Biology; Immunology SC Biochemistry & Molecular Biology; Immunology GA HM513 UT WOS:A1992HM51300010 PM 1565100 ER PT J AU NEUFELD, EJ SKALNIK, DG LIEVENS, PMJ ORKIN, SH AF NEUFELD, EJ SKALNIK, DG LIEVENS, PMJ ORKIN, SH TI HUMAN CCAAT DISPLACEMENT PROTEIN IS HOMOLOGOUS TO THE DROSOPHILA HOMEOPROTEIN, CUT SO NATURE GENETICS LA English DT Article ID GENE PROMOTER; HOMEODOMAIN; EXPRESSION; LOCUS; MELANOGASTER; SPECIFICITY; MUTATIONS; SET AB Human CCAAT displacement protein (CDP), a putative repressor of developmentally regulated gene expression, was purified from HeLa cells by DNA binding-site affinity chromatography. cDNA encoding CDP was obtained by immunoscreening a lambda-gt11 library with antibody raised against purified protein. The deduced primary amino acid sequence of CDP reveals remarkable homology to Drosophila cut with respect to the presence of a unique homeodomain and "cut repeats". As cut participates in determination of cell fate in several tissues in Drosophila, the similarity predicts a broad role for CDP in mammalian development. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. INDIANA UNIV,JAMES WHITCOMB RILEY HOSP CHILDREN,SCH MED,WELLS RES CTR,INDIANAPOLIS,IN 46223. RI Neufeld, Ellis/F-9331-2011 NR 37 TC 181 Z9 183 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD APR PY 1992 VL 1 IS 1 BP 50 EP 55 DI 10.1038/ng0492-50 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA JC978 UT WOS:A1992JC97800012 PM 1301999 ER PT J AU IONASESCU, VV TROFATTER, J HAINES, JL IONASESCU, R SEARBY, C AF IONASESCU, VV TROFATTER, J HAINES, JL IONASESCU, R SEARBY, C TI MAPPING OF THE GENE FOR X-LINKED DOMINANT CHARCOT-MARIE-TOOTH NEUROPATHY SO NEUROLOGY LA English DT Article ID SENSORY NEUROPATHY; HEREDITARY MOTOR; DUFFY LOCUS; DNA PROBES; LINKAGE; DISEASE; LOCALIZATION; FAMILY; CHROMOSOME-17 AB We performed a clinical study and linkage analysis on 278 subjects (66 affected) belonging to eight families with X-linked dominant Charcot-Marie-Tooth (CMT) neuropathy. This form affects 11.8% of CMT patients in Iowa. Motor nerve conduction velocities (MNCVs) were significantly slowed consistent with type 1 CMT. Fifty-six obligate carriers manifested mild distal weakness, localized areflexia, pes cavus, and slowing on MNCVs. Seven X-linked restriction fragment length polymorphisms mapping in the Xp11-q21 region were tested for linkage against CMT. Two-point linkage results showed the highest lod scores with PGK1, DXS159, and DXYS1. Multipoint linkage analysis excluded the CMT gene from being telomeric to either DXS14 or DXYS1, with over 1,000:1 odds. The highest location scores were at PGK1 and 1 cM proximal to DXS159. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP IONASESCU, VV (reprint author), UNIV IOWA HOSP & CLIN,DEPT PEDIAT,PEDIAT GENET MUSCLE LAB,IOWA CITY,IA 52242, USA. RI Haines, Jonathan/C-3374-2012 NR 27 TC 32 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR PY 1992 VL 42 IS 4 BP 903 EP 908 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA HP855 UT WOS:A1992HP85500039 PM 1565250 ER PT J AU SANTORO, N SCHNEYER, AL IBRAHIM, J SCHMIDT, CL AF SANTORO, N SCHNEYER, AL IBRAHIM, J SCHMIDT, CL TI GONADOTROPIN AND INHIBIN CONCENTRATIONS IN EARLY-PREGNANCY IN WOMEN WITH AND WITHOUT CORPORA-LUTEA SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID RADIOIMMUNOASSAY; SERUM AB We compared serum concentrations of immunoreactive inhibin, hCG, and FSH in normal women with those of two groups of women lacking endogenous luteal function. Twelve functionally agonadal, hypergonadotropic women with premature ovarian failure were given replacement ovarian steroids. Donor oocytes were fertilized in vitro with the husband's semen, and embryos were transferred into these women. A second group of 12 women were normogonadotropic but anovulatory, had undergone previously unsuccessful in vitro fertilization, and possessed cryopreserved embryos. These women were suppressed with a GnRH agonist before sex hormone replacement. Serum samples collected at weeks 2, 3, 4-6, 8-10, and 12-14 of pregnancy were measured for FSH, hCG, and immunoreactive inhibin. Data were compared with concentrations in normally ovulating women with well-established dates of conception. Sex steroid replacement hormone levels did not differ between the ovarian-failure and agonist-suppressed women and approximated that of normal cycles until pregnancy; thereafter, estradiol and progesterone levels remained higher than normal. Despite excessive steroid replacement FSH remained higher in women with ovarian failure than in agonist-suppressed or normal women. On immunoassay, inhibin failed to show an early rise at 4-6 weeks of pregnancy in either group of aluteal women (0.52 +/- 0.05 ng/mL), whereas normal women demonstrated 0.9 +/- 0.05 ng/mL inhibin in their sera (P < .001). By 8-10 weeks of pregnancy, women with ovarian failure demonstrated inhibin concentrations identical to those of normal women (1.2 +/- 0.1 and 1.2 +/- 0.15 ng/mL, respectively), whereas agonist-suppressed women lagged behind (0.7 +/- 0.1 ng/mL) (P < .02). In all groups, hCG followed a pattern identical to inhibin. Normal hCG levels were observed in ovarian-failure women by 8-10 weeks, but not in agonist-suppressed women. We conclude the following: 1) Women lacking a corpus luteum do not appear to secrete inhibin until at least 8 weeks of gestation, indicating a luteal source of immunoreactive inhibin in normal early pregnancy; 2) detectable placental inhibin in ovarian failure increases by 8-10 weeks, as does hCG, and appears to be associated with suppressed FSH concentrations, suggesting that placental immunoreactive inhibin may be a biologically active dimer; and 3) both hCG and inhibin secretion are suppressed in GnRH agonist-suppressed women, suggesting a placental "lag" in pregnancies derived from cryopreserved embryos or in chronically anovulatory infertile women. C1 MASSACHUSETTS GEN HOSP,DEPT MED,REPROD ENDOCRINE UNIT,BOSTON,MA 02114. RP SANTORO, N (reprint author), UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT OBSTET & GYNECOL,185 S ORANGE AVE,NEWARK,NJ 07103, USA. FU NICHD NIH HHS [HD-00923, HD-25941] NR 23 TC 17 Z9 17 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0029-7844 J9 OBSTET GYNECOL JI Obstet. Gynecol. PD APR PY 1992 VL 79 IS 4 BP 579 EP 585 PG 7 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HL511 UT WOS:A1992HL51100021 PM 1553181 ER PT J AU EGAN, KM GRAGOUDAS, ES SEDDON, JM WALSH, SM AF EGAN, KM GRAGOUDAS, ES SEDDON, JM WALSH, SM TI SMOKING AND THE RISK OF EARLY METASTASES FROM UVEAL MELANOMA SO OPHTHALMOLOGY LA English DT Article ID PROTON-BEAM IRRADIATION; MALIGNANT-MELANOMA AB Smoking is suspected of altering host immunity and may therefore hasten the development of metastases among cancer patients. The authors followed 946 patients with melanomas of the choroid and/or ciliary body who had been treated with proton beam irradiation and who had provided a smoking history during their evaluation before treatment. After a mean follow-up of 33 months, 98 patients were diagnosed with metastatic disease. Metastasis-free survival rates 3 years after irradiation were similar in association with never, past, and current cigarette smoking (86%, 89%, and 90%, respectively; P = 0.90). Rates also were similar with increasing pack-years of exposure and when the product smoked was cigarettes versus pipes or cigars only. Estimates for smoking effects were unchanged after adjusting for established prognostic factors for metastases. Results suggest that smoking does not alter the risk of metastases during the first few years after irradiation of choroidal melanomas. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EPIDEMIOL UNIT,BOSTON,MA 02114. NR 19 TC 9 Z9 9 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1992 VL 99 IS 4 BP 537 EP 541 PG 5 WC Ophthalmology SC Ophthalmology GA HM532 UT WOS:A1992HM53200017 PM 1584571 ER PT J AU RUBIN, PAD SHORE, JW YAREMCHUK, MJ AF RUBIN, PAD SHORE, JW YAREMCHUK, MJ TI COMPLEX ORBITAL FRACTURE REPAIR USING RIGID FIXATION OF THE INTERNAL ORBITAL SKELETON SO OPHTHALMOLOGY LA English DT Article ID ENOPHTHALMOS AB Large orbital fractures involving more than one orbital wall are frequently associated with enophthalmos and vertical globe dystopia. The authors repaired 22 orbits in 20 patients using the technique of rigid fixation of the internal orbital skeleton. Eleven orbits were reconstructed with titanium or vitallium implants that were custom-shaped to span the bony defect and fixed to the orbital rim. Seven orbits were reconstructed with bone grafts rigidly supported by a miniplate, and, in four cases, direct lag screw support of bone grafts was used. The intraoperative goal was to restore the native orbital anatomy and volume. Autologous calvarial bone grafts were used to supplement the repair to achieve the desired volumetric effect and to cover additional wall defects. A reoperation for additional orbital augmentation was needed in one enophthalmic and one anophthalmic orbit. There were no cases of overcorrection, migration, infection, or extraocular muscle entrapment. In complex orbital fractures, the technique of rigid internal orbital fixation appears to yield a stable and predictable result with the prevention of postoperative globe malposition. C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. NR 11 TC 27 Z9 28 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD APR PY 1992 VL 99 IS 4 BP 553 EP 559 PG 7 WC Ophthalmology SC Ophthalmology GA HM532 UT WOS:A1992HM53200020 PM 1584574 ER PT J AU GOODSON, JM TANNER, A AF GOODSON, JM TANNER, A TI ANTIBIOTIC-RESISTANCE OF THE SUBGINGIVAL MICROBIOTA FOLLOWING LOCAL TETRACYCLINE THERAPY SO ORAL MICROBIOLOGY AND IMMUNOLOGY LA English DT Article DE TETRACYCLINE; DRUG RESISTANCE, MICROBIAL; BACTERIA, ANAEROBIC; DRUG IMPLANT; PERIODONTAL DISEASE AB The antibiotic resistance of the subgingival microbiota was studied by 3 approaches. First, we assessed the ability of subgingival isolates taken following therapy to grow on media containing tetracycline (TC). Higher percentages of TC-resistant organisms appeared at TC fiber-treated periodontal sites and within the saliva 1 week after treatment as compared with pre-treatment levels. By 1 month, the percentage of TC-resistant organisms had returned to levels comparable to those seen before treatment. In the second approach, subgingival isolates taken following therapy were grown on media without antibiotics, and isolates were selected for Gram-stain and cell morphology determination. This study indicated that subgingival sites became colonized with gram-positive cocci in the same time period that an increase of TC-resistant isolates was observed in the first study. This may account for the transient increase in TC resistance, because many gram-positive cocci are intrinsically resistant to TC. In the third approach, the antibiotic resistance of subgingival gram-negative species was determined. The predominant cultivable microbiota of 9 sites from 3 subjects were isolated immediately before and 6 months after TC fiber treatment. Gram-negative rods were characterized and tested for sensitivity to TC (minimum inhibitory concentration [MIC] 1-128-mu-g/ml), penicillin at 80-mu-g/ml, and erythromycin at 8-mu-g/ml. None of the gram-negative rods were resistant to TC (MIC greater-than-or-equal-to 16-mu-g/ml), either before or after treatment. Before treatment 98% of the gram-negative rods were susceptible to TC at 1-2-mu-g/ml and after therapy 88% were susceptible. The percentage of gram-negative rods exhibiting intermediate TC susceptibility (MIC 4-8-mu-g/ml) changed from 2.0% before therapy to 5.2% after therapy. In no case was either penicillin or erythromycin resistance associated with increased resistance to TC. RP GOODSON, JM (reprint author), FORSYTH DENT CTR,DEPT PHARMACOL,140 THE FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE05334, DE03448] NR 0 TC 52 Z9 52 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0055 J9 ORAL MICROBIOL IMMUN JI Oral Microbiol. Immunol. PD APR PY 1992 VL 7 IS 2 BP 113 EP 117 DI 10.1111/j.1399-302X.1992.tb00520.x PG 5 WC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology SC Dentistry, Oral Surgery & Medicine; Immunology; Microbiology GA HP942 UT WOS:A1992HP94200010 PM 1528631 ER PT J AU BUZZI, MG MOSKOWITZ, MA AF BUZZI, MG MOSKOWITZ, MA TI THE TRIGEMINOVASCULAR SYSTEM AND MIGRAINE SO PATHOLOGIE BIOLOGIE LA English DT Article DE MIGRAINE; TRIGEMINOVASCULAR SYSTEM; DIHYDROERGOTAMINE; SUMATRIPTAN ID GENE-RELATED PEPTIDE; PLASMA-PROTEIN EXTRAVASATION; SUBSTANCE-P; DURA MATER; VASCULAR HEADACHES; BLOOD-VESSELS; VASOACTIVE PEPTIDES; TRIGEMINAL GANGLION; CEREBRAL-ARTERIES; PAIN MECHANISMS AB Neurogenic inflammation has been proposed as a possible pathogenetic mechanism for migraine and cluster headache. Antidromic stimulation of trigeminal fibers causes plasma protein extravasation, mast cell activation and degranulation, vacuolation and increase in endothelial vesicle number within post capillary venules in rat dura mater. The antimigraine drugs sumatriptan and dihydroergotamine block the development of plasma extravasation and ultrastructural changes, as well as plasma calcitonin gene-related peptide (CGRP) increase in the superior sagittal sinus following electrical trigeminal ganglion stimulation. Sumatriptan and dihydroergotamine bind with high affinity to the 5-HT1D/1B receptors, thus suggesting that their neurogenic antiinflammatory activity is mediated by activation of 5-HT autoreceptors present on sensory fibers innervating blood vessels in dura mater. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV ROME LA SAPIENZA,DIPARTIMENTO SCI NEUROL,NEUROL CLIN 1,I-00185 ROME,ITALY. RP BUZZI, MG (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL & NEUROSURG,STROKE RES LAB,WELLMAN 423,BOSTON,MA 02114, USA. NR 42 TC 63 Z9 66 U1 1 U2 2 PU EXPANSION SCI FRANCAISE PI PARIS PA 31 BLVD LATOUR MAUBOURG, 75007 PARIS, FRANCE SN 0369-8114 J9 PATHOL BIOL JI Pathol. Biol. PD APR PY 1992 VL 40 IS 4 BP 313 EP 317 PG 5 WC Pathology SC Pathology GA HY518 UT WOS:A1992HY51800008 PM 1379707 ER PT J AU VIETTI, TJ LAND, V SHUSTER, JJ AMYLON, M LINK, M BERARD, C CRIST, W BOROWITZ, M FALLETTA, J BOWMAN, WP BRECHER, M CASTLEBERRY, R FRANKEL, L GOORIN, A HAYES, FA HVIZDALA, E KRISCHER, JP POLLOCK, BH MCWILLIAMS, N MURPHY, S PICK, T PULLEN, J RAVINDRANATH, Y SMITH, EI STEUBER, CP SULLIVAN, M VANEYS, J WHARAM, M AF VIETTI, TJ LAND, V SHUSTER, JJ AMYLON, M LINK, M BERARD, C CRIST, W BOROWITZ, M FALLETTA, J BOWMAN, WP BRECHER, M CASTLEBERRY, R FRANKEL, L GOORIN, A HAYES, FA HVIZDALA, E KRISCHER, JP POLLOCK, BH MCWILLIAMS, N MURPHY, S PICK, T PULLEN, J RAVINDRANATH, Y SMITH, EI STEUBER, CP SULLIVAN, M VANEYS, J WHARAM, M TI PROGRESS AGAINST CHILDHOOD-CANCER - THE PEDIATRIC ONCOLOGY GROUP EXPERIENCE SO PEDIATRICS LA English DT Article DE CANCER; COOPERATIVE GROUP; NEOPLASM ID ACUTE LYMPHOBLASTIC-LEUKEMIA; CHILDREN AB The sequential outcome was evaluated for all childhood cancers in which the Pediatric Oncology Group has conducted a series of clinical trials, with constant eligibility, on patients with newly diagnosed cancer. The analysis was applied to more than 7000 patients with cancer diagnosed between 1976 and 1989. These include acute leukemia (4 subgroups), non-Hodgkins lymphoma (4 subgroups), osteogenic sarcoma, and advanced neuroblastoma. In 8 of these 10 disease areas, significant improvement in outcome has occurred. In rare diseases such as pediatric cancer, collaborative studies may be the only way to conduct therapeutic trials of sufficient statistical power. A cooperative group has distinct advantages over a series of ad hoc collaborative studies in that it can maintain a unified data base, study its history with minimal confounding effects of changing institutional participants, and develop long-term research relationships among its participants. C1 UNIV FLORIDA, DEPT STAT, GAINESVILLE, FL 32611 USA. CHILDRENS HOSP STANFORD, PALO ALTO, CA 94304 USA. ST JUDE CHILDRENS RES HOSP, MEMPHIS, TN 38101 USA. DUKE UNIV, MED CTR, DURHAM, NC 27710 USA. COOK FT WORTH CHILDRENS MED CTR, FT WORTH, TX USA. NEW YORK STATE DEPT HLTH, ROSWELL PK MEM INST, DIV PEDIAT, BUFFALO, NY 14263 USA. UNIV ALABAMA, CHILDRENS HOSP, BIRMINGHAM, AL USA. SCOTT & WHITE MEM HOSP & CLIN, DEPT PEDIAT, TEMPLE, TX 76501 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT PEDIAT, BOSTON, MA 02115 USA. BERLEN LABS INC, ALAMEDA, CA USA. UNIV S FLORIDA, MED CTR, DEPT PEDIAT, TAMPA, FL 33620 USA. UNIV FLORIDA, DEPT PEDIAT, GAINESVILLE, FL 32611 USA. EASTERN MAINE MED CTR, DEPT PEDIAT, BANGOR, ME 04401 USA. CHILDRENS MEM HOSP, CHICAGO, IL 60614 USA. BROOKE ARMY MED CTR, DEPT PEDIAT, FT SAM HOUSTON, TX 78234 USA. UNIV MISSISSIPPI, MED CTR, DEPT PEDIAT, JACKSON, MS 39216 USA. WAYNE STATE UNIV, CHILDRENS HOSP MICHIGAN, DETROIT, MI 48202 USA. UNIV TEXAS, SW MED CTR, DEPT SURG, DALLAS, TX 75230 USA. BAYLOR COLL MED, DEPT PEDIAT, HOUSTON, TX 77030 USA. UNIV TEXAS, MD ANDERSON CANC CTR, DEPT PEDIAT, HOUSTON, TX 77025 USA. JOHNS HOPKINS UNIV, DEPT RADIAT ONCOL, BALTIMORE, MD 21218 USA. RP VIETTI, TJ (reprint author), WASHINGTON UNIV, SCH MED,DEPT PEDIAT,POG OPERAT OFF,SUITE 2A, 4949 W PINE BLVD, ST LOUIS, MO 63108 USA. NR 9 TC 30 Z9 30 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD APR PY 1992 VL 89 IS 4 BP 597 EP 600 PG 4 WC Pediatrics SC Pediatrics GA HM251 UT WOS:A1992HM25100004 ER PT J AU FOUTY, HE YEO, RA OTTO, MW BRIGGS, CR AF FOUTY, HE YEO, RA OTTO, MW BRIGGS, CR TI A NOVEL CONTACT-LENS SYSTEM TO ASSESS VISUAL HEMISPHERIC ASYMMETRIES SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID INPUT; PERCEPTION; DIRECTION AB A soft contact-lens system for achieving unilateral visual stimulation in a free vision format is described. Initial testing with light transmittance and visual perimetry indicated that the lenses created artificial visual-field deficits. The efficacy of the lenses as a technique for lateralizing visual input was evaluated by examining within-subject differences in performance on two visuospatial tasks. Speed and accuracy of performance were greater with visual input directed to the right hemisphere. These data support the lens design as a useful alternative to tachistoscopic procedures and previous lens systems. C1 UNIV NEW MEXICO,ALBUQUERQUE,NM 87131. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. SUNSOFT CORP,ALBUQUERQUE,NM. NR 20 TC 3 Z9 3 U1 0 U2 0 PU PERCEPTUAL MOTOR SKILLS PI MISSOULA PA PO BOX 9229, MISSOULA, MT 59807 SN 0031-5125 J9 PERCEPT MOTOR SKILL JI Percept. Mot. Skills PD APR PY 1992 VL 74 IS 2 BP 567 EP 575 PG 9 WC Psychology, Experimental SC Psychology GA HQ716 UT WOS:A1992HQ71600045 PM 1594418 ER PT J AU ARA, G VARSHNEY, A HA, CS OSEROFF, AR HERMAN, TS TEICHER, BA AF ARA, G VARSHNEY, A HA, CS OSEROFF, AR HERMAN, TS TEICHER, BA TI MULTIPLE MODALITY TREATMENT OF CARCINOMA-CELLS WITH PT(RH-123)2 PLUS X-RAY PLUS LIGHT SO PHOTOCHEMISTRY AND PHOTOBIOLOGY LA English DT Article ID LASER PHOTOTHERAPY; GAMMA-RADIATION; RHODAMINE-123; DYE; PHOTOSENSITIZATION; PHOTOCHEMOTHERAPY; MITOCHONDRIAL; INVITRO; FIBROBLASTS; RETENTION AB A complex of platinum tetrachloride with two molecules of rhodamine-123 (Rh-123), Pt(Rh-123)2, has been reported to act as hypoxic cell radiosensitizer of carcinoma cells in vitro and in vivo. In the present paper we report that Pt(Rh-123)2 photosensitizes human mammary carcinoma (MCF-7) cells and cis-platinum resistant human mammary carcinoma (MCF-7/CP) cells to 400-800 nm light in vitro. The efficiency of photosensitization by Pt(Rh-123)2 was 10 times greater than for Rh-123. Combination therapy using Pt(Rh-123)2 plus x-ray plus light was also much more effective compared to the combination therapy using Rh-123 plus x-ray plus light. After 15-mu-M of Rh-123 plus x-ray (0-8 Gy) plus light (5 J/cm2) treatment, cell survival curve was parallel to the x-ray cell survival curve with an initial decrease in the surviving fraction corresponding to the drug plus light mediated killing. Cell killing caused by Rh-123 (15-mu-M) plus x-ray (0-8 Gy) plus light (5 J/cm2) was additive as determined by the product of the surviving fraction after Rh-123 plus light and x-ray. In contrast, for 15-mu-M of Pt(Rh-123)2 plus x-ray (8 Gy) plus light (5 J/cm2) treatment, whereas additive killing predicts a survival fraction of approximately 0.024, in reality, the combination therapy caused the survival fraction to decrease to 0.0012, implying that the cell killing was enhanced by a factor of 20. Using Pt(Rh-123)2 plus x-ray plus light, supraadditive cell killing was also observed under hypoxic conditions, although compared to normally oxygenated conditions the degree of cytotoxicity was significantly reduced. These results indicate that the platinum-Rh-123 complex acts as a photo- and radiosensitizer and should be a highly effective drug for use with combined photo and x-irradiation. C1 NEW YORK STATE DEPT HLTH,ROSWELL PK MEM INST,DEPT DERMATOL,BUFFALO,NY 14263. RP ARA, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [R01-CA47379, R01-CA36508] NR 27 TC 10 Z9 11 U1 0 U2 0 PU AMER SOC PHOTOBIOLOGY PI AUGUSTA PA BIOTECH PARK, 1021 15TH ST, SUITE 9, AUGUSTA, GA 30901-3158 SN 0031-8655 J9 PHOTOCHEM PHOTOBIOL JI Photochem. Photobiol. PD APR PY 1992 VL 55 IS 4 BP 561 EP 567 DI 10.1111/j.1751-1097.1992.tb04278.x PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HK374 UT WOS:A1992HK37400013 PM 1620732 ER PT J AU SCHULZ, RJ VERHEY, LJ HUQ, MS VENKATARAMANAN, N AF SCHULZ, RJ VERHEY, LJ HUQ, MS VENKATARAMANAN, N TI WATER CALORIMETER DOSIMETRY FOR 160-MEV PROTONS SO PHYSICS IN MEDICINE AND BIOLOGY LA English DT Article AB The absorbed dose to water from a 160 MeV proton beam as determined by a flexible, temperature regulated, sealed glass core, water calorimeter was compared to that determined from ionization chambers used in accordance with AAPM Report 16. The ratios of these doses as obtained from two experiments done over four months apart, are 0.992 +/- 0.004 and 0.990 +/- 0.004. As there are no radiation dependent parameters required for the water calorimeter, these data add to the growing body of evidence which supports the use of the calorimeter as a reliable absorbed dose standard. They also support the use of Co-60-calibrated ionization chambers used in accordance with AAPM Report 16 for the dosimetry of proton beams. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. RP SCHULZ, RJ (reprint author), YALE UNIV,SCH MED,DEPT THERAPEUT RADIOL,NEW HAVEN,CT 06510, USA. FU NCI NIH HHS [2T 32 CA 09259, R01-CA 38563] NR 14 TC 23 Z9 23 U1 0 U2 1 PU IOP PUBLISHING LTD PI BRISTOL PA TECHNO HOUSE, REDCLIFFE WAY, BRISTOL, ENGLAND BS1 6NX SN 0031-9155 J9 PHYS MED BIOL JI Phys. Med. Biol. PD APR PY 1992 VL 37 IS 4 BP 947 EP 953 DI 10.1088/0031-9155/37/4/009 PG 7 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA HP768 UT WOS:A1992HP76800009 PM 1317036 ER PT J AU ABOUSAMRA, AB JUPPNER, H FORCE, T FREEMAN, MW KONG, XF SCHIPANI, E URENA, P RICHARDS, J BONVENTRE, JV POTTS, JT KRONENBERG, HM SEGRE, GV AF ABOUSAMRA, AB JUPPNER, H FORCE, T FREEMAN, MW KONG, XF SCHIPANI, E URENA, P RICHARDS, J BONVENTRE, JV POTTS, JT KRONENBERG, HM SEGRE, GV TI EXPRESSION CLONING OF A COMMON RECEPTOR FOR PARATHYROID-HORMONE AND PARATHYROID HORMONE-RELATED PEPTIDE FROM RAT OSTEOBLAST-LIKE CELLS - A SINGLE RECEPTOR STIMULATES INTRACELLULAR ACCUMULATION OF BOTH CAMP AND INOSITOL TRISPHOSPHATES AND INCREASES INTRACELLULAR FREE CALCIUM SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PROTEIN-KINASE; SARCOMA CELLS; BONE-CELLS; MEMBRANES; HYPERCALCEMIA; METABOLISM; NUCLEOTIDE; ACTIVATION; BIND AB Parathyroid hormone (PTH), a major regulator of mineral ion metabolism, and PTH-related peptide (PTHrP), which causes hypercalcemia in some cancer patients, stimulate multiple signals (cAMP, inositol phosphates, and calcium) probably by activating common receptors in bone and kidney. Using expression cloning, we have isolated a cDNA clone encoding rat bone PTH/PTHrP receptor from rat osteosarcoma (ROS 17/2.8) cells. The rat bone PTH/PTHrP receptor is 78% identical to the opossum kidney receptor; this identity indicates striking conservation of this receptor across distant mammalian species. Additionally, the rat bone PTH/PTHrP receptor has significant homology to the secretin and calcitonin receptors but not to any other G protein-linked receptor. When expressed in COS cells, a single cDNA clone, expressing either rat bone or opossum kidney PTH/PTHrP receptor, mediates PTH and PTHrP stimulation of both adenylate cyclase and phospholipase C. These properties could explain the diversity of PTH action without the need to postulate other receptor subtypes. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,RENAL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT UNIT,BOSTON,MA 02114. RP ABOUSAMRA, AB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. OI Abou-Samra, Abdul/0000-0001-8735-1142 NR 32 TC 899 Z9 904 U1 0 U2 17 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2732 EP 2736 DI 10.1073/pnas.89.7.2732 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600046 PM 1313566 ER PT J AU WILLIAMS, NG ROBERTS, TM LI, P AF WILLIAMS, NG ROBERTS, TM LI, P TI BOTH P21(RAS) AND PP60(V-SRC) ARE REQUIRED, BUT NEITHER ALONE IS SUFFICIENT, TO ACTIVATE THE RAF-1 KINASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SIGNAL TRANSDUCTION; BACULOVIRUS; ONCOGENES; PROTEIN SERINE; THREONINE KINASE; PHOSPHORYLATION ID PROTEIN-KINASE; SIGNAL TRANSDUCTION; BIOLOGICAL-ACTIVITY; RAS PROTEINS; C-RAF; V-RAF; ONCOGENE; PHOSPHORYLATION; TRANSFORMATION; PROTOONCOGENE AB The raf genes encode a family of cytoplasmic proteins with intrinsic protein-serine/threonine kinase activity. The c-raf gene is the cellular homolog of v-raf, the transforming gene of murine sarcoma virus 3611. The constitutive kinase activity of the v-Raf protein has been implicated in transformation and mitogenesis. The activity of Raf-1, the protein product of the c-raf gene, is normally suppressed by a regulatory N-terminal domain. Activation of various tyrosine-kinase growth factor receptors results in activation of Raf-1 and its hyperphosphorylation. Further, Raf-1 has been shown to act either downstream or independently of the p21ras protein, as indicated by experiments involving microinjection of anti-Ras antibodies. To investigate the potential role of p21ras in the activation of Raf-1 by tyrosine kinases, we have used the baculovirus/Sf9 cell system to overproduce various wild-type and mutant forms of pp60src, p21ras, and Raf-1 proteins. We show that either pp60v-src or p21c-ras can independently activate the autokinase activity of Raf-1, but only to a limited extent. Surprisingly, both pp60v-src and p21c-ras are required to fully activate Raf-1. Analysis of the Raf-1 autokinase activity in vitro shows that Raf-1 autophosphorylation sites are distributed equally on serine and threonine residues. When Raf-1 is analyzed by immunoblotting, as previously reported for mammalian cell experiments, a marked increase in the apparent molecular weight of Raf-1 is seen only when it is coexpressed with both pp60v-src and p21ras. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. BASF BIORES CORP,CAMBRIDGE,MA 02139. FU NCI NIH HHS [CA5066, CA43803] NR 36 TC 158 Z9 158 U1 0 U2 0 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD APR 1 PY 1992 VL 89 IS 7 BP 2922 EP 2926 DI 10.1073/pnas.89.7.2922 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL816 UT WOS:A1992HL81600085 PM 1372995 ER PT J AU BENMANSOUR, S TEJANIBUTT, SM HAUPTMANN, M BRUNSWICK, DJ AF BENMANSOUR, S TEJANIBUTT, SM HAUPTMANN, M BRUNSWICK, DJ TI LACK OF EFFECT OF HIGH-DOSE COCAINE ON MONOAMINE UPTAKE SITES IN RAT-BRAIN MEASURED BY QUANTITATIVE AUTORADIOGRAPHY SO PSYCHOPHARMACOLOGY LA English DT Article DE NEUROTOXICITY; COCAINE; DOPAMINE; SEROTONIN; NOREPINEPHRINE; UPTAKE SITES ID TYROSINE-HYDROXYLASE IMMUNOREACTIVITY; NOREPINEPHRINE UPTAKE SITES; SEROTONIN UPTAKE SITES; PARA-CHLOROAMPHETAMINE; H-3 CYANOIMIPRAMINE; FRONTAL-CORTEX; D-AMPHETAMINE; DOPAMINE; METHAMPHETAMINE; FENFLURAMINE AB There have been a number of claims that high-dose administration of cocaine to rats leads to neurotoxic effects on dopamine neurons. In this study possible neurotoxic effects on monoamine neurons were examined by measuring the effects of cocaine (35 mg/kg daily for 10 days) on the binding of radioligands to uptake sites for dopamine, serotonin and norepinephrine using quantitative autoradiography. No effects of cocaine on any of the binding sites were observed and therefore, it is concluded that cocaine, unlike amphetamine derivatives which have similar pharmacologic properties, does not produce neurotoxic effects on monoamine neurons. C1 UNIV PENN,SCH MED,DEPT PSYCHIAT,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,NEUROPSYCHOPHARMACOL UNIT,PHILADELPHIA,PA 19104. FU NIDA NIH HHS [DA05137] NR 27 TC 53 Z9 53 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0033-3158 J9 PSYCHOPHARMACOLOGY JI Psychopharmacology PD APR PY 1992 VL 106 IS 4 BP 459 EP 462 DI 10.1007/BF02244815 PG 4 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA HF491 UT WOS:A1992HF49100005 PM 1579620 ER PT J AU KANABROCKI, EL BREMNER, WF SOTHERN, RB GRUBER, SA THIRD, JLHC BUSHNELL, DL OLWIN, JH AF KANABROCKI, EL BREMNER, WF SOTHERN, RB GRUBER, SA THIRD, JLHC BUSHNELL, DL OLWIN, JH TI A QUEST FOR THE RELIEF OF ATHEROSCLEROSIS - POTENTIAL ROLE OF INTRAPULMONARY HEPARIN - A HYPOTHESIS SO QUARTERLY JOURNAL OF MEDICINE LA English DT Article ID ACUTE MYOCARDIAL-INFARCTION; MOLECULAR-WEIGHT HEPARIN; CORONARY-ARTERY DISEASE; SUDDEN CARDIAC DEATH; RANDOMIZED CLINICAL-TRIALS; INDUCED THROMBOCYTOPENIA; CIRCADIAN VARIATION; HEART-DISEASE; SEASONAL-VARIATION; BLOOD-COAGULATION AB Recent progress in the treatment of coronary artery disease is reviewed from the standpoint of changes in lifestyle, surgical techniques to revascularize the myocardium and a variety of medical interventions. Among the medical modalities, heparin appears to have a greater potential than any other agent tested to neutralize the atherogenic process at most of its stages. This potential is supported by success in clinical trials of heparin administered by intravenous, subcutaneous, pulmonary, sublingual and topical routes. The suggested self-administration of low-dose heparin by inhalation appears to be well justified and easily adaptable to home therapy. The summarized evidence suggests the need for further clinical trials to test the use of heparin in the prophylaxis of atherosclerotic disease. C1 CHICAGO MED SCH,DEPT INTERNAL MED,N CHICAGO,IL 60064. VASC DIS RES FDN,SKOKIE,IL 60076. US DEPT VET AFFAIRS,EDWARD J HINES JR VET ADM HOSP,DEPT INTERNAL MED,HINES,IL 60141. LOYOLA UNIV,MED CTR,DEPT INTERNAL MED,MAYWOOD,IL 60153. UNIV MINNESOTA,DEPT SURG,MINNEAPOLIS,MN 55455. RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT SURG,CHICAGO,IL 60612. RP KANABROCKI, EL (reprint author), US DEPT VET AFFAIRS,EDWARD J HINES JR VET ADM HOSP,NUCL MED SERV,HINES,IL 60141, USA. NR 176 TC 4 Z9 4 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0033-5622 J9 Q J MED JI Q. J. Med. PD APR PY 1992 VL 83 IS 300 BP 259 EP 282 PG 24 WC Medicine, General & Internal SC General & Internal Medicine GA HY199 UT WOS:A1992HY19900001 PM 1631260 ER PT J AU ROSENTHAL, DI ALEXANDER, A ROSENBERG, AE SPRINGFIELD, D AF ROSENTHAL, DI ALEXANDER, A ROSENBERG, AE SPRINGFIELD, D TI ABLATION OF OSTEOID OSTEOMAS WITH A PERCUTANEOUSLY PLACED ELECTRODE - A NEW PROCEDURE SO RADIOLOGY LA English DT Article DE BONE NEOPLASMS, CT; ELECTROCOAGULATION; OSTEOMA ID COMPUTED-TOMOGRAPHY; PAIN AB Osteoid osteoma is a benign, self-limited tumor of bone that usually requires surgical excision for relief of pain and to prevent long-term consequences. Radio-frequency electrodes have been successfully and safely used to ablate small areas of the central nervous system and to perform ablation elsewhere in the body. The authors have used this technique in four patients with proved or presumptive osteoid osteoma, completely relieving the symptoms in three. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 24 TC 235 Z9 246 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 APR PY 1992 VL 183 IS 1 BP 29 EP 33 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400007 PM 1549690 ER PT J AU GERARD, EL FERRY, JA AMREIN, PC HARMON, DC MCKINSTRY, RC HOPPEL, BE ROSEN, BR AF GERARD, EL FERRY, JA AMREIN, PC HARMON, DC MCKINSTRY, RC HOPPEL, BE ROSEN, BR TI COMPOSITIONAL CHANGES IN VERTEBRAL BONE-MARROW DURING TREATMENT FOR ACUTE-LEUKEMIA - ASSESSMENT WITH QUANTITATIVE CHEMICAL-SHIFT IMAGING SO RADIOLOGY LA English DT Article DE BONE MARROW, MR; LEUKEMIA, THERAPY; MAGNETIC RESONANCE (MR), CHEMICAL SHIFT ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ACUTE MYELOID-LEUKEMIA; REGENERATION FOLLOWING CHEMOTHERAPY; T1 RELAXATION; DISORDERS; CHILDREN; RELAPSE; THERAPY; INVITRO; CANCER AB A modified Dixon chemical shift imaging technique was used to quantify longitudinal changes in bone marrow that occur during induction chemotherapy in patients with acute leukemia. Results were correlated with those of bone marrow biopsy. Forty-seven quantitative images were obtained with a 0.6-T whole body imager in a total of 11 patients over the course of treatment. Quantitative measures of fat fractions and water and fat component T1 and T2 relaxation times were determined, as well as average relaxation times. Imaging results showed sequential increases in fat fractions among responding patients (n = 9), consistent with biopsy-confirmed clinical remission. In the two patients who later relapsed, sharp decreases in fat fractions were noted. In the two patients who failed to regenerate normal marrow, unchanging, low fat fractions were seen. Water component T1 values reflected posttherapeutic changes in the hematopoietic elements. Quantitative chemical shift imaging proved useful in assessing treatment response in acute leukemia during early bone marrow regeneration and, later, in ascertaining remission or relapse. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT HEMATOL ONCOL,BOSTON,MA 02114. RP GERARD, EL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,CTR NUCL MAGNET RESONANCE,BLDG 149,BOSTON,MA 02129, USA. FU NCI NIH HHS [R01-CA-40303] NR 28 TC 50 Z9 54 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1992 VL 183 IS 1 BP 39 EP 46 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400009 PM 1549692 ER PT J AU LEE, MJ RATTNER, DW LEGEMATE, DA SAINI, S DAWSON, SL HAHN, PF WARSHAW, AL MUELLER, PR AF LEE, MJ RATTNER, DW LEGEMATE, DA SAINI, S DAWSON, SL HAHN, PF WARSHAW, AL MUELLER, PR TI ACUTE COMPLICATED PANCREATITIS - REDEFINING THE ROLE OF INTERVENTIONAL RADIOLOGY SO RADIOLOGY LA English DT Article DE ABSCESS, PERCUTANEOUS DRAINAGE; INTERVENTIONAL PROCEDURES; PANCREAS, ABSCESS; PANCREAS, NECROSIS; PANCREATITIS ID PERCUTANEOUS DRAINAGE; FLUID COLLECTIONS; CT; ABSCESSES; PSEUDOCYSTS AB Computed tomographic (CT) scans in 30 patients who had undergone percutaneous drainage for acute complicated pancreatitis were retrospectively studied to determine the role of percutaneous drainage. Fifty-nine collections were percutaneously drained in these 30 patients. Eighty-one catheters were placed in the 59 collections (average, 1.4 catheters per patient). Patients required an average of three catheter manipulations, seven abdominal CT scans, 5 weeks of catheter drainage, a mean hospital stay of 82 days (range, 42-122 days), and a mean intensive care unit stay of 31 days (range, 1-62 days). Percutaneous intervention was successful in 14 patients, partially successful in four, and unsuccessful in eight. A temporizing effect was seen in four patients. Percutaneous intervention was successful in one of 10 central (pancreas and lesser sac areas) collections and 28 of 49 peripheral collections. Surgical debridement was necessary in 16 patients because of failed or incomplete percutaneous drainage. Complications occurred in five patients, and the mortality rate was 33%. Drainage of central areas should initially be performed by a surgeon, while peripheral collections should be drained percutaneously as they develop. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 58 Z9 58 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD APR PY 1992 VL 183 IS 1 BP 171 EP 174 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400032 PM 1549667 ER PT J AU STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, ER MROSE, HE WHITE, G CARDENOSA, G SAWICKA, J MAHONEY, E KOPANS, DB AF STACEYCLEAR, A MCCARTHY, KA HALL, DA PILESPELLMAN, ER MROSE, HE WHITE, G CARDENOSA, G SAWICKA, J MAHONEY, E KOPANS, DB TI CALCIFIED SUTURE MATERIAL IN THE BREAST AFTER RADIATION-THERAPY SO RADIOLOGY LA English DT Article DE BREAST, CALCIFICATION; BREAST NEOPLASMS, DIAGNOSIS; BREAST NEOPLASMS, POSTOPERATIVE; BREAST NEOPLASMS, THERAPY ID IRRADIATED BREAST; CALCIFICATIONS; CANCER; RECURRENCE; EXCISION AB Of 335 women who underwent lumpectomy and radiation therapy for breast cancer, 42 subsequently developed calcifications. Particles typical of calcified suture material were identified in 21 of the 42 women (50%). No obvious calcified suture material was found in approximately 1,140 women of 38,000 (3%) who had undergone mammography after they had previously undergone breast biopsy for a benign lesion and thus had not undergone radiation therapy. Calcified suture material rarely develops in the nonirradiated breast, but it is common after radiation therapy and should not be confused with recurrent breast cancer. These calcifications are likely the result of delayed resorption of catgut sutures, which provide a matrix on which calcium can precipitate in a suitable local environment. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. NIH,DEPT RADIOL,BETHESDA,MD 20892. ILLINOIS MASONIC MED CTR,DEPT RADIAT MED,CHICAGO,IL 60657. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. SUSAN KOMEN BREAST CTR,PEORIA,IL. NR 13 TC 6 Z9 6 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 APR PY 1992 VL 183 IS 1 BP 207 EP 208 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HJ874 UT WOS:A1992HJ87400038 PM 1549672 ER PT J AU LEISENRING, W RYAN, L AF LEISENRING, W RYAN, L TI STATISTICAL PROPERTIES OF THE NOAEL SO REGULATORY TOXICOLOGY AND PHARMACOLOGY LA English DT Article ID QUANTITATIVE RISK ANALYSIS; TOXICOLOGY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP LEISENRING, W (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA48061]; NIEHS NIH HHS [5T32ES07142] NR 16 TC 77 Z9 79 U1 0 U2 6 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0273-2300 J9 REGUL TOXICOL PHARM JI Regul. Toxicol. Pharmacol. PD APR PY 1992 VL 15 IS 2 BP 161 EP 171 DI 10.1016/0273-2300(92)90047-D PN 1 PG 11 WC Medicine, Legal; Pharmacology & Pharmacy; Toxicology SC Legal Medicine; Pharmacology & Pharmacy; Toxicology GA HT560 UT WOS:A1992HT56000005 PM 1626067 ER PT J AU WASIK, MA AF WASIK, MA TI PREFERENTIAL INTERACTION OF THE CD4+29+/45RA-SUBSET OF HUMAN CD4+ T LYMPHOCYTES WITH AN ANTIBODY AGAINST THE CELL-MEMBRANE GANGLIOSIDE GD3 SO SCANDINAVIAN JOURNAL OF IMMUNOLOGY LA English DT Article ID DIFFERENTIATION ANTIGENS HB-10; PHASE-I TRIAL; MONOCLONAL-ANTIBODY; INDUCER CELLS; EXPRESSION; ACTIVATION; RESPONSES; SUBSETS; SURFACE; HELPER AB This study shows that the two major subpopulations of CD4+ T lymphoyctes, defined on the basis of differential expression of the CD29 and CD45RA antigens, show significant differences in reactivity with a monoclonal antibody against the G(D3) ganglioside. Double staining studies showed that the G(D3) ganglioside is predominantly expressed on cells from the CD4+29+/45RA- subsets. The preferential interaction of the CD4+29+/45RA- cell subset with the anti-G(D3) MoAb was further confirmed by the proliferative and calcium-flux studies. Accordingly, the reciprocal, CD4+(29-)/45RA+ subset was unable to proliferate in response to the anti-G(D3) MoAb alone. Although it did show a significant mobilization of calcium ions and proliferation to IL-2 when stimulated with the anti-G(D3) MoAb, these responses were much less pronounced than the responses of the CD4+29+/45RA- subset. Finally, when two T-cell stimulating monokines, IL-1 and IL-6, were tested for the ability to modulate the anti-G(D3) Mediated proliferation, only the former, but not the latter was able to enhance the proliferation. Although the natural ligand for the G(D3) ganglioside remains unknown, the data presented here provide further evidence in support of the notion that the T-cell surface molecules different from the T-cell receptor MHC- antigen complex may contribute to the preferential activation of one of the CD4+ T lymphocyte subsets. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. NR 52 TC 12 Z9 12 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0300-9475 J9 SCAND J IMMUNOL JI Scand. J. Immunol. PD APR PY 1992 VL 35 IS 4 BP 421 EP 428 DI 10.1111/j.1365-3083.1992.tb02877.x PG 8 WC Immunology SC Immunology GA HJ788 UT WOS:A1992HJ78800006 PM 1373001 ER PT J AU KOUREMBANAS, S AF KOUREMBANAS, S TI HYPOXIC RESPONSES OF THE NEONATAL ENDOTHELIUM SO SEMINARS IN PERINATOLOGY LA English DT Review ID SMOOTH-MUSCLE; GROWTH-FACTOR; CELLS; RELEASE; MECHANISMS; EXPRESSION; THROMBIN C1 HARVARD UNIV,SCH MED,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV PEDIAT ONCOL,BOSTON,MA 02115. NR 27 TC 8 Z9 8 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0146-0005 J9 SEMIN PERINATOL JI Semin. Perinatol. PD APR PY 1992 VL 16 IS 2 BP 140 EP 146 PG 7 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA HN975 UT WOS:A1992HN97500008 PM 1636128 ER PT J AU ZHAO, LP LIPSITZ, S AF ZHAO, LP LIPSITZ, S TI DESIGNS AND ANALYSIS OF 2-STAGE STUDIES SO STATISTICS IN MEDICINE LA English DT Article ID LOGISTIC-REGRESSION; DISEASE; MODELS AB This paper concerns the design and analysis of two-stage studies, where, at the first stage, the response and the exposure variables are available among a large group of subjects. The other covariables, however, are available in only a subset of the large group, obtained in a second-stage sample. This paper introduces a class of twelve such two-stage designs, including two-stage case-control and case-cohort designs as special cases. In analysing such two-stage data, one objective is to extract information about the relationship between the exposure variable and the response after controlling for other covariables. We discuss three statistical methods to analyse the data and report results of Monte Carlo simulation to study the efficiency of the three methods. C1 UNIV HAWAII,SCH PUBL HLTH,BIOSTAT PROGRAM,HONOLULU,HI 96813. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. RP ZHAO, LP (reprint author), UNIV HAWAII,HAWAII CANC RES CTR,PROGRAM EPIDEMIOL,1236 LAUHALA ST,HONOLULU,HI 96813, USA. FU NCI NIH HHS [CA 23318, P01CA 33619]; NIGMS NIH HHS [GM 29745] NR 14 TC 98 Z9 98 U1 0 U2 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0277-6715 J9 STAT MED JI Stat. Med. PD APR PY 1992 VL 11 IS 6 BP 769 EP 782 DI 10.1002/sim.4780110608 PG 14 WC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Medicine, Research & Experimental; Statistics & Probability SC Mathematical & Computational Biology; Public, Environmental & Occupational Health; Medical Informatics; Research & Experimental Medicine; Mathematics GA HU098 UT WOS:A1992HU09800006 PM 1594816 ER PT J AU FAVA, M ROSENBAUM, JF MCCARTHY, M PAVA, JA STEINGARD, R FOX, R AF FAVA, M ROSENBAUM, JF MCCARTHY, M PAVA, JA STEINGARD, R FOX, R TI CORRELATIONS BETWEEN PERCEIVED STRESS AND DEPRESSIVE SYMPTOMS AMONG DEPRESSIVE OUTPATIENTS SO STRESS MEDICINE LA English DT Article DE PERCEIVED STRESS; DEPRESSION; FLUOXETINE; TREATMENT; CORRELATIONS AB Cognitive distortions associated with depression may amplify the sense of strain and pressure derived from everyday stressors. The Perceived Stress Scale (PSS), designed to assess the degree to which situations are perceived as stressful, was administered before and after open treatment with fluoxetine 20 mg/day for eight weeks to 60 consecutive outpatients with major depression (15 men and 45 women; mean age: 36.9 +/- 10.6 years) and to 22 normal controls (11 men and 11 women; mean age: 34.6 +/- 10.1 years). Pretreatment, the mean PSS score among the depressed patients was 38.8 +/- 6.4, which was significantly higher (z score: 6.33; p < 0.0001) than that (22:4 +/- 7.0) of the group of normal controls. After treatment with fluoxetine, the mean PSS score was 25.1 +/- 8.9, not different from controls but significantly different from baseline (paired t-test = 10.8; p < 0.0001). The correlation between PSS and Hamilton Rating Scale for Depression (HAM-D-17) scores was significant both before (r = 0.33; p < 0.02) and after (r = 0.62; p < 0.0001) treatment with fluoxetine. An even greater correlation was found between differences in pre- and posttreatment PSS scores and differences in pre- and posttreatment HAM-D-17 scores (r = 0.65; p < 0.0001). C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FAVA, M (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 16 TC 11 Z9 11 U1 1 U2 1 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0748-8386 J9 STRESS MEDICINE JI Stress Med. PD APR PY 1992 VL 8 IS 2 BP 73 EP 76 DI 10.1002/smi.2460080203 PG 4 WC Psychiatry; Psychology SC Psychiatry; Psychology GA HU067 UT WOS:A1992HU06700001 ER PT J AU KEARSE, LA BROWN, EN MCPECK, K AF KEARSE, LA BROWN, EN MCPECK, K TI SOMATOSENSORY EVOKED-POTENTIALS SENSITIVITY RELATIVE TO ELECTROENCEPHALOGRAPHY FOR CEREBRAL-ISCHEMIA DURING CAROTID ENDARTERECTOMY SO STROKE LA English DT Article DE CEREBRAL ISCHEMIA; ELECTROENCEPHALOGRAPHY; ENDARTERECTOMY; EVOKED POTENTIALS, SOMATOSENSORY ID BLOOD-FLOW; OCCLUSION; SURGERY; EEG AB Background and Purpose: The relation between electroencephalographic pattern changes and cerebral ischemia during carotid endarterectomy under general anesthesia is well established. Pattern changes seen on somatosensory evoked potentials under the same conditions are reported to be more sensitive indicators of cerebral ischemia. We estimated the sensitivity and specificity of somatosensory evoked potentials relative to electroencephalography for detecting cerebral ischemia during carotid endarterectomy under general anesthesia. Methods: We simultaneously monitored electroencephalographs and somatosensory evoked potentials in 53 carotid endarterectomies performed on 51 patients under general anesthesia, and we determined the extent to which somatosensory evoked potentials detected cerebral ischemia defined by electroencephalographic pattern changes at the time of carotid cross-clamp. Results: Twenty-three of the 53 cases studied had electroencephalographic evidence of ischemia following carotid cross-clamp. Ten of these 23 cases had an increased somatosensory evoked potential latency of 0.1 msec or greater (sensitivity 0.43). One of these 23 patients had a decrease in somatosensory evoked potential amplitude of 50% or greater (sensitivity 0.04). Of the 30 subjects who had no electroencephalographic evidence of ischemia, 13 had either no change or a decrease in somatosensory evoked potential latency (specificity 0.45). None of these 30 cases had a significant decrease in somatosensory evoked potential amplitude (specificity 1.0). If somatosensory evoked potential latencies were a sensitive method for detecting cerebral ischemia (true sensitivity of 0.95 or higher), the probability of only 10 subjects having somatosensory evoked potential latency increases would be less than 0.001. Therefore, our observed sensitivity cannot be attributed to chance. Conclusions: We conclude that measuring somatosensory evoked potentials is not a sensitive method for detecting cerebral ischemia during carotid endarterectomy. RP KEARSE, LA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 27 TC 39 Z9 41 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD APR PY 1992 VL 23 IS 4 BP 498 EP 505 PG 8 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA HN983 UT WOS:A1992HN98300005 PM 1561679 ER PT J AU CAMBRIA, RP IVARSSON, BL FALLON, JT ABBOTT, WM AF CAMBRIA, RP IVARSSON, BL FALLON, JT ABBOTT, WM TI HEPARIN FAILS TO SUPPRESS INTIMAL PROLIFERATION IN EXPERIMENTAL VEIN GRAFTS SO SURGERY LA English DT Article ID MUSCLE CELL-PROLIFERATION; ARTERIAL INJURY; INHIBITION; GROWTH; KINETICS; ENDOTHELIUM; EVOLUTION; ABSENCE; BYPASS; INVIVO AB Heparin has been shown to suppress both vascular smooth muscle cell proliferation in vitro and intimal hyperplasia in animal models of arterial injury. We investigated the effect of heparin on early postoperative smooth muscle cell proliferation and intimal thickening in vein grafts placed in the rat infrarenal aorta. Experimental animals (n = 6) received subcutaneous heparin (800 units/kg with levels monitored by activated factor X assay) every 12 hours for 3 days after surgery to coincide with the known period of maximal vascular wall DNA synthesis after injury. Control animals (n = 7) received identical vein grafts but no heparin. Grafts were harvested with perfusion fixation 14 days after insertion. Tritiated thymidine autoradiography was used to derive a mitotic index in regions of interest along the grafts, and computerized planimetric measurements of intimal and medial thickness were made in the same regions. Evans blue lumenal staining at harvesting revealed confluent endothelial coverage of both experimental and control grafts. The mitotic index of the vein graft's midsection and perianastomotic regions was significantly higher (p < 0.005) than that of the native aorta in all animals, indicating cellular proliferation within all grafts, with no differences noted between heparinzed and control animals. Similarly, both groups exhibited vein graft intimal and medial thickening at the anastomoses relative to the midsection of the vein graft (p < 0.001). Heparin, administered in the equivalent of pharmacologic clinical doses, failed to suppress cellular proliferation and intimal hyperplasia in this model of vein grafting. C1 MASSACHUSETTS GEN HOSP,PATHOL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP CAMBRIA, RP (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 20 TC 17 Z9 17 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0039-6060 J9 SURGERY JI Surgery PD APR PY 1992 VL 111 IS 4 BP 424 EP 429 PG 6 WC Surgery SC Surgery GA HM572 UT WOS:A1992HM57200011 PM 1557688 ER PT J AU BROWN, EN AF BROWN, EN TI THE OUTCOME OF CORONARY-ARTERY BYPASS-SURGERY AS PREDICTED BY DECISION-ANALYSIS - THE INFLUENCE OF AGE, DISEASE SEVERITY AND VENTRICULAR-FUNCTION - COMMENT SO THEORETICAL SURGERY LA English DT Note RP BROWN, EN (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0179-8669 J9 THEOR SURG JI Theor. Surg. PD APR PY 1992 VL 7 IS 2 BP 75 EP 75 PG 1 WC Surgery SC Surgery GA HN530 UT WOS:A1992HN53000005 ER PT J AU YUNIS, I SALAZAR, M ALOSCO, SM GOMEZ, N YUNIS, EJ AF YUNIS, I SALAZAR, M ALOSCO, SM GOMEZ, N YUNIS, EJ TI HLA-DQA1 AND MLC AMONG HLA (GENERIC)-IDENTICAL UNRELATED INDIVIDUALS SO TISSUE ANTIGENS LA English DT Article DE HLA-DQA1; MHC; MLC; PCR-RFLP; HLA ALLELE TYPING ID EXTENDED HAPLOTYPES; CLASS-II; DNA; RESPONSES; VARIANTS AB We modified a previously published PCR-RFLP for DQA1 typing (1) and examined the predictive value of HLA-DQA1 in mixed lymphocyte cultures (MLC) among matched (HLA generic types) pairs of unrelated individuals. There were 61/102 (60%) pairs with positive MLC, one-third of which could be predicted by DQA1* typing alone. DQA1 matching and MLC reactions were classified into 3 groups: 1) DQA1 mismatches showing positive MLC: 19/102 (19%);2) DQA1 matches showing negative MLC: 41/102 (40%); 3) DQA1 identical showing positive MLC: 42/102 (41%). Five different HLA haplotypes that result from non-random association of HLA generic types (high delta haplotypes) were overrepresented in the individuals tested. One of these haplotypes carrying HLA-B7, DR2 was found associated with three different DQA1 alleles (*0201, *0103, *0102). The remaining four high delta haplotypes were associated with one DQA 1 allele in all independent examples tested: HLA-A1, B8, DR3 with DQA1*0501; HLA-A26, B38, DR4 with DQA1*0301; HLA-A2, Bw62, DR4 with DQA1*0301 and HLA-A1, Bw57, DR7 with DQA1*0201. Forty per cent of the negative MLC were explained in part by the excessive number of individuals carrying two of these four haplotypes. which probably carry determinants in linkage disequilibrium with HLA. Nineteen per cent of HLA-identical (generic types) unrelated pairs show positive MLC reactions and all of them are DQA1* mismatched. suggesting that DQA1* allele typing should be used to screen samples prior to performing MLC. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. RP YUNIS, I (reprint author), AMER RED CROSS,DEDHAM,MA 02026, USA. FU NCI NIH HHS [CA20531] NR 18 TC 7 Z9 7 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD APR PY 1992 VL 39 IS 4 BP 182 EP 186 DI 10.1111/j.1399-0039.1992.tb01934.x PG 5 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA HR621 UT WOS:A1992HR62100003 PM 1356281 ER PT J AU SALAZAR, M YUNIS, I ALOSCO, SM CHOPEK, M YUNIS, EJ AF SALAZAR, M YUNIS, I ALOSCO, SM CHOPEK, M YUNIS, EJ TI HLA-DPB1 ALLELE MISMATCHES BETWEEN UNRELATED HLA-A,B,C,DR (GENERIC) DQA1-IDENTICAL UNRELATED INDIVIDUALS WITH UNREACTIVE MLC SO TISSUE ANTIGENS LA English DT Article DE HLA-DPB1; MHC; MLC; PCR-RFLP ID DP-BETA ALLELE; HLA-DP; CELIAC-DISEASE; DNA AB We have used a PCR-RFLP method with one generic amplification of HLA-DPB1 second exon and 6 endonucleases to differentiate the 19 HLA-DPB1 alleles and 171 heterozygous combinations. The set of primers used in our studies produced fragment sizes different from those published before (1). The HLA-DPB1 alleles in Caucasians showed a higher frequency of DPB1*0401 and DPB1*0402, when compared to a small group of Colombians who showed a higher frequency of DPB1*0402 and DPB1*0201. We found three HLA-DPB1 alleles associated with two HLA haplotypes that result from non-random association of alleles: DPB1*0401 with HLA-A26. B38, DR4, DQA1*0301 and DPB1*0101 and DPB1*0401 with HLA-A1. B8, DR3, DQA1*0501. We also report that 70% of combinations between HLA (generic A,B,C,DR) and DQA1-identical MLC-unreactive cell mixtures showed HLA-DPB1 mismatches. suggesting that HLA-DPB1 differences are not important in MLC reactivity. C1 AMER RED CROSS,DEDHAM,MA. RP SALAZAR, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA20531]; NHLBI NIH HHS [HL-29583] NR 18 TC 13 Z9 13 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0001-2815 J9 TISSUE ANTIGENS JI Tissue Antigens PD APR PY 1992 VL 39 IS 4 BP 203 EP 208 DI 10.1111/j.1399-0039.1992.tb01936.x PG 6 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA HR621 UT WOS:A1992HR62100005 PM 1356283 ER PT J AU EMERY, DW SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C AF EMERY, DW SHAFER, GE KARSON, EM SACHS, DH LEGUERN, C TI EXPRESSION OF ALLOGENEIC CLASS-II CDNA IN SWINE BONE-MARROW CELLS TRANSDUCED WITH A RECOMBINANT RETROVIRUS SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL CONGRESS ON XENOTRANSPLANTATION CY AUG 25-28, 1991 CL MINNEAPOLIS, MN SP UNIV MINNESOTA, DEPT SURG C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,BETHESDA,MD 20892. NHLBI,BETHESDA,MD 20892. NR 7 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1992 VL 24 IS 2 BP 468 EP 469 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HN857 UT WOS:A1992HN85700018 PM 1566392 ER PT J AU SYKES, M SACHS, DH AKSENTIJEVICH, I AF SYKES, M SACHS, DH AKSENTIJEVICH, I TI EFFECT OF NATURAL ANTIBODY ON XENOGENEIC BONE-MARROW ENGRAFTMENT SO TRANSPLANTATION PROCEEDINGS LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL CONGRESS ON XENOTRANSPLANTATION CY AUG 25-28, 1991 CL MINNEAPOLIS, MN SP UNIV MINNESOTA, DEPT SURG ID MOUSE C1 NCI,IMMUNOL BRANCH,BETHESDA,MD 20892. RP SYKES, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SURG SERV,TRANSPLANTAT BIOL RES CTR,MGH-E,BLDG 149,BOSTON,MA 02129, USA. NR 8 TC 3 Z9 3 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0041-1345 J9 TRANSPLANT P JI Transplant. Proc. PD APR PY 1992 VL 24 IS 2 BP 497 EP 498 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HN857 UT WOS:A1992HN85700032 PM 1566403 ER PT J AU POLVINOBODNAR, M SCHAFFER, PA AF POLVINOBODNAR, M SCHAFFER, PA TI DNA-BINDING ACTIVITY IS REQUIRED FOR EBNA 1-DEPENDENT TRANSCRIPTIONAL ACTIVATION AND DNA-REPLICATION SO VIROLOGY LA English DT Article ID EPSTEIN-BARR VIRUS; BAMHI-K-FRAGMENT; NUCLEAR ANTIGEN; MAMMALIAN-CELLS; STABLE REPLICATION; PLASMIDS; PROTEINS; SEQUENCES; PROMOTER; ENHANCER C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. RP POLVINOBODNAR, M (reprint author), NORTHEASTERN UNIV,DEPT BIOL,BOSTON,MA 02115, USA. FU NCI NIH HHS [5R37CA20260] NR 31 TC 26 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0042-6822 J9 VIROLOGY JI Virology PD APR PY 1992 VL 187 IS 2 BP 591 EP 603 DI 10.1016/0042-6822(92)90461-W PG 13 WC Virology SC Virology GA HH591 UT WOS:A1992HH59100022 PM 1312270 ER PT J AU STARK, DD AF STARK, DD TI CLINICAL INDICATIONS FOR MRI SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article RP STARK, DD (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 SN 0077-8923 J9 ANN NY ACAD SCI JI Ann. N.Y. Acad. Sci. PD MAR 31 PY 1992 VL 649 BP 332 EP 334 DI 10.1111/j.1749-6632.1992.tb49621.x PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM217 UT WOS:A1992JM21700026 PM 1580504 ER PT J AU DERESIEWICZ, RL CALDERWOOD, SB ROBERTUS, JD COLLIER, RJ AF DERESIEWICZ, RL CALDERWOOD, SB ROBERTUS, JD COLLIER, RJ TI MUTATIONS AFFECTING THE ACTIVITY OF THE SHIGA-LIKE TOXIN-I A-CHAIN SO BIOCHEMISTRY LA English DT Article ID N-GLYCOSIDASE ACTIVITY; ESCHERICHIA-COLI; EUKARYOTIC RIBOSOMES; ENZYMATIC INACTIVATION; GLUTAMIC ACID-177; RICIN; SITE; VEROTOXIN; MECHANISM; SEQUENCE AB Like ricin, Escherichia coli Shiga-like toxin I (SLT-I) inactivates eukaryotic ribosomes by catalytically depurinating adenosine 4324 in 28S rRNA. Although the primary structure of the enzymatic portion of the molecule (Slt-IA) is known to contain regions of significant homology to the ricin A chain (RTA), and although certain residues have been implicated in catalysis, the crystal structure of Slt-IA has not been solved nor has the geometry of its active site been well defined. In order to derive a more complete understanding of the nature of the Slt-IA active site, we placed the slt-IA gene under control of an inducible promoter in Saccharomyces cerevisiae. Induction of the cloned element was lethal to the host. This lethality was the basis for selection of an attenuated mutant of Slt-IA changed at tyrosine 77, a locus not previously linked to the active site. As well, it permitted evaluation of the toxicity of a number of mutant Slt-IA cassettes that we constructed in vitro. Putative active-site residues implicated in this fashion and in other studies were mapped to an energy-minimized computer model of Slt-IA that had been generated on the basis of the known crystal structure of RTA. A cleft was identified on one face of the protein in which all implicated residues clustered, irrespective of their distances from one another in the primary structure of the molecule. Many of the chemical features anticipated in the active site of an RNA N-glycosidase are indeed present on the amino acid side chains occupying the cleft. C1 HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. SHIPLEY INST MED,BOSTON,MA 02115. UNIV TEXAS,DEPT CHEM,AUSTIN,TX 78712. BRIGHAM & WOMENS HOSP,DIV INFECT DIS,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. OI Collier, R John/0000-0002-2427-4239 FU NIAID NIH HHS [AI27329, AI22848, AI22021] NR 25 TC 35 Z9 36 U1 0 U2 2 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD MAR 31 PY 1992 VL 31 IS 12 BP 3272 EP 3280 DI 10.1021/bi00127a032 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HL679 UT WOS:A1992HL67900032 PM 1554712 ER PT J AU BERGELSON, JM SHEPLEY, MP CHAN, BMC HEMLER, ME FINBERG, RW AF BERGELSON, JM SHEPLEY, MP CHAN, BMC HEMLER, ME FINBERG, RW TI IDENTIFICATION OF THE INTEGRIN VLA-2 AS A RECEPTOR FOR ECHOVIRUS-1 SO SCIENCE LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; RHINOVIRUS RECEPTOR; COLLAGEN RECEPTOR; CELLULAR RECEPTOR; LAMININ RECEPTOR; HELA-CELLS; T-CELLS; POLIOVIRUS; PROTEIN; FIBRONECTIN AB Cell surface receptors for echovirus, a common human pathogen, were identified with monoclonal antibodies that protected susceptible cells from infection with echovirus 1. These monoclonal antibodies, which prevented virus attachment to specific receptor sites, recognized the alpha and beta-subunits of the integrin VLA-2 (alpha-2-beta-1), a receptor for collagen and laminin. RD rhabdomyosarcoma cells expressed little VLA-2, did not bind to S-35-labeled virus, and resisted infection until transfected with complementary DNA encoding the alpha-2 subunit of VLA-2. Thus, integrins, adhesion receptors important in interactions between cells and with the extracellular matrix, can mediate virus attachment and infection. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP BERGELSON, JM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI 20382]; NIGMS NIH HHS [GM 38903] NR 38 TC 227 Z9 230 U1 0 U2 4 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD MAR 27 PY 1992 VL 255 IS 5052 BP 1718 EP 1720 DI 10.1126/science.1553561 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HK812 UT WOS:A1992HK81200043 PM 1553561 ER PT J AU SURMAN, OS AF SURMAN, OS TI THE LAW, PUBLIC-POLICY, AND THE PEDDLERS OF TOBACCO SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP SURMAN, OS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAR 25 PY 1992 VL 267 IS 12 BP 1613 EP 1614 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HJ597 UT WOS:A1992HJ59700024 PM 1542168 ER PT J AU ASSARAF, YG FEDER, JN SHARMA, RC WRIGHT, JE ROSOWSKY, A SHANE, B SCHIMKE, RT AF ASSARAF, YG FEDER, JN SHARMA, RC WRIGHT, JE ROSOWSKY, A SHANE, B SCHIMKE, RT TI CHARACTERIZATION OF THE COEXISTING MULTIPLE MECHANISMS OF METHOTREXATE RESISTANCE IN MOUSE 3T6-R50 FIBROBLASTS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID DIHYDROFOLATE-REDUCTASE GENES; SQUAMOUS-CELL CARCINOMA; HAMSTER OVARY CELLS; FLOW-CYTOMETRY; MESSENGER-RNA; AMPLIFICATION; TRIMETREXATE; TRANSPORT; LINE; HEAD AB We have studied the discrepancy in the degree of methotrexate (MTX) resistance that exists between two clonal cell lines, mouse 3T6 R50 cells and Chinese hamster ovary B11 0.5 cells that overexpress comparable levels of dihydrofolate reductase, yet exhibit a 100-fold difference in MTX resistance while maintaining similar sensitivity to the lipophilic antifolates trimetrexate and piritrexim. These data suggested that R50 cells may possess additional mechanism(s) of antifolate resistance, such as MTX transport alteration. Flow cytometric analysis using fluorescein methotrexate revealed comparable levels of fluorescein MTX displacement with lipophilic antifolates in viable R50 and B11 0.5 cells, but marked insensitivity of R50 cells to MTX competition, thus suggesting a poor uptake of MTX into R50 cells. Analysis of the kinetic parameters of dihydrofolate reductase from R50 cells neither showed alterations in enzyme affinities for various antifolates nor in the Michaelis constant for folic acid and NADPH nor a change in the pH activity optimum. R50 cell-free extracts contained wild-type levels of folylpoly-gamma-glutamyl synthetase activity. However, following metabolic labeling with [H-3]MTX, no MTX polyglutamates could be detected in R50 cells. We conclude that the high level of MTX resistance in R50 cells is multifactorial, including overexpression of dihydrofolate reductase, reduced MTX transport, and possibly altered formation of MTX polyglutamates. The potential interactions between the different modalities of MTX resistance in R50 cells are being discussed. C1 UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,DEPT PHYSIOL & BIOCHEM,SAN FRANCISCO,CA 94143. STANFORD UNIV,DEPT BIOL SCI,STANFORD,CA 94305. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV CALIF BERKELEY,DEPT NUTR SCI,BERKELEY,CA 94720. RP ASSARAF, YG (reprint author), TECHNION ISRAEL INST TECHNOL,DEPT BIOL,IL-32000 HAIFA,ISRAEL. FU NCI NIH HHS [CA19589, CA16318, CA41991] NR 42 TC 17 Z9 17 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 25 PY 1992 VL 267 IS 9 BP 5776 EP 5784 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800012 PM 1372892 ER PT J AU DISTEL, RJ ROBINSON, GS SPIEGELMAN, BM AF DISTEL, RJ ROBINSON, GS SPIEGELMAN, BM TI FATTY-ACID REGULATION OF GENE-EXPRESSION - TRANSCRIPTIONAL AND POSTTRANSCRIPTIONAL MECHANISMS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MESSENGER-RNAS; BINDING-PROTEIN; ADIPOCYTE DIFFERENTIATION; 3T3-L1 PREADIPOCYTES; SODIUM-BUTYRATE; C-FOS; 3T3-ADIPOCYTES; COMPLEXES; ENHANCER; INSULIN AB Fatty acids are important metabolic substrates and may also be involved in pathological syndromes such as the insulin resistance of diabetes and obesity. We demonstrate here that fatty acids can regulate specific gene expression; mRNAs encoding the fatty acid binding protein adipocyte P2 (aP2) and the Fos-related transcription factor Fra1 are specifically induced at least 20-fold upon treatment of preadipocytes with oleate. For aP2, the effect requires long chain fatty acids and occurs without a generalized activation of the genes linked to adipocyte differentiation. Other fibroblastic cells without preadipocyte characteristics do not induce aP2 mRNA in response to fatty acids. Unlike aP2, Fra1 induction by fatty acids also can be detected in NIH 3T3 and 3T3-C2 fibroblasts. Nuclear transcription assays in 3T3-F442A preadipocytes demonstrate that fatty acids elicit no transcriptional increase in the aP2 gene. Fra1, on the other hand, shows a 3-4-fold increase in transcription. These results demonstrate at least two distinct mechanisms by which fatty acids may influence gene expression. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MAYER 813,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK31405]; NIGMS NIH HHS [GM13033] NR 25 TC 172 Z9 176 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 25 PY 1992 VL 267 IS 9 BP 5937 EP 5941 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800037 PM 1372897 ER PT J AU GOLDMAN, SJ UNIYAL, S FERGUSON, LM GOLAN, DE BURAKOFF, SJ KIENER, PA AF GOLDMAN, SJ UNIYAL, S FERGUSON, LM GOLAN, DE BURAKOFF, SJ KIENER, PA TI DIFFERENTIAL ACTIVATION OF PHOSPHOTYROSINE PROTEIN PHOSPHATASE-ACTIVITY IN A MURINE T-CELL HYBRIDOMA BY MONOCLONAL-ANTIBODIES TO CD45 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; HUMAN B-CELLS; TYROSINE PHOSPHATASE; SIGNAL TRANSDUCTION; RECEPTOR ANTIBODIES; KINASE-ACTIVITY; IL-2 RECEPTOR; PHOSPHORYLATION; ASSOCIATION; PROLIFERATION AB The effect of two anti-CD45 (T200, LCA, Ly5) antibodies on the activation of the murine T-cell hybridoma 13.13 has been evaluated. These studies have been carried out in a system that did not require cross-linking or coclustering of antibodies. Activation of 13.13 cells with the anti-CD3 monoclonal antibody, 145.2C11, gave rise to rapid increases in intracellular calcium and interleukin-2 production. Additionally, within 1 min, phosphorylation on tyrosine of four major proteins of about 130,000, 110,000, 80,000, and 37,000 daltons could be seen. Pretreatment of the cells with the anti-CD45 mAb M1/89.18.7.HK markedly inhibited all three biological responses, while an alternate anti-CD45 antibody, M1/9.3.4.HL.2, had little effect. The two antibodies bound to CD45 with similar affinities, and no differences in the lateral mobility of antibody-CD45 complexes in the cell membrane were observed. The inhibition of activation of the cells by M1/89.18.7.HK was abrogated significantly both by the phosphotyrosine protein phosphatase inhibitor orthovanadate and by excess M1/9.3.4.HL.2. If M1/89.18.7.HK was added to the 13.13 cells after they had already been activated with anti-CD3, it very effectively stimulated dephosphorylation of substrates that had been phosphorylated on tyrosines prior to adding the anti-CD45 antibody. These results indicate that the phosphotyrosine protein phosphatase activity of CD45 is critical to its biological function and that bivalent (i.e. uncross-linked) anti-CD45 antibodies can give rise to markedly different responses. One of the antibodies, M1/89.18.7.HK, appears to behave much like a receptor ligand and is able to activate the enzymatic activity associated with the CD45 transmembrane protein. C1 BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,DEPT IMMUNOL 205,5 RES PKWY,WALLINGFORD,CT 06492. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-39542]; NHLBI NIH HHS [HL-32854]; NIAID NIH HHS [AI-17258] NR 31 TC 38 Z9 38 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 25 PY 1992 VL 267 IS 9 BP 6197 EP 6204 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HK318 UT WOS:A1992HK31800073 PM 1532579 ER PT J AU FREESE, A FINKLESTEIN, SP DIFIGLIA, M AF FREESE, A FINKLESTEIN, SP DIFIGLIA, M TI BASIC FIBROBLAST GROWTH-FACTOR PROTECTS STRIATAL NEURONS INVITRO FROM NMDA-RECEPTOR MEDIATED EXCITOTOXICITY SO BRAIN RESEARCH LA English DT Note DE FIBROBLAST GROWTH FACTOR; NEUROTOXICITY; QUINOLINIC ACID; KAINIC ACID; GLUTAMATE ID HIPPOCAMPAL-NEURONS; DEGENERATION; GLUTAMATE; SEQUENCE; CULTURES; SURVIVAL; INJURY; SYSTEM; FGF AB Basic fibroblast growth factor (bFGF) promotes the survival and outgrowth of neurons. In this study the neuroprotective effects of bFGF were examined in 12-18-day-old cultured striatal neurons exposed to glutamic acid, kainic acid (KA), and quinolinic acid (QA), an N-methyl-D-aspartate (NMDA)-receptor agonist. Results showed that preincubation with bFGF (6 pM) from the day of plating significantly increased the survival of striatal neurons treated for 3 h with glutamate (3 mM) or QA (1 mM), but had little effect on KA (1 mM) induced toxicity. Moreover, maximum protection by bFGF against glutamate neurotoxicity was observed in cultures treated as little as 2 h before glutamate exposure. These results show that bFGF markedly protects striatal neurons from NMDA-receptor induced neurotoxicity. C1 MASSACHUSETTS GEN HOSP E,CELLULAR NEUROBIOL LAB,149 E 13 ST,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,DEPT NEUROL,CENT NERVOUS SYST GROWTH FACTOR RES LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIA NIH HHS [AG 08207]; NINDS NIH HHS [NS 10828, NS16367] NR 25 TC 145 Z9 145 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 20 PY 1992 VL 575 IS 2 BP 351 EP 355 DI 10.1016/0006-8993(92)90104-H PG 5 WC Neurosciences SC Neurosciences & Neurology GA HM252 UT WOS:A1992HM25200027 PM 1349256 ER PT J AU MUNRO, S BAST, BJEG COLLEY, KJ TEDDER, TF AF MUNRO, S BAST, BJEG COLLEY, KJ TEDDER, TF TI THE LYMPHOCYTE-B SURFACE-ANTIGEN CD75 IS NOT AN ALPHA-2,6-SIALYLTRANSFERASE BUT IS A CARBOHYDRATE ANTIGEN, THE PRODUCTION OF WHICH REQUIRES THE ENZYME SO CELL LA English DT Letter ID MONOCLONAL-ANTIBODIES; LOCALIZATION C1 ACAD ZIEKENHUIS UTRECHT,3508 GA UTRECHT,NETHERLANDS. UNIV ILLINOIS,COLL MED,DEPT BIOCHEM,CHICAGO,IL 60612. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP MUNRO, S (reprint author), MRC,MOLEC BIOL LAB,CAMBRIDGE CB2 2QH,ENGLAND. NR 9 TC 24 Z9 24 U1 1 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 20 PY 1992 VL 68 IS 6 BP 1003 EP 1004 DI 10.1016/0092-8674(92)90070-S PG 2 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK674 UT WOS:A1992HK67400003 PM 1547499 ER PT J AU WOOD, KW SARNECKI, C ROBERTS, TM BLENIS, J AF WOOD, KW SARNECKI, C ROBERTS, TM BLENIS, J TI RAS MEDIATES NERVE GROWTH-FACTOR RECEPTOR MODULATION OF 3 SIGNAL-TRANSDUCING PROTEIN-KINASES - MAP KINASE, RAF-1, AND RSK SO CELL LA English DT Article ID CELL-PROLIFERATION; ONCOGENE PRODUCTS; PC12 CELLS; PHOSPHORYLATION; REQUIREMENT; ACTIVATION; TYROSINE; DIFFERENTIATION; STIMULATION; INHIBITION AB p21c-ras plays a critical role in mediating tyrosine kinase-stimulated cell growth and differentiation. However, the pathways through which p21c-ras propagates these signals remain unknown. We report that in PC12 cells, expression of a dominant inhibitory mutant of ras, c-Ha-ras(Asn-17), antagonizes growth factor- and phorbol ester-induced activation of the erk-encoded family of MAP kinases, the 85-92 kd RSKs, and the kinase(s) responsible for hyperphosphorylation of the proto-oncogene product Raf-1. In addition, we find that expression of the activated ras oncogene is sufficient to stimulate these events. These data indicate that ras mediates nerve growth factor receptor and protein kinase C modulation of MAP kinases, RSKs, and Raf-1. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. RP WOOD, KW (reprint author), HARVARD UNIV,DIV MED SCI,PROGRAM CELL & DEV BIOL,CAMBRIDGE,MA 02138, USA. FU NCI NIH HHS [CA50661, CA43803]; NICHD NIH HHS [HD24926] NR 55 TC 877 Z9 880 U1 0 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 20 PY 1992 VL 68 IS 6 BP 1041 EP 1050 DI 10.1016/0092-8674(92)90076-O PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK674 UT WOS:A1992HK67400008 PM 1312393 ER PT J AU CHAN, BM KASSNER, PD SCHIRO, JA BYERS, HR KUPPER, TS HEMLER, ME AF CHAN, BM KASSNER, PD SCHIRO, JA BYERS, HR KUPPER, TS HEMLER, ME TI DISTINCT CELLULAR FUNCTIONS MEDIATED BY DIFFERENT VLA INTEGRIN ALPHA-SUBUNIT CYTOPLASMIC DOMAINS SO CELL LA English DT Article ID EXTRACELLULAR-MATRIX COMPONENTS; HUMAN-MELANOMA CELLS; FIBRONECTIN RECEPTOR; T-CELLS; MONOCLONAL-ANTIBODY; GENE-EXPRESSION; SIGNAL TRANSDUCTION; ADHESION MOLECULES; COLLAGEN RECEPTOR; LAMININ RECEPTOR AB To characterize VLA alpha-subunit cytoplasmic domain functions, unaltered alpha-2 cDNA (called X2C2) and two chimeric cDNAs (called X2C5 and X2C4) were constructed with extracellular alpha-2 domains and cytoplasmic alpha-2, alpha-5, and alpha-4 domains respectively. Upon transfection into rhabdomyosarcoma (RD) cells, each construct yielded comparable expression levels, immunoprecipitation profiles, and avidity for collagen and laminin. However, while RDX2C2 and RDX2C5 transfectants mediated collagen gel contraction, RDX2C4 and a mock transfectant (RDpF) did not. Conversely, only RDX2C4 cells (but not RDX2C2 or RDX2C5) showed enhanced cell migration on collagen and laminin compared with RDpF cells. This indicates markedly differing roles for integrin alpha-subunit cytoplasmic domains in post-ligand binding events. Furthermore, stable exertion of physical force (collagen gel contraction) may involve fundamentally different cellular machinery than the transient adhesion occurring during cell migration. Finally, these findings provide insight into a functional flexibility perhaps resulting from multiple integrins binding to identical ligands. C1 WASHINGTON UNIV,SCH MED,DIV DERMATOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02129. RP CHAN, BM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115, USA. FU NIAMS NIH HHS [AR40124]; NIGMS NIH HHS [GM38903, GM46526] NR 99 TC 303 Z9 303 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 20 PY 1992 VL 68 IS 6 BP 1051 EP 1060 DI 10.1016/0092-8674(92)90077-P PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HK674 UT WOS:A1992HK67400009 PM 1547502 ER PT J AU ZERVAS, NT CHIAPPA, KH HEDLEYWHYTE, ET GREENBERG, SM HOCHBERG, FH ADAMS, RD PILESPELLMAN, J AF ZERVAS, NT CHIAPPA, KH HEDLEYWHYTE, ET GREENBERG, SM HOCHBERG, FH ADAMS, RD PILESPELLMAN, J TI A 64-YEAR-OLD WOMAN WITH THE ABRUPT ONSET OF PARAPARESIS AFTER 10 MONTHS OF INCREASING EPISODIC LEG WEAKNESS - ARTERIOVENOUS-FISTULA OF SPINAL DURA (TYPE-1) (FOIX-ALAJOUANINE SYNDROME) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID MALFORMATIONS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ZERVAS, NT (reprint author), MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114, USA. NR 11 TC 5 Z9 5 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 19 PY 1992 VL 326 IS 12 BP 816 EP 824 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HJ592 UT WOS:A1992HJ59200008 ER PT J AU DENNY, T YOGEV, R GELMAN, R SKUZA, C OLESKE, J CHADWICK, E CHENG, SC CONNOR, E AF DENNY, T YOGEV, R GELMAN, R SKUZA, C OLESKE, J CHADWICK, E CHENG, SC CONNOR, E TI LYMPHOCYTE SUBSETS IN HEALTHY-CHILDREN DURING THE 1ST 5 YEARS OF LIFE SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID IMMUNODEFICIENCY-VIRUS TYPE-1; CONTROLLED TRIAL; CELL SUBSETS; INFECTION; ZIDOVUDINE AB Objective. - To assess whether relative and absolute values of CD4 and CD8 lymphocytes and CD4/CD8 ratio change in relation to age, and to estimate the fifth and 95th percentiles for these values in children of various ages. Patients and Methods. - Phenotypic analysis of lymphocyte subsets was performed on blood samples from 208 healthy children, aged 1 through 59 months, using standard flow cytometric techniques. Results. - Regression analysis demonstrated that CD4 and CD8 lymphocyte counts declined significantly with advancing age (P < .000001 and P = .03, respectively). Since CD4 and CD8 counts depend on total lymphocyte count, the percentage of total lymphocytes of each phenotype was also analyzed and demonstrated that the CD4 percentage was highly age dependent (P < .000001). The CD8 percentage increased with age (P = .0001) but not as much as the CD4 percentage decreased. Median CD4 counts (fifth and 95th percentiles) for children 2 through 3, 4 through 8, 12 through 23, and 24 through 59 months of age were 2.83 (1.46 to 5.11), 2.95 (1.69 to 4.61), 2.07 (1.02 to 3.60), and 1.80 (0.90 to 2.86) x 10(9)/L, respectively. Conclusion. - Healthy children's CD4 lymphocyte counts are considerably higher than previously established adult values. These data demonstrate that age is an important consideration in interpretation of lymphocyte subsets in children. This may be especially relevant in children who are infected with the human immunodeficiency virus, where CD4 lymphocyte values play a central role in monitoring disease progression and determining thresholds for medical interventions. C1 UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,DEPT PEDIAT,185 S ORANGE AVE,NEWARK,NJ 07103. CHILDRENS HOSP NEW JERSEY,NEWARK,NJ. UNIV MED & DENT NEW JERSEY,NEW JERSEY MED SCH,AIDS CLIN TRIALS UNIT,NEWARK,NJ 07103. NORTHWESTERN UNIV,CHILDRENS MEM HOSP,SCH MED,DEPT PEDIAT,CHICAGO,IL 60614. NORTHWESTERN UNIV,CHILDRENS MEM HOSP,SCH MED,AIDS CLIN TRIALS UNIT,CHICAGO,IL 60614. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. RI Brugnara, Carlo/A-8041-2010; OI Brugnara, Carlo/0000-0001-8192-8713; Denny, Thomas/0000-0002-7364-8276 FU NIAID NIH HHS [1UO1-AI25883, 5UO1-AI27559, N01-AI-95030] NR 25 TC 180 Z9 182 U1 0 U2 2 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 18 PY 1992 VL 267 IS 11 BP 1484 EP 1488 DI 10.1001/jama.267.11.1484 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HH488 UT WOS:A1992HH48800028 PM 1347086 ER PT J AU LIPTON, SA LEIFER, D BARNSTABLE, CJ AF LIPTON, SA LEIFER, D BARNSTABLE, CJ TI SELECTIVITY OF THY-1 MONOCLONAL-ANTIBODIES IN ENHANCING NEURITE OUTGROWTH SO NEUROSCIENCE LETTERS LA English DT Article DE IMMUNOGLOBULIN-LIKE DOMAIN; RODENT RETINAL GANGLION CELL; THY-1 GLYCOPROTEIN; ACTIVE SITE; CENTRAL NERVOUS SYSTEM; CELL CULTURE; AXONAL DENDRITIC REGENERATION ID RETINAL GANGLION-CELLS; ADHESION MOLECULES; NERVOUS-SYSTEM; GLYCOPROTEIN; SURFACE; IMMUNOGLOBULIN; REGENERATION; CULTURE; SURVIVAL; NEURON AB Thy-1 monoclonal antibodies (MAbs) have previously been shown to promote neurite outgrowth from retinal ganglion cells and a variety of other neurons. We have studied the effect on neurite outgrowth of several Thy-1 MAbs with quantitatively similar binding properties and found that only certain Thy-1 MAbs promote neurite outgrowth. This finding suggests that the antibody effects depend on specific interactions with one or more active sites on the Thy-1 glycoprotein. C1 CHILDRENS HOSP MED CTR,DEPT NEUROL,ENDERS BLDG,ROOM 350,300 LONGWOOD AVE,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT NEUROL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. YALE UNIV,SCH MED,DEPT OPHTHALMOL & VISUAL SCI,NEW HAVEN,CT 06510. OI Barnstable, Colin/0000-0002-7011-4068 FU NEI NIH HHS [EY05206, EY06087]; NICHD NIH HHS [CHD00888] NR 24 TC 12 Z9 13 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAR 16 PY 1992 VL 137 IS 1 BP 75 EP 77 DI 10.1016/0304-3940(92)90302-N PG 3 WC Neurosciences SC Neurosciences & Neurology GA HL202 UT WOS:A1992HL20200019 PM 1352632 ER PT J AU MAHONEY, JF URAKAZE, M HALL, S DEGASPERI, R CHANG, HM SUGIYAMA, E WARREN, CD BOROWITZ, M NICHOLSONWELLER, A ROSSE, WF YEH, ETH AF MAHONEY, JF URAKAZE, M HALL, S DEGASPERI, R CHANG, HM SUGIYAMA, E WARREN, CD BOROWITZ, M NICHOLSONWELLER, A ROSSE, WF YEH, ETH TI DEFECTIVE GLYCOSYLPHOSPHATIDYLINOSITOL ANCHOR SYNTHESIS IN PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA GRANULOCYTES SO BLOOD LA English DT Note ID DECAY-ACCELERATING FACTOR; VARIANT SURFACE GLYCOPROTEIN; THY-1 GLYCOPROTEIN; BIOSYNTHESIS; CELLS; GENE; TRANSCRIPTION; PROTEINS; MUTANTS C1 DUKE UNIV,MED CTR,DEPT MED,DIV HEMATOL ONCOL,BOX 3934,DURHAM,NC 27710. DUKE UNIV,DEPT PATHOL,DURHAM,NC 27706. MASSACHUSETTS GEN HOSP,DEPT MED,PAIN CONTROL UNIT,ARTHRIT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,DEPT MED,HARVARD THORNDIKE LAB,BOSTON,MA 02215. FU NHLBI NIH HHS [5T32 HL07057]; NIAMS NIH HHS [P01 AR-03564]; NIDDK NIH HHS [55 R36 DK31379] NR 21 TC 75 Z9 75 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1992 VL 79 IS 6 BP 1400 EP 1403 PG 4 WC Hematology SC Hematology GA HH745 UT WOS:A1992HH74500003 PM 1372185 ER PT J AU MAZIARZ, RT ARCECI, RJ BERNSTEIN, SC FRAZIER, L SMITH, BR KASAI, M TANTRAVAHI, R STROMINGER, JL AF MAZIARZ, RT ARCECI, RJ BERNSTEIN, SC FRAZIER, L SMITH, BR KASAI, M TANTRAVAHI, R STROMINGER, JL TI A GAMMA-DELTA+ T-CELL LEUKEMIA BEARING A NOVEL-T(8-14)(Q24-Q11) TRANSLOCATION DEMONSTRATES SPONTANEOUS INVITRO NATURAL KILLER-LIKE ACTIVITY SO BLOOD LA English DT Article ID ACUTE LYMPHOBLASTIC-LEUKEMIA; ALPHA-CHAIN LOCUS; ACUTE LYMPHOCYTIC-LEUKEMIA; C-MYC ONCOGENE; CHROMOSOMAL TRANSLOCATION; B-CELL; ANTIGEN RECEPTOR; MONOCLONAL-ANTIBODY; MOLECULAR-CLONING; FUSION TRANSCRIPT C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV PEDIAT HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV CYTOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,DEPT BIOCHEM & MOLEC BIOL,CAMBRIDGE,MA 02138. FU NCI NIH HHS [CA45574]; NIGMS NIH HHS [GM38156] NR 67 TC 13 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD MAR 15 PY 1992 VL 79 IS 6 BP 1523 EP 1531 PG 9 WC Hematology SC Hematology GA HH745 UT WOS:A1992HH74500020 PM 1532137 ER PT J AU HASS, R GUNJI, H DATTA, R KHARBANDA, S HARTMANN, A WEICHSELBAUM, R KUFE, D AF HASS, R GUNJI, H DATTA, R KHARBANDA, S HARTMANN, A WEICHSELBAUM, R KUFE, D TI DIFFERENTIATION AND RETRODIFFERENTIATION OF HUMAN MYELOID-LEUKEMIA CELLS IS ASSOCIATED WITH REVERSIBLE INDUCTION OF CELL CYCLE-REGULATORY GENES SO CANCER RESEARCH LA English DT Article ID HUMAN MONOCYTIC DIFFERENTIATION; HUMAN MONONUCLEAR PHAGOCYTES; PROTEIN-KINASE; FISSION YEAST; MESSENGER-RNA; M-PHASE; TYROSINE PHOSPHORYLATION; DNA-REPLICATION; PHORBOL ESTER; HUMAN HOMOLOG AB Treatment of human myeloid leukemia cells (HL-60, U-937, THP-1) with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) is associated with differentiation along the monocytic lineage. This induction by TPA is characterized in part by growth arrest and the appearance of differentiated monocytic phenotype. The present studies demonstrate that myeloid leukemia cells exit the cell cycle to G0-G1 between 24 and 36 h following TPA treatment. This G0-G1 arrest was accompanied by down-regulation of the cell cycle-regulatory genes cdc2, cyclin A, cyclin B, and cdc25. Similar findings were obtained for histones H1 and H4. Cell cycle progression of synchronized U-937 cells revealed low to undetectable mRNA levels for these genes in G1 and maximal transcription in G2-M phase. Results obtained from mRNA half-life studies demonstrate that the stability of cdc2, cyclin A, cyclin B, and cdc25 transcripts is similar in control and TPA-treated U-937 cells. Nuclear run-on assays demonstrated down-regulation of histone gene transcription, while there was no signal detectable for the cell cycle-regulatory genes. The present findings also demonstrate that long term culture of TPA-differentiated U-937 cells is associated with a decrease in G0-G1-arrested cells and an increase of cells in S and G2-M after 25 days. This reentry into the cell cycle was accompanied by loss of adherence, down-regulation of markers for the monocytic phenotype, and induction of the cell cycle-regulatory genes. This process of retrodifferentiation was completed after 36 days when patterns of cell cycle-regulatory and histone gene expression were identical to that in untreated U-937 cells. C1 DEUTSCH KREBSFORSCHUNGSZENTRUM,VIROL ABT,W-6900 HEIDELBERG,GERMANY. UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. UNIV CHICAGO,DEPT RADIAT & CELLULAR ONCOL,CHICAGO,IL 60637. RP HASS, R (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115, USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 FU NCI NIH HHS [CA42802] NR 46 TC 51 Z9 52 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAR 15 PY 1992 VL 52 IS 6 BP 1445 EP 1450 PG 6 WC Oncology SC Oncology GA HJ145 UT WOS:A1992HJ14500012 PM 1531783 ER PT J AU MEIER, AH CINCOTTA, AH LOVELL, WC AF MEIER, AH CINCOTTA, AH LOVELL, WC TI TIMED BROMOCRIPTINE ADMINISTRATION REDUCES BODY-FAT STORES IN OBESE SUBJECTS AND HYPERGLYCEMIA IN TYPE-II DIABETICS SO EXPERIENTIA LA English DT Article ID HAMSTER MESOCRICETUS-AURATUS; DOPAMINERGIC-NEURONS; CIRCADIAN VARIATION; PROLACTIN PERMITS; HORMONE RHYTHMS; ENERGY-BALANCE; GROWTH-HORMONE; SYRIAN-HAMSTER; INSULIN; HEPATOCYTES AB Obese postmenopausal female volunteers were given timed daily oral dosages of bromocriptine, and tested for reduction of body fat stores. This dopamine agonist has been shown to reset circadian rhythms that are altered in obese animals and to reduce body fat levels in several animal models. The participants were instructed not to alter their existing exercise and eating behavior during treatment. Skinfold measurements were taken on 33 subjects as indices of body fat. The measurements (e.g., suprailiac) were reduced after six weeks by about 25%, which represents a reduction of 11.7% of the total body fat. These dramatic decreases in body fat, which are equivalent to that produced by severe caloric restriction, were accompanied by more modest reductions of body weight (2.5%), indicating a possible conservation of protein that is usually lost as a consequence of such caloric restriction. The effects of bromocriptine treatment on body fat and hyperglycemia were also examined in non-insulin dependent diabetics being treated with oral hypoglycemics (7 subjects) or insulin (7 subjects). Total body fat was reduced by 10.7% and 5.1% in diabetics on oral hypoglycemics and insulin, respectively, without any significant reductions in body weight. Hyperglycemia was reduced in most of the 15 diabetic subjects treated leading to euglycemia and even cessation of hypoglycemic drugs in 3 of the 7 subjects during 4-8 weeks of bromocriptine treatment. These findings support the hypothesis that obesity and type II diabetes may be treated effectively with bromocriptine when administered at the proper times and dosages. C1 MASSACHUSETTS GEN HOSP, WELLMAN LABS PHOTOMED, BOSTON, MA 02114 USA. BATON ROUGE MENOPAUSAL CLIN, BATON ROUGE, LA 70806 USA. HARVARD UNIV, SCH MED, DEPT DERMATOL, BOSTON, MA 02114 USA. RP MEIER, AH (reprint author), LOUISIANA STATE UNIV, DEPT ZOOL & PHYSIOL, BATON ROUGE, LA 70803 USA. NR 43 TC 46 Z9 48 U1 0 U2 1 PU BIRKHAUSER VERLAG AG PI BASEL PA VIADUKSTRASSE 40-44, PO BOX 133, CH-4010 BASEL, SWITZERLAND SN 0014-4754 J9 EXPERIENTIA JI Experientia PD MAR 15 PY 1992 VL 48 IS 3 BP 248 EP 253 DI 10.1007/BF01930467 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HL609 UT WOS:A1992HL60900010 PM 1547854 ER PT J AU DELAMAZA, MS DUTT, JE FOSTER, CS AF DELAMAZA, MS DUTT, JE FOSTER, CS TI DISTRIBUTION OF COLLAGENS AND FIBRONECTIN IN HUMAN ADULT AND FETAL SCLERA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 711 EP 711 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500096 ER PT J AU LIN, CP BIRNGRUBER, R FUJIMOTO, JG PULIAFITO, CA AF LIN, CP BIRNGRUBER, R FUJIMOTO, JG PULIAFITO, CA TI EFFECTS OF SINGLE AND MULTIPLE PICOSECOND LASER-PULSES ON RPE CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,WELLMAN LAB PHOTOMED,BOSTON,MA 02114. MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. RI Birngruber, Reginald/Q-2342-2016 NR 1 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 721 EP 721 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500148 ER PT J AU ROIDER, J TROCCOLI, J ANDERSON, RR FLOTTE, TJ BIRNGRUBER, R AF ROIDER, J TROCCOLI, J ANDERSON, RR FLOTTE, TJ BIRNGRUBER, R TI MICROVASCULATURE OCCLUSION BY REPETITIVE SHORT LASER-PULSES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MED UNIV LUBECK,DEPT OPHTHALMOL,LUBECK,GERMANY. MED LASER CTR,LUBECK,GERMANY. RI Roider, Johann/E-4513-2010; Birngruber, Reginald/Q-2342-2016 NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 722 EP 722 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500151 ER PT J AU WONG, J SCHUMAN, JS WANG, N MILLER, JW AF WONG, J SCHUMAN, JS WANG, N MILLER, JW TI MODULATION OF HUMAN FIBROBLAST ACTIVITY BY SELECTED ANGIOINHIBINS 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 EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 735 EP 735 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500221 ER PT J AU LIU, JJ FOSTER, CS CAI, XX LEE, SJ AF LIU, JJ FOSTER, CS CAI, XX LEE, SJ TI ALTERNATIVELY SPLICED FORMS OF FIBRONECTIN IN THE WOUNDED CORNEAL EPITHELIUM - POLYMERASE CHAIN-REACTION ANALYSIS IN A RAT MODEL OF EPITHELIAL WOUNDS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RHOAD MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 779 EP 779 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500430 ER PT J AU JAIN, VK MEAD, MD AF JAIN, VK MEAD, MD TI VISUAL OUTCOME IN PENETRATING OCULAR TRAUMA 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 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 783 EP 783 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500454 ER PT J AU ENDO, EG MEAD, MD AF ENDO, EG MEAD, MD TI AMBULATORY CARE OF TRAUMATIC HYPHEMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 784 EP 784 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500461 ER PT J AU ARRUNATEGUICORREA, VR ZHAO, TZ FOSTER, CS AF ARRUNATEGUICORREA, VR ZHAO, TZ FOSTER, CS TI ROLE OF B-CELLS IN PROTECTION FROM HSV RETINITIS IN THE MOUSE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 785 EP 785 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500462 ER PT J AU HEILIGENHAUS, A LEE, SJ FOSTER, CS AF HEILIGENHAUS, A LEE, SJ FOSTER, CS TI INFLUENCE OF HSV I ON THE T-CELL RECEPTOR V-BETA REPERTOIRE IN A MURINE MODEL OF HERPES-SIMPLEX STROMAL 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. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RHOADS MOLEC LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 785 EP 785 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500463 ER PT J AU NEUMANN, R FOSTER, CS ZILSTRA, M JAENISCH, R AF NEUMANN, R FOSTER, CS ZILSTRA, M JAENISCH, R TI BETA-2-MICROGLOBULIN DEFICIENT MICE ARE RESISTANT TO 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. MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02139. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 785 EP 785 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500464 ER PT J AU MUSARELLA, MA KIRSHGESSNER, C TROFATTER, J MIYAKE, Y DEGENNARO, L AF MUSARELLA, MA KIRSHGESSNER, C TROFATTER, J MIYAKE, Y DEGENNARO, L TI ASSIGNMENT OF THE GENE FOR INCOMPLETE CONGENITAL STATIONARY NIGHT BLINDNESS (CSNB2) TO PROXIMAL XP SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HOSP SICK CHILDREN,RES INST,DEPT OPHTHALMOL,TORONTO M5G 1X8,ONTARIO,CANADA. HOSP SICK CHILDREN,RES INST,DEPT GENET,TORONTO M5G 1X8,ONTARIO,CANADA. UNIV MASSACHUSETTS,MOLEC NEUROGENET LAB,AMHERST,MA 01003. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. NAGOYA UNIV,SCH MED,DEPT OPHTHALMOL,NAGOYA,AICHI 466,JAPAN. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 792 EP 792 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500501 ER PT J AU PAVILACK, MA FOSTER, CS ELNER, SG ELNER, VM AF PAVILACK, MA FOSTER, CS ELNER, SG ELNER, VM TI LEUKOCYTE ADHESION MOLECULE EXPRESSION IN CICATRICIAL PEMPHIGOID SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 795 EP 795 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500518 ER PT J AU BURSELL, SE CLERMONT, A BRITTIS, M SHIBA, T MCGOVERN, T KING, GL AF BURSELL, SE CLERMONT, A BRITTIS, M SHIBA, T MCGOVERN, T KING, GL TI RETINAL BLOOD-FLOW CHANGES - VIDEO FLUORESCEIN ANGIOGRAPHY METHODOLOGY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 811 EP 811 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500596 ER PT J AU KING, GL SHIBA, T GOLDSTEIN, BJ AF KING, GL SHIBA, T GOLDSTEIN, BJ TI CLONING AND EXPRESSION OF ENDOTHELIN-1 (ET-1) RECEPTOR FROM RETINAL PERICYTES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 816 EP 816 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500619 ER PT J AU CHUN, LLY AF CHUN, LLY TI REGULATION OF TROPHIC FACTOR PRODUCTION FOR MAMMALIAN RETINAL GANGLION-CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 817 EP 817 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500626 ER PT J AU LI, ZZ FOSTER, CS LIU, JJ LEE, SJ AF LI, ZZ FOSTER, CS LIU, JJ LEE, SJ TI ELEVATED LEVEL OF SERUM TNF-ALPHA IN OCULAR CICATRICIAL PEMPHIGIOD SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 844 EP 844 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500759 ER PT J AU BERRA, A NOURI, M DUTT, J FOSTER, CS AF BERRA, A NOURI, M DUTT, J FOSTER, CS TI HEAT-SHOCK PROTEIN (HSPS) EXPRESSION IN HUMAN CONJUNCTIVA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 850 EP 850 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500795 ER PT J AU MATSUMOTO, K SHAMS, NBK HANNINEN, LA KENYON, KR AF MATSUMOTO, K SHAMS, NBK HANNINEN, LA KENYON, KR TI DEGRADATION OF CORNEAL PROTEINASES BY PSEUDOMONAS-AERUGINOSA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,DEPT OPHTHALMOL,IMMUNOL UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 850 EP 850 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500792 ER PT J AU MERAYO, J CALONGE, M FOSTER, CS AF MERAYO, J CALONGE, M FOSTER, CS TI EXPERIMENTAL-MODEL OF HAY-FEVER CONJUNCTIVITIS 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. RI Calonge, Margarita/K-2839-2014 OI Calonge, Margarita/0000-0001-8178-4836 NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 850 EP 850 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500794 ER PT J AU AJANI, UA WILLETT, WC SEDDON, JM AF AJANI, UA WILLETT, WC SEDDON, JM TI REPRODUCIBILITY OF A DIET HISTORY QUESTIONNAIRE IN AN EYE DISORDERS 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. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 863 EP 863 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500859 ER PT J AU CONLON, MR YU, JS MESSNER, EJ ROBERTS, KM BRAUNER, E MARTUZA, RL ALBERT, DM AF CONLON, MR YU, JS MESSNER, EJ ROBERTS, KM BRAUNER, E MARTUZA, RL ALBERT, DM TI TREATMENT OF TRANSGENIC MURINE RETINOBLASTOMA WITH RECOMBINANT HERPES-VIRUS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,COGAN EYE PATHOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 876 EP 876 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500918 ER PT J AU ESPAILLAT, A FOSTER, CS COLVIN, RB LIU, J LEE, SJ AF ESPAILLAT, A FOSTER, CS COLVIN, RB LIU, J LEE, SJ TI ALTERNATIVE SPLICED FORMS OF THE V-REGION OF FIBRONECTIN ARE DEMONSTRATED BY POLYMERASE CHAIN-REACTION ANALYSIS OF CORNEAL TISSUE FROM A RAT EPITHELIAL SCRAPE-WOUND MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 888 EP 888 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500978 ER PT J AU KAUFMAN, AH FOSTER, CS PULIAFITO, CA FERRARA, AH LEE, SJ PETERS, JH NICKELEIT, V COLVIN, RB AF KAUFMAN, AH FOSTER, CS PULIAFITO, CA FERRARA, AH LEE, SJ PETERS, JH NICKELEIT, V COLVIN, RB TI ALTERNATIVELY SPLICED EIIIA-FIBRONECTIN IS EXPRESSED IN NORMAL CORNEA AND PARTICIPATES IN CORNEAL WOUND-HEALING FOLLOWING 193NM EXCIMER LASER ANTERIOR KERATECTOMY IN A RAT MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,NEW ENGLAND EYE CTR,BOSTON,MA 02111. MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 889 EP 889 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13500982 ER PT J AU RINEHART, WB GIRARD, MT FINI, ME AF RINEHART, WB GIRARD, MT FINI, ME TI REGULATION OF SERUM AMYLOID-A (SAA3) EXPRESSION IN RABBIT CORNEAL FIBROBLASTS 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 3 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 893 EP 893 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501005 ER PT J AU LEE, SJ LIU, JJ FOSTER, CS AF LEE, SJ LIU, JJ FOSTER, CS TI ANALYSIS OF T-CELL RECEPTOR (TCR) V-BETA REPERTOIRE RESPONDING TO HERPES-SIMPLEX VIRUS (HSV) IN A MURINE MODEL OF HERPES STROMAL KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,RHOADS MOLEC IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 896 EP 896 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501025 ER PT J AU SHAMS, NBK MATSUMOTO, K HANNINEN, LA KENYON, KR AF SHAMS, NBK MATSUMOTO, K HANNINEN, LA KENYON, KR TI LYMPHORETICULAR CELLS PRODUCE SMALL MOLECULAR-WEIGHT CASEINASES - A ROLE IN CORNEAL ULCERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,EYE RES INST,IMMUNOL UNIT,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 977 EP 977 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501427 ER PT J AU DELAPAZ, MA YANDELL, DW BERROCAL, AM GRAGOUDAS, ES MUKAI, S AF DELAPAZ, MA YANDELL, DW BERROCAL, AM GRAGOUDAS, ES MUKAI, S TI SEARCH FOR MUTATIONS IN THE P53 GENE IN CHOROIDAL MELANOMA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,HOWE LAB,BOSTON,MA 02115. HARVARD UNIV,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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 978 EP 978 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501428 ER PT J AU MERCHANT, A WU, H FOSTER, CS AF MERCHANT, A WU, H FOSTER, CS TI SOLUBLE INTERLEUKIN-2 RECEPTOR LEVELS IN CORNEAL TRANSPLANT RECIPIENTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 982 EP 982 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501447 ER PT J AU FILATOV, V TALAMO, JH STEINERT, RF AF FILATOV, V TALAMO, JH STEINERT, RF TI POSTKERATOPLASTY ASTIGMATISM - SINGLE RUNNING SUTURE ADJUSTMENT VERSUS SELECTIVE REMOVAL OF INTERRUPTED SUTURES, A PROSPECTIVE RANDOMIZED TRIAL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 YALE UNIV,DEPT OPHTHALMOL & VISUAL SCI,NEW HAVEN,CT 06520. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 988 EP 988 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501474 ER PT J AU ANDLEY, U CHYLACK, L KOCHEVAR, I REDDAN, J AF ANDLEY, U CHYLACK, L KOCHEVAR, I REDDAN, J TI QUANTITATION OF THE BIOLOGICAL EFFECTS OF UV-RADIATION ON THE LENS EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. OAKLAND UNIV,ROCHESTER,MI 48063. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1038 EP 1038 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501735 ER PT J AU TO, KW ADAMIAN, M BERSON, EL AF TO, KW ADAMIAN, M BERSON, EL TI HISTOPATHOLOGIC FINDINGS IN 3 CARRIERS OF CHOROIDEREMIA SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1067 EP 1067 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501879 ER PT J AU MUKAI, S AF MUKAI, S TI INDIRECT OPHTHALMOSCOPY AND FUNDUS PHOTOGRAPHY OF TRANSGENIC MICE WITH RETINAL DISEASES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,RETINA SERV,BOSTON,MA 02115. HARVARD UNIV,SCH MED,HOWE LAB,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1074 EP 1074 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501915 ER PT J AU DREYER, EB LIPTON, SA AF DREYER, EB LIPTON, SA TI EXCITATORY AMINO-ACIDS IN GLAUCOMA - A POTENTIALLY NOVEL ETIOLOGY OF NEURONAL LOSS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT NEUROL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1092 EP 1092 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13501999 ER PT J AU CHRISTEN, WG GLYNN, RJ SEDDON, JM MANSON, JE BURING, JE HENNEKENS, CH AF CHRISTEN, WG GLYNN, RJ SEDDON, JM MANSON, JE BURING, JE HENNEKENS, CH TI CATARACT AND SUBSEQUENT RISK OF CARDIOVASCULAR-DISEASE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1097 EP 1097 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502023 ER PT J AU ZARATE, J BERRA, A BADIA, A DEGREGORIS, W MONSERRAT, AJ DUTT, J FOSTER, CS AF ZARATE, J BERRA, A BADIA, A DEGREGORIS, W MONSERRAT, AJ DUTT, J FOSTER, CS TI INFLAMMATORY RESPONSE TO INTRAVITREAL PHOSPHOLIPASE-A2 SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 UNIV BUENOS AIRES,FAC MED,DEPT PATHOL,BUENOS AIRES,ARGENTINA. UNIV BUENOS AIRES,FAC MED,DEPT OPHTHALMOL,BUENOS AIRES,ARGENTINA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1114 EP 1114 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502105 ER PT J AU KWONG, K BELLIVEAU, J CHESLER, D GOLDBERG, I CHENG, HM ROSEN, B AF KWONG, K BELLIVEAU, J CHESLER, D GOLDBERG, I CHENG, HM ROSEN, B TI FUNCTIONAL MAGNETIC-RESONANCE-IMAGING OF PRIMARY VISUAL-CORTEX SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02129. MASSACHUSETTS EYE & EAR HOSP,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1132 EP 1132 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502195 ER PT J AU FOSTER, CS LIU, JJ LEE, SJ AF FOSTER, CS LIU, JJ LEE, SJ TI MODULATION OF T-CELL RECEPTOR (TCR) EXPRESSION IN MURINE HERPES STROMAL KERATITIS (HSK) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1135 EP 1135 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502210 ER PT J AU PARK, CH LATINA, MA AF PARK, CH LATINA, MA TI EFFECTS OF CALCIUM IONOPHORE-A23187 AND PHORBOL ESTER ON TRABECULAR MESHWORK PHAGOCYTOSIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,WELLMAN LABS,BOSTON,MA 02114. EYE RES INST,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1165 EP 1165 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502368 ER PT J AU HOUSTON, MS CREAN, EV RICHARDSON, TM AF HOUSTON, MS CREAN, EV RICHARDSON, TM TI GROWTH-FACTOR EFFECTS ON TRABECULAR MESHWORK CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1166 EP 1166 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502372 ER PT J AU FERRARA, AH KAUFMAN, AH PULIAFITO, CA LEE, SJ WOODS, WP COLVIN, RB FOSTER, CS AF FERRARA, AH KAUFMAN, AH PULIAFITO, CA LEE, SJ WOODS, WP COLVIN, RB FOSTER, CS TI ANALYSIS OF CORNEAL WOUND-HEALING FOLLOWING 193NM EXCIMER LASER ANTERIOR KERATECTOMY IN A NOVEL RAT MODEL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. TUFTS UNIV,NEW ENGLAND EYE CTR,BOSTON,MA 02111. 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1197 EP 1197 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502513 ER PT J AU RUBIN, PAD POPHAM, JK SHORE, JW AF RUBIN, PAD POPHAM, JK SHORE, JW TI A COMPARISON OF FIBROVASCULAR INGROWTH INTO HYDROXYAPATITE AND POROUS POLYETHYLENE ORBITAL IMPLANTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1198 EP 1198 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502520 ER PT J AU HETH, CA MARESCALCHI, PA AF HETH, CA MARESCALCHI, PA TI GENERATION OF INOSITOL TRIPHOSPHATE DURING ROD OUTER SEGMENT PHAGOCYTOSIS IS ABNORMAL IN CULTURED RCS RETINAL-PIGMENT EPITHELIUM SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 3 Z9 3 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1203 EP 1203 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502539 ER PT J AU CLAESSENS, DA MILLER, JW WOODS, WJ FOLKMAN, J AF CLAESSENS, DA MILLER, JW WOODS, WJ FOLKMAN, J TI ALPHA-INTERFERON TREATMENT OF EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,MORSE LASER CTR,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1207 EP 1207 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502559 ER PT J AU KOWAL, VO MEAD, MD AF KOWAL, VO MEAD, MD TI COMMUNITY ACQUIRED CORNEAL ULCERS - THE IMPACT OF CULTURES ON MANAGEMENT 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 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1210 EP 1210 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502574 ER PT J AU KIM, AY LAMKIN, JC RIZZO, JF LESSELL, S ALBERT, DM AF KIM, AY LAMKIN, JC RIZZO, JF LESSELL, S ALBERT, DM TI PREVALENCE AND CLINICAL PREDICTORS OF DISCORDANT TEMPORAL ARTERY BIOPSIES IN GIANT-CELL ARTERITIS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 BOSTON UNIV,SCH MED,BOSTON,MA 02118. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1224 EP 1224 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502645 ER PT J AU SANDBERG, MA MILLER, S WEINER, A GAUDIO, AR AF SANDBERG, MA MILLER, S WEINER, A GAUDIO, AR TI ASSOCIATION OF IRIS PIGMENTATION WITH VISUAL-FIELD DEFECTS AND RPE ATROPHY 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 STUDY RETINAL DEGENERAT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1229 EP 1229 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502669 ER PT J AU MATSUBARA, M FINI, ME AF MATSUBARA, M FINI, ME TI THE RABBIT GENE FOR 92-KDA TYPE-IV COLLAGENASE - REGULATED EXPRESSION IN CORNEAL EPITHELIUM 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. 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1237 EP 1237 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502714 ER PT J AU BURNSTINE, MA LEVIN, LA HEDLEYWHYTE, ET KUPSKY, WJ ALBERT, DM AF BURNSTINE, MA LEVIN, LA HEDLEYWHYTE, ET KUPSKY, WJ ALBERT, DM TI THE VALUE OF NUCLEOLAR ORGANIZER REGIONS IN OPTIC-NERVE GLIOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROPATHOL,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,DEPT NEUROPATHOL,BOSTON,MA 02115. NR 2 TC 2 Z9 2 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1245 EP 1245 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502760 ER PT J AU MELAMED, S KOTASNEUMANN, R BARAK, A EPSTEIN, DL AF MELAMED, S KOTASNEUMANN, R BARAK, A EPSTEIN, DL TI THE EFFECT OF INTRACAMERAL ETHACRYNIC-ACID ON INTRAOCULAR-PRESSURE IN GLAUCOMA PATIENTS - A PILOT-STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TEL AVIV UNIV,SACKLER FAC MED,SHEBA MED CTR,GOLDSCHLEGER EYE INST,IL-52621 TEL HASHOMER,ISRAEL. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,GLAUCOMA SERV,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1247 EP 1247 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502769 ER PT J AU HU, LK HUH, K GRAGOUDAS, ES YOUNG, LHY AF HU, LK HUH, K GRAGOUDAS, ES YOUNG, LHY TI ESTABLISHMENT OF PIGMENTED CHOROIDAL MELANOMAS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1252 EP 1252 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502791 ER PT J AU SCHMIDT, U BAUMAN, W SCHOMACKER, K BIRNGRUBER, R GRAGOUDAS, E HASAN, T AF SCHMIDT, U BAUMAN, W SCHOMACKER, K BIRNGRUBER, R GRAGOUDAS, E HASAN, T TI PHOTOSENSITIZING POTENCY OF BENZOPORPHYRIN DERIVATIVE (BPD) ASSOCIATED WITH HUMAN LOW-DENSITY-LIPOPROTEIN (LDL) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. RI Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1253 EP 1253 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502796 ER PT J AU WEAVER, YK LIN, CP SCHUMAN, S WOODS, WJ FUJIMOTO, JG BIRNGRUBER, R PULIAFITO, CA AF WEAVER, YK LIN, CP SCHUMAN, S WOODS, WJ FUJIMOTO, JG BIRNGRUBER, R PULIAFITO, CA TI EXPERIMENTAL IRIDOTOMY WITH A PICOSECOND NEODYMIUM-AG LASER SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139. RI Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1265 EP 1265 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502854 ER PT J AU FINI, ME BURGESON, RE MATSUBARA, M AF FINI, ME BURGESON, RE MATSUBARA, M TI KALININ IS DEPOSITED IN THE BASEMENT-MEMBRANE ZONE OF HEALING CORNEAL BURNS 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 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1274 EP 1274 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502903 ER PT J AU GIRARD, MT FINI, ME AF GIRARD, MT FINI, ME TI STIMULATION OF PHOSPHOLIPASE-D ACTIVITY BY IONOMYCIN AND PHORBOL ESTERS IN BOVINE CORNEAL EPITHELIAL-CELLS 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1275 EP 1275 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502907 ER PT J AU HOSOI, J GRABBE, S KNISELY, TL GRANSTEIN, RD AF HOSOI, J GRABBE, S KNISELY, TL GRANSTEIN, RD TI AQUEOUS-HUMOR INHIBITS TUMOR-ANTIGEN PRESENTATION BY FRESH LANGERHANS CELLS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1284 EP 1284 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502948 ER PT J AU KNISELY, TL GRABBE, S GRANSTEIN, RD AF KNISELY, TL GRABBE, S GRANSTEIN, RD TI PRODUCTION OF GRANULOCYTE/MACROPHAGE-COLONY STIMULATING FACTOR (GM-CSF) AND INTERLEUKIN-6 (IL-6) BY MURINE IRIS/CILIARY BODY TISSUE INVITRO SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HARVARD CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1284 EP 1284 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502947 ER PT J AU WU, HK ZHAO, TZ FOSTER, CS AF WU, HK ZHAO, TZ FOSTER, CS TI THE ROLE OF CD4 AND CD8 LYMPHOCYTE-T IN THE VON SZILY HERPES-SIMPLEX VIRUS RETINITIS MODEL IN SCID MICE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HILLES IMMUNOL LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1284 EP 1284 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13502950 ER PT J AU ROSENTHAL, P COTTER, JM AF ROSENTHAL, P COTTER, JM TI RIGID GAS PERMEABLE SCLERAL CONTACT-LENSES ARE A USEFUL MODALITY FOR THE VISUAL REHABILITATION AND THERAPEUTIC MANAGEMENT OF CERTAIN CORNEAL DISORDERS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 POLYMER TECHNOL CORP,WILMINGTON,MA. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1296 EP 1296 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503012 ER PT J AU GILBERT, MM MANGIONE, CM COOK, EF SEDDON, JM AF GILBERT, MM MANGIONE, CM COOK, EF SEDDON, JM TI INFLUENCE OF SURGICAL APPROACH AND TYPE OF CATARACT ON INCIDENCE OF POSTOPERATIVE YAG CAPSULOTOMY IN PATIENTS UNDERGOING CATARACT-EXTRACTION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1302 EP 1302 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503036 ER PT J AU BIRNGRUBER, R DEUTSCH, T FLOTTE, T FUJIMOTO, J PULIAFITO, C AF BIRNGRUBER, R DEUTSCH, T FLOTTE, T FUJIMOTO, J PULIAFITO, C TI RETINAL DAMAGE INDUCED BY SINGLE PICOSECOND LASER-PULSES SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MED LASER CTR,LUBECK,GERMANY. MIT,CAMBRIDGE,MA 02139. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. RI Birngruber, Reginald/Q-2342-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1309 EP 1309 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503074 ER PT J AU BRITTIS, M MCGOVERN, T CLERMONT, A SHIBA, T KING, GL BURSELL, SE AF BRITTIS, M MCGOVERN, T CLERMONT, A SHIBA, T KING, GL BURSELL, SE TI PREVENTION OF ABNORMAL RETINAL HEMODYNAMICS IN DIABETIC RATS BY STRICT GLYCEMIC CONTROL SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1361 EP 1361 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503326 ER PT J AU NAYAK, RC ATTAWIA, MA CARTER, J AF NAYAK, RC ATTAWIA, MA CARTER, J TI CIRCULATING ANTIPERICYTE ANTIBODIES IN DIABETIC-RETINOPATHY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1361 EP 1361 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503331 ER PT J AU CLERMONT, A BURSELL, SE KING, GL AIELLO, LM AF CLERMONT, A BURSELL, SE KING, GL AIELLO, LM TI INDICATION OF RETINAL CIRCULATION CHANGES IN EARLY STAGE DIABETIC-PATIENTS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 JOSLIN DIABET CTR,BOSTON,MA. NR 0 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1366 EP 1366 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503357 ER PT J AU HAHN, LB BERSON, EL DRYJA, TP AF HAHN, LB BERSON, EL DRYJA, TP TI SEARCH FOR MUTATIONS IN THE GAMMA-SUBUNIT OF THE HUMAN PHOSPHODIESTERASE GENE IN PATIENTS WITH HEREDITARY RETINAL DEGENERATION SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB,BOSTON,MA 02114. 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1396 EP 1396 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503516 ER PT J AU MCGEE, TL BERSON, EL DRYJA, TP AF MCGEE, TL BERSON, EL DRYJA, TP TI SEARCH FOR POINT MUTATIONS IN THE INTERSTITIAL RETINOID-BINDING PROTEIN GENE IN PATIENTS WITH HEREDITARY RETINAL DEGENERATIONS SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. 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 SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1396 EP 1396 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503515 ER PT J AU ROSENFELD, PJ COWLEY, GS HAHN, LB SANDBERG, MA BERSON, EL DRYJA, TP AF ROSENFELD, PJ COWLEY, GS HAHN, LB SANDBERG, MA BERSON, EL DRYJA, TP TI A NULL MUTATION WITHIN THE RHODOPSIN GENE IN A FAMILY WITH AUTOSOMAL RECESSIVE RETINITIS-PIGMENTOSA 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 3 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1397 EP 1397 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503519 ER PT J AU OLSSON, JE PAWLYK, BS GORDON, JW BERSON, EL AF OLSSON, JE PAWLYK, BS GORDON, JW BERSON, EL TI TRANSGENIC MICE THAT CARRY A MUTANT COPY OF THE HUMAN RHODOPSIN GENE (PRO347SER) SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. NR 1 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1398 EP 1398 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503523 ER PT J AU OKADA, AA JOHNSON, RP DAMICO, DJ BAKER, AS AF OKADA, AA JOHNSON, RP DAMICO, DJ BAKER, AS TI ENDOGENOUS BACTERIAL ENDOPHTHALMITIS - A 10-YEAR RETROSPECTIVE STUDY SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Meeting Abstract C1 MASSACHUSETTS EYE & EAR HOSP,DEPT OPHTHALMOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR HOSP,INFECT DIS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,INFECT DIS UNIT,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0146-0404 J9 INVEST OPHTH VIS SCI JI Invest. Ophthalmol. Vis. Sci. PD MAR 15 PY 1992 VL 33 IS 4 BP 1420 EP 1420 PG 1 WC Ophthalmology SC Ophthalmology GA HK135 UT WOS:A1992HK13503629 ER PT J AU AUGER, KR CARPENTER, CL SHOELSON, SE PIWNICAWORMS, H CANTLEY, LC AF AUGER, KR CARPENTER, CL SHOELSON, SE PIWNICAWORMS, H CANTLEY, LC TI POLYOMA-VIRUS MIDDLE-T ANTIGEN-PP60C-SRC COMPLEX ASSOCIATES WITH PURIFIED PHOSPHATIDYLINOSITOL 3-KINASE INVITRO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID KINASE-ACTIVITY; TYROSINE PHOSPHORYLATION; TRANSFORMING PROTEIN; PDGF RECEPTOR; ANTIGEN; PP60C-SRC; PRODUCT; BINDING; CELLS; GENE AB Reconstitution of the polyoma virus middle T antigen (mT)-pp60-src complex and phosphatidylinositol 3-kinase (PtdIns 3-kinase) has been accomplished in vitro with immunopurified baculovirus-expressed mT-pp60c-src and PtdIns 3-kinase purified from rat liver. Both the 110- and 85-kDa subunits of the PtdIns 3-kinase associated with the mT-pp60c-src complex. The association of PtdIns 3-kinase with the mT-pp60c-src complex was dependent on the protein-tyrosine kinase activity of pp60c-src as a kinase-inactive mutant (pp60(295c-src)) still complexed with mT, but the mT-pp60(295c-src) complex was unable to bind PtdIns 3-kinase. The mT-pp60c-src complex phosphorylated both subunits of PtdIns 3-kinase on tyrosine residues. The immunopurified mT-pp60c-src complex also associated with PtdIns 3-kinase activity from whole cell lysates, and this association was dependent upon the protein-tyrosine kinase activity of pp60c-src. Comparison of S-35-labeled proteins from whole cell lysates which associated with immunopurified mT-pp60c-src and mT-pp60(295c-src) revealed proteins of 110 and 85 kDa as the major peptides dependent on protein-tyrosine kinase activity for association with the complex. In addition, a synthetic phosphopeptide (13-mer) containing sequences conserved between the major tyrosine phosphorylation site of murine polyoma virus mT, hamster polyoma virus mT, and the insulin receptor substrate (IRS-1) specifically blocked the association of the 85- and 110-kDa polypeptides with the mT-pp60c-src complex. The ability to block the association was dependent on the tyrosine phosphorylation of the peptide. Association of PtdIns 3-kinase activity was blocked concurrently. This is the first demonstration that the 110-kDa subunit of PtdIns 3-kinase can associate with mT-pp60c-src. This association in vitro is a step toward understanding protein-protein interactions important in the signal transduction pathway of oncogenic proteins. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. RP AUGER, KR (reprint author), TUFTS UNIV,SCH MED,DEPT PHYSIOL,136 HARRISON AVE,BOSTON,MA 02111, USA. RI Piwnica-Worms, Helen/C-5214-2012; Cantley, Lewis/D-1800-2014 OI Cantley, Lewis/0000-0002-1298-7653 FU NCI NIH HHS [CA 50767]; NIGMS NIH HHS [GM 36624, GM 41890, R01 GM041890] NR 44 TC 74 Z9 74 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 15 PY 1992 VL 267 IS 8 BP 5408 EP 5415 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700063 PM 1372000 ER PT J AU TOWLE, CA TREADWELL, BV AF TOWLE, CA TREADWELL, BV TI IDENTIFICATION OF A NOVEL MAMMALIAN ANNEXIN - CDNA CLONING, SEQUENCE-ANALYSIS, AND UBIQUITOUS EXPRESSION OF THE ANNEXIN-XI GENE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID FACTOR RECEPTOR KINASE; DEPENDENT 35-KILODALTON SUBSTRATE; PLACENTAL ANTICOAGULANT PROTEIN; PHOSPHOLIPID-BINDING-PROTEINS; AMINO-ACID-SEQUENCE; LIGHT-CHAIN BINDING; CALPACTIN-I; LIPOCORTIN-I; HEAVY-CHAIN; DIFFERENTIAL EXPRESSION AB Annexins (or lipocortins) are a family of at least 10 structurally related calcium- and phospholipid-binding proteins. Each protein consists of a conserved core domain having four (or eight) repeats of a segment approximately 70 amino acids in length and a nonconserved, usually short, amino-terminal domain. To date, amino acid sequences for eight distinct mammalian annexins have been predicted from cDNAs. This report describes an additional member of this family, bovine annexin XI, identified by cDNA cloning and sequence analysis. The 503-amino acid deduced protein consists of a core domain of four annexin repeats and a long amino-terminal domain rich in glycine, proline, and tyrosine. This novel annexin gene is expressed in a wide variety of tissues and isolated cells in culture. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TOWLE, CA (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [2R01AR16265-17A3] NR 72 TC 40 Z9 41 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 15 PY 1992 VL 267 IS 8 BP 5416 EP 5423 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HH747 UT WOS:A1992HH74700064 PM 1372001 ER PT J AU SPECTOR, NL SAMSON, W RYAN, C GRIBBEN, J URBA, W WELCH, WJ NADLER, LM AF SPECTOR, NL SAMSON, W RYAN, C GRIBBEN, J URBA, W WELCH, WJ NADLER, LM TI GROWTH ARREST OF HUMAN LYMPHOCYTES-B IS ACCOMPANIED BY INDUCTION OF THE LOW-MOLECULAR-WEIGHT MAMMALIAN HEAT-SHOCK PROTEIN (HSP28) SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CELL-CYCLE PROGRESSION; SACCHAROMYCES-CEREVISIAE; RESTRICTED ANTIGEN; PHORBOL ESTER; TUMOR-ANTIGEN; EXPRESSION; ACTIVATION; GENE; PHOSPHORYLATION; STIMULATION AB A large number of protein and molecular markers have been identified that delineate the early stages of human B cell activation and proliferation. In contrast, few if any molecules are transiently expressed precisely as activated B cells stop proliferating and undergo growth arrest. We demonstrate that the low molecular weight heat shock protein (hsp28) exhibits unique induction kinetics that specifically demarcates this interval. After mitogenic activation of unstimulated splenic B cells, hsp28 protein and phosphorylation transiently increase coinciding precisely with the peak of cellular proliferation and the onset of growth arrest. Although most neoplastic B cells constitutively express hsp28, three cell lines were identified that were hsp28-. No differences in phenotype or growth kinetics were detected between hsp28+ and hsp28- neoplastic B cells demonstrating that hsp28 expression is not essential for cell growth. However, when treated with phorbol ester or heat shock, these hsp28- cell lines synthesize hsp28 followed by the onset growth arrest. The consistency with which hsp28 induction transiently delineates the interval from peak proliferation to the onset of growth arrest suggests hsp28 itself is likely to be involved in regulating this process. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NCI,FREDERICK CANC RES & DEV CTR,FREDERICK,MD 21702. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,DEPT MED,SAN FRANCISCO,CA 94110. RP SPECTOR, NL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [1F32CA08954-01, CA-40216-06] NR 35 TC 82 Z9 82 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 MAR 15 PY 1992 VL 148 IS 6 BP 1668 EP 1673 PG 6 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600010 PM 1541812 ER PT J AU HASUNUMA, T TSUBOTA, H WATANABE, M CHEN, ZW LORD, CI BURKLY, LC DALEY, JF LETVIN, NL AF HASUNUMA, T TSUBOTA, H WATANABE, M CHEN, ZW LORD, CI BURKLY, LC DALEY, JF LETVIN, NL TI REGIONS OF THE CD4-MOLECULE NOT INVOLVED IN VIRUS BINDING OR SYNCYTIA FORMATION ARE REQUIRED FOR HIV-1 INFECTION OF LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; HTLV-III/LAV ENVELOPE; T-CELLS; MONOCLONAL-ANTIBODIES; CD4 MOLECULE; FUSION; RECEPTOR; GLYCOPROTEIN; ACTIVATION; MEMBRANE AB Cell surface-expressed CD4 binds to the envelope glycoprotein of HIV-1 and mediates syncytia formation through interacting with membrane expressed HIV-1 gpl20. Further possible roles of the CD4 molecule in the process of cell infection by HIV-1 remain poorly understood. In our study we describe two mAb that recognize the V3/V4 domain of the CD4 molecule. Although these mAb do not inhibit gpl20-CD4 binding or HIV-1-induced syncytia formation, they inhibit HIV-1 infection of human PBL. These findings suggest that discrete, definable domains of the CD4 molecule may be involved in interactions after HIV-1 envelope binding that lead to virus entry into the cell. C1 HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,1 PINE HILL DR,SOUTHBOROUGH,MA 01772. BIOGEN INC,CAMBRIDGE,MA 02142. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RI Hasunuma, Tomoko/F-3533-2011 FU NCI NIH HHS [CA50139]; NCRR NIH HHS [RR00168]; NIAID NIH HHS [AI20729] NR 26 TC 23 Z9 23 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 MAR 15 PY 1992 VL 148 IS 6 BP 1841 EP 1846 PG 6 WC Immunology SC Immunology GA HH746 UT WOS:A1992HH74600036 PM 1371792 ER PT J AU WILSON, RA MCDONALD, RW BRISTOW, JD CHEITLIN, M NAUMAN, D MASSIE, B GREENBERG, B AF WILSON, RA MCDONALD, RW BRISTOW, JD CHEITLIN, M NAUMAN, D MASSIE, B GREENBERG, B TI CORRELATES OF AORTIC DISTENSIBILITY IN CHRONIC AORTIC REGURGITATION AND RELATION TO PROGRESSION TO SURGERY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID VENTRICULAR EJECTION FRACTION; VALVE-REPLACEMENT; NATURAL-HISTORY; THORACIC AORTA; AGE; INSUFFICIENCY; HYPERTENSION; VALIDATION; STIFFNESS; EXERCISE AB Aortic distensibility decreases with increasing age. Patients with chronic aortic regurgitation eject a large stroke volume into the proximal aorta. A decrease in distensibility of the aorta may impose a higher afterload on the left ventricle and may contribute to deterioration of left ventricular function over time. Accordingly, aortic distensibility was measured in 33 patients aged 13 to 73 years who had chronic isolated aortic regurgitation with minimal or no symptoms. Ascending aortic diameter was measured 4 cm above the aortic valve by two-dimensional echocardiography and pulse pressure was measured simultaneously by sphygmomanometry. Aortic distensibility was calculated as (Change in aortic diameter between systole and diastole/End-diastolic diameter)/Pulse pressure. Left ventricular systolic wall stress and mass were derived from standard M-mode echocardiographic measurements. Left ventricular volumes and ejection fraction were measured by radionuclide ventriculography. Aortic distensibility decreased logarithmically with increasing age (r = -0.62, p < 0.001) and also correlated inversely with systolic wall stress, left ventricular mass and end-diastolic volume. Patients who eventually underwent aortic valve replacement for symptoms of left ventricular dysfunction had significantly lower aortic distensibility than did those who did not yet require valve replacement: 0.09 +/- 0.08 vs. 0.22 +/- 0.19 x 1/100 (1/mm Hg) (p < 0.05). Thus, the reduced aortic distensibility that occurs with increasing age may contribute to the gradual left ventricular dilation and dysfunction seen in patients with chronic aortic regurgitation. C1 SAN FRANCISCO GEN HOSP,DEPT MED,DIV CARDIOL,SAN FRANCISCO,CA 94110. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO VET AFFAIRS MED CTR,DEPT MED,SAN FRANCISCO,CA 94143. RP WILSON, RA (reprint author), OREGON HLTH SCI UNIV,DEPT MED,DIV CARDIOL,3181 SW SAM JACKSON PK RD,PORTLAND,OR 97201, USA. FU NHLBI NIH HHS [HL-28146, HL-07192]; NIGMS NIH HHS [GM07546] NR 42 TC 11 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAR 15 PY 1992 VL 19 IS 4 BP 733 EP 738 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HJ636 UT WOS:A1992HJ63600002 PM 1545067 ER PT J AU SHOELSON, SE CHATTERJEE, S CHAUDHURI, M WHITE, MF AF SHOELSON, SE CHATTERJEE, S CHAUDHURI, M WHITE, MF TI YMXM MOTIFS OF IRS-1 DEFINE SUBSTRATE-SPECIFICITY OF THE INSULIN-RECEPTOR KINASE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE SIGNAL TRANSDUCTION; PHOSPHATIDYLINOSITOL 3'-KINASE; ONCOGENE; TYROSINE KINASE; SRC HOMOLOGY DOMAIN-2 ID STIMULATES TYROSINE PHOSPHORYLATION; PROTEIN-KINASE; BETA-SUBUNIT; SEQUENCE; RECOGNITION; ACTIVATION; PEPTIDES; CELLS; AUTOPHOSPHORYLATION; INVITRO AB Of 34 tyrosine residues in insulin receptor substrate 1 (IRS-1), 14 are adjacent to acidic residues, suggesting that they might be phosphorylation sites. Synthetic peptides corresponding to sequences surrounding these tyrosines were used as substrates of the insulin receptor kinase. Surprisingly six of these, each within YMXM motifs, were phosphorylated with greatest efficiency (K(m), 24-92-mu-M; k(cat)/K(m), 0.6-2.1 x 10(4) M-1.sec-1). Substituted YMXM peptides revealed a strong preference of the insulin receptor kinase for methionine at Y + 1 and Y + 3 positions. When phosphorylated, related YMXM sequences are recognition motifs for binding to proteins with src-homology (SH2) domains. The combined hydrophobic and flexible nature of methionine side chains adjacent to the targeted tyrosines provides a versatile contact for recognition by diverse proteins involved in signal transduction. C1 HARVARD UNIV,SCH MED,SCH MED,BOSTON,MA 02115. RP SHOELSON, SE (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK08366] NR 45 TC 156 Z9 156 U1 0 U2 3 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2027 EP 2031 DI 10.1073/pnas.89.6.2027 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300007 PM 1312712 ER PT J AU HUA, QX KOCHOYAN, M WEISS, MA AF HUA, QX KOCHOYAN, M WEISS, MA TI STRUCTURE AND DYNAMICS OF DES-PENTAPEPTIDE-INSULIN IN SOLUTION - THE MOLTEN-GLOBULE HYPOTHESIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID RECEPTOR; CONFORMATION; ASSIGNMENTS; RESONANCE; HELIX; CHAIN; NMR AB Structures of insulin in different crystal forms exhibit significant local and nonlocal differences, including correlated displacement of elements of secondary structure. Here we describe the solution structure and dynamics of a monomeric insulin analogue, des-pentapeptide-(B26-B30)-insulin (DPI), as determined by two-dimensional NMR spectroscopy and distance geometry/restrained molecular dynamics (DG/RMD). Although the solution structure of DPI exhibits a general similarity to its crystal structure, individual DG/RMD structures in the NMR ensemble differ by rigid-body displacements of alpha-helices that span the range of different crystal forms. These results suggest that DPI exists as a partially folded state formed by coalescence of distinct alpha-helix-associated microdomains. The physical reality of this model is investigated by comparison of the observed two-dimensional nuclear Overhauser enhancement (NOE) spectroscopy (NOESY) spectrum with that predicted from crystal and DG/RMD structures. The observed NOESY spectrum contains fewer tertiary contacts than predicted by any single simulation, but it matches their shared features; such "ensemble correspondence" is likely to reflect the effect of protein dynamics on observed NOE intensities. We propose (i) that the folded state of DPI is analogous to that of a compact protein-folding intermediate rather than a conventional native state and (ii) that the molten state is the biologically active species. This proposal (the molten-globule hypothesis) leads to testable thermodynamic predictions and has general implications for protein design. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. BIOP POLYTECH,CNRS,URA 32,F-91128 PALAISEAU,FRANCE. CHINESE ACAD SCI,INST BIOPHYS,BEIJING,PEOPLES R CHINA. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 27 TC 38 Z9 41 U1 0 U2 1 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2379 EP 2383 DI 10.1073/pnas.89.6.2379 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300079 PM 1549601 ER PT J AU LEE, SW TOMASETTO, C SWISSHELM, K KEYOMARSI, K SAGER, R AF LEE, SW TOMASETTO, C SWISSHELM, K KEYOMARSI, K SAGER, R TI DOWN-REGULATION OF A MEMBER OF THE S100 GENE FAMILY IN MAMMARY-CARCINOMA CELLS AND REEXPRESSION BY AZADEOXYCYTIDINE TREATMENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CELL CYCLE; CHROMOSOME-1; SUBTRACTIVE HYBRIDIZATION; TUMOR SUPPRESSOR; DEMETHYLATION ID CALCIUM-BINDING PROTEIN; HUMAN-BREAST CANCER; EPITHELIAL-CELLS; GROWTH; CLONING; CHROMOSOME-1Q; IDENTIFICATION; SEQUENCES; CALCYCLIN; HOMOLOGY AB A cDNA clone, designated CaN19 (originally called clone 19), isolated by subtractive hybridization, contains sequences that are preferentially expressed in normal mammary epithelial cells but not in breast tumor cells. Comparison of its deduced amino acid sequence with sequences in the GenBank data base revealed similarity with the S100 protein family, a group of small Ca2+-binding modulator proteins involved in cell cycle progression and cell differentiation. CaN19 expression is down-regulated in normal cells by A23187, a calcium ionophore, suggesting that its regulation is calcium-dependent. We have assigned CaNl9 to human chromosome 1q21-q24, a region containing four other S100-related genes. In contrast to CaN19 mRNA expression, most members of the S100 protein family are activated or overexpressed in tumor cells. Synchronization experiments by growth-factor deprivation demonstrated a biphasic induction of CaN19 expression in normal cells, almost-equal-to 2-fold in early G1 phase and another 2- to 3-fold at the G1/S boundary. Exposure of mammary tumor cells to 5-aza-2'-deoxycytidine, an inhibitor of DNA methylation, reactivated the expression of CaN19 mRNA. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC GENET,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELL GROWTH & REGULAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Tomasetto, Catherine/J-2783-2014 OI Tomasetto, Catherine/0000-0002-1811-5848 FU NCI NIH HHS [CA39814] NR 48 TC 148 Z9 152 U1 0 U2 3 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAR 15 PY 1992 VL 89 IS 6 BP 2504 EP 2508 DI 10.1073/pnas.89.6.2504 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HJ053 UT WOS:A1992HJ05300105 PM 1372446 ER PT J AU ROSEN, FS AF ROSEN, FS TI METCHNIKOFF AND THE ORIGINS OF IMMUNOLOGY - FROM METAPHOR TO THEORY - TAUBER,AI, CHERNYAK,L SO NATURE LA English DT Book Review RP ROSEN, FS (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES INC,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU MACMILLAN MAGAZINES LTD PI LONDON PA PORTERS SOUTH, 4 CRINAN ST, LONDON, ENGLAND N1 9XW SN 0028-0836 J9 NATURE JI Nature PD MAR 12 PY 1992 VL 356 IS 6365 BP 119 EP 119 DI 10.1038/356119a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HH731 UT WOS:A1992HH73100043 ER PT J AU JOHNSON, DC MCLOUD, TC MARK, EJ DAHLBERG, CGW AF JOHNSON, DC MCLOUD, TC MARK, EJ DAHLBERG, CGW TI INCREASING DYSPNEA AND COUGH IN A 77-YEAR-OLD MAN WITH INTERSTITIAL LUNG-DISEASE - BRONCHIOLOALVEOLAR CARCINOMA OF LUNG - PULMONARY INTERSTITIAL FIBROSIS, CONSISTENT WITH USUAL INTERSTITIAL PNEUMONITIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID ATYPICAL ADENOMATOUS HYPERPLASIA; ALVEOLAR CELL-CARCINOMA; LYMPHOMATOID GRANULOMATOSIS; BRONCHIOLITIS OBLITERANS; ORGANIZING PNEUMONIA; COMPUTED-TOMOGRAPHY; BRONCHOALVEOLAR LAVAGE; RADIOLOGIC FINDINGS; CONVERTING-ENZYME; CT FINDINGS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JOHNSON, DC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 83 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 12 PY 1992 VL 326 IS 11 BP 750 EP 758 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HH064 UT WOS:A1992HH06400007 ER PT J AU KISTLER, JP BUONANNO, FS GRESS, DR AF KISTLER, JP BUONANNO, FS GRESS, DR TI CAROTID ENDARTERECTOMY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter ID CEREBRAL VASCULAR-DISEASE; ATHEROTHROMBOSIS; THERAPY RP KISTLER, JP (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 9 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 12 PY 1992 VL 326 IS 11 BP 764 EP 765 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HH064 UT WOS:A1992HH06400016 ER PT J AU TAKAHASHI, LK TURNER, JG KALIN, NH AF TAKAHASHI, LK TURNER, JG KALIN, NH TI PRENATAL STRESS ALTERS BRAIN CATECHOLAMINERGIC ACTIVITY AND POTENTIATES STRESS-INDUCED BEHAVIOR IN ADULT-RATS SO BRAIN RESEARCH LA English DT Article DE PRENATAL STRESS; HYPOTHALAMIC-PITUITARY-ADRENAL SYSTEM; ADRENOCORTICOTROPIN; CORTICOSTERONE; CATECHOLAMINE; NOREPINEPHRINE; DOPAMINE; DEFENSIVE FREEZING; STRESS ID LOCUS COERULEUS; EXPLORATORY-BEHAVIOR; ULTRASONIC VOCALIZATIONS; CORTICOSTERONE LEVELS; TEGMENTAL-A10 REGION; CEREBRAL-CORTEX; NORADRENALINE; DOPAMINE; NOREPINEPHRINE; CORTICOTROPIN AB Previous studies demonstrated that throughout the preweaning period prenatally stressed rats have an overactive hypothalamic-pituitary-adrenal (HPA) system. This increased HPA activity was accompanied by an increase in defensive behavior. This study examined whether these alterations in HPA activity and defensive behavior continued into adulthood. Brain catecholamines in the cerebral cortex and locus coeruleus were also measured in prenatally stressed and control rats. Shock-induced levels of defensive freezing were significantly higher in prenatally stressed rats than in controls. However, plasma ACTH and corticosterone concentrations did not differ between groups either in the basal state or after exposure to foot shock. Concentrations of norepinephrine (NE) in the cerebral cortex and locus coeruleus region were significantly reduced in prenatally stressed rats. In addition, concentrations of NE metabolites were significantly elevated in prenatally stressed rats, suggesting an increased turnover of brain NE. Prenatally stressed rats also had, in the locus coeruleus region, significantly reduced dopamine (DA) levels but elevated concentration of DA metabolites. Results indicate that prenatal stress produces an increased behavioral responsiveness to stress that is evident in early life and continues into adulthood. The early hyperactivity of the HPA system in prenatally stressed rats, however, appears to normalize in adulthood. The increased turnover in brain catecholamines measure in the cerebral cortex and locus coeruleus region of prenatally stressed rats may be associated with the heightened expression of stress-induced behavior. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR, MADISON, WI 53705 USA. 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 50 TC 178 Z9 183 U1 1 U2 8 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD MAR 6 PY 1992 VL 574 IS 1-2 BP 131 EP 137 DI 10.1016/0006-8993(92)90809-N PG 7 WC Neurosciences SC Neurosciences & Neurology GA HK089 UT WOS:A1992HK08900018 PM 1322219 ER PT J AU MOMBAERTS, P IACOMINI, J JOHNSON, RS HERRUP, K TONEGAWA, S PAPAIOANNOU, VE AF MOMBAERTS, P IACOMINI, J JOHNSON, RS HERRUP, K TONEGAWA, S PAPAIOANNOU, VE TI RAG-1-DEFICIENT MICE HAVE NO MATURE LYMPHOCYTES-B AND LYMPHOCYTES-T SO CELL LA English DT Article ID SEVERE COMBINED IMMUNODEFICIENCY; CELL ANTIGEN RECEPTOR; MURINE LEUKEMIA-VIRUS; SCID MICE; V(D)J RECOMBINATION; GENE REARRANGEMENTS; MOUSE; DIFFERENTIATION; EXPRESSION; GENERATION AB The V(D)J recombination activation gene RAG-1 was isolated on the basis of its ability to activate V(D)J recombination on an artificial substrate in fibroblasts. This property and the expression pattern in tissues and cell lines indicate that RAG-1 either activates or catalyzes the V(D)J recombination reaction of immunoglobulin and T cell receptor genes. We here describe the introduction of a mutation in RAG-1 into the germline of mice via gene targeting in embryonic stem cells. RAG-1 -deficient mice have small lymphoid organs that do not contain mature B and T lymphocytes. The arrest of B and T cell differentiation occurs at an early stage and correlates with the inability to perform V(D)J recombination. The immune system of the RAG-1 mutant mice can be described as that of nonleaky scid mice. Although RAG-1 expression has been reported in the central nervous system of the mouse, no obvious neuroanatomical or behavioral abnormalities have been found in the RAG-1-deficient mice. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. SHRIVER CTR MENTAL RETARDAT,WALTHAM,MA 02254. TUFTS UNIV,SCH MED & VET MED,DEPT PATHOL,BOSTON,MA 02111. RP MOMBAERTS, P (reprint author), MIT,CTR CANC RES,HOWARD HUGHES MED INST,CAMBRIDGE,MA 02139, USA. OI Johnson, Randall/0000-0002-4084-6639 FU NICHD NIH HHS [HD27295]; NINDS NIH HHS [NS18381] NR 50 TC 1881 Z9 1909 U1 8 U2 60 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 6 PY 1992 VL 68 IS 5 BP 869 EP 877 DI 10.1016/0092-8674(92)90030-G PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HH748 UT WOS:A1992HH74800006 PM 1547488 ER PT J AU ROMEO, C AMIOT, M SEED, B AF ROMEO, C AMIOT, M SEED, B TI SEQUENCE REQUIREMENTS FOR INDUCTION OF CYTOLYSIS BY THE T-CELL ANTIGEN/FC RECEPTOR ZETA-CHAIN SO CELL LA English DT Article ID NATURAL-KILLER-CELLS; FC-GAMMA-RIII; TRIGGER MOLECULES; CYTO-TOXICITY; TUMOR-CELLS; COMPLEX; EXPRESSION; CD16; RECOGNITION; LYMPHOCYTES AB The zeta-chain of the T cell antigen receptor is a dimeric transmembrane protein with a very short extracellular domain and an extended cytoplasmic tail that triggers T cell effector function when aggregated by extracellular stimuli. We have reduced the active site of zeta to an 18 residue motif that can be appended to the intracellular domain of other transmembrane proteins to endow them with receptor-like activity. The compact size of the motif appears to eliminate zeta-mechanisms based on enzymatic activity and suggests that one or at most a few cellular proteins interact with the zeta-intracellular domain to initiate signal transduction. Analysis of individual amino acids within the 18 residue element reveals two phylogenetically conserved tyrosines that are absolutely required for activity and other residues that are less essential but contribute to the efficacy of receptor-directed cytolysis. RP ROMEO, C (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI27849] NR 42 TC 308 Z9 308 U1 0 U2 4 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD MAR 6 PY 1992 VL 68 IS 5 BP 889 EP 897 DI 10.1016/0092-8674(92)90032-8 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HH748 UT WOS:A1992HH74800008 PM 1547489 ER PT J AU AUSIELLO, DA STOW, JL CANTIELLO, HF DEALMEIDA, JB BENOS, DJ AF AUSIELLO, DA STOW, JL CANTIELLO, HF DEALMEIDA, JB BENOS, DJ TI PURIFIED EPITHELIAL NA+ CHANNEL COMPLEX CONTAINS THE PERTUSSIS TOXIN-SENSITIVE G-ALPHA-I-3 PROTEIN SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID BINDING PROTEIN; SODIUM-CHANNEL; ALPHA-SUBUNIT; CELL LINE; LOCALIZATION; INHIBITION; ANTIBODIES; TRANSPORT; LLC-PK1; CYCLASE AB We have recently demonstrated that the amiloride-sensitive Na+ channel in the apical membrane of the renal epithelial cell line, A6, is modulated by the alpha(i-3) subunit of the G(i-3) protein. We also showed that a 700-kDa protein complex can be purified from the membranes of A6 epithelia which (a) can reconstitute the amiloride-sensitive Na+ influx in liposomes and planar bilayer membranes and (b) consists of six major protein bands observed on reducing sodium dodecyl sulfate-polyacrylamide gels with molecular masses ranging from 35 to 320 kDa. The present study was undertaken to determine if the alpha(i-3) subunit was a member of this Na+ channel complex. G-alpha(i) structure and function were identified by Western blotting with specific G-alpha(i) subunit antibodies and Na+ channel antibodies, through ADP-ribosylation with pertussis toxin, and by immunocytochemical localization of the Na+ channel and G-alpha(i) proteins. We demonstrate that two protein substrates are ADP-ribosylated in the 700-kDa complex in the presence of pertussis toxin and are specifically immunoprecipitated with an anti-Na+ channel polyclonal antibody. One of these substrates, a 41-kDa protein, was identified as the alpha(i-3) subunit of the G(i-3) protein on Western blots with specific antibodies. Na+ channel antibodies do not recognize G-alpha(i-3) on Western blots of Golgi membranes which contain alpha(i-3) but not Na+ channel proteins, nor do they immunoprecipitate alpha(i-3) from solubilized Golgi membranes; however, alpha(i-3) is coprecipitated as part of the Na+ channel complex from A6 cell membranes by polyclonal Na+ channel antibodies. Both alpha(i-3) and the Na+ channel have been localized in A6 cells by confocal imaging and immunofluorescence with specific antibodies and are found to be in distinct but adjacent domains of the apical cell surface. In functional studies, alpha(i-3), but not alpha(i-2), stimulates Na+ channel activity. These data are therefore consistent with the localization of Na+ channel activity and modulatory alpha(i-3) protein at the apical plasma membrane, which together represent a specific signal transduction pathway for ion channel regulation. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02114. UNIV ALABAMA,DEPT PHYSIOL & BIOPHYS,BIRMINGHAM,AL 35294. RP AUSIELLO, DA (reprint author), MASSACHUSETTS GEN HOSP,RENAL UNIT,149 13TH ST,8TH FL,BOSTON,MA 02129, USA. FU NIDDK NIH HHS [DK19406, DK37206] NR 25 TC 90 Z9 91 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAR 5 PY 1992 VL 267 IS 7 BP 4759 EP 4765 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HF642 UT WOS:A1992HF64200072 PM 1311319 ER PT J AU CHEN, F HABER, E MATSUEDA, GR AF CHEN, F HABER, E MATSUEDA, GR TI AVAILABILITY OF THE B-BETA(15-21) EPITOPE ON CROSS-LINKED HUMAN FIBRIN AND ITS PLASMIC DEGRADATION PRODUCTS SO THROMBOSIS AND HAEMOSTASIS LA English DT Article ID MONOCLONAL-ANTIBODIES; ACTIVATOR; BINDING; INVIVO; CLOTS AB The binding of radiolabeled monoclonal antifibrin antibody 59D8 (specific for fibrin but not fibrinogen) to a series of degraded fibrin clots showed that the availability of the B-beta(15-21) epitope (against which 59D8 had been raised) was inversely proportional to the extent of clot lysis. Examination of digest supernatants revealed that the B-beta(15-21) epitope was released from clots as a high molecular weight degradation product in the presence of calcium ions but that the generation of low molecular weight peptides occurred in the absence of calcium ions. To address the question of epitope accessibility, we compared levels of fibrin clot binding among four radioactively labeled antibodies: antifibrin monoclonal antibody 59D8, two antifibrinogen monoclonal antibodies that cross-reacted with fibrin, and an affinity-purified polyclonal antifibrinogen antibody. We expected that the antifibrinogen antibodies would show enhanced binding to clots in comparison with the antifibrin antibody. However, the epitope accessibility experiments showed that all four antibody preparations bound fibrin clots at comparable levels. Taken together, these studies demonstrated that one fibrin-specific epitope, B-beta(15-21), remains available on clots as they undergo degradation by plasmin and, importantly, that the epitope is not solubilized at a rate faster than the rate at which the clot is itself solubilized. The availability of the B-beta(15-21) epitope during the course of plasminolysis assures the potential utility of antifibrin antibodies such as 59D8 for detecting thrombi and targeting plasminogen activators. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-28015] NR 27 TC 7 Z9 7 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD MAR 2 PY 1992 VL 67 IS 3 BP 335 EP 340 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA HH209 UT WOS:A1992HH20900011 PM 1379385 ER PT J AU PITMAN, MB SZYFELBEIN, WM NILES, J FIENBERG, R AF PITMAN, MB SZYFELBEIN, WM NILES, J FIENBERG, R TI CLINICAL UTILITY OF FINE NEEDLE ASPIRATION BIOPSY IN THE DIAGNOSIS OF WEGENERS GRANULOMATOSIS - A REPORT OF 2 CASES SO ACTA CYTOLOGICA LA English DT Article ID CRESCENTIC GLOMERULONEPHRITIS; CYTOPLASMIC AUTOANTIBODIES; HUMAN-NEUTROPHILS AB In two patients, pulmonary lesions of Wegener's granulomatosis (WG) were sampled by fine needle aspiration biopsy: one with the clinical diagnosis of primary pulmonary malignancy and the other with a clinical suspicion of WG. In the latter case the smears showed distinctive eosinophilic, collagen necrosis (pathergic necrosis), poorly formed granulomata composed of loose aggregates of elongated, often palisading epithelioid histiocytes, and multinucleate histiocytes. A cell block preparation in this case contained minute tissue fragments illustrating the distinctive, pathergic-type necrosis. In the former case, many of these features were present, but additionally there were several groups, atypical bronchial epithelial cells that, in light of the clinical impression, initially led to an incorrect diagnosis of bronchoalveolar carcinoma. Subsequent review of this case led to the diagnosis of WG. Antineutrophil cytoplasmic antibody (ANCA) serology was later obtained, confirming the diagnosis of WG in both cases. In our experience, the cytomorphologic findings of granular collagen necrosis, granulomata and multinucleate cells, although not specific, should alert the cytopathologist to consider the diagnosis of WG, especially when special stains for microorganisms are negative. A recommendation for ANCA serology testing early in the disease process, particularly in the limited forms of the disease, may lead to early recognition of WG, resulting in prompt institution of immunosuppressive therapy, greatly improving the patient's prognosis. RP PITMAN, MB (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114, USA. NR 20 TC 11 Z9 11 U1 0 U2 0 PU SCI PRINTERS & PUBL INC PI ST LOUIS PA P.O. DRAWER 12425 8342 OLIVE BLVD, ST LOUIS, MO 63132 SN 0001-5547 J9 ACTA CYTOL JI Acta Cytol. PD MAR-APR PY 1992 VL 36 IS 2 BP 222 EP 229 PG 8 WC Pathology SC Pathology GA HK367 UT WOS:A1992HK36700021 PM 1543006 ER PT J AU CARTER, EA AF CARTER, EA TI EFFECT OF ETHANOL ADMINISTRATION ON PLASMA GLYCEROL LEVELS IN THE RAT SO ALCOHOL LA English DT Article DE FATTY LIVER; ETHANOL; PLASMA GLYCEROL AB Many mechanisms have been postulated as being responsible for the fatty liver resulting from ethanol ingestion. Lipid mobilization has been strongly implicated in both acute and chronic ethanol administration-the difference between the two lying in the source of the fat. In the acute situation, the lipid is mobilized from depot fat, whereas in the chronic situation, it apparently comes from the diet. One possibility not explored is the mobilization of glycerol. This substance is the backbone of triglyceride. Hence, an influx of glycerol to the liver coupled with increased amounts of fatty acids could help explain, in part, the fatty liver resulting from alcohol administration. The purpose of the following study was to determine if such an effect does occur. C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP CARTER, EA (reprint author), MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 11 TC 1 Z9 1 U1 1 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0741-8329 J9 ALCOHOL JI Alcohol PD MAR-APR PY 1992 VL 9 IS 2 BP 93 EP 94 DI 10.1016/0741-8329(92)90017-5 PG 2 WC Substance Abuse; Pharmacology & Pharmacy; Toxicology SC Substance Abuse; Pharmacology & Pharmacy; Toxicology GA HM972 UT WOS:A1992HM97200002 PM 1599631 ER PT J AU RIVITZ, SM DELUCA, SA AF RIVITZ, SM DELUCA, SA TI POSTERIOR MEDIASTINAL MASSES IN CHILDREN - GANGLIONEUROBLASTOMA SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Ganglioneuroblastoma, although a rare neoplasm, is one of the most common causes of posterior mediastinal masses in children. This tumor occurs in children from one to 10 years of age. With intrathoracic involvement, the tumor may remain asymptomatic until it is large. The case reported illustrates a typical presentation of intrathoracic ganglioneuroblastoma. RP RIVITZ, SM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,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 1992 VL 45 IS 3 BP 1153 EP 1156 PG 4 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HH556 UT WOS:A1992HH55600012 PM 1543100 ER PT J AU BLISS, DZ GUENTER, PA SETTLE, RG AF BLISS, DZ GUENTER, PA SETTLE, RG TI DEFINING AND REPORTING DIARRHEA IN TUBE-FED PATIENTS - WHAT A MESS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE TUBE-FEEDING DIARRHEA; DIARRHEA DEFINITIONS; REPORTING THE EXTENT OF DIARRHEA ID CRITICALLY ILL PATIENTS; FECAL BULKING AGENT; ENTERAL NUTRITION; ELEMENTAL DIET; BURN PATIENTS; FEEDING FORMULAS; BOWEL FUNCTION; TOLERANCE; CONTAMINATION; SUPPORT AB The frequency and consistency of stools of all patients at a VA Medical Center who were tube-fed during a 3-mo period were recorded prospectively and analyzed in terms of eight definitions of diarrhea derived from the literature. The extent of diarrhea, reported. as incidence and as percentage of days with diarrhea, was used to determine differences among the definitions. The relationship between extent of diarrhea and duration of monitoring patients was also determined. Results of 29 patients monitored for 13.0 d (6.5 d) [median (interquartile range)] indicated that the definition of diarrhea significantly influenced the reported incidence of and percentage of days with diarrhea. Duration of monitoring showed a significant, positive relationship to the incidence of diarrhea (ie, the longer the duration, the more likely that diarrhea was observed). When diarrhea was reported as the percentage of days with diarrhea, the influence of monitoring duration virtually disappeared. C1 PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. UNIV PENN,SCH NURSING,PHILADELPHIA,PA 19104. GRAD HOSP PHILADELPHIA,DEPT OTORHINOLARYNGOL,PHILADELPHIA,PA 19146. NR 47 TC 67 Z9 71 U1 0 U2 1 PU AMER SOC CLINICAL NUTRITION PI BETHESDA PA 9650 ROCKVILLE PIKE, SUBSCRIPTIONS, RM L-2310, BETHESDA, MD 20814-3998 SN 0002-9165 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD MAR PY 1992 VL 55 IS 3 BP 753 EP 759 PG 7 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HG351 UT WOS:A1992HG35100024 PM 1550053 ER PT J AU NATOWICZ, MR ALPER, JK ALPER, JS AF NATOWICZ, MR ALPER, JK ALPER, JS TI GENETIC DISCRIMINATION AND THE LAW SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article AB The use of genetic tests can lead to genetic discrimination, discrimination based solely on the nature of an individual's genotype. Instances of the discriminatory uses of genetic tests by employers and insurance companies have already been reported. The recently enacted Americans with Disabilities Act of 1990 (ADA), together with other federal and state laws, can be used to combat some forms of this discrimination. In this article we define and characterize genetic discrimination, discuss the applicability of the various relevant federal and state laws, including the ADA, in the areas of employment and insurance discrimination, explore the limitations of these laws, and, finally, suggest some means of overcoming these limitations. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. UNIV MASSACHUSETTS,CTR DISABIL LAW,BOSTON,MA 02125. UNIV MASSACHUSETTS,DEPT CHEM,BOSTON,MA 02125. RP NATOWICZ, MR (reprint author), SHRIVER CTR MENTAL RETARDAT,DIV MED GENET,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 23 TC 87 Z9 87 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAR PY 1992 VL 50 IS 3 BP 465 EP 475 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA HH974 UT WOS:A1992HH97400003 PM 1342778 ER PT J AU BILLINGS, PR KOHN, MA DECUEVAS, M BECKWITH, J ALPER, JS NATOWICZ, MR AF BILLINGS, PR KOHN, MA DECUEVAS, M BECKWITH, J ALPER, JS NATOWICZ, MR TI DISCRIMINATION AS A CONSEQUENCE OF GENETIC TESTING SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID HUNTINGTONS-DISEASE; LINKAGE MAP; IMPACT AB Genetic discrimination refers to discrimination directed against an individual or family based solely on an apparent or perceived genetic variation from the "normal" human genotype. We describe here the results of a case history study designed to assess whether or not genetic discrimination exists. Using the above definition of genetic discrimination and applying stringent criteria for case selection, we find that genetic discrimination exists and is manifested in many social institutions, especially in the health and life insurance industries. Stigmatization, and denial of services or entitlements to individuals who have a genetic diagnosis but who are asymptomatic or who will never become significantly impaired, is noted. Follow-up comprehensive studies on the significance and varieties of genetic discrimination are needed. In order to avoid creating a new social underclass based on genetic discrimination (the "asymptomatic ill"), existing and future genetic testing or screening programs need review by medical, scientific, legal, and social policy experts, as well as the public, and may require modification. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV MASSACHUSETTS,DEPT CHEM,AMHERST,MA 01003. MASSACHUSETTS GEN HOSP,MASSACHUSETTS EYE & EAR INFIRM,DEPT PATHOL,BOSTON,MA 02114. SHRIVER CTR MENTAL RETARDAT,DIV MED GENET,WALTHAM,MA. RP BILLINGS, PR (reprint author), CALIF PACIFIC MED CTR,DEPT MED,DIV GENET MED,POB 7999,SAN FRANCISCO,CA 94120, USA. NR 35 TC 313 Z9 314 U1 2 U2 22 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 1992 VL 50 IS 3 BP 476 EP 482 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA HH974 UT WOS:A1992HH97400004 PM 1539589 ER PT J AU TANZI, RE WATKINS, PC STEWART, GD WEXLER, NS GUSELLA, JF HAINES, JL AF TANZI, RE WATKINS, PC STEWART, GD WEXLER, NS GUSELLA, JF HAINES, JL TI A GENETIC-LINKAGE MAP OF HUMAN CHROMOSOME-21 - ANALYSIS OF RECOMBINATION AS A FUNCTION OF SEX AND AGE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID FAMILIAL ALZHEIMERS-DISEASE; HUMAN-BREAST CANCER; BETA-PROTEIN GENE; DEFECT; CDNA; REGION; CELLS AB A genetic linkage map of human chromosome 21 has been constructed using 22 anonymous DNA markers and five complementary DNAs (cDNAs) encoding the amyloid beta-protein precursor (APP), superoxide dismutase 1 (SOD1), the ets-2 proto-oncogene (ETS2), the estrogen inducible breast cancer locus ((BCEI), and the leukocyte antigen, CD18 (CD18). Segregation of RFLPs detected by these DNA markers was traced in the Venezuelan Reference Pedigree (VRP). A comprehensive genetic linkage map consisting of the 27 DNA markers spans 102 cM on the long arm of chromosome 21. We have confirmed our initial findings of a dramatically increased rate of recombination at the telomere in both females and males and of significantly higher recombination in females in the pericentromeric region. By comparing patterns of recombination in specific regions of chromosome 21 with regard to both parental sex and age, we have now identified a statistically significant downward trend in the frequency of crossovers in the most telomeric portion of chromosome 21 with increasing maternal age. A less significant decrease in recombination with increasing maternal age was observed in the pericentromeric region of the chromosome. These results may help in ultimately understanding the physical relationship between recombination and nondisjunction in the occurrence of trisomy 21. C1 COLUMBIA UNIV,INST PSYCHIAT,NEW YORK,NY 10027. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. LIFE TECHNOL INC,GAITHERSBURG,MD. UNIV MICHIGAN,DEPT PEDIAT & COMMUNICABLE DIS,ANN ARBOR,MI 48109. RI Haines, Jonathan/C-3374-2012 FU NHGRI NIH HHS [HG00169, HG00324]; NINDS NIH HHS [NS30428] NR 35 TC 75 Z9 77 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAR PY 1992 VL 50 IS 3 BP 551 EP 558 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA HH974 UT WOS:A1992HH97400014 PM 1347193 ER PT J AU OZELIUS, LJ KRAMER, PL DELEON, D RISCH, N BRESSMAN, SB SCHUBACK, DE BRIN, MF KWIATKOWSKI, DJ BURKE, RE GUSELLA, JF FAHN, S BREAKEFIELD, XO AF OZELIUS, LJ KRAMER, PL DELEON, D RISCH, N BRESSMAN, SB SCHUBACK, DE BRIN, MF KWIATKOWSKI, DJ BURKE, RE GUSELLA, JF FAHN, S BREAKEFIELD, XO TI STRONG ALLELIC ASSOCIATION BETWEEN THE TORSION DYSTONIA GENE (DYTI) AND LOCI ON CHROMOSOME 9Q34 IN ASHKENAZI JEWS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID AUTOSOMAL DOMINANT INHERITANCE; FAMILIAL DYSAUTONOMIA; SEGREGATION ANALYSIS; DNA POLYMORPHISMS; LINKAGE ANALYSIS; COMPLEX; MAP AB The DYT1 gene responsible for early-onset, idiopathic torsion dystonia (ITD) in the Ashkenazi Jewish population, as well as in one large non-Jewish family, has been mapped to chromosome 9q32-34. Using (GT)n and RFLP markers in this region, we have identified obligate recombination events in some of these Jewish families, which further delineate the area containing the DYT1 gene to a 6-cM region bounded by loci AK1 and ASS. In 52 unrelated, affected Ashkenazi Jewish individuals, we have found highly significant linkage disequilibrium between a particular extended haplotype at the ABL-ASS loci and the DYT1 gene. The 4/A12 haplotype for ABL-ASS is present on 69% of the disease-bearing chromosomes among affected Jewish individuals and on only 1% of control Jewish chromosomes (chi-2 = 91.07, P << .001). The allelic association between this extended haplotype and DYT1 predicts that these three genes lie within 1-2 cM of each other; on the basis of obligate recombination events, the DYT1 gene is centromeric to ASS. Furthermore, this allelic association supports the idea that a single mutation event is responsible for most hereditary cases of dystonia in the Jewish population. Of the 53 definitely affecteds typed, 13 appear to be sporadic, with no family history of dystonia. However, the proportion of sporadic cases which potentially carry the A12 haplotype at ASS (8/13 [62%]) is similar to the proportion of familial cases with A12 (28/40 [70%]). This suggests that many sporadic cases are hereditary, that the disease gene frequency is greater than 1115,000, and that the penetrance is lower than 30%, as previously estimated in this population. Most affected individuals were heterozygous for the ABL-ASS haplotype, a finding supporting autosomal dominant inheritance of the DYT1 gene. The ABL-ASS extended-haplotype status will provide predictive value for carrier status in Jewish individuals. This information can be used for molecular diagnosis, evaluation of subclinical expression of the disease, and elucidation of environmental factors which may modify clinical symptoms. C1 MASSACHUSETTS GEN HOSP E,NEUROSCI CTR NEUROL,MOLEC NEUROGENET UNIT,13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. COLUMBIA PRESBYTERIAN MED CTR,DEPT NEUROL,DYSTONIA CLIN RES CTR,NEW YORK,NY 10032. YALE UNIV,SCH MED,DEPT EPIDEMIOL,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT PUBL HLTH,NEW HAVEN,CT 06510. YALE UNIV,SCH MED,DEPT HUMAN GENET,NEW HAVEN,CT 06510. RI Burke, Robert/B-7226-2011 OI Burke, Robert/0000-0002-4760-8553 FU NINDS NIH HHS [NS26656, NS26836, NS28384] NR 40 TC 119 Z9 119 U1 0 U2 3 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 1992 VL 50 IS 3 BP 619 EP 628 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA HH974 UT WOS:A1992HH97400022 PM 1347197 ER PT J AU SPRINCE, NL OLIVER, LC MCLOUD, TC GINNS, LC AF SPRINCE, NL OLIVER, LC MCLOUD, TC GINNS, LC TI T-CELL ALVEOLITIS IN LUNG LAVAGE OF ASBESTOS-EXPOSED SUBJECTS SO AMERICAN JOURNAL OF INDUSTRIAL MEDICINE LA English DT Article DE ASBESTOSIS; T-CELL SUBSETS; BRONCHOALVEOLAR LAVAGE ID BRONCHOALVEOLAR LAVAGE; PULMONARY SARCOIDOSIS; HYPERSENSITIVITY PNEUMONITIS; MONOCLONAL-ANTIBODIES; WORKERS; BLOOD; SUBPOPULATIONS; LYMPHOCYTES; MACROPHAGES; EXPRESSION AB In sarcoidosis and idiopathic pulmonary fibrosis, it has been reported that lymphocyte proportions in lung lavage predict the subsequent clinical course. Recent evidence has suggested that lymphocytes are important in the alveolitis of asbestosis. We hypothesized that a greater relative proportion of T-lymphocytes in lung lavage of asbestos-exposed subjects is associated with immune activation and may predict die subsequent clinical course. We assessed lymphocyte subsets in lung lavage and peripheral blood (PB) of 97 asbestos-exposed subjects and 10 unexposed normals, using flow cytometry analysis of monoclonal antibody-treated cells. T-cell alveolitis was defined as follows: [%lymphocytes in lavage X %CD3 in lavage] > 2 SD above that product in normals. Eighteen subjects had T-cell alveolitis (group 1) and 79 did not (group 2). There were no significant differences between the groups in age, smoking status, duration of exposure, lung function results, or frequency of plaques or profusion greater-than-or-equal-to 1/0. Percent CD2 was higher in lavage of group 1 compared with group 2. There was a trend for higher %Ia in lavage of group 1 compared with group 2. These results identify a subgroup of asbestos-exposed subjects with T-cell alveolitis but no present excess of asbestos-related disease who may be at risk for future asbestos-related disease. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,PULM & CRIT CARE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SPRINCE, NL (reprint author), UNIV IOWA,COLL MED,DEPT PREVENT MED & ENVIRONM HLTH,INST AGR MED & OCCUPAT HLTH,IOWA CITY,IA 52242, USA. FU NIEHS NIH HHS [ES03301] NR 30 TC 3 Z9 3 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0271-3586 J9 AM J IND MED JI Am. J. Ind. Med. PD MAR PY 1992 VL 21 IS 3 BP 311 EP 319 DI 10.1002/ajim.4700210304 PG 9 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HF886 UT WOS:A1992HF88600003 PM 1585942 ER PT J AU IONASESCU, VV TROFATTER, J HAINES, JL IONASESCU, R SEARBY, C AF IONASESCU, VV TROFATTER, J HAINES, JL IONASESCU, R SEARBY, C TI CHARCOT-MARIE-TOOTH NEUROPATHY RELATED TO CHROMOSOME-1 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE DEMYELINATING NEUROPATHY; CHROMOSOME-1Q; CMT SUBTYPES; LINKAGE ID HMSN TYPE-I; SENSORY NEUROPATHY; HEREDITARY MOTOR; GENETIC-LINKAGE; DISEASE; MARKERS; HETEROGENEITY; ABSENCE AB One family with documented male-to-male transmission of Charcot-Marie-Tooth (CMT) neuropathy was studied clinically and by genetic linkage. Patients had progressive distal weakness and atrophy, areflexia, and distal sensory loss, but early onset (before age 3 years) in all 5 cases, and phrenic nerve involvement in the propositus (a 39-year-old woman) requiring CPAP ventilator support during the night. Motor-nerve conduction velocities (MNCVs) were significantly slow, consistent with severe demyelinating neuropathy. Electromyography (EMG) data were normal. Two-point and multipoint linkage analyses strongly suggested the presence of a CMT gene on chromosome 1q. A maximum multipoint lod score of 2.70 was obtained at MUC1 (theta = 0), with the locus order centromere-MUC1-SPTA1-Fc(gamma)RII-AT3-telomere. Multipoint linkage analysis excluded the CMT locus from chromosome 17 markers in this family. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RP IONASESCU, VV (reprint author), UNIV IOWA HOSP & CLIN,DEPT PEDIAT,DIV MED GENET,PEDIAT GENET MUSCLE LAB,IOWA CITY,IA 52242, USA. RI Haines, Jonathan/C-3374-2012; OI Searby, Charles/0000-0002-8108-8782 NR 25 TC 10 Z9 10 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD MAR 1 PY 1992 VL 42 IS 5 BP 728 EP 732 DI 10.1002/ajmg.1320420521 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA HJ087 UT WOS:A1992HJ08700020 PM 1632448 ER PT J AU EMANUEL, EJ AF EMANUEL, EJ TI SECURING PATIENTS RIGHT TO REFUSE MEDICAL-CARE - IN PRAISE OF THE CRUZAN DECISION SO AMERICAN JOURNAL OF MEDICINE LA English DT Article RP EMANUEL, EJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. NR 8 TC 8 Z9 8 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD MAR PY 1992 VL 92 IS 3 BP 307 EP 312 DI 10.1016/0002-9343(92)90081-L PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HH566 UT WOS:A1992HH56600013 PM 1546730 ER PT J AU CUNNINGHAM, MJ AF CUNNINGHAM, MJ TI THE MANAGEMENT OF CONGENITAL NECK MASSES SO AMERICAN JOURNAL OF OTOLARYNGOLOGY LA English DT Review RP CUNNINGHAM, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 16 Z9 16 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0196-0709 J9 AM J OTOLARYNG JI Am. J. Otolaryngol. PD MAR-APR PY 1992 VL 13 IS 2 BP 78 EP 92 DI 10.1016/0196-0709(92)90004-D PG 15 WC Otorhinolaryngology SC Otorhinolaryngology GA HW730 UT WOS:A1992HW73000004 PM 1642331 ER PT J AU MCKENNA, MJ HALPIN, C OJEMANN, RG NADOL, JB MONTGOMERY, WW LEVINE, RA CARLISLE, E MARTUZA, R AF MCKENNA, MJ HALPIN, C OJEMANN, RG NADOL, JB MONTGOMERY, WW LEVINE, RA CARLISLE, E MARTUZA, R TI LONG-TERM HEARING RESULTS IN PATIENTS AFTER SURGICAL REMOVAL OF ACOUSTIC TUMORS WITH HEARING PRESERVATION SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article; Proceedings Paper CT MEETING OF THE AMERICAN OTOLOGICAL SOC CY MAY 05-06, 1991 CL WAIKOLOA, HI SP AMER OTOL SOC ID AUDITORY EVOKED-POTENTIALS; NEUROMA SURGERY; NEURINOMA; ANGLE AB Long-term hearing results are described in 1 8 patients after suboccipital removal of unilateral acoustic neurinomas. Follow-up ranged from 3.4 to 10.4 years with a mean of 5.4 years. Fourteen patients (78%) experienced no significant decline in long-term hearing. Four patients (22%) experienced a significant decline in long-term hearing as defined by a drop in pure-tone average (0.5, 1, and 2 kHz), or a significant decline in Speech Discrimination Scores (SDS). Changes in hearing did not correlate with tumor size, preoperative hearing, intraoperative change in hearing, the interval between initial symptoms and surgery, sex, or age. C1 HARVARD UNIV,SCH MED,DEPT OTOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT LARYNGOL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,EATON PEABODY LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROSURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS EYE & EAR HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT AGR & RESOURCE ECON,BOSTON,MA 02114. RP MCKENNA, MJ (reprint author), MASSACHUSETTS EYE & EAR HOSP,DEPT OTOLARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. NR 18 TC 32 Z9 32 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1992 VL 13 IS 2 BP 134 EP 136 PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA HJ274 UT WOS:A1992HJ27400008 PM 1599004 ER PT J AU KANG, S BARNHILL, RL GRAEMECOOK, F RANDOLPH, G NADOL, JB SOBER, AJ AF KANG, S BARNHILL, RL GRAEMECOOK, F RANDOLPH, G NADOL, JB SOBER, AJ TI PRIMARY MALIGNANT-MELANOMA OF THE EXTERNAL AUDITORY-CANAL - A CASE-REPORT WITH PRESENTATION AS AN AURAL POLYP SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article AB A case of primary cutaneous melanoma of the external auditory canal and a review of the literature are reported. This is the first reported case with microstaging of the tumor. The tumor presented as a polypoid obstructive lesion of the external ear canal. Although occurrence of melanoma in this location is extremely rare, differential diagnosis of an external ear canal polyp should be expanded to include primary malignant melanoma. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02115. RP KANG, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BARTLETT-410,FRUIT ST,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5T 32 AR07098-16] NR 7 TC 7 Z9 7 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD MAR PY 1992 VL 13 IS 2 BP 194 EP 196 PG 3 WC Otorhinolaryngology SC Otorhinolaryngology GA HJ274 UT WOS:A1992HJ27400017 PM 1599012 ER PT J AU ALROY, J ORGAD, U DEGASPERI, R RICHARD, R WARREN, CD KNOWLES, K THALHAMMER, JG RAGHAVAN, SS AF ALROY, J ORGAD, U DEGASPERI, R RICHARD, R WARREN, CD KNOWLES, K THALHAMMER, JG RAGHAVAN, SS TI CANINE GM1-GANGLIOSIDOSIS - A CLINICAL, MORPHOLOGICAL, HISTOCHEMICAL, AND BIOCHEMICAL-COMPARISON OF 2 DIFFERENT MODELS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID LYSOSOMAL STORAGE DISEASE; PERFORMANCE LIQUID-CHROMATOGRAPHY; BETA-GALACTOSIDASE DEFICIENCY; VISCERAL GM1 GANGLIOSIDOSIS; PORTUGUESE WATER DOGS; LECTIN HISTOCHEMISTRY; ALPHA-NEURAMINIDASE; OLIGOSACCHARIDES; MANNOSIDOSIS; HYDROLYSIS AB The clinical, morphologic, histochemical, and biochemical features of G(M1)-gangliosidosis in two canine models, English Springer Spaniel (ESS) and Portuguese Water Dog (PWD), have been compared. The disease onset, its clinical course, and survival period of the affected dogs were similar in both models. Skeletal dysplasia was noted radiographically at 2 months of age, whereas at 4 1/2 months of age there was progressive neurologic impairment. However, dwarfism and coarse facial features were seen only in ESS. Both models had similar deficiency in activity of lysosomal beta-galactosidase, but possessed a normal protein activator for G(M1)-beta-galactosidase. Both models stored G(M1)-ganglioside, asialo-G(M1), and oligosaccharides in brain. Furthermore, only the PWD stored glycoproteins containing polylactosaminoglycans in visceral organs, and neither model stored them in the brain. Morphologically, both models demonstrated similar storage material in multiple tissues and cell types. The ultrastructure of the storage material was cell-type specific and identical in both models. However, some differences in the lectin staining pattern were noted. Our clinical, biochemical, and histochemical findings indicate that PWD and ESS may represent two different mutations of the beta-galactosidase gene. Moreover, the authors conclude that it is difficult, and inappropriate, to apply the human classification of G(M1)-gangliosidosis (i.e., infantile, juvenile, and adult forms) to these canine models. C1 TUFTS UNIV,SCH VET MED,DEPT PATHOL,BOSTON,MA 02111. HEBREW UNIV JERUSALEM,KORET SCH VET MED,DEPT PATHOL,JERUSALEM,ISRAEL. MASSACHUSETTS GEN HOSP,CARBOHYDRATE RES LAB,BOSTON,MA 02114. TUFTS UNIV,SCH VET MED,GRAFTON,MA. EK SHRIVER CTR,DEPT BIOCHEM,WALTHAM,MA. RP ALROY, J (reprint author), TUFTS UNIV,SCH MED,DEPT PATHOL,136 HARRISON AVE,BOSTON,MA 02111, USA. FU NICHD NIH HHS [HD 21087]; NINDS NIH HHS [NS 21765] NR 47 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAR PY 1992 VL 140 IS 3 BP 675 EP 689 PG 15 WC Pathology SC Pathology GA HH120 UT WOS:A1992HH12000017 PM 1546746 ER PT J AU PAUL, SR PEREZATAYDE, A WILLIAMS, DA AF PAUL, SR PEREZATAYDE, A WILLIAMS, DA TI INTERSTITIAL PULMONARY-DISEASE ASSOCIATED WITH DYSKERATOSIS-CONGENITA SO AMERICAN JOURNAL OF PEDIATRIC HEMATOLOGY ONCOLOGY LA English DT Letter C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP PAUL, SR (reprint author), HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. NR 7 TC 17 Z9 17 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-8562 J9 AM J PEDIAT HEMATOL PD SPR PY 1992 VL 14 IS 1 BP 89 EP 92 PG 4 WC Oncology; Hematology; Pediatrics SC Oncology; Hematology; Pediatrics GA GZ931 UT WOS:A1992GZ93100015 PM 1550271 ER PT J AU BURLACU, S JANMEY, PA BOREJDO, J AF BURLACU, S JANMEY, PA BOREJDO, J TI DISTRIBUTION OF ACTIN FILAMENT LENGTHS MEASURED BY FLUORESCENCE MICROSCOPY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE MUSCLE PROTEINS; LENGTH DISTRIBUTION; CORRELATION LENGTH; OPTICAL MICROSCOPY ID F-ACTIN; CYTOCHALASIN-B; DNA-MOLECULES; MUSCLE ACTIN; PHALLOIDIN; MYOSIN; POLYMERIZATION; ATP; STABILIZATION; CONTRACTION AB We analyzed the distribution of actin filament lengths by optical microscopy (OM). OM avoids possible alterations in the size or structure of actin filaments occurring during sample preparation for electron microscopy (EM). Images of F-actin labeled with tetramethylrhodamine isothiocyanate (TRITC)-phalloidin were analyzed for both size distribution and flexibility. In the standard buffer [25 mM potassium acetate, 4 mM MgSO4, 25 mM tris(hydroxymethyl)aminomethane acetate, pH 7.5, 20 mM beta-mercaptoethanol] filaments did not aggregate into bundles and remained stable at nanomolar concentrations for at least 1 h. At the same concentration, actin labeled directly with rhodamine (no phalloidin) formed unstable filaments whose average length decreased with time. The number average length of TRITC-phalloidin labeled filaments (L(n)) was 4.90-mu-m, the ratio (rho) of the weight average length to the number average length was 2.06, and the correlation length (1/lambda) was 8.33-mu-m. These parameters were in good agreement with the values determined by EM for filaments shorter than 8-mu-m. Passing G-actin through a Sephadex G-150 column before polymerization did not have a significant effect on the distribution of lengths but made filaments more stiff (1/lambda = 12.5-mu-m). Millimolar concentration of ATP increased the correlation length, and gelsolin had the expected fragmenting effect on filaments. These results show that OM can be used as a fast and reliable method to analyze the distribution and flexibility of actin filaments and suggest that, in spite of extensive manipulation of actin filaments during sample preparation, EM is a valid tool for determination of size parameters of actin filaments. C1 BAYLOR UNIV,MED CTR,BAYLOR RES INST,3812 ELM ST,DALLAS,TX 75226. MASSACHUSETTS GEN HOSP,HEMATOL UNIT,BOSTON,MA 02114. HARVARD UNIV,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,DEPT BIOL CHEM,BOSTON,MA 02114. HARVARD UNIV,DEPT MOLEC PHARMACOL,BOSTON,MA 02114. FU NIAMS NIH HHS [AR-40095-01] NR 48 TC 54 Z9 54 U1 2 U2 7 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP C569 EP C577 PN 1 PG 9 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200005 PM 1312777 ER PT J AU ODA, A DRUKER, BJ SMITH, M SALZMAN, EW AF ODA, A DRUKER, BJ SMITH, M SALZMAN, EW TI INHIBITION BY SODIUM-NITROPRUSSIDE OR PGE1 OF TYROSINE PHOSPHORYLATION INDUCED IN PLATELETS BY THROMBIN OR ADP SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE CALCIUM; GUANINE NUCLEOTIDE-BINDING PROTEIN; PP60SRC ID PROTEIN-PHOSPHORYLATION; COMMON SET; CYCLIC-AMP; ACTIVATION; ADENOSINE-3',5'-MONOPHOSPHATE; AGGREGATION; ELEVATION; VANADATE AB Upon platelet activation, numerous proteins are known to be tyrosine phosphorylated. To investigate the mechanisms of the regulation of tyrosine phosphorylation and its physiological significance, the effects on tyrosine phosphorylation of agents that elevate the platelet level of the cyclic nucleotides cAMP and cGMP were examined in aspirin-treated gel-filtered platelets by Western blotting with a specific anti-phosphotyrosine antibody. The effects of these agents on other aspects of platelet activation, i.e., aggregation, secretion, and elevation of the concentration of cytosolic ionized calcium ([Ca2+]i), were also examined in parallel experiments. Tyrosine phosphorylation in platelets activated by alpha-thrombin (1 nM) was inhibited by prostaglandin (PG) E1 (2-mu-M) or by sodium nitroprusside (100-mu-M). Elevation of [Ca2+]i, aggregation, and serotonin secretion was also strongly inhibited. On the other hand, a higher concentration of alpha-thrombin (10 nM) induced tyrosine phosphorylation of the same proteins, elevation of [Ca2+]i, platelet aggregation, and serotonin secretion, irrespective of pretreatment of platelets by either PGE1 or sodium nitroprusside. Inhibition by sodium nitroprusside of tyrosine phosphorylation induced by alpha-thrombin (1 nM) was accompanied by an increased concentration of cGMP. 8-BrcGMP (2 mM) also inhibited tyrosine phosphorylation and aggregation, although less than sodium nitroprusside. ADP (20-mu-M) induced platelet shape change and tyrosine phosphorylation of only a few proteins; these effects were also inhibited by either PGE1 or sodium nitroprusside. Thus tyrosine phosphorylation in platelets can be inhibited by elevation of either cAMP or cGMP, an effect that is overcome by a high concentration of thrombin, resulting in granule secretion and aggregation. Some of the proteins that are tyrosine phosphorylated may be important in the regulation of platelet functions. C1 BETH ISRAEL HOSP,DEPT SURG,330 BROOKLINE AVE,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR MOLEC BIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-38820, HL-33014] NR 33 TC 19 Z9 19 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP C701 EP C707 PN 1 PG 7 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200021 PM 1372480 ER PT J AU DENEKE, SM LAWRENCE, RA JENKINSON, SG AF DENEKE, SM LAWRENCE, RA JENKINSON, SG TI ENDOTHELIAL-CELL CYSTINE UPTAKE AND GLUTATHIONE INCREASE WITH N,N-BIS(2-CHLOROETHYL)-N-NITROSOUREA EXPOSURE SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE AMINO ACID TRANSPORT; PULMONARY ENDOTHELIUM; ANTIOXIDANTS; GLUTATHIONE REDUCTASE ID HUMAN-DIPLOID FIBROBLASTS; GLUTAMIC-ACID UPTAKE; TRANSPORT ACTIVITY; DIETHYL MALEATE; ELECTROPHILIC AGENTS; RAT HEPATOCYTES; HYPEROXIA; CULTURE; INDUCTION; ENHANCEMENT AB Glutathione (gamma-glutamylcysteinylglycine, GSH) is an important cellular antioxidant. In typical cultured cell preparations GSH synthesis is limited by the availability of intracellular cysteine. Because extracellular cystine is the chief source of intracellular cysteine in cultured cells, increasing cystine transport can result in increased intracellular GSH. Depletion of GSH or exposure to oxidants has been shown to stimulate cystine transport in bovine pulmonary endothelial cells and other cell types. BCNU [N,N-bis(2-chloroethyl)-N-nitrosourea] is a potent inhibitor of glutathione reductase (GSSG-Red). We examined the effects of BCNU on cystine uptake by bovine pulmonary artery endothelial cells (BPAEC). We hypothesized that blocking GSSG-Red could result in increased cellular uptake of cystine to replenish decreases in GSH caused by oxidation. Levels of BCNU between 0.005 and 0.05 mM added to the cell culture medium inhibited GSSG-Red at 2, 4, and 24 h after addition. BCNU treatment resulted in concentration-dependent increases in both cystine uptake and GSH levels after 24 h of exposure. The increases in uptake were specific for cystine and glutamate and were sodium independent, suggesting induction of a x(c)--like transport system. No intracellular accumulation of GSSG was measured nor was any significant depletion of GSH noted at any time of BCNU exposure. C1 AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX 78284. RP DENEKE, SM (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV PULM,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NHLBI NIH HHS [HL-32824] NR 21 TC 10 Z9 10 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0002-9513 J9 AM J PHYSIOL JI Am. J. Physiol. PD MAR PY 1992 VL 262 IS 3 BP L301 EP L304 PN 1 PG 4 WC Physiology SC Physiology GA HK362 UT WOS:A1992HK36200089 PM 1550253 ER PT J AU MCCARTHY, KM GONG, JL TELFORD, JR SCHNEEBERGER, EE AF MCCARTHY, KM GONG, JL TELFORD, JR SCHNEEBERGER, EE TI ONTOGENY OF IA+ ACCESSORY CELLS IN FETAL AND NEWBORN RAT LUNG SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID DENDRITIC CELLS; ALVEOLAR MACROPHAGES; MONOCLONAL-ANTIBODY; LYMPHOID-CELLS; IDENTIFICATION; HETEROGENEITY; POPULATIONS; INHALATION; RESPONSES; TOLERANCE AB In the adult mammalian lung, Ia+ dendritic cells (DC) constitute a significant population of immunologically potent accessory cells that are important in the regulation of immune responses to inhaled antigens. The newborn, in most species, displays an increased susceptibility to sensitization by inhaled antigens; whether an immaturity of pulmonary accessory cells is involved has not been determined. In the present study, the ontogeny and function of these cells were examined in fetal and newborn rats. Cells identified as DC in fetal and newborn rat lungs were Ia+, C11b +/-, OX41-, OX43-, W3/13-, W3/25-, and OX8-. They were characterized ultrastructurally by an eccentric, lobulated nucleus, a paucity of lysosomes, delicate cytoplasmic processes, and abundant membrane-associated Ia. Ia+ DC were first detected within the pulmonary mesenchyme at day 15 and by day 17 of gestation they were also present within the epithelium lining airways. The appearance of Ia+ DC preceded the migration of either T4 or T8 subclasses of T cells to the lung, the latter becoming significant only after birth, when the newborn was exposed to environmental antigens. In none of the fetal or newborn animals was Ia detected on alveolar type II cells. The accessory cell function of rat pulmonary DC, isolated from fetuses at 20 and 21 days of gestation and from newborns, was tested by an autologous mixed leukocyte reaction. At 20 and 21 days of gestation, pulmonary DC were 40 and 60% as effective, respectively, in stimulating cell proliferation in purified autologous adult splenic T cells as those isolated from adults. Immediately after birth, the accessory cell function of pulmonary DC was the same as or exceeded that of adults. It is concluded that Ia+ DC populate the fetal lung early in gestation and, although they are functionally immature in the fetal rat, at the time of birth these accessory cells are immunologically competent. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,COX BLDG 5,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-36781] NR 40 TC 31 Z9 31 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD MAR PY 1992 VL 6 IS 3 BP 349 EP 356 PG 8 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA HH869 UT WOS:A1992HH86900014 PM 1540399 ER PT J AU KOPANS, DB AF KOPANS, DB TI THE POSITIVE PREDICTIVE VALUE OF MAMMOGRAPHY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material ID NONPALPABLE BREAST-LESIONS; FINE-NEEDLE ASPIRATION; NON-PALPABLE LESIONS; OCCULT LESIONS; TUMOR SIZE; CANCER; BIOPSY; LOCALIZATION; TRIAL; DIAGNOSIS RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 41 TC 337 Z9 351 U1 0 U2 2 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1992 VL 158 IS 3 BP 521 EP 526 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HE964 UT WOS:A1992HE96400007 PM 1310825 ER PT J AU PRINCE, MR CHEW, FS AF PRINCE, MR CHEW, FS TI RENAL LYMPHOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 5 TC 1 Z9 1 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1992 VL 158 IS 3 BP 570 EP 570 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HE964 UT WOS:A1992HE96400017 PM 1738996 ER PT J AU GUTTENTAG, AR SHEPARD, JAO MCLOUD, TC AF GUTTENTAG, AR SHEPARD, JAO MCLOUD, TC TI CATHETER-INDUCED PULMONARY-ARTERY PSEUDOANEURYSM - THE HALO SIGN ON CT SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID ANEURYSM C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. NR 8 TC 13 Z9 13 U1 0 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAR PY 1992 VL 158 IS 3 BP 637 EP 639 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HE964 UT WOS:A1992HE96400031 PM 1739010 ER PT J AU FERRY, JA ZUKERBERG, LR HARRIS, NL AF FERRY, JA ZUKERBERG, LR HARRIS, NL TI FLORID PROGRESSIVE TRANSFORMATION OF GERMINAL-CENTERS - A SYNDROME AFFECTING YOUNG MEN, WITHOUT EARLY PROGRESSION TO NODULAR LYMPHOCYTE PREDOMINANCE HODGKINS-DISEASE SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE HODGKINS DISEASE; LYMPHOCYTE-PREDOMINANCE HODGKINS DISEASE; PROGRESSIVE TRANSFORMATION OF GERMINAL CENTERS; FOLLICLE LYSIS; LYMPH NODES ID PARAGRANULOMA; EXPERIENCE AB Progressive transformation of germinal centers (PTGC) occurs focally in reactive lymph nodes, and has been reported with increased frequency in patients with nodular lymphocyte predominance Hodgkin's disease (NLPHD). It has been suggested that patients with lymph node biopsy samples showing PTGC are at increased risk for the development of NLPHD, and that Hodgkin's disease may evolve from PTGC. We report five young men (ages 14-24 years, mean 18) with prominent lymphadenopathy and florid PTGC, in whom careful examination and follow-up showed no progression to Hodgkin's disease. Three patients developed adenopathy that involved several node groups and two had localized adenopathy. Cervical (2), inguinal (2) and axillary (1) nodes ranging from 3 to 4 cm were excised. The number of progressively transformed germinal centers (PTGCs) ranged from 10 to 123 per specimen (mean 67); single sections contained nine to 29 PTGCs (mean 19). In three cases the nodal architecture was significantly distorted, suggestive of NLPHD, but Reed-Sternberg cells were absent. Follow-up is available for all patients (all untreated): three patients had persistent adenopathy 1 year 4 months to 10 years after diagnosis. Results of repeat biopsy in two patients (2 and 3 years after diagnosis) showed florid PTGC with no evidence of Hodgkin's disease. One of these patients had one subsequent biopsy 8 years after presentation; results showed only rare PTGCs. The fourth and fifth patients, who had presented with isolated adenopathy, were free of recurrent adenopathy at 2 and 5 years. These cases suggest a syndrome of lymphoid hyperplasia with florid PTGC in adolescent boys and young men. Although adenopathy can persist, there has been no progression to Hodgkin's disease. Recognition of this syndrome is important to avoid overdiagnosis of LPHD. Close follow-up of these patients will be necessary to evaluate the relationship of this disorder to NLPHD. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FERRY, JA (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,FRUIT ST,BOSTON,MA 02114, USA. NR 17 TC 40 Z9 41 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD MAR PY 1992 VL 16 IS 3 BP 252 EP 258 DI 10.1097/00000478-199203000-00005 PG 7 WC Pathology; Surgery SC Pathology; Surgery GA HF371 UT WOS:A1992HF37100005 PM 1599017 ER PT J AU LESSER, M PADILLA, ML CARDOZO, C AF LESSER, M PADILLA, ML CARDOZO, C TI INDUCTION OF EMPHYSEMA IN HAMSTERS BY INTRATRACHEAL INSTILLATION OF CATHEPSIN-B SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID HUMAN ALVEOLAR MACROPHAGES; BRONCHOALVEOLAR LAVAGE FLUID; ELASTOLYTIC ACTIVITY; ALPHA-1-PROTEINASE INHIBITOR; PLASMINOGEN-ACTIVATOR; CIGARETTE SMOKERS; HUMAN NEUTROPHIL; ELASTASE; DEGRADATION; PROTEINASE AB Current theories of pathogenesis suggest that pulmonary emphysema develops in humans because of progressive loss or derangement of lung elastin through a process mediated by elastolytic enzymes released by inflammatory cells. Neutrophils are considered primary etiologic factors because these cells produce and release two potent serine proteinases that cause emphysema when instilled into the lungs of animals. It has been suggested that alveolar macrophages also contribute to the development of emphysema through production of several enzymes with elastolytic activity, including the lysosomal cysteine proteinases cathepsin B and cathepsin L, but this has not been verified experimentally. In the current study, we instilled 115-mu-g of active cathepsin B into the lungs of hamsters three times at 48-h intervals. After 6 wk microscopic evaluation revealed that lung sections of five of seven animals given cathepsin B contained focal areas of enlarged and distorted alveoli, in the absence of fibrosis, which were similar to changes seen in the lungs of animals given papain intratracheally. Morphometrically, mean linear intercept (mu-m) values were significantly higher (p < 0.025) in animals given cathepsin B (204.4 +/- 20.8) as compared with control animals (173.2 +/- 7.8), and internal surface area (sqcm) values were significantly lower (935 +/- 120 versus 1,083 +/- 56 in control animals), thereby confirming that airspace enlargement had developed after instillation of the enzyme. Lung volumes (ml) and compliance (ml/cm H2O) were not significantly higher in animals given cathepsin B. The current findings, along with additional observations that the number of alveolar macrophages are increased in the lungs of cigarette smokers and that the cells contain higher levels of cathepsin B, suggest that alveolar macrophages may participate in the development of emphysema and that cysteine proteinases contained within these cells could exert elastolytic activity thereby contributing to the process. C1 MT SINAI MED CTR,DEPT MED,NEW YORK,NY 10029. RP LESSER, M (reprint author), BRONX VET AFFAIRS MED CTR,PULM SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 49 TC 26 Z9 26 U1 1 U2 2 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD MAR PY 1992 VL 145 IS 3 BP 661 EP 668 PG 8 WC Respiratory System SC Respiratory System GA HH281 UT WOS:A1992HH28100030 PM 1546848 ER PT J AU GREENBERG, PD AF GREENBERG, PD TI DECISION-ANALYSIS COMPARING THE TUBERCULIN SCREENING STRATEGY WITH BCG VACCINE - REPLY SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Letter RP GREENBERG, PD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 0003-0805 J9 AM REV RESPIR DIS JI Am. Rev. Respir. Dis. PD MAR PY 1992 VL 145 IS 3 BP 732 EP 733 PG 2 WC Respiratory System SC Respiratory System GA HH281 UT WOS:A1992HH28100043 ER PT J AU ZWASS, MS FISHER, DM WELBORN, LG COTE, CJ DAVIS, PJ DINNER, M HANNALLAH, RS LIU, LMP SARNER, J MCGILL, WA ALIFIMOFF, JK EMBREE, PB COOK, DR AF ZWASS, MS FISHER, DM WELBORN, LG COTE, CJ DAVIS, PJ DINNER, M HANNALLAH, RS LIU, LMP SARNER, J MCGILL, WA ALIFIMOFF, JK EMBREE, PB COOK, DR TI INDUCTION AND MAINTENANCE CHARACTERISTICS OF ANESTHESIA WITH DESFLURANE AND NITROUS-OXIDE IN INFANTS AND CHILDREN SO ANESTHESIOLOGY LA English DT Article DE ANESTHESIA, PEDIATRIC, DESFLURANE; HALOTHANE; ANESTHETICS, NITROUS OXIDE; ANESTHETICS, VOLATILE, DESFLURANE; HALOTHANE; COMPLICATIONS, HYPOXEMIA; LARYNGOSPASM ID ISOFLURANE; HALOTHANE AB To determine the induction and maintenance characteristics of desflurane in pediatric patients, the authors anesthetized 206 infants and children aged 1 month to 12 yr with nitrous oxide plus desflurane and/or halothane in oxygen. Patients were assigned to one of four groups: anesthesia was 1) induced and maintained with desflurane after premedication with an oral combination of meperidine, diazepam, and atropine; 2) induced and maintained with desflurane; 3) induced with halothane and maintained with desflurane; or 4) induced and maintained with halothane. An unblinded observer recorded time to loss of consciousness (lid reflex), time to intubation, and clinical characteristics of the induction and maintenance of anesthesia. Moderate-to-severe laryngospasm (49%) and moderate-to-severe coughing (58%) occurred frequently during induction of anesthesia with desflurane; the incidence of these was not altered by premedication. In contrast, laryngospasm and coughing were rare during induction of anesthesia with halothane. In unpremedicated patients, time to loss of lid reflex (mean +/- SD) was similar for desflurane (2.4 +/- 1.2 min) and halothane (2.1 +/- 0.8 min). During induction of anesthesia, before laryngoscopy and intubation, mean arterial pressure < 80% of baseline was more common with halothane; heart rate and mean arterial pressure > 120% of baseline were more common with desflurane. Intraoperatively, heart rate > 120% of baseline was more common with desflurane; blood pressures were similar for the two anesthetics. The authors conclude that the high incidence of airway complications during induction of anesthesia with desflurane limits its utility for inhalation induction in pediatric patients. Anesthesia can be safely maintained with desflurane if induced with a different anesthetic. C1 UNIV CALIF SAN FRANCISCO,DEPT ANESTHESIA,SAN FRANCISCO,CA 94143. CHILDRENS HOSP,NATL MED CTR,DEPT ANESTHESIA,WASHINGTON,DC 20010. HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT ANAESTHESIA,BOSTON,MA 02114. UNIV PITTSBURGH,DEPT ANESTHESIA,PITTSBURGH,PA 15260. CORNELL UNIV,MED CTR,DEPT ANESTHESIA,NEW YORK,NY 10021. NR 10 TC 77 Z9 82 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1992 VL 76 IS 3 BP 373 EP 378 DI 10.1097/00000542-199203000-00009 PG 6 WC Anesthesiology SC Anesthesiology GA HG476 UT WOS:A1992HG47600009 PM 1539848 ER PT J AU ALSTON, TA AF ALSTON, TA TI ANTAGONISM OF SULFONAMIDES BY BENZOCAINE AND CHLOROPROCAINE SO ANESTHESIOLOGY LA English DT Letter RP ALSTON, TA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAR PY 1992 VL 76 IS 3 BP 475 EP 476 DI 10.1097/00000542-199203000-00027 PG 2 WC Anesthesiology SC Anesthesiology GA HG476 UT WOS:A1992HG47600027 PM 1539864 ER PT J AU POWELL, AC GOLD, MR BROOKS, R GARAN, H RUSKIN, JN MCGOVERN, BA AF POWELL, AC GOLD, MR BROOKS, R GARAN, H RUSKIN, JN MCGOVERN, BA TI ELECTROPHYSIOLOGIC RESPONSE TO MORICIZINE IN PATIENTS WITH SUSTAINED VENTRICULAR ARRHYTHMIAS SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID CONGESTIVE HEART-FAILURE; LONG-TERM; ETHMOZINE; EFFICACY; HCL; TACHYCARDIA; SAFETY; DRUG; TACHYARRHYTHMIAS; FLECAINIDE AB Objective: To assess the short-term efficacy and safety of moricizine in patients receiving electrophysiologically guided therapy for sustained ventricular arrhythmias refractory to treatment with class IA antiarrhythmic agents. Design: Uncontrolled clinical trial. Setting: Referral-based teaching medical center. Patients: Twenty-one patients (18 of whom had coronary artery disease) with a mean left ventricular ejection fraction of 32% +/- 11% who presented with sustained ventricular tachycardia (13 patients), syncope (4 patients), or cardiac arrest (4 patients). Interventions: Moricizine, 743 +/- 85 mg daily. Measurements: Electrophysiologic testing in the drug-free state and after administration of moricizine unless sustained arrhythmias occurred. Main Results: Sustained ventricular tachycardia was inducible in the absence of antiarrhythmic drugs in 20 patients and was not suppressed by moricizine in any patient. Four patients had six episodes of spontaneous ventricular tachycardia while receiving moricizine. A probable proarrhythmic response occurred in four patients. Conclusion: In patients with compromised left ventricular function caused by coronary artery disease in whom class IA antiarrhythmics were ineffective, moricizine was ineffective in suppressing sustained ventricular arrhythmias and resulted in proarrhythmic effects in some patients. C1 MASSACHUSETTS GEN HOSP, CARDIAC ARRHYTHMIA SERV, 32 FRUIT ST, BOSTON, MA 02114 USA. NR 31 TC 9 Z9 9 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 USA SN 0003-4819 EI 1539-3704 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 1 PY 1992 VL 116 IS 5 BP 382 EP 387 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HF268 UT WOS:A1992HF26800006 PM 1736771 ER PT J AU STOECKLE, JD REISER, SJ AF STOECKLE, JD REISER, SJ TI THE CORPORATE ORGANIZATION OF HOSPITAL WORK - BALANCING PROFESSIONAL AND ADMINISTRATIVE RESPONSIBILITIES SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID HEALTH-CARE; PHYSICIANS; DOCTOR AB The development of the hospital into a corporation has influenced the care of patients and the work of the professional staff. As a corporate enterprise, the modern hospital has a private agenda aimed at increasing growth and efficiency with an emphasis on technical services, professionals as employees, and patients as customers. These changes have resulted in a decrease in trustee and professional authority and an increase in administrative control. This shift in the control structure has continued in response to the need for accounting and regulation of services and in response to demands for increased growth and efficiency made by an increasingly competitive market environment. Strategies for the reorganization of hospital staff aimed at improving both inpatient and outpatient care are reviewed. The reorganization of the institution and staff, using either a staff group-practice corporation or an administrative staff model, is proposed. Clinicians have new responsibilities for developing collective arrangements for institutional governance, for allocating institutional resources, for providing public accountability regarding the use of these resources, and for defining the missions of care. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV TEXAS,HLTH SCI CTR,HOUSTON,TX 77225. RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,SERV MED,32 FRUIT ST,BOSTON,MA 02114, USA. NR 61 TC 15 Z9 15 U1 0 U2 7 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAR 1 PY 1992 VL 116 IS 5 BP 407 EP 413 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HF268 UT WOS:A1992HF26800011 PM 1736774 ER PT J AU RENSHAW, PF STERN, TA WELCH, C SCHOUTEN, R KOLODNY, EH AF RENSHAW, PF STERN, TA WELCH, C SCHOUTEN, R KOLODNY, EH TI ELECTROCONVULSIVE-THERAPY TREATMENT OF DEPRESSION IN A PATIENT WITH ADULT GM2 GANGLIOSIDOSIS SO ANNALS OF NEUROLOGY LA English DT Note ID HEXOSAMINIDASE-A DEFICIENCY; DISEASE AB Adult GM2 gangliosidosis is a rare disorder that often presents with both neurological and psychiatric syndromes. Effective treatment of the psychotic and affective symptoms associated with this disorder has been complicated by poor treatment response and the concern that many psychotropic agents may worsen the underlying gangliosidosis. We report he successful use of electroconvulsive therapy for treatment of severe depression in a young man with adult GM2 gangliosidosis. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP RENSHAW, PF (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114, USA. NR 10 TC 15 Z9 15 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD MAR PY 1992 VL 31 IS 3 BP 342 EP 344 DI 10.1002/ana.410310320 PG 3 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA HQ121 UT WOS:A1992HQ12100019 PM 1386210 ER PT J AU CHAN, KH DOYLE, WJ SWARTS, JD KARDATZKE, D HASHIDA, Y WOLF, GL AF CHAN, KH DOYLE, WJ SWARTS, JD KARDATZKE, D HASHIDA, Y WOLF, GL TI EXPERIMENTAL OTITIS-MEDIA EVALUATED BY MAGNETIC-RESONANCE-IMAGING - AN INVIVO MODEL SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE ANIMAL MODEL; INFLAMMATION; MAGNETIC RESONANCE IMAGING; OTITIS MEDIA AB The use of magnetic resonance imaging in otitis media research is being explored in our laboratory. In this study, we present a new method for studying changes in the middle ear cleft due to an episode of induced otitis media in the chinchilla model. It uses gadolinium-diethylenetriamine pentaacetic acid, a magnetic resonance imaging contrast agent, to examine the uptake and washout characteristics of middle ear mucosa during an inflammatory episode. Parameters such as the time to maximum intensity of the mucosa and the washout rate of the contrast agent from the mucosa were significantly correlated to the duration of the infection. C1 UNIV PITTSBURGH,CHILDRENS HOSP PITTSBURGH,SCH MED,DEPT PATHOL,PITTSBURGH,PA 15213. MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02114. RP CHAN, KH (reprint author), UNIV PITTSBURGH,CHILDRENS HOSP PITTSBURGH,SCH MED,DEPT OTOLARYNGOL,PITTSBURGH,PA 15213, USA. FU NIDCD NIH HHS [DC00158, DC00561] NR 7 TC 10 Z9 10 U1 0 U2 0 PU ANNALS PUBL CO PI ST LOUIS PA 4507 LACLEDE AVE, ST LOUIS, MO 63108 SN 0003-4894 J9 ANN OTO RHINOL LARYN JI Ann. Otol. Rhinol. Laryngol. PD MAR PY 1992 VL 101 IS 3 BP 248 EP 254 PG 7 WC Otorhinolaryngology SC Otorhinolaryngology GA HH873 UT WOS:A1992HH87300008 PM 1543334 ER PT J AU BAETHGE, BA LIDSKY, MD GOLDBERG, JW AF BAETHGE, BA LIDSKY, MD GOLDBERG, JW TI A STUDY OF ADVERSE-EFFECTS OF HIGH-DOSE INTRAVENOUS (PULSE) METHYLPREDNISOLONE THERAPY IN PATIENTS WITH RHEUMATIC DISEASE SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; METHYL PREDNISOLONE; UNPROVED THERAPY; ARTHRITIS; TRIAL AB OBJECTIVE: To determine the frequency of significant adverse effects associated with high-dose intravenous methylprednisolone therapy (HIVMP) given as methylprednisolone 1 g/d for three consecutive days. DESIGN: Retrospective study of consecutive patients. SETTING: Department of Veterans Affairs Medical Center (VAMC), university teaching hospital, and private outpatient clinic. PATIENTS: Eighty-four patients given HIVMP for systemic rheumatic disease. MEASUREMENTS: Subjective complaints were elicited via a standardized questionnaire that identified adverse effects through organ system review. Medical records were reviewed for adverse effects occurring within two weeks of HIVMP therapy. RESULTS: Two hundred seventy-five HIVMP treatments were examined by either patient questionnaire (76 patients) and/or chart review (78 patients). Sixty-five patients described symptoms after HIVMP treatment. Most symptoms were transient in duration, mild in severity, and required no medical treatment. Chart review found 42 possible complications occurring within two weeks of HIVMP therapy. In 18 instances medical intervention was required for problems that included hypertension, seizures, gastric erosions, sepsis, and other infections. It is impossible to attribute all of the complications to HIVMP alone because of underlying disease, use of other medications at the time of therapy, or both. CONCLUSIONS: HIVMP has an acceptably low risk of significant adverse effects. C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,DEPT MED,RHEUMATOL SECT,HOUSTON,TX 77030. MARSHFIELD CLIN FDN MED RES & EDUC,MED,MARSHFIELD,WI 54449. RP BAETHGE, BA (reprint author), LOUISIANA STATE UNIV,MED CTR,CTR EXCELLENCE ARTHRIT & RHEUMATOL,POB 33932,SHREVEPORT,LA 71130, USA. NR 21 TC 34 Z9 35 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 1992 VL 26 IS 3 BP 316 EP 320 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ266 UT WOS:A1992HJ26600001 PM 1554949 ER PT J AU HERRERA, CR MOSS, JT REVES, RR BUFFLER, PA AF HERRERA, CR MOSS, JT REVES, RR BUFFLER, PA TI FEASIBILITY STUDY OF SURVEYING THE ADVERSE DRUG REACTION SURVEILLANCE SYSTEMS IN A LARGE COMMUNITY OF HOSPITALS SO ANNALS OF PHARMACOTHERAPY LA English DT Article ID PROGRAM; PHARMACIST AB OBJECTIVE: To determine the feasibility of accurately assessing the types of hospital adverse drug reaction (ADR) surveillance systems. DESIGN: Cross-sectional survey by mailed, self-administered questionnaire followed by selected verification interviews. SETTING: Harris County, Texas. PARTICIPANTS: All hospitals in the county with different pharmacy directors. MAIN OUTCOME MEASURE: Self description of surveillance system and number of ADRs reported. RESULTS: Forty-nine of 61 hospitals (80 percent) responded to a questionnaire. Forty-seven (96 percent) of the responding hospitals collected information on ADRs with 11 (22 percent) describing their surveillance system as active. Those individuals most often cited as responsible for ADR surveillance included pharmacists, quality assurance personnel, and nurses. Data were verified by personal interviews for 10 hospitals. The number of ADRs reported during the interviews was significantly lower than that reported in the questionnaires. Overall, the reporting of fatal and severe ADRs were more reliable than the reporting of moderate ADRs. These differences were the result of inadequate documentation and the lack of a uniform definition of ADRs. CONCLUSIONS: These data suggest that a large-scale ongoing survey of surveillance systems and reported adverse event rates has limitations and the reliability of data derived from a questionnaire should be verified. To improve the accuracy of surveys used to monitor hospital ADR surveillance systems, it is essential to develop reliable definitions for classifying ADRs and surveillance methods, as well as accurate measures of ADR documentation procedures. C1 DEPT VET AFFAIRS MED CTR,PHARM SERV,DRUG UTILIZAT & INFORMAT ANAL SECT,HOUSTON,TX. UNIV CALIF BERKELEY,SCH PUBL HLTH,BERKELEY,CA 94720. RP HERRERA, CR (reprint author), UNIV TEXAS,HLTH SCI CTR,MSB 1122,643 FANNIN,HOUSTON,TX 77030, USA. NR 34 TC 4 Z9 4 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 1992 VL 26 IS 3 BP 384 EP 391 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HJ266 UT WOS:A1992HJ26600016 PM 1554961 ER PT J AU STILL, RJ HILGENBERG, AD AKINS, CW DAGGETT, WM BUCKLEY, MJ AF STILL, RJ HILGENBERG, AD AKINS, CW DAGGETT, WM BUCKLEY, MJ TI INTRAOPERATIVE AORTIC DISSECTION SO ANNALS OF THORACIC SURGERY LA English DT Article ID ROOT DISSECTION; SURGERY AB Intraoperative aortic dissection is a rare but potentially fatal complication of open heart operations. If the dissection is promptly recognized and repaired, however, the outcome may be significantly better. In this study, we reviewed the hospital records of patients with dissection of the aortic arch occurring as a complication of a cardiac operation at Massachusetts General Hospital and Mt. Auburn Hospital from January 1980 through June 1990. During this period, 14,877 surgical procedures with the use of cardiopulmonary bypass and aortic cannulation were performed, and 24 patients (0.16%) with iatrogenic aortic dissection were identified. Dissection was discovered intraoperatively in 20 patients and postoperatively after complications developed in 4. Of the 20 patients whose injuries were discovered intraoperatively and repaired, 4 (20%) died. Of the 4 whose injuries were discovered after operation, 2 (50%) died. The primary cause of death was ventricular dysfunction resulting from myocardial ischemia. Dissections originated at the aortic cannulation site in 10 patients, at the cross-clamp site in 8, at the site of the partial-occlusion clamp in 7, at the proximal anastomosis in 1 patient, and as a result of direct injury in 1. Three of these patients had simultaneous injuries at the aortic cannulation site and at the heel of the partial-occlusion clamp. Two techniques of repair were used: primary repair and patch or tube graft insertion. There were two deaths in the patients who underwent primary repair and four deaths in patients requiring graft replacement. Although it is uncommon, intraoperative aortic dissection can be a lethal complication of cardiac operations. Prompt recognition and repair are necessary to limit the extent of dissection and minimize patient morbidity and mortality. C1 MASSACHUSETTS GEN HOSP,SURG CARDIOVASC UNIT,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 13 TC 71 Z9 74 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD MAR PY 1992 VL 53 IS 3 BP 374 EP 380 PG 7 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA HH119 UT WOS:A1992HH11900004 PM 1540051 ER PT J AU WALLACE, JE HARRIS, SC GALLEGOS, J FOULDS, G CHEN, TJH RINALDI, MG AF WALLACE, JE HARRIS, SC GALLEGOS, J FOULDS, G CHEN, TJH RINALDI, MG TI ASSAY OF FLUCONAZOLE BY HIGH-PERFORMANCE LIQUID-CHROMATOGRAPHY WITH A MIXED-PHASE COLUMN SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Article ID HUMANS AB A mixed-phase liquid chromatographic column was used to assay fluconazole in plasma, serum, and cerebrospinal fluid. The assay was linear from 0.2 to 20-mu-g/ml, with an average coefficient of variation of less than 5%. The partitioning of the drug between serum and cerebrospinal fluid was determined for 34 patients. The method was demonstrated to be suitable for both pharmacokinetic studies and monitoring of patients receiving treatment with this antifungal agent. C1 AUDIE L MURPHY MEM VET ADM MED CTR,LAB SERV,SAN ANTONIO,TX 78284. PRECIS ANALYT LABS INC,SAN ANTONIO,TX 78216. PFIZER INC,CENT RES,DEPT DRUG METAB,GROTON,CT 06340. RP WALLACE, JE (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284, USA. NR 8 TC 32 Z9 32 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD MAR PY 1992 VL 36 IS 3 BP 603 EP 606 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA HH283 UT WOS:A1992HH28300015 PM 1622169 ER PT J AU BERRY, AJ RINALDI, MG GRAYBILL, JR AF BERRY, AJ RINALDI, MG GRAYBILL, JR TI USE OF HIGH-DOSE FLUCONAZOLE AS SALVAGE THERAPY FOR CRYPTOCOCCAL MENINGITIS IN PATIENTS WITH AIDS SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID ACQUIRED IMMUNODEFICIENCY SYNDROME AB Eight patients with AIDS were treated orally with 800 mg of fluconazole daily for cryptococcal meningitis for a mean duration of 4.5 months. Previous antifungal treatment had failed for all of the patients. No major toxicity was observed. Three patients died from cryptococcal infection. High-dose fluconazole may be effective salvage therapy for cryptococcal meningitis. C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP BERRY, AJ (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 12 TC 65 Z9 67 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0066-4804 J9 ANTIMICROB AGENTS CH JI Antimicrob. Agents Chemother. PD MAR PY 1992 VL 36 IS 3 BP 690 EP 692 PG 3 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA HH283 UT WOS:A1992HH28300036 PM 1622188 ER PT J AU LILLOMARTIN, DC HANSON, VL SMITH, ST AF LILLOMARTIN, DC HANSON, VL SMITH, ST TI DEAF READERS COMPREHENSION OF RELATIVE CLAUSE STRUCTURES SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID POOR READERS; LANGUAGE; SENTENCES; SIGNERS; HEARING AB It is commonly found that most deaf readers display an overall depressed level of reading performance in conjunction with specific difficulties in complex syntax. In this study, deaf good and poor readers' comprehension of relative clause structures was tested in written English, signed English, and American Sign Language. It was found that the behavior of deaf good and poor readers was parallel across relative clause sentence types, and that the deaf readers generally performed similarly to hearing readers tested in a different study. These results support the hypothesis that a specific syntactic disability does not differentiate deaf good and poor readers. Instead, it is suggested that a processing deficit may underlie the poor readers' comprehension difficulties. C1 IBM CORP,THOMAS J WATSON RES CTR,DIV RES,YORKTOWN HTS,NY 10598. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HASKINS LABS INC,NEW HAVEN,CT 06511. RP LILLOMARTIN, DC (reprint author), UNIV CONNECTICUT,DEPT LINGUIST,U-145,341 MANSFIELD RD,RM 230,STORRS,CT 06269, USA. NR 27 TC 12 Z9 12 U1 0 U2 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 SN 0142-7164 J9 APPL PSYCHOLINGUIST JI Appl. Psycholinguist. PD MAR PY 1992 VL 13 IS 1 BP 13 EP 30 DI 10.1017/S0142716400005403 PG 18 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA HU690 UT WOS:A1992HU69000002 ER PT J AU KAYE, ET BLANK, IH ANDERSON, RR ARNDT, KA LEVIN, JA AF KAYE, ET BLANK, IH ANDERSON, RR ARNDT, KA LEVIN, JA TI DURABLE PROTECTION AGAINST LONG-WAVELENGTH UV-A RADIATION AND BLUE-LIGHT - REPLY SO ARCHIVES OF DERMATOLOGY LA English DT Letter C1 BETH ISRAEL HOSP,DEPT DERMATOL,BOSTON,MA 02215. RP KAYE, ET (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,DEPT DERMATOL,BOSTON,MA 02114, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1992 VL 128 IS 3 BP 409 EP 409 PG 1 WC Dermatology SC Dermatology GA HH855 UT WOS:A1992HH85500020 ER PT J AU GREEN, HA MOSCHELLA, S AF GREEN, HA MOSCHELLA, S TI MULTIPLE INVASIVE SQUAMOUS-CELL CARCINOMAS AND COMMON VARIABLE IMMUNODEFICIENCY SO ARCHIVES OF DERMATOLOGY LA English DT Letter ID CANCER C1 LAHEY CLIN FDN,MED CTR,DEPT DERMATOL,BURLINGTON,MA 01805. RP GREEN, HA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN 2,BOSTON,MA 02114, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAR PY 1992 VL 128 IS 3 BP 412 EP 413 PG 2 WC Dermatology SC Dermatology GA HH855 UT WOS:A1992HH85500026 PM 1550383 ER PT J AU KASHKET, S YASKELL, T AF KASHKET, S YASKELL, T TI EFFECT OF TIMING OF ADMINISTERED CALCIUM LACTATE ON THE SUCROSE-INDUCED INTRAORAL DEMINERALIZATION OF BOVINE ENAMEL SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE CALCIUM; INTRAORAL; DEMINERALIZATION; ENAMEL; PHOSPHATE; STREPTOCOCCUS-MUTANS; PLAQUE ID DENTAL PLAQUE; CARIES; FLUORIDE; MOUTHRINSE; FLUID AB A number of soluble calcium salts are known to reduce the demineralization of enamel in the mouth. The present study was undertaken to examine the effects of rinses containing different concentrations of calcium lactate, and the time of giving the rinses with respect to sucrose challenges. Subjects wore palatal appliances containing blocks of bovine enamel whose surfaces were covered with Streptococcus mutans IB 1600, and rinsed with 10% sucrose for 1 min. Changes in iodide penetrability of the enamel, and the pH and extracellular ion concentrations of the streptococcal plaque were determined. When added to the sucrose rinse, 100 or 150 mM calcium lactate reduced demineralization by about 35%, although the plaque pH was not affected. Plaque calcium was elevated but diffused away rapidly so that concentrations after 45 min were close to control values. Plaque inorganic phosphate and lactate were not affected. Ongoing demineralization appeared to be stopped when 100 mM calcium lactate was given 15 min after the sucrose rinse. When the lactate was given 15 min before the sucrose rinse, demineralization was reduced by only about 25%, consistent with the rapid diffusion of plaque calcium. The combination of (i) pretreatment with calcium lactate and (ii) admixture of calcium lactate with sucrose was most effective. Demineralization was reduced about 55% with 100 mM calcium lactate under these conditions, and protective effects were seen with as little as 25 mM. In summary, the findings demonstrate the enamel-protective effect of relatively low concentrations of calcium lactate, and point to the need to sustain a high plaque calcium during periods of maximum acidogenicity. C1 FORSYTH DENT CTR,CTR RES ORAL & BIOL EFFECTS FOODS,BOSTON,MA 02115. RP KASHKET, S (reprint author), FORSYTH DENT CTR,DEPT BIOCHEM,BOSTON,MA 02115, USA. NR 26 TC 5 Z9 6 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0003-9969 J9 ARCH ORAL BIOL JI Arch. Oral Biol. PD MAR PY 1992 VL 37 IS 3 BP 187 EP 191 DI 10.1016/0003-9969(92)90088-P PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HM457 UT WOS:A1992HM45700004 PM 1586281 ER PT J AU GOLDMACHER, VS SENTER, PD LAMBERT, JM BLATTLER, WA AF GOLDMACHER, VS SENTER, PD LAMBERT, JM BLATTLER, WA TI PHOTOACTIVATION OF TOXIN CONJUGATES SO BIOCONJUGATE CHEMISTRY LA English DT Article ID RICIN-A-CHAIN; CYTO-TOXICITY; PROTEIN; INTERNALIZATION; IMMUNOTOXINS; ANTIBODIES; GELONIN; CELLS AB A novel photocleavable protein cross-linking reagent has been used for conjugation of the ribosome-inactivating protein pokeweed antiviral protein from seeds of Phytolacca americana (PAP-S), with either the monoclonal antibody 5E9 directed against the human transferrin-receptor or the B-chain of ricin that binds to cell-surface oligosaccharides bearing terminal D-galactose residues. When irradiated with near-UV light (350 nm), the linker of these conjugates undergoes photolytic degradation, resulting in the release of native toxin that is fully functional. The cytotoxicities of these 5E9-PAP-S and ricin B-chain-PAP-S conjugates for HeLa cells could be enhanced by irradiating the cells with light after they had internalized the conjugates. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GOLDMACHER, VS (reprint author), IMMUNOGEN INC,148 SIDNEY ST,CAMBRIDGE,MA 02139, USA. NR 20 TC 19 Z9 19 U1 0 U2 11 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 1043-1802 J9 BIOCONJUGATE CHEM JI Bioconjugate Chem. PD MAR-APR PY 1992 VL 3 IS 2 BP 104 EP 107 DI 10.1021/bc00014a003 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Multidisciplinary; Chemistry, Organic SC Biochemistry & Molecular Biology; Chemistry GA HL948 UT WOS:A1992HL94800003 PM 1515463 ER PT J AU RYAN, L AF RYAN, L TI QUANTITATIVE RISK ASSESSMENT FOR DEVELOPMENTAL TOXICITY SO BIOMETRICS LA English DT Article DE MULTINOMIAL MODEL; OVERDISPERSION; QUASI-LIKELIHOOD; RISK ASSESSMENT; TERATOLOGY ID GLYCOL DIMETHYL ETHER; DOSE-RESPONSE MODEL; TERATOLOGICAL EXPERIMENTS; MICE; RATS AB Pharmaceutical companies and governmental regulatory agencies are becoming increasingly aware of the need for improved statistical methods for developmental toxicity experiments. Although a number of statisticians have become interested in this area, activity has centered mostly on the development of methods to analyze binary outcomes, such as malformations among live pups, while accounting appropriately for the correlation induced by the litter effect. In contrast, the topic of quantitative risk assessment has received relatively little attention. This paper addresses the specific question of how to assess risk appropriately when exposure causes a variety of adverse effects, including resorption and fetal death, in addition to malformations. It will be seen that risk assessments based on a single developmental outcome, such as malformation, may be conservative. A method is proposed for estimating an exposure level at which the overall risk of any adverse effect is acceptably low. The method is based on a continuation ratio formulation of a multinomial distribution, with an additional scale parameter to account for overdispersion. Comparisons are made with binary models on prenatal death and malformation, as well as a binary model that makes no distinction between death and malformation, but simply classifies each fetus as normal or abnormal. Data from several developmental toxicity studies illustrate the results and findings. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP RYAN, L (reprint author), HARVARD UNIV,SCH PUBL HLTH,44 BINNEY ST,BOSTON,MA 02115, USA. RI Ryan, Louise/A-4562-2009 OI Ryan, Louise/0000-0001-5957-2490 FU NCI NIH HHS [CA48061] NR 19 TC 76 Z9 76 U1 0 U2 4 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1992 VL 48 IS 1 BP 163 EP 174 DI 10.2307/2532747 PG 12 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA HR666 UT WOS:A1992HR66600014 PM 1581483 ER PT J AU LIPSITZ, SR AF LIPSITZ, SR TI METHODS FOR ESTIMATING THE PARAMETERS OF A LINEAR-MODEL FOR ORDERED CATEGORICAL-DATA SO BIOMETRICS LA English DT Article DE GENERALIZED LEAST SQUARES; ORDERED CATEGORICAL DATA; SCORE; VARIANCE CORRECTION ID REGRESSION AB In many empirical analyses, the response of interest is categorical with an ordinal scale attached. Many investigators prefer to formulate a linear model, assigning scores to each category of the ordinal response and treating it as continuous. When the covariates are categorical, Haber (1985, Computational Statistics and Data Analysis 3, 1-10) has developed a method to obtain maximum likelihood (ML) estimates of the parameters of the linear model using Lagrange multipliers. However, when the covariates are continuous, the only method we found in the literature is ordinary least squares (OLS), performed under the assumption of homogeneous variance. The OLS estimates are unbiased and consistent but, since variance homogeneity is violated, the OLS estimates of variance can be biased and may not be consistent. We discuss a variance estimate (White, 1980, Econometrica 48, 817-838) that is consistent for the true variance of the OLS parameter estimates. The possible bias encountered by using the naive OLS variance estimate is discussed. An estimated generalized least squares (EGLS) estimator is proposed and its efficiency relative to OLS is discussed. Finally, an empirical comparison of OLS, EGLS, and ML estimators is made. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP LIPSITZ, SR (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,677 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI24643]; NIGMS NIH HHS [GM29745]; OID CDC HHS [CH39929] NR 19 TC 12 Z9 12 U1 0 U2 0 PU INTERNATIONAL BIOMETRIC SOC PI WASHINGTON PA 808 17TH ST NW SUITE 200, WASHINGTON, DC 20006-3910 SN 0006-341X J9 BIOMETRICS JI Biometrics PD MAR PY 1992 VL 48 IS 1 BP 271 EP 281 DI 10.2307/2532755 PG 11 WC Biology; Mathematical & Computational Biology; Statistics & Probability SC Life Sciences & Biomedicine - Other Topics; Mathematical & Computational Biology; Mathematics GA HR666 UT WOS:A1992HR66600022 PM 1581487 ER PT J AU POTTS, JT AF POTTS, JT TI CHEMISTRY OF THE CALCITONINS SO BONE AND MINERAL LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP CELEBRATING THE 30TH ANNIVERSARY OF THE DISCOVERY OF CALCITONIN CY AUG 29, 1991 CL UNIV BRIT COLUMBIA, VANCOUVER, CANADA SP MED RES COUNCIL CANADA, ROYAL SOC CANADA, RHONE POULENC RORER PHARM HO UNIV BRIT COLUMBIA ID SALMON-CALCITONIN; ANALOGS C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP POTTS, JT (reprint author), MASSACHUSETTS GEN HOSP,GEN MED SERV,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [P01-DK11794-23] NR 11 TC 9 Z9 9 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0169-6009 J9 BONE MINER JI Bone Miner. PD MAR PY 1992 VL 16 IS 3 BP 169 EP 173 DI 10.1016/0169-6009(92)90894-J PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HH298 UT WOS:A1992HH29800008 PM 1314120 ER PT J AU SHARABI, Y ABRAHAM, VS SYKES, M SACHS, DH AF SHARABI, Y ABRAHAM, VS SYKES, M SACHS, DH TI MIXED ALLOGENEIC CHIMERAS PREPARED BY A NON-MYELOABLATIVE REGIMEN - REQUIREMENT FOR CHIMERISM TO MAINTAIN TOLERANCE SO BONE MARROW TRANSPLANTATION LA English DT Article ID BONE-MARROW; MONOCLONAL-ANTIBODIES; TRANSPLANTATION TOLERANCE; HOST DISEASE; CELLS; GRAFT; SURFACE; SPECIFICITY; IRRADIATION; ENGRAFTMENT AB We have recently described a non-myeloablative conditioning regimen permitting engraftment of allogeneic bone marrow in mice which involves administration of anti-CD4 (GK1.5) plus anti-CD8 (2.43) monoclonal antibodies in vivo, 3 Gy whole body irradiation, plus 7 Gy thymic irradiation. B10 (H-2b) mice prepared by this regimen and infused with unmanipulated B10.D2 (H-2d) bone marrow develop permanent mixed lymphohematopoietic chimerism and specific tolerance to donor skin grafts. We now demonstrate that mixed chimerism persists longer than 170 days in the lymphoid tissues including spleen, thymus and bone marrow of such animals, and that equivalent levels of donor chimerism are observed in both T and B cell compartments. In addition stable mixed chimeras were found to be unresponsive to host (B10) and donor (B10.D2) stimulator cells in mixed lymphocyte reaction and in cell mediated lympholysis assays, while responses to a third party (B10.BR, H-2k) were intact. Persistent chimerism was found to be necessary for the maintenance of skin graft tolerance in these animals, since in vivo depletion of donor cells by treatment with an anti-H-2d (34-2-12) monoclonal antibody resulted in the subsequent rejection of donor skin grafts. These studies demonstrate that mixed allogeneic chimeras produced using this regimen are specifically tolerant to donor in vitro and in vivo, and that persistence of donor chimerism is critical for the maintenance of tolerance. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. FU NCI NIH HHS [R01 CA5590]; PHS HHS [R01 A131158] NR 23 TC 124 Z9 124 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0268-3369 J9 BONE MARROW TRANSPL JI Bone Marrow Transplant. PD MAR PY 1992 VL 9 IS 3 BP 191 EP 197 PG 7 WC Biophysics; Oncology; Hematology; Immunology; Transplantation SC Biophysics; Oncology; Hematology; Immunology; Transplantation GA HL770 UT WOS:A1992HL77000007 PM 1387333 ER PT J AU SIMON, LS BASCH, CM YOUNG, DY ROBINSON, DR AF SIMON, LS BASCH, CM YOUNG, DY ROBINSON, DR TI EFFECTS OF NAPROXEN ON RENAL-FUNCTION IN OLDER PATIENTS WITH MILD TO MODERATE RENAL DYSFUNCTION SO BRITISH JOURNAL OF RHEUMATOLOGY LA English DT Article DE NONSTEROIDAL ANTIINFLAMMATORY DRUGS (NSAID); THE ELDERLY; RENAL DYSFUNCTION; RENAL HEMODYNAMICS; SERUM THROMBOXANE B-2 (TXB2); URINARY PROSTAGLANDINS E2 (PGE2) AND I-2 (PROSTACYCLIN; 6-KETO-PGF1-ALPHA) ID ANTI-INFLAMMATORY DRUGS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; PROSTAGLANDIN EXCRETION; SULINDAC; IBUPROFEN; FAILURE; NSAID; NEPHROTOXICITY; IDENTIFICATION; INSUFFICIENCY C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,ARTHRITIS UNIT,BOSTON,MA 02114. SYNTEX RES LABS INC,PALO ALTO,CA. RP SIMON, LS (reprint author), NEW ENGLAND DEACONESS HOSP,MED SERV,110 FRANCIS ST,SUITE 5A,BOSTON,MA 02215, USA. FU NCRR NIH HHS [RR01066-12]; NIAMS NIH HHS [AR03564-03] NR 31 TC 8 Z9 8 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0263-7103 J9 BRIT J RHEUMATOL JI Br. J. Rheumatol. PD MAR PY 1992 VL 31 IS 3 BP 163 EP 168 PG 6 WC Rheumatology SC Rheumatology GA HG592 UT WOS:A1992HG59200005 PM 1540783 ER PT J AU ROSENBAUM, JF AF ROSENBAUM, JF TI EVALUATION AND MANAGEMENT OF THE TREATMENT-RESISTANT ANXIETY DISORDER PATIENT SO BULLETIN OF THE MENNINGER CLINIC LA English DT Article; Proceedings Paper CT 1992 ANNUAL MEETING OF THE AMERICAN PSYCHIATRIC ASSOC : INTEGRATED TREATMENT OF PANIC DISORDER AND SOCIAL PHOBIA CY MAY 02, 1992 CL WASHINGTON, DC SP MENNINGER, ROCHE LAB ID PANIC DISORDER; BEHAVIORAL-INHIBITION; LIFE EVENTS; AGORAPHOBIA; DEPRESSION; CHILDREN; ONSET AB Effective evaluation and management of patients with anxiety disorders require an integrated theoretical model that predicts risk for the disorder as a consequence of constitutional vulnerability shaped by developmental experience and activated or influenced by environmental factors. From this perspective, the author describes a rational therapeutic strategy with treatment-resistant patients. He particularly urges a careful evaluation of risk factors and associated conditions that may contribute to persisting distress. RP ROSENBAUM, JF (reprint author), MASSACHUSETTS GEN HOSP,15 PARKMAN ST,WACC 815,BOSTON,MA 02114, USA. NR 25 TC 2 Z9 2 U1 0 U2 0 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 1992 VL 56 IS 2 SU A BP A50 EP A60 PG 11 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA HW009 UT WOS:A1992HW00900006 PM 1623340 ER PT J AU AOBA, T MORENO, EC AF AOBA, T MORENO, EC TI CHANGES IN THE SOLUBILITY OF ENAMEL MINERAL AT VARIOUS STAGES OF PORCINE AMELOGENESIS SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE AMELOGENESIS; ENAMEL MINERAL; CARBONATOAPATITE; SOLUBILITY ID DENTAL ENAMEL; CARBONATE; APATITES; FLUID AB The solubility of enamel mineral (a carbonated apatite) formed at various stages of porcine amelogenesis was investigated at controlled partial pressures of CO2. Enamel samples were obtained from the outer (young) secretory, inner (old) secretory, early (soft) and late (hard) mature enamel of the permanent dentition of slaughtered piglets. The dissected enamel was pulverized and subjected to a plasma ashing at low temperature to remove organic matter. The composition (Ca, total P, HPO4, and CO3) of the enamel mineral was determined chemically. The enamel mineral contained significant amounts of carbonate and acid phosphate; the model adopted for its stoichiometry was [Ca]5-x [HPO4]v[CO3]w[PO4]3-x[OH]1-x. Each enamel sample was equilibrated in dilute phosphoric acid solutions (0.01-1.2 mM) under Pco2 = 1.86 and 1.75%. Equilibration of the enamel samples usually took 20-25 days; the solution composition (pH, concentrations of Ca, P, Mg, Na, and K, and activity of Ca2+) was determined periodically. The composition of the solution at equilibrium showed that (1) the outer (younger) secretory mineral was the most soluble and the solubility of enamel mineral decreased with advancing developmental stages; (2) the mean activity product in the saturated solutions for the outer secretory enamel was the same as that calculated on the basis of the reported composition of the enamel fluid; and (3) the solubility data obtained with most of the enamel samples were consistent with a model in which the equilibration includes two processes: dissolution of the original enamel mineral and precipitation of a new carbonatoapatite. Analyses of the equilibrated samples, particularly the mature enamel, by electron microscopy, supported the precipitation of carbonatoapatite. The overall results are in good agreement with previous results indicating that significant changes in the composition and structure of porcine enamel mineral occur with the mineralization progress. RP AOBA, T (reprint author), FORSYTH DENT CTR,DEPT PHYS CHEM,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-8670, DE-3187, DE-7009] NR 26 TC 17 Z9 18 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0171-967X J9 CALCIFIED TISSUE INT JI Calcif. Tissue Int. PD MAR PY 1992 VL 50 IS 3 BP 266 EP 272 DI 10.1007/BF00296292 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HD540 UT WOS:A1992HD54000011 PM 1617502 ER PT J AU PANDOLFI, F TRENTIN, L BOYLE, LA STAMENKOVIC, I BYERS, HR COLVIN, RB KURNICK, JT AF PANDOLFI, F TRENTIN, L BOYLE, LA STAMENKOVIC, I BYERS, HR COLVIN, RB KURNICK, JT TI EXPRESSION OF CELL-ADHESION MOLECULES IN HUMAN-MELANOMA CELL-LINES AND THEIR ROLE IN CYTOTOXICITY MEDIATED BY TUMOR-INFILTRATING LYMPHOCYTES SO CANCER LA English DT Article ID METASTATIC MELANOMA; AUTOLOGOUS MELANOMA; LYMPH-NODE; IMMUNOGLOBULIN SUPERFAMILY; LEUKOCYTE DIFFERENTIATION; MONOCLONAL-ANTIBODY; INTEGRIN RECEPTORS; ENDOTHELIAL-CELLS; CLONAL ANALYSIS; IV COLLAGEN AB The role of cell adhesion molecules (CAM) LFA1, ICAM-1, LFA3, VLA1, VLA4, CD29, CD44, and CD56 in tumor-infiltrating lymphocyte (TIL) and natural killer cell (NK)-mediated killing of target cells was studied. Melanoma cell lines and autologous TIL were derived from seven patients with metastatic melanoma, and cytotoxicity assays were done in the presence and absence of monoclonal antibodies (MoAb) to CAM expressed on melanoma cells or TIL. The melanoma cell lines analyzed were all positive for CD29 and LFA3 expression, negative for LFA1 expression, but showed variable expression of ICAM-1, VLA1, VLA4, CD44, and CD56. The effects of anti-CAM antibodies on TIL-mediated melanoma killing fell into three categories: (1) consistent inhibition of TIL-mediated killing was observed when melanoma cells were pretreated with anti-ICAM1 and anti-LFA-3 MoAb or when TIL were pretreated with anti-LFA1; (2) no effect was observed when melanoma cells were pretreated with anti-CD56; or (3) a discreet, but significant, inhibition was observed when target cells were pretreated with anti-CD29, anti-VLA1, anti-VLA4, and anti-CD44. Cytotoxicity was significantly enhanced by pretreatment of target cells with gamma-interferon (gamma-IFN), although gamma-IFN did not augment surface expression of the CAM studied. The NK-mediated killing of K562 cells was blocked by anti-LFA1, anti-CD18, and anti-ICAM, and partially inhibited by anti-CD44 MoAb. Together, these results suggest that several accessory CAM may play a role in regulating cellular cytotoxicity. Because cytotoxicity generally correlated with the level of expression of CAM in melanoma cells, weak CAM surface expression may provide a means for melanomas to escape immune surveillance. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RI TRENTIN, LIVIO/J-7676-2016 OI TRENTIN, LIVIO/0000-0003-1222-6149 FU NCI NIH HHS [CA 44324]; NIAMS NIH HHS [AR 39993] NR 51 TC 67 Z9 67 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 1992 VL 69 IS 5 BP 1165 EP 1173 PG 9 WC Oncology SC Oncology GA HF672 UT WOS:A1992HF67200016 PM 1739916 ER PT J AU PARRY, RL CHIN, T EPSTEIN, J HUDSON, PL POWELL, DM DONAHOE, PK AF PARRY, RL CHIN, T EPSTEIN, J HUDSON, PL POWELL, DM DONAHOE, PK TI RECOMBINANT HUMAN MULLERIAN INHIBITING SUBSTANCE INHIBITS HUMAN OCULAR MELANOMA CELL-LINES INVITRO AND INVIVO SO CANCER RESEARCH LA English DT Article ID HUMAN OVARIAN-CANCER; COLONY GROWTH; ASSAY; MODEL; SPHEROIDS; CULTURE; CAPSULE; BOVINE; GENE; MICE AB Since Mullerian Inhibiting Substance (MIS) causes regression of the Mullerian duct, the anlagen of the uterus, vagina, and fallopian tube, we expected and have previously observed that purified recombinant human MIS causes regression of gynecological tumors. However, recent experiments indicating that neural crest derivatives might be responsive to MIS prompted study of a group of human ocular melanoma cell lines in 4 in vitro inhibition assays, and a subrenal capsule assay in vivo. Ocular melanoma cell lines that grew well in a respective assay were studied with MIS to determine whether this biological modifier could inhibit growth. Three human ocular melanomas, OM431 (P < 0.01), OM467 (P < 0.02), and OM482 (P < 0.03), were growth-inhibited by highly purified human recombinant MIS in soft agarose. A dose-dependent tumor inhibition was noted when OM431 cells were incubated with MIS in a liquid colony inhibition assay (P < 0.05). In addition, OM467 was inhibited (P < 0.05) by MIS in a multicellular tumor spheroid assay. Cell cycle analysis indicated that OM431 cells were inhibited in monolayer by MIS while in G1. At 100-fold lower serum concentrations than required in the media of in vitro assays, MIS delivered via i.p. osmotic pumps inhibited (P < 0.05) in vivo the growth of OM431 implanted beneath the renal capsule of nude and CD-1 irradiated mice when compared to mice given implants of pumps containing no MIS. The responsiveness of ocular melanoma to MIS broadens the spectrum of tumors that might be treated with MIS and suggests further investigation of other neural crest tumors. C1 MASSACHUSETTS GEN HOSP,PEDIAT SURG RES LAB,WARREN 11,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 17393] NR 37 TC 24 Z9 26 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 1992 VL 52 IS 5 BP 1182 EP 1186 PG 5 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700020 PM 1531323 ER PT J AU GATTONICELLI, S KIRSCH, K TIMPANE, R ISSELBACHER, KJ AF GATTONICELLI, S KIRSCH, K TIMPANE, R ISSELBACHER, KJ TI BETA-2-MICROGLOBULIN GENE IS MUTATED IN A HUMAN COLON CANCER CELL-LINE (HCT) DEFICIENT IN THE EXPRESSION OF HLA CLASS-I ANTIGENS ON THE CELL-SURFACE SO CANCER RESEARCH LA English DT Article ID HYBRIDIZATION PROBES; MESSENGER-RNA; HISTOCOMPATIBILITY; TUMORS; DIFFERENTIATION; INTERFERON; HLA-A,B,C; CARCINOMA; MOLECULES; SEQUENCES AB The human colon cancer cell line HCT does not express any detectable HLA class I antigens on the cell surface. RNA blot analyses showed that HCT cells synthesize easily detectable levels of heavy chains as well as beta-2-microglobulin (beta-2m) transcripts. Experiments of immunoprecipitation revealed the presence of intracellular HLA heavy chains and the absence of beta-2m molecules. Sequencing studies, Performed on Polymerase chain reaction-mediated amplification of beta-2m-specific complementary DNAs, indicated that in HCT cells both beta-2m genes are mutated. The first mutation consists of an 11-base deletion, corresponding to the first 11 base pairs of the second exon of the beta-2m gene. This mutation alters the reading frame, starting from the third amino acid residue of the mature beta-2m protein, resulting in the synthesis of a 31-amino acid peptide with no remarkable homology to any of the sequences stored in the protein database. The second mutation is a point mutation (C --> A), resulting in a UAA stop codon corresponding to the 10th amino acid residue of the mature beta-2m. Therefore, it would appear that in HCT cells the beta-2m genes have undergone two different mutational changes. This is the first molecular demonstration of beta-2m mutations in a human epithelial cell line. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 28 TC 49 Z9 50 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 1992 VL 52 IS 5 BP 1201 EP 1204 PG 4 WC Oncology SC Oncology GA HF637 UT WOS:A1992HF63700024 PM 1737380 ER PT J AU ROSENBAUM, DS WILBER, DJ SMITH, JM DU, D RUSKIN, JN GARAN, H AF ROSENBAUM, DS WILBER, DJ SMITH, JM DU, D RUSKIN, JN GARAN, H TI LOCAL ACTIVATION VARIABILITY DURING MONOMORPHIC VENTRICULAR-TACHYCARDIA IN THE DOG SO CARDIOVASCULAR RESEARCH LA English DT Article DE VENTRICULAR TACHYCARDIA; LOCAL ACTIVATION TIME, ELECTROPHYSIOLOGICAL MAPPING; ALTERNANS; MYOCARDIAL INFARCTION; REENTRY ID ACTION-POTENTIAL DURATION; CANINE MYOCARDIAL-INFARCTION; MUSCLE-FIBERS; MECHANISMS; ALTERNANS; PURKINJE; REFRACTORINESS; PATTERNS AB Objective: The aim was to determine the beat to beat variability in local activation time during sustained monomorphic ventricular tachycardia in a canine model of experimental myocardial infarction. Methods: A digital template matching algorithm was developed for detecting subtle beat to beat variability in local activation timing at each of multiple ventricular sites. Ten electrically induced sustained ventricular tachycardia episodes. mean cycle length 211 (SD 40) ms, were endocardially and epicardially mapped in mongrel dogs weighing 15-20 kg. Digitised data were analysed for beat to beat local activation time variability. Similar data recorded during ventricular pacing at comparable rates and during sinus rhythm served as controls. Results: The overall mean variability of local activation time for all 10 ventricular tachycardias was 3.2(1.6) ms, range 1.8(1.1) ms to 4.7(2.8) ms, in contrast to the overall mean variability of 0.2(0.4) ms (p = 0.0001) for ventricular pacing and 0.7(0.6) ms (p = 0.0001) for sinus rhythm. Oscillations in local activation time manifested alternans type periodicity during seven of 10 ventricular tachycardias independent of any alternans in local electrogram morphology. Conclusions: During sustained, monomorphic ventricular tachycardia, beat to beat variability and alternans type oscillations in local activation time are common and may be an intrinsic property of re-entry since they are negligibly small during ventricular pacing. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02138. NR 21 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0008-6363 J9 CARDIOVASC RES JI Cardiovasc. Res. PD MAR PY 1992 VL 26 IS 3 BP 237 EP 243 DI 10.1093/cvr/26.3.237 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HH717 UT WOS:A1992HH71700007 PM 1423418 ER PT J AU KASHKET, S YASKELL, T AF KASHKET, S YASKELL, T TI LIMITATIONS IN THE INTRAORAL DEMINERALIZATION OF BOVINE ENAMEL SO CARIES RESEARCH LA English DT Article DE CALCIUM; ENAMEL DEMINERALIZATION, INTRAORAL; IODIDE PENETRABILITY; PHOSPHATE; PLAQUE PH; SATURATION; STREPTOCOCCUS-MUTANS ID PLAQUE-PH DATA; FOOD CARIOGENICITY; CARIES; FLUORIDE; INGESTION; CLEARANCE; SUCROSE; SUGAR; RAT; PHOSPHATE AB A model system was used to examine the relation between the duration of plaque pH fall and enamel demineralization following the intake of dietary carbohydrate in humans. Subjects wore palatal appliances containing blocks of bovine enamel covered with Streptococcus mutans IB 1600, and rinsed with 5 or 10% sucrose. Changes in iodide penetrability (delta Ip) of the enamel, and the pH and extracellular calcium and inorganic phosphate (Pi) concentrations of the streptococcal plaque were determined. Following rinses with 5% sucrose, delta Ip increased with time and reached a maximum (11.2 +/- 2.2 units) at 45-60 min although the S. mutans plaque remained acidic (pH = 4.8 +/- 0.6). After 10% sucrose, the maximum (14.7 +/- 3.1 units) was reached while the plaque pH was 4.0 +/- 0.3. Second rinses with sucrose increased delta Ip at most by 30%. Thus, demineralization did not persist throughout the period of low plaque pH, but occurred primarily during the early phase of plaque acidogenesis. Enamel demineralization appeared to be limited by factors other than the pH of the streptococcal plaque. Calcium concentrations in the S. mutans plaque rose to a maximum of 10.9 +/- 2.8 mEq/l at 30 min after the 5% sucrose rinses, then fell; Pi reached a stable level of 12.2 +/- 2.3 mEq/l by 60 min. Calculations showed that conditions approached saturation with respect to enamel and dicalcium phosphate dihydrate as demineralization reached a maximum. Demineralization appeared to be limited at low plaque pH, therefore, by the accumulation of high levels of mineral ions in the streptococcal plaque. These findings suggest that the effects on the natural dentition will be limited when consuming a number of carbohydrate-containing foods during a meal. C1 FORSYTH DENT CTR,CTR RES ORAL & BIOL EFFECTS FOODS,BOSTON,MA 02115. RP KASHKET, S (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE-05253] NR 41 TC 6 Z9 6 U1 0 U2 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6568 J9 CARIES RES JI Caries Res. PD MAR-APR PY 1992 VL 26 IS 2 BP 98 EP 103 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HP616 UT WOS:A1992HP61600006 PM 1521313 ER PT J AU EPSTEIN, RJ DRUKER, BJ IRMINGER, JC JONES, SD ROBERTS, TM STILES, CD AF EPSTEIN, RJ DRUKER, BJ IRMINGER, JC JONES, SD ROBERTS, TM STILES, CD TI EXTRACELLULAR CALCIUM MIMICS THE ACTIONS OF PLATELET-DERIVED GROWTH-FACTOR ON MOUSE FIBROBLASTS SO CELL GROWTH & DIFFERENTIATION LA English DT Article ID MOLECULAR-CLONING; PHOSPHATE CRYSTAL; HUMAN-NEUTROPHILS; FACTOR RECEPTORS; BETA-INTERFERON; 3T3 CELLS; MODULATION; KINASE; GENE; PYROPHOSPHATE AB Microprecipitates of calcium phosphate (CaPO4) can substitute for platelet-derived growth factor (PDGF) to stimulate the growth of cultured 3T3 cells. In two-part complementation assays, CaPO4 behaves as a PDGF-like "competence factor"-that is, the mitogenic response to CaPO4 is enhanced synergistically by "progression factors" contained in platelet-poor plasma. In studies described here, we show that early cytoplasmic and intranuclear events in the mitogenic response to CaPO4 are equivalent to those induced by PDGF. However, no net increase in tyrosine kinase activity of either the PDGF-alpha or PDGF-beta receptor is seen following exposure to CaPO4. Our data suggest that calcium acts within the cell, regulating events which normally proceed from activation of PDGF receptors. Alternatively, microprecipitates Of CaPO4 could act externally by activating a growth factor receptor which escapes detection with available reagents. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. RP EPSTEIN, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,DIV CELL & MOLEC BIOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 28 TC 15 Z9 15 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 1044-9523 J9 CELL GROWTH DIFFER JI Cell Growth Differ. PD MAR PY 1992 VL 3 IS 3 BP 157 EP 164 PG 8 WC Cell Biology SC Cell Biology GA HH538 UT WOS:A1992HH53800003 PM 1352989 ER PT J AU FLETCHER, EC DONNER, CF MIDGREN, B ZIELINSKI, J LEVIVALENSI, P BRAGHIROLI, A RIDA, Z MILLER, CC AF FLETCHER, EC DONNER, CF MIDGREN, B ZIELINSKI, J LEVIVALENSI, P BRAGHIROLI, A RIDA, Z MILLER, CC TI SURVIVAL IN COPD PATIENTS WITH A DAYTIME PAO2-GREATER-THAN-60 MM HG WITH AND WITHOUT NOCTURNAL OXYHEMOGLOBIN DESATURATION SO CHEST LA English DT Article ID OBSTRUCTIVE PULMONARY-DISEASE; LONG-TERM OXYGEN; SLEEP; THERAPY AB There have been few studies examining the relationship between NOD and mortality in patients with COPD and none examining this relationship in those patients with a daytime PaO2 > 60 mm Hg. Is NOD related to early death, and if so, should nocturnal supplemental oxygen be considered as therapy for altering survival? We examined survival in 169 COPD subjects. Two definitions were used to classify subjects as NOD and non-NOD, one considering episodic desaturation associated mainly with REM sleep (definition 1) and one considering > 30 percent of time in bed spent below an SaO2 of 90 percent (definition 2) to be significant. Survival corrected for age was significantly better in non-NOD subjects. However, when stratified for supplemental oxygen use, survival remained better only in subjects separated by definition 1. There was a trend toward increased survival in 35 oxygen-treated vs 38 non-oxygen-treated NOD subjects (definition 1), but this difference was not statistically significant. C1 BAYLOR COLL MED,HOUSTON,TX 77030. RP FLETCHER, EC (reprint author), HOUSTON VET AFFAIRS MED CTR,DEPT MED,PULM DIS SECT,2002 HOLCOMBE BLVD,HOUSTON,TX 77030, USA. NR 20 TC 107 Z9 110 U1 2 U2 7 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD MAR PY 1992 VL 101 IS 3 BP 649 EP 655 DI 10.1378/chest.101.3.649 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA HG784 UT WOS:A1992HG78400016 PM 1541127 ER PT J AU TUZCU, EM BLOCK, PC GRIFFIN, BP NEWELL, JB PALACIOS, IF AF TUZCU, EM BLOCK, PC GRIFFIN, BP NEWELL, JB PALACIOS, IF TI IMMEDIATE AND LONG-TERM OUTCOME OF PERCUTANEOUS MITRAL VALVOTOMY IN PATIENTS 65 YEARS AND OLDER SO CIRCULATION LA English DT Article DE MITRAL STENOSES; AGING; VALVULOPLASTY; VALVES ID CATHETER BALLOON VALVULOPLASTY; FOLLOW-UP; CONSECUTIVE PATIENTS; ACTUARIAL ANALYSIS; VALVE-REPLACEMENT; COMMISSUROTOMY; STENOSIS; PREDICTORS; SURVIVAL; FEATURES AB Background. We analyzed the immediate and long-term outcome of percutaneous balloon mitral valvotomy (PMV) in 99 patients who were greater-than-or-equal-to 65 years of age (81 women and 18 men; mean +/- SEM age, 72 +/- 0.5 years). Methods and Results. There were 84 patients in New York Heart Association (NYHA) class III or IV; 26 patients had previous surgical commissurotomy; 64 had one or more comorbidities; 73 had fluoroscopically visible mitral valve (MV) calcification; and 63 had echocardiographic score > 8 (mean +/- SEM score, 9.2 +/- 0.2). There were three procedural deaths, all occurring in our early experience. Pericardial tamponade occurred in five patients, thromboembolism in three, and transient atrioventricular block in one. After PMV, MV area was greater-than-or-equal-to 1 cm2 in 86 patients and greater-than-or-equal-to 1.5 cm2 in 56. A successful outcome (defined as MV area greater-than-or-equal-to 1.5 cm2 without a greater-than-or-equal-to 2-grade increase in mitral regurgitation and without left-to-right shunt with a pulmonary-to-systemic flow ratio of greater-than-or-equal-to 1.5:1) was achieved in 46 patients. The best multivariate predictor of success was the combination of echocardiographic score, NYHA functional class, and inverse of MV area. Mean follow-up was 16 +/- 1 months. Actuarial survival (79 +/- 7% versus 62 +/- 10%, p = 0.04), survival without MV replacement (71 +/- 8% versus 41 +/- 8%, p = 0.002), and survival without MV replacement and NYHA class III or IV (54 +/- 12% versus 38 +/- 8%, p = 0.01) at 3 years were significantly better in the successful group of 46 patients than in the unsuccessful group of 53 patients. Low echocardiographic score was the only independent predictor of survival. Lack of MV calcification and low NYHA class, low mean left atrial pressure, and low pulmonary artery pressure were the independent predictors of event-free survival. Conclusions. PMV can be performed safely in selected patients greater-than-or-equal-to 65 years old with good immediate and long-term results. In addition to clinical examination, echocardiographic evaluation of the mitral valve and fluoroscopic screening for valvular calcification are the most important steps in patient selection for successful outcome. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 31 TC 74 Z9 75 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 963 EP 971 PG 9 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100011 PM 1537133 ER PT J AU ORTU, P LAMURAGLIA, GM ROBERTS, WG FLOTTE, TJ HASAN, T AF ORTU, P LAMURAGLIA, GM ROBERTS, WG FLOTTE, TJ HASAN, T TI PHOTODYNAMIC THERAPY OF ARTERIES - A NOVEL-APPROACH FOR TREATMENT OF EXPERIMENTAL INTIMAL HYPERPLASIA SO CIRCULATION LA English DT Article DE INTIMA; HYPERPLASIA; PHOTODYNAMIC THERAPY; PHTHALOCYANINES ID MUSCLE CELL-PROLIFERATION; ALUMINUM SULFONATED PHTHALOCYANINE; LUMINAL CORONARY ANGIOPLASTY; RAT CAROTID-ARTERY; ATHEROMATOUS PLAQUES; VASCULAR INJURY; PHOTOSENSITIZATION; TUMOR; FLUORESCENCE; PREVENTION AB Background. Photodynamic therapy (PDT) uses light activation of otherwise nontoxic dyes for the production of reactive oxygen species that cause cell injury and death. Methods and Results. The inhibition of intimal hyperplasia (IH) by PDT was studied in the balloon injury model of the rat carotid artery. Chloroaluminum-sulfonated phthalocyanine (CASPc) was the drug chosen for PDT because it does not produce skin photosensitivity and has a high absorption peak of light at 675 nm, a wavelength with good tissue penetration. A pilot study indicated that CASPc administration with laser radiant exposure of 100 J/cm2 resulted in a homogeneous, circumferential effect on the whole artery. Male Sprague-Dawley rats received the balloon catheter injury to the left common carotid artery (day 0) and were equally divided into two groups. Nine rats received either CASPc (5 mg/kg i.v., n = 6) or saline (n = 3) at day 2, before IH was present, and nine rats received CASPc or saline in the same manner on day 7, when IH was already present. Twenty minutes after drug injection, the distal left common carotid artery was irradiated under saline with 675-nm laser light at 100 mW/cm2 for 10(3) seconds (100 J/cm2). At this low laser irradiance, there are no thermal effects, but photoactivation of CASPc occurs. The rats were killed at day 14 after balloon injury when IH reaches a maximum. The arteries were harvested after perfusion-fixation for light microscopy, histological and computerized morphometric evaluation, and transmission electron microscopy (TEM) analysis. The cross-sectional areas of the neointima were measured in the PDT-treated arteries and in the laser-only control arteries. There was a significant mean +/- SD decrease of IH in the PDT-irradiated segments of the arteries (0.06 +/- 0.05 mm2) versus the laser-only control ones (0.17 +/- 0.07 mm2) (t test, p < 0.001), with no statistical difference between the day 2 and day 7 treated rats. Lack of IH was correlated in 90% of cases with histological absence of medial smooth muscle cells or inflammatory cells, but no other structural injury was identified. TEM analysis showed early evidence of PDT-mediated cytotoxic effects at 4 hours and the absence of collagen or elastic tissue structural alterations. Conclusions. These data demonstrated that PDT can effectively inhibit the IH response when it is used before or during induction of cellular proliferation in this acute model. Although the long-term implications of PDT in arteries need to be defined, this technique may offer a new method for understanding and treating IH. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,GEN SURG SERV,VASC SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. FU NHLBI NIH HHS [K08-HL-02583-01] NR 46 TC 92 Z9 93 U1 0 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1189 EP 1196 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100038 PM 1537115 ER PT J AU GARABEDIAN, HD GOLD, HK AF GARABEDIAN, HD GOLD, HK TI CORONARY THROMBOLYSIS, CONJUNCTIVE HEPARIN INFUSION, AND THE EFFECT ON SYSTEMIC THROMBIN ACTIVITY SO CIRCULATION LA English DT Editorial Material DE RECOMBINANT PROTEINS; HEPARIN; THROMBOLYSIS; THROMBIN; EDITORIAL COMMENTS ID ACUTE MYOCARDIAL-INFARCTION; TISSUE PLASMINOGEN-ACTIVATOR; THERAPY; REPERFUSION; TRIAL; FIBRINOPEPTIDE; STREPTOKINASE C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. NR 25 TC 10 Z9 10 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAR PY 1992 VL 85 IS 3 BP 1205 EP 1207 PG 3 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HG541 UT WOS:A1992HG54100040 PM 1537116 ER PT J AU FLESCHER, E BOWLIN, TL TALAL, N AF FLESCHER, E BOWLIN, TL TALAL, N TI REGULATION OF IL-2 PRODUCTION BY MONONUCLEAR-CELLS FROM RHEUMATOID-ARTHRITIS SYNOVIAL-FLUIDS SO CLINICAL AND EXPERIMENTAL IMMUNOLOGY LA English DT Article DE IL-2; RHEUMATOID ARTHRITIS; POLYAMINES ID PERIPHERAL-BLOOD; INTERLEUKIN-2; POLYAMINES; RESPONSES; OXIDATION; GROWTH AB Products of polyamine oxidation down-regulate IL-2 production by peripheral blood T cells. We show here that the production of IL-2 by rheumatoid arthritis synovial fluid mononuclear cells is inversely correlated with the concentrations of polyamines in these cells. In addition. the inhibition of polyamine biosynthesis or oxidation in cultures of these cells enhances their ability to produce IL-2. Our findings suggest that polyamine oxidation plays an important role in the suppression of T cell function characteristic of rheumatoid arthritis synovial fluids. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. MARION MERRELL DOW RES INST,CINCINNATI,OH. RP FLESCHER, E (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDCR NIH HHS [R01 DE09311-01] NR 12 TC 10 Z9 10 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9104 J9 CLIN EXP IMMUNOL JI Clin. Exp. Immunol. PD MAR PY 1992 VL 87 IS 3 BP 435 EP 437 PG 3 WC Immunology SC Immunology GA HG588 UT WOS:A1992HG58800018 PM 1544227 ER PT J AU MALKIN, D FRIEND, S AF MALKIN, D FRIEND, S TI DETECTION OF GERM LINE P53 MUTATIONS IN HEREDITARY CANCER SO CLINICAL CHEMISTRY LA English DT Article; Proceedings Paper CT 1991 SAN DIEGO CONF ON NUCLEIC ACIDS : THE LEADING EDGE CY 1991 CL SAN DIEGO, CA SP AMER ASSOC CLIN CHEM, SAN DIEGO SECT, AMER ASSOC CLIN CHEM, MOLEC PATHOL DIV RP MALKIN, D (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,BLDG 149,13TH ST,BOSTON,MA 02114, USA. NR 9 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD MAR PY 1992 VL 38 IS 3 BP 452 EP 453 PG 2 WC Medical Laboratory Technology SC Medical Laboratory Technology GA HJ870 UT WOS:A1992HJ87000043 ER PT J AU ADAMS, M NAGAYA, T TONE, Y JAMESON, JL CHATTERJEE, VKK AF ADAMS, M NAGAYA, T TONE, Y JAMESON, JL CHATTERJEE, VKK TI FUNCTIONAL-PROPERTIES OF A NOVEL MUTANT THYROID-HORMONE RECEPTOR IN A FAMILY WITH GENERALIZED THYROID-HORMONE RESISTANCE SYNDROME SO CLINICAL ENDOCRINOLOGY LA English DT Article ID NEGATIVE REGULATION; GENE; BETA; FIBROBLASTS; MUTATIONS; KINDREDS; TISSUES; BINDING; DOMAIN AB OBJECTIVE We wished to ascertain whether a mutation in the thyroid hormone receptor beta-gene was present in a family with generalized thyroid hormone resistance syndrome and to characterize the functional properties of this mutant receptor. DESIGN Blood samples were obtained from family members for hormone assays and genomic DNA was isolated from leucocytes for genetic analyses. PATIENTS Three members (B,C,E) of a family with possible thyroid hormone resistance and two normal family members (A,D) were studied. MEASUREMENTS Basal thyroid function tests together with serum sex hormone binding globulin (SHBG) levels were measured. The thyroid hormone receptor beta-gene was amplified using the polymerase chain reaction and the receptor mutation identified by sequence analysis. The ability of mutant receptor to bind T3, interact with a specific DNA sequence and to modulate target gene expression was tested. The effects of mutant receptor on co-expressed wild type receptor action were determined. RESULTS Patients with resistance had raised levels of T4 and T3 together with inappropriately normal serum TSH and SHBG whereas unaffected individuals had a normal hormone profile. A single nucleotide substitution corresponding to a glycine to serine mutation at codon 340 (G340S) in the hormone binding domain was identified in one of the two beta-receptor gene alleles in patients with resistance, but not in the normal family members. When expressed in vitro, this receptor protein (G340S), as well as a related (G340R) mutant identified in another family, retained the ability to bind to a specific DNA sequence but were unable to bind ligand or to activate or repress target gene expression. In addition both receptor mutants were capable of inhibiting the function of wild type thyroid hormone receptor in a co-expression assay but differed in their inhibitory potential. CONCLUSIONS We report a second type of mutation (Gly to Ser) in codon 340 of hTR-beta in a family with generalized thyroid hormone resistance. Mutations at this site eliminate T3 binding, causing a loss of hormone-stimulated receptor function. However, the mutant receptors retain the ability to block normal receptor action. The occurrence of different mutations at the same site suggests that alterations in this region of the receptor may be important for generating the clinical phenotype of this disorder. C1 UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT MED,HILLS RD,LEVEL 5,CAMBRIDGE CB2 2QQ,ENGLAND. MASSACHUSETTS GEN HOSP,THYROID UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Perez , Claudio Alejandro/F-8310-2010; OI Perez , Claudio Alejandro/0000-0001-9688-184X; Jameson, James/0000-0001-9538-4059 FU NIDDK NIH HHS [DK 42144]; Wellcome Trust NR 27 TC 34 Z9 35 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0300-0664 J9 CLIN ENDOCRINOL JI Clin. Endocrinol. PD MAR PY 1992 VL 36 IS 3 BP 281 EP 289 DI 10.1111/j.1365-2265.1992.tb01444.x PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HF551 UT WOS:A1992HF55100011 PM 1563081 ER PT J AU DEKEYSER, F HOCH, SO TAKEI, M DANG, H DEKEYSER, H ROKEACH, LA TALAL, N AF DEKEYSER, F HOCH, SO TAKEI, M DANG, H DEKEYSER, H ROKEACH, LA TALAL, N TI CROSS-REACTIVITY OF THE B/B'-SUBUNIT OF THE SM RIBONUCLEOPROTEIN AUTOANTIGEN WITH PROLINE-RICH POLYPEPTIDES SO CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY LA English DT Article ID SYSTEMIC LUPUS-ERYTHEMATOSUS; ANTI-SM; PEPTIDE ANTIGENS; AUTO-ANTIGEN; PROTEINS; ANTIBODIES; EPITOPE; CDNA; AUTOANTIBODIES; U1 C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CLIN IMMUNOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,CLIN IMMUNOL SECT,SAN ANTONIO,TX 78284. AGOURON INST,LA JOLLA,CA 92037. FU FIC NIH HHS [FO5 TWD4264-01-BI-5]; NIAID NIH HHS [AI21083]; NIDCR NIH HHS [DE-09311] NR 37 TC 32 Z9 32 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-1229 J9 CLIN IMMUNOL IMMUNOP JI Clin. Immunol. Immunopathol. PD MAR PY 1992 VL 62 IS 3 BP 285 EP 290 DI 10.1016/0090-1229(92)90104-V PG 6 WC Immunology; Pathology SC Immunology; Pathology GA HH787 UT WOS:A1992HH78700006 PM 1371727 ER PT J AU HIRSCHHORN, LR MCINTOSH, K ANDERSON, KG DERMODY, TS AF HIRSCHHORN, LR MCINTOSH, K ANDERSON, KG DERMODY, TS TI INFLUENZAL PNEUMONIA AS A COMPLICATION OF AUTOLOGOUS BONE-MARROW TRANSPLANTATION SO CLINICAL INFECTIOUS DISEASES LA English DT Letter ID CELLS C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. NR 7 TC 12 Z9 12 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1992 VL 14 IS 3 BP 786 EP 787 PG 2 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HE701 UT WOS:A1992HE70100026 PM 1562672 ER PT J AU RINALDI, MG AF RINALDI, MG TI LABORATORY EVALUATION OF ANTIFUNGAL AGENTS - A BRIEF OVERVIEW SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID SUSCEPTIBILITY AB The increasing incidence and significance of human mycotic diseases has prompted concurrent interest in the development and evaluation of antifungal drugs. There has never been a period in medicine when the number of antimycotic agents, either commercially available or undergoing clinical investigation, is as great as at present. An integral part of new antimicrobial development is the laboratory evaluation, both in vivo and in vitro, of such agents. Each of these aspects of laboratory testing offers distinct limitations and advantages; however, such evaluation is critical for continued success in the quest for nontoxic, inexpensive, and efficacious antifungal agents. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT VET AFFAIRS,MYCOL REFERENCE LAB,LAB SERV,SAN ANTONIO,TX 78284. RP RINALDI, MG (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,FUNGUS TESTING LAB,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 14 TC 15 Z9 16 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAR PY 1992 VL 14 SU 1 BP S130 EP S133 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HF382 UT WOS:A1992HF38200019 PM 1562685 ER PT J AU HARDIN, TC DIPIRO, JT AF HARDIN, TC DIPIRO, JT TI WHO SHOULD RECEIVE ANTIENDOTOXIN MONOCLONAL-ANTIBODY THERAPY SO CLINICAL PHARMACY LA English DT Editorial Material RP HARDIN, TC (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0278-2677 J9 CLIN PHARMACY PD MAR PY 1992 VL 11 IS 3 BP 255 EP 256 PG 2 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HF678 UT WOS:A1992HF67800005 PM 1611815 ER PT J AU MATHISEN, DJ AF MATHISEN, DJ TI SURGICAL-MANAGEMENT OF TRACHEOBRONCHIAL DISEASE SO CLINICS IN CHEST MEDICINE LA English DT Article ID TRACHEAL SLEEVE PNEUMONECTOMY; BRONCHOGENIC-CARCINOMA C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MATHISEN, DJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT THORAC SURG,DIV GEN THORAC SURG,WARREN 1109,44 FRUIT ST,BOSTON,MA 02114, USA. NR 17 TC 10 Z9 13 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-5231 J9 CLIN CHEST MED JI Clin. Chest Med. PD MAR PY 1992 VL 13 IS 1 BP 151 EP 171 PG 21 WC Respiratory System SC Respiratory System GA HM158 UT WOS:A1992HM15800015 PM 1582144 ER PT J AU POLLACK, MH OTTO, MW ROSENBAUM, JF SACHS, GS AF POLLACK, MH OTTO, MW ROSENBAUM, JF SACHS, GS TI PERSONALITY-DISORDERS IN PATIENTS WITH PANIC DISORDER - ASSOCIATION WITH CHILDHOOD ANXIETY DISORDERS, EARLY TRAUMA, COMORBIDITY, AND CHRONICITY SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID BEHAVIORAL-INHIBITION; AGORAPHOBIA; CHILDREN; INTERVIEW; PARENTS RP POLLACK, MH (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,ANXIETY CLIN RES UNIT,ACC-815,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 29 TC 42 Z9 42 U1 1 U2 5 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 1992 VL 33 IS 2 BP 78 EP 83 DI 10.1016/0010-440X(92)90002-8 PG 6 WC Psychiatry SC Psychiatry GA HH791 UT WOS:A1992HH79100002 PM 1544300 ER PT J AU CALONGE, M FOSTER, CS RICE, BA BAER, JC AF CALONGE, M FOSTER, CS RICE, BA BAER, JC TI MANAGEMENT OF CORNEAL COMPLICATIONS IN XERODERMA-PIGMENTOSUM SO CORNEA LA English DT Article DE CONJUNCTIVAL RESECTION; CORNEAL DYE LASER PHOTOCOAGULATION; CORNEAL TRANSPLANTATION; CYCLOSPORINE; MITOMYCIN-C; PHOTOPHOBIA-ULTRAVIOLET RADIATION; XERODERMA-PIGMENTOSUM AB Xeroderma pigmentosum is an uncommon, recessively inherited disorder characterized by hypersensitivity to ultraviolet (UV) radiation, with defective repair of DNA damage caused by short-wavelength radiation. Patients with this disease experience progressive and precancerous changes in sun-exposed areas of the skin and mucous membranes. Some patients develop progressive neurologic degeneration. Eye involvement includes lid, conjunctiva, and corneal disorders. We report clinical, histopathologic findings, and complex management strategies used for a 33-year-old woman with xeroderma pigmentosum and recurrent corneal ulcerations that required corneal transplantation, topical cyclosporin, perilimbic conjunctival resection followed by topical mitomycin C, and corneal dye-laser photocoagulation of neovascularization in the left eye. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,IMMUNOL SERV,243 CHARLES ST,BOSTON,MA 02114. RI Calonge, Margarita/K-2839-2014 OI Calonge, Margarita/0000-0001-8178-4836 NR 0 TC 5 Z9 5 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD MAR PY 1992 VL 11 IS 2 BP 173 EP 182 DI 10.1097/00003226-199203000-00014 PG 10 WC Ophthalmology SC Ophthalmology GA HE714 UT WOS:A1992HE71400014 PM 1582221 ER PT J AU SPRUNG, CL ARMSTRONG, JC BAILEY, MA CIVETTA, JM DAGI, TF DANIS, M DUNBAR, S ENGELHARDT, HT GRENVIK, A HOFMANN, PB HOYT, JW JAMETON, A KLEIN, RL KOFKE, WA LEVINEARIFF, J LIEBERMAN, J LYNN, J MARSHALL, MF MCCARTNEY, JJ NELSON, R NINOS, NP NOLAN, K PEDUZZI, P PEREZSTABLE, E RAPHAELY, RC REARDON, F RIE, MA ROSENBAUM, SH SCHWARTZ, S SIEGLER, M SOTTILLE, FD SPANIER, A STEINBERG, A TENDLER, MD TRUOG, RD WIKLER, D YEH, TS AF SPRUNG, CL ARMSTRONG, JC BAILEY, MA CIVETTA, JM DAGI, TF DANIS, M DUNBAR, S ENGELHARDT, HT GRENVIK, A HOFMANN, PB HOYT, JW JAMETON, A KLEIN, RL KOFKE, WA LEVINEARIFF, J LIEBERMAN, J LYNN, J MARSHALL, MF MCCARTNEY, JJ NELSON, R NINOS, NP NOLAN, K PEDUZZI, P PEREZSTABLE, E RAPHAELY, RC REARDON, F RIE, MA ROSENBAUM, SH SCHWARTZ, S SIEGLER, M SOTTILLE, FD SPANIER, A STEINBERG, A TENDLER, MD TRUOG, RD WIKLER, D YEH, TS TI ATTITUDES OF CRITICAL CARE MEDICINE PROFESSIONALS CONCERNING FORGOING LIFE-SUSTAINING TREATMENTS SO CRITICAL CARE MEDICINE LA English DT Article DE ETHICS; CRITICAL CARE; LIFE-SUPPORT SYSTEMS; HEALTH-CARE TEAM; VEGETATIVE STATE; TERMINAL ILLNESS; PALLIATIVE TREATMENT; INTENSIVE CARE UNIT; DO-NOT-RESUSCITATE ORDERS ID RESUSCITATE ORDER; ILL PATIENTS; PHYSICIANS; PREFERENCES AB Objective: To evaluate the attitudes of critical care professionals concerning forgoing life-sustaining treatments in critically ill patients. Design and Setting: Questionnaires (n = 1148) were distributed to all registrants at the annual Society of Critical Care Medicine meeting, and 600 (52%) were returned and analyzed. Patients: None. Interventions: None. Measurements and Main Results: When confronted with an actual patient whose condition was deemed to be irreversible and terminal, 334 (56%) of 600 respondents were not disturbed by withholding or withdrawing treatment, whereas 156 (26%) of 600 respondents were more disturbed by withdrawing than withholding treatment. Five hundred thirty-six (89%) respondents had withheld and 519 (87%) had withdrawn life-prolonging treatments. Forgoing treatments was more common for academic physicians (329/343, 96%) and professionals responsible for the decision to forgo treatments (389/404, 96%). Respondents believed the physician's professional duty to his or her patient was to preserve life foremost, but evaluate quality of life (342, 57%) or ensure quality of life foremost, but evaluate preservation of life (188, 31%). Conclusions: Critical care professionals evaluate both the preservation of life and quality of life in their patients. Despite some discomfort in forgoing treatment, the majority of critical care professionals decide to forgo treatment in irreversibly, terminally ill patients. C1 HADASSAH HEBREW UNIV,JERUSALEM,ISRAEL. ST FRANCIS MED CTR,PITTSBURGH,PA. ST LUKES HOSP,NEW YORK,NY. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA. CHILDRENS HOSP BOSTON,BOSTON,MA. CHILDRENS HOSP OAKLAND,OAKLAND,CA. LETTERMAN ARMY MED CTR,SAN FRANCISCO,CA 94129. HASTINGS CTR,HASTINGS ON HUDSON,NY 10706. VET ADM MED CTR,W HAVEN,CT 06516. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. PENN STATE UNIV,MILTON S HERSHEY MED CTR,HERSHEY,PA 17033. UNIV VIRGINIA,MED CTR,SCH MED,CHARLOTTESVILLE,VA 22901. VILLANOVA UNIV,VILLANOVA,PA 19085. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. US SENATE,SPECIAL COMM AGING,WASHINGTON,DC 20510. ST VINCENT HOSP,WORCESTER,MA 01604. UNIV CHICAGO,PRITZKER SCH MED,CHICAGO,IL 60637. SIR MORTIMER B DAVIS JEWISH HOSP,MONTREAL H3T 1E2,QUEBEC,CANADA. HEBREW UNIV JERUSALEM,JERUSALEM,ISRAEL. YESHIVA UNIV,NEW YORK,NY 10033. EMORY UNIV,SCH NURSING,ATLANTA,GA 30322. BAYLOR COLL MED,HOUSTON,TX 77030. UNIV PITTSBURGH,SCH MED,PITTSBURGH,PA 15261. UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. UNIV WISCONSIN,MADISON,WI 53706. GEORGE WASHINGTON UNIV,SCH MED,WASHINGTON,DC 20052. UNIV N CAROLINA,CHAPEL HILL,NC 27514. EMORY UNIV,SCH MED,ATLANTA,GA 30322. RP SPRUNG, CL (reprint author), SOC CRIT CARE MED,COMM ETH,8101 E KAISER BLVD,ANAHEIM,CA 92808, USA. NR 16 TC 73 Z9 75 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 1992 VL 20 IS 3 BP 320 EP 326 PG 7 WC Critical Care Medicine SC General & Internal Medicine GA HJ672 UT WOS:A1992HJ67200005 ER PT J AU ROSEN, HR VLAHAKES, GJ RATTNER, DW AF ROSEN, HR VLAHAKES, GJ RATTNER, DW TI FULMINANT PEPTIC-ULCER DISEASE IN CARDIAC SURGICAL PATIENTS - PATHOGENESIS, PREVENTION, AND MANAGEMENT SO CRITICAL CARE MEDICINE LA English DT Article DE STRESS ULCER; DUODENAL ULCER; GASTRIC ULCER; HISTAMINE ANTAGONISTS; CARDIAC SURGERY; CARDIOPULMONARY BYPASS; GASTROINTESTINAL HEMORRHAGE; GASTRIC ACID; PEPTIC ULCER; STRESS ID CRITICALLY ILL PATIENTS; INTENSIVE-CARE UNIT; NOSOCOMIAL PNEUMONIA; RANDOMIZED TRIAL; CIMETIDINE; SUCRALFATE; ANTACIDS; SURGERY; COMPLICATIONS AB Objectives: To identify pathogenetic factors associated with the development of peptic ulcers in patients following cardiac surgery and to examine the efficacy of medical and surgical therapy of peptic ulcers in this setting. Design: Retrospective study with randomly selected case controls. Setting: University hospital referral practice. Patients: A total of 9,199 consecutive patients undergoing procedures requiring cardiopulmonary bypass between January 1, 1980 through September 30, 1988, were reviewed. Life-threatening ulcer complications were defined as hemorrhage of > 2 units of packed red blood cells which prompted subspecialty consultation and required a therapeutic intervention. Patients who developed life-threatening complications of peptic ulcers (32/9199, 0.35%) (group 1) were compared with 32 randomly selected patients (group 2) for differences in potential pathogenetic factors and outcome. Main Outcome Measures: Gastrointestinal hemorrhage, perforated ulcers, death. Results: Patients in group 1 were significantly older than patients in group 2 (66.7 +/- 7.9 vs. 54 +/- 10 yrs, p < .01). Complications following cardiopulmonary bypass requiring further surgery or causing prolonged hypotension were significantly more frequent in patients with ulcers than in controls (10/32 vs. 1/32, p < .005). The mortality rate for patients in group 1 was 34.3% (11/32) compared with 0% in group 2 (p < .001). Perioperative ulcer prophylaxis was employed with equal frequency in groups 1 and 2 and did not correlate with outcome. Conclusions: The development of complications of postoperative peptic ulcers following cardiac surgery correlates with age, need for reoperation, and hypoperfusion, but not with the use of prophylactic regimens to suppress acid secretion. These results suggest that impairment of gastric and duodenal mucosal defense mechanisms is a critical factor in the development of postoperative peptic ulcers. C1 HANUSCH MED CTR,DEPT SURG,VIENNA,AUSTRIA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP ROSEN, HR (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114, USA. NR 16 TC 23 Z9 24 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 1992 VL 20 IS 3 BP 354 EP 359 DI 10.1097/00003246-199203000-00011 PG 6 WC Critical Care Medicine SC General & Internal Medicine GA HJ672 UT WOS:A1992HJ67200011 PM 1347261 ER PT J AU EPSTEIN, DL HOOSHMAND, LB EPSTEIN, MPM AF EPSTEIN, DL HOOSHMAND, LB EPSTEIN, MPM TI THIOL ADDUCTS OF ETHACRYNIC-ACID INCREASE OUTFLOW FACILITY IN ENUCLEATED CALF EYES SO CURRENT EYE RESEARCH LA English DT Article AB Ethacrynic acid (ECA), a sulfhydryl (SH)-reactive diuretic drug, has been shown to increase outflow facility (C) both in living monkey eyes and in the calf eye, in vitro (Epstein et al. 1987). In an attempt to increase the therapeutic index of this drug for potential clinical use in glaucoma, we explored the effect of various thiol adducts of ECA on C in the calf eye in vitro. These adducts might be expected to liberate ECA by a reversible retro-Micheal type reaction. Enucleated calf eyes were perfused at 25-degrees-C at 15 mm Hg for 5 hours with various ECA-thiol adducts. ECA-cysteine at 0.25 mM (for each) increased outflow facility 104% compared to 38% in sham manipulated eyes (n-10; p < .005). A dose response effect was demonstrated from 0.01 mM to 0.25 mM. A relative potency table (for increasing C) was established for several ECA-thiol adducts: Cysteine = cysteamine > glutathione > N-Acetyl cysteine > thiosalicylic acid > N-Acetyl cysteamine. This study identifies the potential of utilizing various derivatives of ECA as outflow pathway acting agents. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY01894] NR 12 TC 17 Z9 18 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD MAR PY 1992 VL 11 IS 3 BP 253 EP 258 DI 10.3109/02713689209001776 PG 6 WC Ophthalmology SC Ophthalmology GA HQ148 UT WOS:A1992HQ14800007 PM 1587147 ER PT J AU HUDSON, AP MCENTEE, CM REACHER, M WHITTUMHUDSON, JA TAYLOR, HR AF HUDSON, AP MCENTEE, CM REACHER, M WHITTUMHUDSON, JA TAYLOR, HR TI INAPPARENT OCULAR INFECTION BY CHLAMYDIA-TRACHOMATIS IN EXPERIMENTAL AND HUMAN TRACHOMA SO CURRENT EYE RESEARCH LA English DT Note ID ANIMAL-MODEL AB There is substantial indirect evidence which suggests that Chlamydia trachomatis can generate inapparent, persistent infections in human. To confirm this directly, we examined ocular chlamydial infection in both the cynomolgus monkey model of trachoma and in patient samples from a trachoma-endemic area. In monkeys, ocular infection was studied over time using direct immunofluorescence cytology (DFA) and a molecular hybridization screening system which targets chlamydial ribosomal RNA. In eleven animals infected once with B serovar, DFA and probe screening of parallel conjunctival swabs gave congruent results through day 42 post-infection. Thereafter, DFA showed clearing of chlamydia and was negative by day 70, as in previous studies. In contrast, hybridization analysis indicated a continuing presence of chlamydial RNA in all samples from all animals through the end of the experiment at day 84 post-infection. Similarly, analysis of swabs from trachoma patients showed that a number of DFA-negative samples gave clear positive signal for chlamydial RNA. Taken together these data indicate that ocular chlamydial infection persists for longer periods than previously thought, judging solely on the basis of DFA, and they support the idea that inapparent ocular chlamydial infection occurs in vivo. C1 MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. JOHNS HOPKINS UNIV,SCH MED,DEPT OPHTHALMOL,BALTIMORE,MD 21205. RP HUDSON, AP (reprint author), DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104, USA. OI Taylor, Hugh/0000-0002-9437-784X FU NEI NIH HHS [EYO3240] NR 19 TC 18 Z9 18 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0271-3683 J9 CURR EYE RES JI Curr. Eye Res. PD MAR PY 1992 VL 11 IS 3 BP 279 EP 283 DI 10.3109/02713689209001780 PG 5 WC Ophthalmology SC Ophthalmology GA HQ148 UT WOS:A1992HQ14800011 PM 1375138 ER PT J AU CANTWELL, R MCENTEE, CM HUDSON, AP AF CANTWELL, R MCENTEE, CM HUDSON, AP TI REGULATION OF MITOCHONDRIAL TRANSCRIPTION DURING THE STRINGENT RESPONSE IN YEAST SO CURRENT GENETICS LA English DT Article DE YEAST; TRANSCRIPTION; MITOCHONDRIA; RNA ID LARGE RIBOSOMAL-RNA; SACCHAROMYCES-CEREVISIAE; INVITRO TRANSCRIPTION; PROTEIN-SYNTHESIS; ESCHERICHIA-COLI; POLYMERASE; PROMOTER; GENE; GENOME; DNA AB In yeast (S. cerevisiae) the stringent response is known to include rapid, selective, and severe transcriptional curtailment for genes specifying cytoplasmic rRNAs and r-proteins. We have shown that transcription of the mitochondrial 21S rRNA gene is also congruently and selectively curtailed during the yeast stringent response. Using an in vitro transcription assay with intact organelles from both rho+ and rho--strains, we show here that the mitochondrial stringent response includes not only transcription of the 21S and 16S rRNA genes, but also that of organellar genes specifying non-mitoribosome-related products. Stringent organellar transcriptional curtailment is identical when cells are starved for a required (marker) amino acid or when they are subjected to nutritional downshift, and the relative level of that transcriptional curtailment following either perturbation is the same in cells growing on fermentative (repressing) or purely respiratory carbon sources. These results confirm that the mechanism governing mitochondrial gene expression during a stringent response is specified outside the organelle, and they show that this transcriptional control mechanism is not immediately subject to glucose repression. In all strains examined, stringent organellar gene expression requires a mitochondrial promoter, suggesting that the regulatory mechanism which functions during the stringent response operates primarily at transcriptional initiation. C1 DEPT VET AFFAIRS MED CTR,RES SERV,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. NR 42 TC 13 Z9 13 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0172-8083 J9 CURR GENET JI Curr. Genet. PD MAR PY 1992 VL 21 IS 3 BP 241 EP 247 DI 10.1007/BF00336848 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA HJ475 UT WOS:A1992HJ47500011 PM 1563050 ER PT J AU GIANANI, R PUGLIESE, A BONNERWEIR, S SHIFFRIN, AJ SOELDNER, JS ERLICH, H AWDEH, Z ALPER, CA JACKSON, RA EISENBARTH, GS AF GIANANI, R PUGLIESE, A BONNERWEIR, S SHIFFRIN, AJ SOELDNER, JS ERLICH, H AWDEH, Z ALPER, CA JACKSON, RA EISENBARTH, GS TI PROGNOSTICALLY SIGNIFICANT HETEROGENEITY OF CYTOPLASMIC ISLET CELL ANTIBODIES IN RELATIVES OF PATIENTS WITH TYPE-I DIABETES SO DIABETES LA English DT Article ID TARGET ANTIGEN; PROGRESSION; EXPRESSION AB A significant proportion of relatives of patients with insulin-dependent (type I) diabetes with high titers of cytoplasmic islet cell autoantibodies (ICAs) do not progress to overt diabetes with up to 8 yr of follow-up. This may reflect that follow-up of such relatives has not been long enough to observe diabetes, that despite expression of identical ICAs, some relatives will not progress to diabetes; or that there is heterogeneity in what is identified as ICA. We identified a subset of ICA that was restricted in its species (not reacting with mouse islets) and cell-type reactivity within islets (beta-cell specific). Only one of eight relatives whose sera had the restricted pattern of reactivity progressed to overt diabetes, and on sequential evaluation, all but the one relative who progressed to diabetes have maintained normal first-phase insulin secretion to intravenous glucose. In contrast, by life-table analysis, 70% of relatives expressing nonrestricted ICA became diabetic within 5 yr of follow-up (1 of 8 vs. 16 of 25 diabetic at last follow-up, P < 0.02). Moreover, preliminary data suggest a significant association of the human leukocyte antigen DQB1*0602 allele of DR2 haplotypes with the restricted ICA pattern (4 of 5 DQB1*0602 restricted vs. 0 nonrestricted ICA, P = 0.006). We propose that expression of a genetically determined restricted ICA pattern confers a markedly lower risk for progression to diabetes. Our studies suggest that relatives with restricted ICA may comprise most ICA+ relatives who do not develop diabetes or abnormal first-phase insulin secretion on follow-up of > 5 yr and that expression of such autoantibodies may be associated with the "protective" DQB1*0602 allele. C1 BRIGHAM & WOMENS HOSP,JOSLIN DIABETES CTR,IMMUNOL & IMMUNOGENET SECT,1 JOSLIN PL,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA. MCGILL UNIV,MONTREAL H3A 2T5,QUEBEC,CANADA. NEW ENGLAND DEACONESS HOSP,BOSTON,MA 02215. UNIV CALIF DAVIS,DAVIS,CA 95616. CETUS CORP,EMERYVILLE,CA 94608. FU NIDDK NIH HHS [DK-32082, DK-33790, DK-39233] NR 20 TC 143 Z9 144 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 1992 VL 41 IS 3 BP 347 EP 353 DI 10.2337/diabetes.41.3.347 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HQ276 UT WOS:A1992HQ27600014 PM 1551494 ER PT J AU DEFRONZO, RA BONADONNA, RC FERRANNINI, E AF DEFRONZO, RA BONADONNA, RC FERRANNINI, E TI PATHOGENESIS OF NIDDM - A BALANCED OVERVIEW SO DIABETES CARE LA English DT Review ID DEPENDENT DIABETES-MELLITUS; HEPATIC GLUCOSE-PRODUCTION; INSULIN-RECEPTOR GENE; ISLET-AMYLOID POLYPEPTIDE; MUSCLE GLYCOGEN-SYNTHASE; HUMAN SKELETAL-MUSCLE; FREE FATTY-ACID; CONTINUOUS INDIRECT CALORIMETRY; PRIMARY CULTURED ADIPOCYTES; CHRONIC GLYBURIDE THERAPY AB Non-insulin-dependent diabetes mellitus (NIDDM) results from an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have demonstrated that the earliest detectable abnormality in NIDDM is an impairment in the body's ability to respond to insulin. Because the pancreas is able to appropriately augment its secretion of insulin to offset the insulin resistance, glucose tolerance remains normal. With time, however, the beta-cell fails to maintain its high rate of insulin secretion and the relative insulinopenia (i.e., relative to the degree of insulin resistance) leads to the development of impaired glucose tolerance and eventually overt diabetes mellitus. The cause of pancreatic "exhaustion" remains unknown but may be related to the effect of glucose toxicity in a genetically predisposed beta-cell. Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered beta-cell function in NIDDM. Insulin resistance in NIDDM involves both hepatic and peripheral, muscle, tissues. In the postabsorptive state hepatic glucose output is normal or increased, despite the presence of fasting hyperinsulinemia, whereas the efficiency of tissue glucose uptake is reduced. In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. The accelerated rate of hepatic glucose output is due entirely to augmented gluconeogenesis. In muscle many. cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. The abnormalities account for disturbances in the two major intracellular pathways of glucose disposal, glycogen synthesis, and glucose oxidation. In the earliest stages of NIDDM, the major defect involves the inability of insulin to promote glucose uptake and storage as glycogen. Other potential mechanisms that have been put forward to explain the insulin resistance, include increased lipid oxidation, altered skeletal muscle capillary density/fiber type/blood flow, impaired insulin transport across the vascular endothelium, increased amylin, calcitonin gene-related peptide levels, and glucose toxicity. C1 CNR,INST PHYSIOL,I-56100 PISA,ITALY. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP DEFRONZO, RA (reprint author), UNIV TEXAS,HLTH SCI CTR,DIV DIABET,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 432 TC 1641 Z9 1664 U1 3 U2 74 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD MAR PY 1992 VL 15 IS 3 BP 318 EP 368 DI 10.2337/diacare.15.3.318 PG 51 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HF323 UT WOS:A1992HF32300002 PM 1532777 ER PT J AU LEAHY, JL BONNERWEIR, S WEIR, GC AF LEAHY, JL BONNERWEIR, S WEIR, GC TI BETA-CELL DYSFUNCTION INDUCED BY CHRONIC HYPERGLYCEMIA - CURRENT IDEAS ON MECHANISM OF IMPAIRED GLUCOSE-INDUCED INSULIN-SECRETION SO DIABETES CARE LA English DT Review ID DEPENDENT DIABETES-MELLITUS; RAT PANCREATIC-ISLETS; SHR/N-CP RATS; B-CELL; PHOSPHOINOSITIDE HYDROLYSIS; INVIVO HYPERGLYCEMIA; ELEVATED PROINSULIN; DOWN-REGULATION; PIMA-INDIANS; INFUSED RATS AB Non-insulin-dependent diabetes mellitus is characterized by abnormal beta-cell function. The characteristic secretory defect is a selective loss of glucose-induced insulin secretion. Substantial data have been generated in animal models to support the concept that chronic hyperglycemia causes the loss of glucorecognition (the so-called glucose toxicity hypothesis). This review summarizes the data supporting the concept of hyperglycemia-induced beta-cell dysfunction and then focuses on the ideas for the mechanism of the glucose unresponsiveness. The lack of access to islet tissue in humans means that these studies have all been conducted in animal models. Another major stumbling block continues to be the lack of in vitro systems that faithfully reproduce the secretory abnormalities that occur in vivo. Despite these limitations, many hypotheses are being investigated that span most of the major intracellular steps for glucose-induced insulin secretion, including abnormalities in glucose Port, storage, metabolism/oxidation, and the second messengers. No single hypothesis stands out as being able to explain all of the characteristics of the secretory abnormalities. In the last few years major advances have occurred in our knowledge about the events that normally cause glucose-induced insulin secretion. Similarly, biochemical and molecular tools have become available to probe the different steps. As better in vitro models of the selective glucose unresponsiveness become available, rapid Progress can be expected in unraveling the biochemical basis for the loss of glucose responsiveness in diabetic rat. models. The long-term hope is that this information will lead to innovative new strategies for the therapy of non-insulin-dependent diabetes mellitus. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LEAHY, JL (reprint author), JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NIDDK NIH HHS [DK-35449, DK-36836, DK-38543] NR 109 TC 349 Z9 352 U1 0 U2 10 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD MAR PY 1992 VL 15 IS 3 BP 442 EP 455 DI 10.2337/diacare.15.3.442 PG 14 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HF323 UT WOS:A1992HF32300007 PM 1559411 ER PT J AU POLONSKY, WH DAVIS, CL JACOBSON, AM ANDERSON, BJ AF POLONSKY, WH DAVIS, CL JACOBSON, AM ANDERSON, BJ TI HYPERGLYCEMIA, HYPOGLYCEMIA, AND BLOOD-GLUCOSE CONTROL IN DIABETES - SYMPTOM PERCEPTIONS AND TREATMENT STRATEGIES SO DIABETIC MEDICINE LA English DT Article DE HYPERGLYCEMIA; DIABETES; SYMPTOM PERCEPTION; SELF-CARE STRATEGIES AB Recent research has suggested that patients with Type 1 diabetes who are in chronically poor blood glucose control perceive hyperglycaemia differently from those who are in good control. To extend these observations 181 insulin-treated patients with Type 1 or Type 2 diabetes were studied. Patients completed a self-report questionnaire which included items concerning feelings about high and low blood glucose levels and strategies for maintaining blood glucose control. Glycosylated haemoglobin levels were also measured. We hypothesized that level of blood glucose control would: (1) be associated with perceptions of hyperglycaemia and treatment strategies for managing hyperglycaemia and (2) not be associated with perceptions and strategies concerning hypoglycaemia. In comparison with those in 'acceptable' or 'poor' blood glucose control, those in 'good' control perceived symptoms of hyperglycaemia at lower blood glucose levels (p < 0.001) and felt physically best at lower blood glucose levels (p < 0.001). They also began treatment for hyperglycaemia at lower glucose levels (p < 0.05), set lower minimal (p < 0.001) and maximal (p < 0.001) glucose levels as treatment goals, and tested their blood glucose levels more frequently (p < 0.05). Among Type 1 diabetic patients, those in 'good' control reported experiencing hypoglycaemia at lower glucose levels than those in 'acceptable' or 'poor' control (p < 0.05). No differences in treatment strategies of hypoglycaemic symptoms were apparent. This study suggests an influence of patients' perceptions of symptoms and treatment in self-care of diabetes. RP POLONSKY, WH (reprint author), JOSLIN DIABET CTR,PSYCHOSOCIAL UNIT,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 0 TC 13 Z9 13 U1 0 U2 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0742-3071 J9 DIABETIC MED JI Diabetic Med. PD MAR PY 1992 VL 9 IS 2 BP 120 EP 125 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG630 UT WOS:A1992HG63000005 PM 1563245 ER PT J AU STREULI, M KRUEGER, NX ARINIELLO, PD TANG, M MUNRO, JM BLATTLER, WA ADLER, DA DISTECHE, CM SAITO, H AF STREULI, M KRUEGER, NX ARINIELLO, PD TANG, M MUNRO, JM BLATTLER, WA ADLER, DA DISTECHE, CM SAITO, H TI EXPRESSION OF THE RECEPTOR-LINKED PROTEIN TYROSINE PHOSPHATASE LAR - PROTEOLYTIC CLEAVAGE AND SHEDDING OF THE CAM-LIKE EXTRACELLULAR REGION SO EMBO JOURNAL LA English DT Article DE HUMAN CHROMOSOME-1; IMMUNOHISTOCHEMISTRY; PAIRED BASIC AMINO ACID SITE; PROTEIN TYROSINE PHOSPHORYLATION ID LEUKOCYTE COMMON ANTIGEN; HUMAN INSULIN-RECEPTOR; IMMUNOGLOBULIN SUPERFAMILY; MONOCLONAL-ANTIBODIES; POINT MUTATION; FAMILY; SITE; CLONING; KINASE; CELLS AB The human transmembrane molecule LAR is a protein tyrosine phosphatase (PTPase) with a cell adhesion molecule-like extracellular receptor region. The structure of LAR hinted at its involvement in the regulation of tyrosine phosphorylation through cell - cell or cell - matrix interactions. We show here that LAR is expressed on the cell surface as a complex of two non-covalently associated subunits derived from a proprotein. The LAR E-subunit contains the cell adhesion molecule-like receptor region, while the LAR P-subunit contains a short segment of the extracellular region, the transmembrane peptide and the cytoplasmic PTPase domains. Proprotein processing occurs intracellularly. Analysis of LAR mutants suggested that cleavage occurs in the LAR extracellular region at a paired basic amino acid site by a subtilisin-like endoprotease. A single amino acid substitution at this site blocked LAR proprotein cleavage. The LAR E-subunit is shed during cell growth, suggesting that LAR receptor shedding may be a mechanism for regulating PTPase function. The use of immunohistochemistry techniques on human tissues demonstrated the expression of LAR by various cell lineages, including epithelial cells, smooth muscle cells and cardiac myocytes. The LAR gene is mapped to chromosome 1, region p32-33, which contains candidate tumor suppressor genes. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. UNIV WASHINGTON,DEPT PATHOL,SEATTLE,WA 98195. IMMUNOGEN INC,CAMBRIDGE,MA 02139. RP STREULI, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA51132]; NIA NIH HHS [AG01751]; NIAID NIH HHS [AI26598] NR 60 TC 150 Z9 150 U1 0 U2 0 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD MAR PY 1992 VL 11 IS 3 BP 897 EP 907 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HH082 UT WOS:A1992HH08200013 PM 1547787 ER PT J AU PETER, ME HALL, C RUHLMANN, A SANCHO, J TERHORST, C AF PETER, ME HALL, C RUHLMANN, A SANCHO, J TERHORST, C TI THE T-CELL RECEPTOR ZETA-CHAIN CONTAINS A GTP/GDP BINDING-SITE SO EMBO JOURNAL LA English DT Article DE GTP BINDING PROTEIN; INSITU AFFINITY LABELING; MUTAGENESIS; P21H-RAS; T-CELL RECEPTOR ZETA-CHAIN ID ELONGATION-FACTOR-TU; ANTIGEN RECEPTOR; TYROSINE PHOSPHORYLATION; MOLECULAR-CLONING; ESCHERICHIA-COLI; ETA-CHAIN; ACTIVATION; PROTEINS; COMPLEX; CONFORMATION AB In a search for nucleotide binding proteins associated with the T-cell receptor (TCR) - CD3 complex, a novel labeling technique involving introduction of [alpha-P-32]GTP or [alpha-P-32]ATP into permeabilized cells followed by in situ periodate oxidation was developed. To test the method we first demonstrated that p21ras and other classical GTP binding proteins could be labeled in a GTP-specific manner. In human T lymphocytes the TCR zeta-chain was found to be specifically labeled by GTP(oxi) but not by ATP(oxi) or CTP(oxi). Labeling kinetics and competition experiments demonstrated that zeta had a capacity to bind GTP and GDP but not GMP or ATP. Proteolytic cleavage experiments identified lysine 128 as the GTP crosslinking site. This result was confirmed by studies using oligonucleotide-directed mutagenesis. Lysine residues 128, 135 and 149 were each replaced by arginine and glycine 134 by valine and mutated proteins were expressed in CHO celts. Labeling of mutants K128R and G134V was abrogated whereas mutant proteins K135R and K148R could still be specifically crosslinked to GTP. We conclude that Lys128 and Gly134 are part of a GTP/GDP binding site suggesting that zeta is a unique GTP/GDP binding structure. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MOLEC IMMUNOL LAB,BOSTON,MA 02115. RI Sancho, Jaime/O-3228-2013 OI Sancho, Jaime/0000-0003-3852-7951 FU NIAID NIH HHS [AI 15066] NR 46 TC 60 Z9 60 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD MAR PY 1992 VL 11 IS 3 BP 933 EP 941 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HH082 UT WOS:A1992HH08200017 PM 1547789 ER PT J AU GIORGINO, F CHEN, JH SMITH, RJ AF GIORGINO, F CHEN, JH SMITH, RJ TI CHANGES IN TYROSINE PHOSPHORYLATION OF INSULIN-RECEPTORS AND A 170,000 MOLECULAR-WEIGHT NONRECEPTOR PROTEIN INVIVO IN SKELETAL-MUSCLE OF STREPTOZOTOCIN-INDUCED DIABETIC RATS - EFFECTS OF INSULIN AND GLUCOSE SO ENDOCRINOLOGY LA English DT Article ID GROWTH FACTOR-I; KINASE-ACTIVITY; ENDOGENOUS SUBSTRATE; 3T3-L1 ADIPOCYTES; ADIPOSE-TISSUE; HUMAN-PLACENTA; CELLS; AUTOPHOSPHORYLATION; STIMULATE; BINDING AB The effects of experimental diabetes on in vivo tyrosine phosphorylation of the insulin receptor (IR) and nonreceptor proteins were investigated in rat skeletal muscle. Diabetes was induced in male Sprague-Dawley rats (200 g) by streptozotocin administration (100 mg/kg, ip). Diabetic animals were subsequently anesthetized, insulin was injected via cardiac puncture, and hindlimb skeletal muscles were removed, frozen in liquid N2, and homogenized in sodium dodecyl sulfate. Tyrosine phosphoproteins were first immunoprecipitated and then identified by immunoblotting with antiphosphotyrosine antibodies. In both control and diabetic rats, insulin stimulated tyrosine phosphorylation of the IR beta-subunit and a major nonreceptor 170,000 mol wt (M(r)) endogenous protein (pp170) in a dose- and time-dependent manner. Total IR number (determined by immunoprecipitation and immunoblotting with an anti-IR antibody) increased 2.4-fold in diabetic muscle, but there was little change in phosphorylated insulin receptor beta-subunit (157 +/- 12% of control value; P < 0.001). In contrast, pp170 phosphorylation increased markedly in diabetes (500 +/- 119% of control value; P < 0.005), and the time course of its disappearance was delayed compared to that in control rats. These changes were reversed by insulin therapy (5 U, sc, twice daily), but not by correction of hyperglycemia with phlorizin (0.4 g/kg.day, sc). In conclusion, in rat skeletal muscle in vivo, streptozotocin-diabetes results in 1) increased total IR number, 2) reduced efficiency of IR phosphorylation, and 3) markedly enhanced tyrosine phosphorylation of a 170,000 M(r) putative IR substrate. Hypoinsulinemia, but not hyperglycemia, appears to increase the level of the phophorylated 170,000 M(r) protein in streptozotocin-diabetes. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,1 JOSLIN PL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. RI Giorgino, Francesco/K-7262-2016 OI Giorgino, Francesco/0000-0001-7372-2678 FU NIDDK NIH HHS [DK-36836]; NIGMS NIH HHS [GM-36428] NR 51 TC 66 Z9 68 U1 0 U2 0 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAR PY 1992 VL 130 IS 3 BP 1433 EP 1444 DI 10.1210/en.130.3.1433 PG 12 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HG161 UT WOS:A1992HG16100047 PM 1531627 ER PT J AU HUOVINEN, P WOLFSON, JS HOOPER, DC AF HUOVINEN, P WOLFSON, JS HOOPER, DC TI SYNERGISM OF TRIMETHOPRIM AND CIPROFLOXACIN INVITRO AGAINST CLINICAL BACTERIAL ISOLATES SO EUROPEAN JOURNAL OF CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES LA English DT Note ID ESCHERICHIA-COLI; QUINOLONE RESISTANCE; DNA GYRASE; MECHANISMS; EMERGENCE AB For the first time, the effects of combinations of trimethoprim and a fluoroquinolone (ciprofloxacin) against gram-positive and gram-negative bacterial isolates were evaluated in vitro. Synergism was found in 31 % (fractional inhibitory concentration, FIC) and 33 % (fractional bactericidal concentration, FBC) of 121 clinical isolates of various bacterial strains, most often in Escherichia coli, staphylococci, and enterococci. Antagonism occurred in 1 % (FIC) and 3 % (FBC). The combination of trimethoprim and ciprofloxacin merits further evaluation for potential usefulness as a clinical regimen. C1 UNIV TURKU,DEPT MED MICROBIOL,SF-20500 TURKU 50,FINLAND. MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. RP HUOVINEN, P (reprint author), NATL PUBL HLTH INST,ANTIMICROBIAL RES UNIT,SF-20520 TURKU,FINLAND. RI Huovinen, Pentti/C-1917-2009 NR 13 TC 9 Z9 9 U1 0 U2 0 PU FRIEDR VIEWEG SOHN VERLAG GMBH PI WIESBADEN 1 PA PO BOX 5829, W-6200 WIESBADEN 1, GERMANY SN 0934-9723 J9 EUR J CLIN MICROBIOL JI Eur. J. Clin. Microbiol. Infect. Dis. PD MAR PY 1992 VL 11 IS 3 BP 255 EP 257 DI 10.1007/BF02098092 PG 3 WC Infectious Diseases; Microbiology SC Infectious Diseases; Microbiology GA HT713 UT WOS:A1992HT71300010 PM 1597204 ER PT J AU LUND, T SHAIKH, S HATTORI, M MAKINO, S AF LUND, T SHAIKH, S HATTORI, M MAKINO, S TI ANALYSIS OF THE T-CELL RECEPTOR (TCR) REGIONS IN THE NOD, NON AND CTS MOUSE STRAINS DEFINE NEW TCR V-ALPHA HAPLOTYPES AND NEW DELETIONS IN THE TCR V-BETA REGION SO EUROPEAN JOURNAL OF IMMUNOLOGY LA English DT Note ID NONOBESE DIABETIC MICE; MAJOR HISTOCOMPATIBILITY COMPLEX; FRAGMENT-LENGTH-POLYMORPHISMS; GENE FAMILIES; CHAIN; PREVENTION; INSULITIS; MELLITUS AB We have analyzed the T cell receptor (TcR) V(alpha) and TcR V(beta) regions in the spontaneous mouse model for insulin-dependent diabetes mellitus. the NOD mouse, and compared it to the regions in the two sister strains, the NON and CTS strains. Based on restriction fragment length polymorphism analysis the TcR V(alpha) region in the NOD mouse is essentially identical to that of the SJL/J strain. In contrast both the NON and CTS strains have a unique TcR V(alpha) haplotype. Whereas the NOD and NON strains apparently contains all the TcR V(beta) genes, the CTS mouse has three deletions in the V(beta) region. Our analysis does not give any indications for the diabetic phenotype of the NOD mouse. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. SHIONOGI ABURAHI LABS,SHIGA,JAPAN. RP LUND, T (reprint author), UNIV COLL & MIDDLESEX SCH MED,DEPT IMMUNOL,MED MOLEC BIOL UNIT,40-50 TOTTENHAM ST,LONDON W1P 9PG,ENGLAND. NR 30 TC 3 Z9 3 U1 0 U2 0 PU VCH PUBLISHERS INC PI DEERFIELD BEACH PA 303 NW 12TH AVE, DEERFIELD BEACH, FL 33442-1788 SN 0014-2980 J9 EUR J IMMUNOL JI Eur. J. Immunol. PD MAR PY 1992 VL 22 IS 3 BP 871 EP 874 DI 10.1002/eji.1830220337 PG 4 WC Immunology SC Immunology GA HK529 UT WOS:A1992HK52900036 PM 1532150 ER PT J AU JUWEID, M STRAUSS, HW YAOITA, H RUBIN, RH FISCHMAN, AJ AF JUWEID, M STRAUSS, HW YAOITA, H RUBIN, RH FISCHMAN, AJ TI ACCUMULATION OF IMMUNOGLOBULIN-G AT FOCAL SITES OF INFLAMMATION SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE INFECTION; IMMUNOGLOBULIN; IGG; RATE CONSTANTS ID POLYCLONAL HUMAN-IMMUNOGLOBULIN; LOCALIZATION; MACROMOLECULES; INFECTION; HISTAMINE; IGG; RAT AB To evaluate the factors responsible for the accumulation of indium-111 immunoglobulin Gr (In-111-IgG) at sites of inflammation, sequential measurements of tissue blood volume, interstitial fluid volume and accumulation of radiolabelled albumin and IgG were made in rats following Escherichia coli infection in the thigh. Compared with normal thigh muscle, there was approximately two-fold increase in interstitial fluid volume and approximately 1.5-fold increase in plasma and red blood cell volumes in infected muscle. For both proteins, there was a fivefold increase in influx rate constant (k(in)) in infected muscle. In normal muscle, the interstitial fluid concentration of labelled human serum albumin (In-111-HSA) was significantly higher than that of In-111-IgG (P < 0.01). In contrast, the concentrations in infected muscle were nearly identical. The concentration ratios (infected to normal muscle) were 1.7:1 for HSA and 3:1 for IgG. These data suggest that the infection imaging properties of In-111-IgG are related to expansion of the space available to macromolecules in infected tissue and increased transport into this space. At clinically important imaging times (24-48 h after injection), the higher target-to-background ratio of In-111-IgG compared with In-111-HSA is not due to the higher accumulation IgG in infected tissue but rather to the higher accumulation of HSA in normal tissue. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 23 TC 56 Z9 56 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD MAR PY 1992 VL 19 IS 3 BP 159 EP 165 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HK245 UT WOS:A1992HK24500002 PM 1572378 ER PT J AU SENDA, M FISCHMAN, AJ WEISE, S ALPERT, NM CORREIA, JA RUBIN, RH STRAUSS, HW AF SENDA, M FISCHMAN, AJ WEISE, S ALPERT, NM CORREIA, JA RUBIN, RH STRAUSS, HW TI REGIONAL PERFUSION, OXYGEN-METABOLISM, BLOOD-VOLUME AND IMMUNOGLOBULIN-G ACCUMULATION AT FOCAL SITES OF INFECTION IN RABBITS SO EUROPEAN JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE REGIONAL PERFUSION; OXYGEN METABOLISM; BLOOD VOLUME; IMMUNOGLOBULIN-G; INFECTION SITES; RABBIT ID ENHANCED VASCULAR-PERMEABILITY; POSITRON EMISSION TOMOGRAPHY; NONSPECIFIC POLYCLONAL IGG; ACUTE-INFLAMMATION; QUANTITATION; FLOW; HEMORRHAGE; BRAIN; O-15 AB Infection causes remarkable changes in extracellular fluid volume, blood flow and oxygen consumption in the region of the lesion. To determine the sequence and magnitude of these changes, we performed serial scintigraphic measurements in 10 rabbits with experimental Escherichia coli abscesses. Positron emission tomography with (CO2)-O-15 O-15(2) and (CO)-11 was used to measure regional blood flow, oxygen extraction (OEF) and blood volume; extracellular fluid volume was evaluated by single photon scintigraphy with indium-111 immunoglobulin G (IgG). Images were recorded following tracer administration at 1 and 7-10 days after infection. At the first imaging time, blood flow to infected muscle had increased by 40% compared with control sites (7.4 +/- 0.6 to 10.8 +/- 3.8 ml/min.100 g), OEF had decreased from 55% +/- 34% to 45% +/- 14%, and the infected-to-contralateral (I/C) ratio of IgG had increased to 3.34 +/- 1.85. At the later imaging time, flow had increased by almost threefold compared with day 1 (29.4 +/- 9.8 ml/min.100 g), OEF had decreased to 29% +/- 14%, and the I/C ratio for IgG had remained constant. Although OEF fell, oxygen delivery (OEF x flow) increased from 4.07 ml/min (control value) to 4.86 ml/min on day 1 and 8.64 ml/min on days 7-9. The infected-to-contralateral (IC) ratio of O-15(2)/(CO2)-O-15 was 0.74 +/- 0.15 on day 1 and 0.77 +/- 0.10 at 7-9 days. These studies indicate that expansion of the extracellular fluid volume increases early in the evolution of the infection and exceeds changes in regional perfusion and oxygen delivery. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,32 FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. NR 22 TC 10 Z9 10 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0340-6997 J9 EUR J NUCL MED JI Eur. J. Nucl. Med. PD MAR PY 1992 VL 19 IS 3 BP 166 EP 172 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HK245 UT WOS:A1992HK24500003 PM 1572379 ER PT J AU STARK, DD AF STARK, DD TI PHYSIOLOGICAL PRINCIPLES FOR THE DESIGN OF HEPATIC CONTRAST AGENTS SO EUROPEAN JOURNAL OF RADIOLOGY LA English DT Article DE MAGNETIC RESONANCE, CONTRAST MEDIA; MAGNETIC RESONANCE, PHYSIOLOGY; CONTRAST MEDIA, MRI RP STARK, DD (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0720-048X J9 EUR J RADIOL JI Eur. J. Radiol. PD MAR-APR PY 1992 VL 14 IS 2 BP 124 EP 127 DI 10.1016/0720-048X(92)90225-X PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HM510 UT WOS:A1992HM51000007 PM 1314179 ER PT J AU HUANG, Q VONSATTEL, JP SCHAFFER, PA MARTUZA, RL BREAKEFIELD, XO DIFIGLIA, M AF HUANG, Q VONSATTEL, JP SCHAFFER, PA MARTUZA, RL BREAKEFIELD, XO DIFIGLIA, M TI INTRODUCTION OF A FOREIGN GENE (ESCHERICHIA-COLI-LACZ) INTO RAT NEOSTRIATAL NEURONS USING HERPES-SIMPLEX VIRUS MUTANTS - A LIGHT AND ELECTRON-MICROSCOPIC STUDY SO EXPERIMENTAL NEUROLOGY LA English DT Article ID LATENCY-ASSOCIATED TRANSCRIPT; BETA-GALACTOSIDASE; CHOLINERGIC NEURONS; SENSORY NEURONS; NERVOUS-SYSTEM; TYPE-1; MOUSE; GANGLIA; INFECTION; ORGANIZATION C1 MASSACHUSETTS GEN HOSP,DEPT SURG,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HUANG, Q (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114, USA. FU NINDS NIH HHS [NS 16367, NS24279] NR 36 TC 54 Z9 54 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0014-4886 J9 EXP NEUROL JI Exp. Neurol. PD MAR PY 1992 VL 115 IS 3 BP 303 EP 316 DI 10.1016/0014-4886(92)90196-W PG 14 WC Neurosciences SC Neurosciences & Neurology GA HH294 UT WOS:A1992HH29400001 PM 1311266 ER PT J AU SCHREIBER, RA KLEINMAN, RE BARKSDALE, EM MAGANARO, TF DONAHOE, PK AF SCHREIBER, RA KLEINMAN, RE BARKSDALE, EM MAGANARO, TF DONAHOE, PK TI REJECTION OF MURINE CONGENIC BILE-DUCTS - A MODEL FOR IMMUNE-MEDIATED BILE-DUCT DISEASE SO GASTROENTEROLOGY LA English DT Article ID REOVIRUS TYPE-3 INFECTION; PRIMARY BILIARY-CIRRHOSIS; TRANSPLANTATION IMMUNOLOGY; EPITHELIAL-CELLS; ATRESIA; EXPRESSION; ANTIGENS; CHOLANGITIS; SURVIVAL; PRODUCTS C1 HARVARD UNIV,CHILDRENS HOSP,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02115. RP SCHREIBER, RA (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,PEDIAT SURG RES LABS,BOSTON,MA 02114, USA. FU NICHD NIH HHS [HD 20810] NR 37 TC 23 Z9 26 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAR PY 1992 VL 102 IS 3 BP 924 EP 930 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HF721 UT WOS:A1992HF72100024 PM 1537528 ER PT J AU ISRAEL, EJ AF ISRAEL, EJ TI PAF-ACETHER IN NECROTIZING ENTEROCOLITIS - REPLY SO GASTROENTEROLOGY LA English DT Letter C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP ISRAEL, EJ (reprint author), HARVARD UNIV,SCH MED,DIV PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAR PY 1992 VL 102 IS 3 BP 1092 EP 1092 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HF721 UT WOS:A1992HF72100057 ER PT J AU HAHN, PF STARK, DD FERRUCCI, JT AF HAHN, PF STARK, DD FERRUCCI, JT TI ACCUMULATION OF IRON-OXIDE PARTICLES AROUND LIVER METASTASES DURING MR IMAGING SO GASTROINTESTINAL RADIOLOGY LA English DT Article DE LIVER, MR STUDIES; MAGNETIC RESONANCE, CONTRAST ENHANCEMENT; COLON CARCINOMA, METASTASES ID CLINICAL-APPLICATION AB The histologic nature of the bright ring ("peritumoral edema") around some liver metastases on T2-weighted magnetic resonance (MR) images is controversial. In the case reported, particles of the iron oxide contrast agent AMI-25 are retained in the peritumoral zone of a colon cancer metastasis, causing the bright ring to disappear. The location of iron particles in resected specimens could be used systematically to study peritumoral edema. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HAHN, PF (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [R01-CA 50353] NR 7 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2356 J9 GASTROINTEST RADIOL PD SPR PY 1992 VL 17 IS 2 BP 173 EP 174 DI 10.1007/BF01888539 PG 2 WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical Imaging SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical Imaging GA HD812 UT WOS:A1992HD81200022 PM 1551515 ER PT J AU RON, D HABENER, JF AF RON, D HABENER, JF TI CHOP, A NOVEL DEVELOPMENTALLY REGULATED NUCLEAR-PROTEIN THAT DIMERIZES WITH TRANSCRIPTION FACTORS C/EBP AND LAP AND FUNCTIONS AS A DOMINANT-NEGATIVE INHIBITOR OF GENE-TRANSCRIPTION SO GENES & DEVELOPMENT LA English DT Article DE CHOP-10; NUCLEAR PROTEIN; DOMINANT-NEGATIVE INHIBITOR; TRANSCRIPTION FACTORS ID LEUCINE ZIPPER PROTEINS; ENHANCER-BINDING-PROTEIN; PHASE RESPONSE ELEMENT; DNA-BINDING; ANGIOTENSINOGEN GENE; FAMILY; EXPRESSION; ACTIVATOR; CLONING; MEMBER AB We report on the identification of a nuclear protein that serves as a dominant-negative inhibitor of the transcription factors C/EBP and LAP. A P-32-labeled LAP DNA-binding and dimerization domain "zipper probe" was used to isolate a clone that encodes a new C/EBP-homologous protein: CHOP-10. CHOP-10 has strong sequence similarity to C/EBP-like proteins within the bZIP region corresponding to the DNA-binding domain consisting of a leucine zipper and a basic region. Notably, however, CHOP-10 contains 2 prolines substituting for 2 residues in the basic region, critical for binding to DNA. Thus, heterodimers of CHOP-10 and C/EBP-like proteins are unable to bind their cognate DNA enhancer element. CHOP-10 mRNA is expressed in many different rat tissues. Antisera raised against CHOP-10 recognize a nuclear protein with an apparent molecular mass of 29 kD. CHOP-10 is induced upon differentiation of 3T3-L1 fibroblasts to adipocytes, and cytokine-induced dedifferentiation of adipocytes is preceded by the loss of nuclear CHOP-10. Coimmunoprecipitation of CHOP-10 and LAP from transfected COS-1 cells demonstrated a direct interaction between the two proteins, in vivo. Consistent with the structure of its defective basic region, bacterially expressed CHOP-10 inhibits the DNA-binding activity of C/EBP and LAP by forming heterodimers that cannot bind DNA. In transfected HepG2 cells, expression of CHOP-10 attenuates activation of C/EBP- and LAP-driven promoters. We suggest that CHOP-10 is a negative modulator of the activity of C/EBP-like proteins in certain terminally differentiated cells, similar to the regulatory function of Id on the activity of MyoD and MyoD-related proteins important in the development of muscle cells. RP RON, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK25532] NR 42 TC 916 Z9 939 U1 2 U2 15 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD MAR PY 1992 VL 6 IS 3 BP 439 EP 453 DI 10.1101/gad.6.3.439 PG 15 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA HM444 UT WOS:A1992HM44400010 PM 1547942 ER PT J AU REICHARDT, JKV BELMONT, JW LEVY, HL WOO, SLC AF REICHARDT, JKV BELMONT, JW LEVY, HL WOO, SLC TI CHARACTERIZATION OF 2 MISSENSE MUTATIONS IN HUMAN GALACTOSE-1-PHOSPHATE URIDYLTRANSFERASE - DIFFERENT MOLECULAR MECHANISMS FOR GALACTOSEMIA SO GENOMICS LA English DT Article ID URIDYL TRANSFERASE; SEQUENCE; CLONING; GENE C1 BAYLOR COLL MED,TEXAS MED CTR,DEPT CELL BIOL,HOUSTON,TX 77030. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. HARVARD UNIV,SCH MED,JOSEPH P KENNEDY JR LABS,BOSTON,MA 02129. BAYLOR COLL MED,TEXAS MED CTR,INST MOLEC GENET,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02129. RP REICHARDT, JKV (reprint author), HOWARD HUGHES MED INST,HOUSTON,TX 77030, USA. NR 16 TC 24 Z9 26 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD MAR PY 1992 VL 12 IS 3 BP 596 EP 600 DI 10.1016/0888-7543(92)90453-Y PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HD434 UT WOS:A1992HD43400024 PM 1373122 ER PT J AU PRESSLEY, RH MUNTZ, HG FALKENBERRY, S RICE, LW AF PRESSLEY, RH MUNTZ, HG FALKENBERRY, S RICE, LW TI SERUM LACTIC-DEHYDROGENASE AS A TUMOR-MARKER IN DYSGERMINOMA SO GYNECOLOGIC ONCOLOGY LA English DT Article ID OVARIAN DYSGERMINOMA; CHEMOTHERAPY C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP PRESSLEY, RH (reprint author), MASSACHUSETTS GEN HOSP,DIV GYNECOL ONCOL,VINCENT GYNECOL SERV,BOSTON,MA 02114, USA. NR 19 TC 18 Z9 19 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0090-8258 J9 GYNECOL ONCOL JI Gynecol. Oncol. PD MAR PY 1992 VL 44 IS 3 BP 281 EP 283 DI 10.1016/0090-8258(92)90058-Q PG 3 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA HK179 UT WOS:A1992HK17900016 PM 1541442 ER EF