FN Thomson Reuters Web of Science™ VR 1.0 PT J AU LASALLE, JM TOLENTINO, PJ FREEMAN, GJ NADLER, LM HAFLER, DA AF LASALLE, JM TOLENTINO, PJ FREEMAN, GJ NADLER, LM HAFLER, DA TI EARLY SIGNALING DEFECTS IN HUMAN T-CELLS ANERGIZED BY T-CELL PRESENTATION OF AUTOANTIGEN SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; KINASE-C ACTIVATION; COSTIMULATORY SIGNAL; TRANSGENIC MICE; SELF-TOLERANCE; CLONAL ANERGY; LYMPHOCYTES-T; ANTIGEN; INDUCTION; UNRESPONSIVENESS AB Major histocompatibility complex class 11-positive human T cell clones are nontraditional antigen-presenting cells (APCs) that are able to simultaneously present and respond to peptide or degraded antigen, but are unable to process intact protein. Although T cell presentation of peptide antigen resulted in a primary proliferative response, T cells that had been previously stimulated by T cells presenting antigen were completely unresponsive to antigen but not to interleukin 2 (IL-2). In contrast, peptide antigen presented by B cells or DP2+ L cell transfectants resulted in T cell activation and responsiveness to restimulation. The anergy induced by T cell presentation of peptide could not be prevented by the addition of either autologous or allogeneic B cells or B7+DR2+ L cell transfectants, suggesting that the induction of anergy could occur in the presence of costimulation. T cell anergy was induced within 24 h of T cell presentation of antigen and was long lasting. Anergized T cells expressed normal levels of T cell receptor/CD3 but were defective in their ability to release [C2+] to both alpha-CD3 and APCs. Moreover, anergized T cells did not proliferate to alpha-CD2 monoclonal antibodies or alpha-CD3 plus phorbol myristate acetate (PMA), nor did they synthesize IL-2, IL-4, or interferon-gamma mRNA in response to either peptide or peptide plus PMA. In contrast, ionomycin plus PMA induced both normal proliferative responses and synthesis of cytokine mRNA, suggesting that the signaling defect in anergized cells occurs before protein kinase C activation and [Ca2+]i release. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP LASALLE, JM (reprint author), BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,221 LONGWOOD AVE,BOSTON,MA 02115, USA. RI LaSalle, Janine/A-4643-2008 OI LaSalle, Janine/0000-0002-3480-2031 FU NINDS NIH HHS [R01 NS-24247] NR 37 TC 130 Z9 130 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 JUL 1 PY 1992 VL 176 IS 1 BP 177 EP 186 DI 10.1084/jem.176.1.177 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA JA759 UT WOS:A1992JA75900019 PM 1535366 ER PT J AU HARDING, PM MCMURRAY, MC LAESSIG, RH SIMLEY, DO CORRELL, PJ TSUNEHIRO, JK AF HARDING, PM MCMURRAY, MC LAESSIG, RH SIMLEY, DO CORRELL, PJ TSUNEHIRO, JK TI THE EFFECT OF DENTURES AND DENTURE ADHESIVES ON MOUTH ALCOHOL RETENTION SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE TOXICOLOGY; BREATH-ALCOHOL TESTING; MOUTH ALCOHOL; DENTURES AB A total of 24 alcohol-free, denture-wearing subjects were tested for mouth-alcohol retention times with an Intoxilyzer(TM) 5000. The subjects were given 30 mL doses of 80 proof brandy to swish in their mouths without swallowing for 2 min prior to expectorating the dose. Subjects were tested under three conditions: 1) with dentures removed, 2) with dentures held loosely in place without an adhesive, and 3) with dentures plus an adhesive. Beyond 20 min following expectoration, mouth alcohol made no significant contribution to the apparent breath alcohol concentration (BrAC), with trace (less-than-or-equal-to 0.01 g/210 L) readings found in only two of the subjects. Denture use, both with and without the concurrent use of adhesives does not significantly affect BrAC as long as a pretest alcohol deprivation period of 20 min is observed. C1 WISCONSIN STATE LAB HYG,MADISON,WI. WISCONSIN STATE CRIME LAB,MILWAUKEE,WI. UNIV WISCONSIN,PATHOL,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,DENT SERV,MADISON,WI 53705. NR 15 TC 13 Z9 14 U1 0 U2 1 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD JUL PY 1992 VL 37 IS 4 BP 999 EP 1007 PG 9 WC Medicine, Legal SC Legal Medicine GA JY405 UT WOS:A1992JY40500009 PM 1506841 ER PT J AU CARR, P FRIEDMAN, RH MOSKOWITZ, MA KAZIS, LE WEED, HG AF CARR, P FRIEDMAN, RH MOSKOWITZ, MA KAZIS, LE WEED, HG TI RESEARCH, ACADEMIC RANK, AND COMPENSATION OF WOMEN AND MEN FACULTY IN ACADEMIC GENERAL INTERNAL-MEDICINE SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Article DE WOMEN; GENERAL INTERNAL MEDICINE; RANK; RESEARCH; COMPENSATION; FACULTY AB Objective: To evaluate the status of men and women faculty in academic general internal medicine, including their professional training, faculty responsibilities, research performance, academic rank and compensation, to determine whether systematic differences exist by gender. Design/setting: The authors analyzed responses to a 55-part questionnaire sent to all full-time general internal medicine faculty at the major teaching hospitals in the United States. Unadjusted means were generated for men versus women faculty in demographics, training background, hours of work, professional time allocations, institutional support, professional self-assessment, research performance, academic rank, and compensation. Means were recalculated after adjusting for other variables using multivariate methods. Results: The authors found no significant difference in the frequency of fellowship training between men and women faculty Women and men perform similar professional activities, but even after multivariate adjustment, women devote less time to research and perceive less research skill and institutional support for their research, but have similar numbers of grants, abstracts, and publications in refereed journals and have similar academic ranks. Women faculty, however, receive lower compensation than do men faculty, even after adjustment. Conclusion: While the characteristics of men and women faculty are quite similar, including those defining their academic productivity, important differences exist in research time, perceived institutional support, and compensation. These differences cannot be explained by such obvious factors as age differentials, academic rank, or hours of work per week. RP CARR, P (reprint author), MASSACHUSETTS GEN HOSP,GEN MED UNIT,BULFINCH 1,FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 59 Z9 59 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD JUL-AUG PY 1992 VL 7 IS 4 BP 418 EP 423 DI 10.1007/BF02599159 PG 6 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA JE266 UT WOS:A1992JE26600007 PM 1506948 ER PT J AU DEC, GW SEMIGRAN, MJ VLAHAKES, G SOUTHERN, J FALLON, JT AF DEC, GW SEMIGRAN, MJ VLAHAKES, G SOUTHERN, J FALLON, JT TI LYMPHOMA MIMICS CYTOMEGALOVIRUS-INDUCED HEPATITIS IN A HEART-TRANSPLANT RECIPIENT SO JOURNAL OF HEART AND LUNG TRANSPLANTATION LA English DT Article AB A 56-year-old diabetic man underwent heart transplantation for end-stage ischemic heart disease; fever, progressive thrombocytopenia, and hepatitis developed 8 weeks after transplantation. Cytomegalovirus was cultured from the serum buffy coat. In spite of therapy with high-dose ganciclovir sodium, the patient died on the seventy-seventh postoperative day. Autopsy revealed a previously unsuspected high-grade B-cell lymphoma with extensive hepatic replacement. RP DEC, GW (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULFINCH 1,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1053-2498 J9 J HEART LUNG TRANSPL JI J. Heart Lung Transplant. PD JUL-AUG PY 1992 VL 11 IS 4 BP 778 EP 780 PN 1 PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery; Transplantation SC Cardiovascular System & Cardiology; Respiratory System; Surgery; Transplantation GA JJ434 UT WOS:A1992JJ43400027 PM 1323329 ER PT J AU FUNAKI, N TANAKA, Y MAK, KM LIEBER, CS AF FUNAKI, N TANAKA, Y MAK, KM LIEBER, CS TI URIDINE DIPHOSPHOGLUCOSE RESTORES LIPOCYTE PROLIFERATION IN THE REGENERATING LIVER OF ETHANOL-TREATED RATS SO JOURNAL OF HEPATOLOGY LA English DT Article DE URIDINE DIPHOSPHOGLUCOSE; ETHANOL; RAT; HEPATECTOMY; LIPOCYTE ID TISSUES AB The effect of continuous intraperitoneal infusion of uridine diphosphoglucose on ethanlol-induced suppression of lipocyte proliferation was studied in regenerating rat livers from 1 4 days after hepatectomy. Proliferating lipocytes were positively identified using a two-sequence immunohistochemical staining for cytoplasmic desmin and bromodeoxyuridine-labelled nuclei. Hepatectomy rapidly stimulated lipocyte proliferation which peaked 2 days after hepatectomy (labelling index, 17.9 +/- 0.81%). uridine diphosphoglucose or glucose infusion did not modify the time course of lipocyte proliferation. Ethanol feeding to hepatectomized rats receiving saline or glucose infusion resulted in a 71% (p < 0.005) and 61% (p < 0.005) inhibition of lipocyte proliferation, respectively, 2 days after hepatectomy, thereby abolishing the characteristic proliferative peak observed in rats not treated with ethanol. In contrast, uridine diphosphoglucose infusion doubled the labelling index (13.1 +/- 2.34%) in ethanol-fed rats compared to that in corresponding rats treated with saline (5.28 +/- 1.29%; p < 0.005) or glucose (6.51 +/- 0.64%; p < 0.005). This resulted in the appearance of a proliferative peak, albeit smaller than normal, 2 days after hepatectomy. In sham-operated rats, lipocyte proliferation was low with a labelling index of 1.88 +/- 0.13% at the time of operation and of 1.69 +/- 0.23% 2 days thereafter. Uridine diphosphoglucose infusion to sham-operated rats for 2 days did not significantly affect lipocyte proliferation (labelling index 1.79 +/- 0.06%). The present study demonstrated that uridine diphosphoglucose does not affect lipocyte proliferation in the regenerating or sham-operated livers, but that it artially reverses the ethanol-induced suppression of lipocyte proliferation after hepatectomy. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,130 W KINGSBRIDGE RD,BRONX,NY 10468. CUNY MT SINAI SCH MED,DEPT MED,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT PATHOL,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,DEPT CELL BIOL ANAT,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY 10468. FU NIAAA NIH HHS [AA 03508]; NIDDK NIH HHS [DK 32810] NR 14 TC 2 Z9 2 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0168-8278 J9 J HEPATOL JI J. Hepatol. PD JUL PY 1992 VL 15 IS 3 BP 367 EP 371 DI 10.1016/0168-8278(92)90070-6 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA JP510 UT WOS:A1992JP51000016 PM 1447504 ER PT J AU HERNANDEZMUNOZ, R MA, XL BARAONA, E LIEBER, CS AF HERNANDEZMUNOZ, R MA, XL BARAONA, E LIEBER, CS TI METHOD OF ACETALDEHYDE MEASUREMENT WITH MINIMAL ARTIFACTUAL FORMATION IN RED-BLOOD-CELLS AND PLASMA OF ACTIVELY DRINKING SUBJECTS WITH ALCOHOLISM SO JOURNAL OF LABORATORY AND CLINICAL MEDICINE LA English DT Article ID ETHANOL; CHROMATOGRAPHY; INTERFERENCE; ELIMINATION AB After alcohol consumption, a substantial amount of acetaldehyde that is reversibly bound to protein and nonprotein components of the red blood cells circulates in the blood and could cause extrahepatic toxicity. However, acetaldehyde measurement in human red blood cells is hampered by considerable ex vivo artifactual formation as a result of nonenzymatic oxidation of ethanol during protein precipitation. To eliminate this source of artifactual formation, free and reversibly bound acetaldehyde were trapped with semicarbazide from red blood cell hemolysates, and both the stroma and the hemoglobin were sequentially removed by centrifugation and ion-exchange chromatography in carboxymethyl Sephadex, respectively. The eluted semicarbazone was dissociated with perchloric acid, and the acetaldehyde that was released in the protein-free supernatants was measured by head-space gas chromatography. Maximal retention of hemoglobin by carboxymethyl Sephadex and complete recovery of acetaldehyde and ethanol were achieved at a pH of 5.3. The artifactual formation decreased from 2.62 +/- 0.32-mu-mol of acetaldehyde per millimole of ethanol in the initial hemolysates to 1.38 +/- 0.20-mu-mol after removal of the stroma and to a level that is comparable to measurements in plasma (0.09 +/- 0.02-mu-mol) after removal of both the stroma and the hemoglobin. In 12 actively drinking subjects with alcoholism, with blood ethanol levels that ranged between 9 and 81 mmol/L, the concentrations of acetaldehyde in red blood cells (11.50 +/- 1.46-mu-mol/L; range: 7.5 to 22-mu-mol/L) were minimally affected by blood ethanol levels and were three times as high as those in the plasma (3.74 +/- 1.49-mu-mol/L). This improved method, with a 29-fold reduction in artifactual formation, is suitable for the elucidation of the respective contributions of red blood cell and plasma acetaldehyde to the toxicity of this reactive metabolite on cells other than the hepatocyte. C1 BRONX VET AFFAIRS MED CTR,ALCOHOL RES CTR,BRONX,NY. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,LIVER DIS & NUTR SECT,BRONX,NY 10468. FU NIAAA NIH HHS [AA-03508, AA-07802] NR 26 TC 29 Z9 30 U1 0 U2 2 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 JUL PY 1992 VL 120 IS 1 BP 35 EP 41 PG 7 WC Medical Laboratory Technology; Medicine, General & Internal; Medicine, Research & Experimental SC Medical Laboratory Technology; General & Internal Medicine; Research & Experimental Medicine GA JB784 UT WOS:A1992JB78400008 PM 1613325 ER PT J AU TUOHY, VK SOBEL, RA LU, ZJ LAURSEN, RA LEES, MB AF TUOHY, VK SOBEL, RA LU, ZJ LAURSEN, RA LEES, MB TI MYELIN PROTEOLIPID PROTEIN - MINIMUM SEQUENCE REQUIREMENTS FOR ACTIVE INDUCTION OF AUTOIMMUNE ENCEPHALOMYELITIS IN SWR/J AND SJL/J MICE SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE MYELIN PROTEOLIPID PROTEIN; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; T-CELL EPITOPE; ENCEPHALITOGENIC; DEMYELINATION; MULTIPLE SCLEROSIS ID EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; T-CELL EPITOPE; BASIC-PROTEIN; ENCEPHALITOGENIC DETERMINANT; SYNTHETIC PEPTIDE; LYMPHOCYTES-T; LARGE NUMBERS; SITE; IDENTIFICATION; RECOGNITION AB Proteolipid protein (PLP) is the major protein constituent of mammalian central nervous system myelin. We have previously identified two different PLP encephalitogenic T cell epitopes in two mouse strains. Murine PLP peptides 103-116 YKTTICGKGLSATV and 139-151 HCLGKWLGHPDKF are encephalitogenic determinants in SWR/J (H-2q) and SJL/J (H-2s) mice, respectively. The purpose of the present study was to determine the minimum sequence requirements for each of these PLP encephalitogens. In SWR/J mice, at least two distinct overlapping peptides can induce experimental autoimmune encephalomyelitis (EAE). The eleven residue sequences PLP 105-115 TTICGKGLSAT and PLP 106-116 TICGKGLSATV are encephalitogenic in SWR/J mice, but PLP 106-115 TICGKGLSAT, the decapeptide indigenous to both sequences, is non-encephalitogenic. In contrast, the shortest PLP sequence capable of inducing EAE in SJL/J mice is the nonapeptide 141-149 LGKWL-GHPD. These data indicate that encephalitogenic determinants of PLP are short contiguous peptide sequences similar in length and diversity to those of MBP. C1 EK SHRIVER CTR,DEPT BIOCHEM,WALTHAM,MA. BOSTON UNIV,DEPT CHEM,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,IMMUNOPATHOL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROPATHOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NICHD NIH HHS [HD 04147]; NINDS NIH HHS [NS 16945, NS 26773] NR 39 TC 56 Z9 56 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0165-5728 J9 J NEUROIMMUNOL JI J. Neuroimmunol. PD JUL PY 1992 VL 39 IS 1-2 BP 67 EP 74 DI 10.1016/0165-5728(92)90175-K PG 8 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA JB483 UT WOS:A1992JB48300007 PM 1377711 ER PT J AU HAWLEY, RJ SCHEIBE, RJ WAGNER, JA AF HAWLEY, RJ SCHEIBE, RJ WAGNER, JA TI NGF INDUCES THE EXPRESSION OF THE VGF GENE THROUGH A CAMP RESPONSE ELEMENT SO JOURNAL OF NEUROSCIENCE LA English DT Article ID NERVE GROWTH-FACTOR; PC12 PHEOCHROMOCYTOMA CELLS; DEPENDENT PROTEIN-KINASES; TRANSCRIPTION FACTOR CREB; NUCLEAR FACTOR CREB; CYCLIC-AMP; ORNITHINE DECARBOXYLASE; RAT PHEOCHROMOCYTOMA; SOMATOSTATIN GENE; C-FOS AB NGF is a peptide growth factor that plays a key role in the differentiation and survival of neurons in both the PNS and CNS. NGF acts through both transcription-dependent and transcription-independent mechanisms to regulate the differentiation of PC12 cells. To better understand the regulation of gene expression by NGF, we have defined a cis-acting sequence that is immediately upstream of the transcription start site of the VGF (a2/NGF33.1) gene that is required for induction by NGF. Within this sequence is a consensus cAMP response element (CRE) embedded in a 14 base pair palindrome. Mutations in this CRE eliminate induction of the VGF gene both by NGF and by agents that act via cAMP. Although this sequence confers transcriptional induction by both NGF and cAMP, it is not sufficient to allow induction by epidermal growth factor, acidic or basic fibroblast growth factor, or phorbol 12-myristate 13-acetate (PMA). Thus, this sequence defines an element that is selectively activated by NGF and cAMP. Promoter fragments from the VGF gene that include the core CRE efficiently bind the inducible transcription factor CREB, while fragments bearing mutations that eliminate NGF and cAMP inducibility fail to do so. Sequence comparisons and hybridization studies indicate that there are at least two alternatively spliced forms of VGF mRNA, and the accumulation of both of these forms is similarly regulated by NGF and cAMP. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA22427, CA40929]; NEI NIH HHS [EY06454] NR 81 TC 65 Z9 67 U1 0 U2 0 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JUL PY 1992 VL 12 IS 7 BP 2573 EP 2581 PG 9 WC Neurosciences SC Neurosciences & Neurology GA JC512 UT WOS:A1992JC51200014 PM 1377233 ER PT J AU BUNKER, C AF BUNKER, C TI ESOPHAGEAL DISORDERS AND SCINTIGRAPHY - ONE CLINICIAN PERSPECTIVE SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material ID DIAGNOSIS RP BUNKER, C (reprint author), MASSACHUSETTS GEN HOSP,O EMERSON PL,SUITE 2H,BOSTON,MA 02114, USA. NR 12 TC 1 Z9 1 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 JUL PY 1992 VL 33 IS 7 BP 1301 EP 1303 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JB807 UT WOS:A1992JB80700012 PM 1613569 ER PT J AU HOLMAN, BL GARADA, B JOHNSON, KA MENDELSON, J HALLGRING, E TEOH, SK WORTH, J NAVIA, B AF HOLMAN, BL GARADA, B JOHNSON, KA MENDELSON, J HALLGRING, E TEOH, SK WORTH, J NAVIA, B TI A COMPARISON OF BRAIN PERFUSION SPECT IN COCAINE ABUSE AND AIDS DEMENTIA COMPLEX SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HIV-1 AB Intravenous drug use is a major risk factor for HIV-1 infection. Since both AIDS dementia complex (ADC) and cocaine have been associated with abnormal brain perfusion imaging, we compared the scintigraphic patterns of ADC patients and cocaine polydrug users with normal control subjects using Tc-99m-HMPAO SPECT. We found a high incidence of cortical defects in both ADC (100%) and cocaine-dependent (90%) subjects. In the cocaine and ADC patients, cortical defects were most frequent in the frontal, temporal and parietal lobes and occurred with similar frequency in the two populations. In both groups, the number of cortical defects per subject was higher than normal subjects (10.0 +/- 5.0 for ADC, 10.1 +/- 5.2 for cocaine and 0.7 +/- 1.5 for normal), background activity was high (a 65% and 60% incidence for ADC and cocaine, respectively), and basal ganglia involvement was frequent (40% and 65% for ADC and cocaine). We conclude that the brain perfusion pattern, while a sensitive indicator of ADC, cannot be distinguished from chronic cocaine polydrug use and caution should therefore be applied before entertaining a specific diagnosis. C1 MCLEAN HOSP,ALCOHOL & DRUG ABUSE RES CTR,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. RP HOLMAN, BL (reprint author), BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIDA NIH HHS [DA06116, DA00064] NR 16 TC 85 Z9 87 U1 1 U2 1 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 JUL PY 1992 VL 33 IS 7 BP 1312 EP 1315 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JB807 UT WOS:A1992JB80700014 PM 1613571 ER PT J AU SAINI, S AF SAINI, S TI DIAGNOSTIC-IMAGING OF THE LIVER SO JOURNAL OF NUCLEAR MEDICINE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SAINI, S (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 8 TC 1 Z9 1 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 JUL PY 1992 VL 33 IS 7 BP 1344 EP 1345 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JB807 UT WOS:A1992JB80700019 PM 1613575 ER PT J AU FISCHMAN, AJ FUCELLO, AJ PELLEGRINOGENSEY, JL GELTOFSKY, J YARMUSH, ML RUBIN, RH STRAUSS, HW AF FISCHMAN, AJ FUCELLO, AJ PELLEGRINOGENSEY, JL GELTOFSKY, J YARMUSH, ML RUBIN, RH STRAUSS, HW TI EFFECT OF CARBOHYDRATE MODIFICATION ON THE LOCALIZATION OF HUMAN POLYCLONAL IGG AT FOCAL SITES OF BACTERIAL-INFECTION SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID HUMAN-IMMUNOGLOBULIN; MONOCLONAL-ANTIBODIES; INFLAMMATION; FC; BINDING; CELLS; U937 AB Radiolabeled human polyclonal IgG localizes at focal sites of infection/inflammation. Previous studies have sought to identify the mechanism of localization, but the relative importance of specific antigen recognition by individual antibody molecules, binding to Fc receptors on inflammatory cells and nonspecific processes such as increased tissue permeability remains uncertain. This study was performed to evaluate the specific role of Fc receptor binding as a mechanism of localization. The Fc region of IgG was modified by endoglycosidase-F digestion and periodate oxidation to reduce the binding of IgG to Fc receptors. In-vitro binding was tested in an Fc receptor binding assay using the human monocyte-like cell line, U937. The in-vivo ability of the modified antibodies to localize at focal sites of E. coli infection was tested by biodistribution studied with the In-111-labeled proteins. Modification of the carbohydrate moiety of the Fc region of IgG resulted in a marked decrease in Fc receptor binding in vitro; with antibody concentrations of 1-mu-g/ml (which is presumed to exist at infected sites) showing no binding for endoglycosidase modified IgG and 50% binding for periodate modified IgG. In contrast, in-vivo infection localization as measured by level of accumulation or target-to-background ratio was not significantly effected by carbohydrate modification. These studies suggest that the contribution of Fc receptor binding to IgG localization at sites of infection is minimal. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,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 SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RW JOHNSON PHARMACEUT RES INST,RARITAN,NJ. RP FISCHMAN, AJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV NUCL MED,FRUIT ST,BOSTON,MA 02114, USA. NR 26 TC 31 Z9 31 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 JUL PY 1992 VL 33 IS 7 BP 1378 EP 1382 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA JB807 UT WOS:A1992JB80700025 PM 1613581 ER PT J AU CINTI, S SBARBATI, A MORRONI, M CARBONI, V ZANCANARO, C LOCASCIO, V DICKERSIN, GR AF CINTI, S SBARBATI, A MORRONI, M CARBONI, V ZANCANARO, C LOCASCIO, V DICKERSIN, GR TI PARATHYROID-GLANDS IN PRIMARY HYPERPARATHYROIDISM - AN ULTRASTRUCTURAL MORPHOMETRIC STUDY OF 25 CASES SO JOURNAL OF PATHOLOGY LA English DT Article DE PARATHYROID GLAND; PRIMARY HYPERPARATHYROIDISM; ELECTRON MICROSCOPY; MORPHOMETRY; CELL COUNT ID PRIMARY HYPER-PARATHYROIDISM; CALCIUM-CONCENTRATION; HORMONE; CELLS; FAT; FRAGMENTS; ADENOMA; INVITRO; RELEASE; SERUM AB In parathyroid glands removed from patients with primary hyperparathyroidism (pHPT), hyperplasias and adenomas cannot be distinguished from one another by light microscopy when only one gland is available for examination. When a second gland is available, it is necessary to establish whether it is normal, suppressed, or hyperplastic. This distinction may be difficult, and the main criterion is the amount of cytoplasmic lipid in the parenchymal cells. If the lipid is abundant, the gland is considered normal or suppressed, and if it is scanty, the gland is interpreted as hyperplastic. We have performed a morphometric ultrastructural study to test the reliability of this criterion. Twenty-five adenomatous glands removed from patients with pHPT, when compared with glands of normal size from euparathyroid patients, showed a significant increase in the parameters indicative of metabolic activity, namely the size of the Golgi apparatus, the amount of rough endoplasmic reticulum, and the length of plasmalemmas. In addition, the amount of cytoplasmic lipid was significantly reduced. Furthermore, 25 glands of normal size removed from the same patients with pHPT showed an amount of lipid similar to that of normal glands from euparathyroid patients. However, all the parameters indicative of metabolic activity were significantly higher than those in glands from euparathyroid patients and comparable to those found in adenomatous glands. These results suggest that in pHPT, normal-size glands are as active as adenomatous glands, regardless of a higher lipid content. C1 UNIV VERONA,INST HUMAN ANAT & HISTOL,I-37100 VERONA,ITALY. UNIV VERONA,INST MED SEMEIOT & NEPHROL,I-37100 VERONA,ITALY. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT LABS,BOSTON,MA 02114. RP CINTI, S (reprint author), UNIV ANCONA,IST MORFOL UMANA NORMALE,SERV MICROSCOPIA ELETTR,USL 12,VIA RANIERI,I-60131 ANCONA,ITALY. NR 48 TC 6 Z9 6 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0022-3417 J9 J PATHOL JI J. Pathol. PD JUL PY 1992 VL 167 IS 3 BP 283 EP 290 DI 10.1002/path.1711670305 PG 8 WC Oncology; Pathology SC Oncology; Pathology GA JF685 UT WOS:A1992JF68500004 PM 1381434 ER PT J AU BURTON, PBJ MONIZ, C QUIRKE, P MALIK, A BUI, TD JUPPNER, H SEGRE, GV KNIGHT, DE AF BURTON, PBJ MONIZ, C QUIRKE, P MALIK, A BUI, TD JUPPNER, H SEGRE, GV KNIGHT, DE TI PARATHYROID HORMONE-RELATED PEPTIDE - EXPRESSION IN FETAL AND NEONATAL DEVELOPMENT SO JOURNAL OF PATHOLOGY LA English DT Article DE PTH-RELATED PEPTIDE; FETAL DEVELOPMENT; IMMUNOCYTOCHEMISTRY; GROWTH FACTORS ID GROWTH-FACTOR-BETA; HUMORAL HYPERCALCEMIA; PROTEIN; MALIGNANCY; RECEPTOR; INVITRO; SYSTEM; NUMBER; GENE; RAT AB Hypercalcaemia frequently complicates the clinical management of cancer. Many factors have been implicated in the pathogenesis of this humoral hypercalcaemia of malignancy, the most recent candidate being parathyroid hormone-related peptide (PTHrP). Until now, this peptide has been detected only in some normal and transformed adult tissues. In recent years, it has become apparent that tumours are capable of expressing and secreting factors previously elaborated only during fetal life. Many of these factors act to stimulate the growth of both tumour and fetal cells in an autocrine manner. The data presented here demonstrate that PTHrP is expressed in the human and rat fetus throughout gestation. Immunocytochemistry reveals a gestationally related, changing pattern of expression which is paralleled by changes in mRNA transcription. These data support the hypothesis that PTHrP may function as a fetal growth factor. C1 KINGS COLL,DIV BIOMED SCI,LONDON W8 7AH,ENGLAND. UNIV LONDON KINGS COLL HOSP,DEPT CLIN BIOCHEM,LONDON SE5 9RS,ENGLAND. UNIV LEEDS,DEPT PATHOL,LEEDS LS2 9JT,W YORKSHIRE,ENGLAND. UNIV LONDON KINGS COLL HOSP,DEPT MED,LONDON SE5 9RS,ENGLAND. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. RI Malik, Afshan /F-5652-2011 NR 35 TC 63 Z9 63 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0022-3417 J9 J PATHOL JI J. Pathol. PD JUL PY 1992 VL 167 IS 3 BP 291 EP 296 DI 10.1002/path.1711670306 PG 6 WC Oncology; Pathology SC Oncology; Pathology GA JF685 UT WOS:A1992JF68500005 PM 1517900 ER PT J AU LISTGARTEN, MA COHN, S PHILSTROM, B HORROWITZ, B HORROWITZ, HS DAGOSTINO, RB ZIMMERMAN, SO CHILTON, NW GOODSON, JM DEROUEN, T HOBERMAN, D BEST PAGE, RC KENT, RL LASTER, LL HUJOEL, PP VANDEROUDERAA, F SOUTHARD, GL AF LISTGARTEN, MA COHN, S PHILSTROM, B HORROWITZ, B HORROWITZ, HS DAGOSTINO, RB ZIMMERMAN, SO CHILTON, NW GOODSON, JM DEROUEN, T HOBERMAN, D BEST PAGE, RC KENT, RL LASTER, LL HUJOEL, PP VANDEROUDERAA, F SOUTHARD, GL TI PRINCIPLES AND CHOICES IN STATISTICAL-ANALYSIS OF DENTAL ORAL RESEARCH STUDIES (OR CLINICAL-TRIALS) GENERAL DISCUSSION SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Discussion C1 FED TRADE COMMISS,WASHINGTON,DC 20580. UNIV ILLINOIS,URBANA,IL 61801. UNIV MINNESOTA,MINNEAPOLIS,MN 55455. UNIV TEXAS,HOUSTON,TX 77025. TASK FORCE DESIGN & ANAL,LAWRENCEVILLE,NJ. FORSYTH DENT CTR,BOSTON,MA. UNIV WASHINGTON,SEATTLE,WA 98195. US FDA,SAN FRANCISCO,CA 94102. UNILEVER RES LABS,WIRRAL L62 4XN,CHESHIRE,ENGLAND. ATRIX LABS,FT COLLINS,CO. RP LISTGARTEN, MA (reprint author), UNIV PENN,PHILADELPHIA,PA 19104, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1992 VL 27 IS 4 BP 358 EP 361 PN 2 PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JF125 UT WOS:A1992JF12500013 ER PT J AU GOODSON, JM AF GOODSON, JM TI DESIGN ISSUES SPECIFIC TO STUDIES OF PERIODONTITIS - DISCUSSION SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Discussion DE PERIODONTAL DISEASE; CLINICAL TRIALS ID ROOT DEBRIDEMENT; SUBGINGIVAL MICROFLORA; PLAQUE CONTROL; THERAPY; TETRACYCLINE; SINGLE; METRONIDAZOLE; ATTACHMENT; DISEASE; POCKETS RP GOODSON, JM (reprint author), FORSYTH DENT CTR,DEPT PHARMACOL,140 FENWAY,BOSTON,MA 02115, USA. NR 21 TC 6 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 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1992 VL 27 IS 4 BP 412 EP 416 DI 10.1111/j.1600-0765.1992.tb01706.x PN 2 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JF125 UT WOS:A1992JF12500024 ER PT J AU IMREY, PB DEROUEN, T BEST LISGARTEN, MA PAGE, R HOBERMAN, D PHILSTROM, BL JEFFCOAT, M POLSON, AM CASSINGHAM, JR CHILTON, NW BURRELL, KH KENT, RL GOODSON, JM AF IMREY, PB DEROUEN, T BEST LISGARTEN, MA PAGE, R HOBERMAN, D PHILSTROM, BL JEFFCOAT, M POLSON, AM CASSINGHAM, JR CHILTON, NW BURRELL, KH KENT, RL GOODSON, JM TI SPECIFIC STATISTICAL CONSIDERATIONS RELEVANT TO DESIGN AND ANALYSIS OF GINGIVITIS TRIALS - DESIGN ISSUES SPECIFIC TO STUDIES OF PERIODONTITIS - GENERAL DISCUSSION SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Discussion C1 US FDA, ROCKVILLE, MD 20857 USA. UNIV WASHINGTON, SEATTLE, WA 98195 USA. UNIV PENN, PHILADELPHIA, PA 19104 USA. UNIV WASHINGTON, SEATTLE, WA 98195 USA. UNIV MINNESOTA, MINNEAPOLIS, MN 55455 USA. UNIV ALABAMA, BIRMINGHAM, AL 35294 USA. ARRIX LABS, FT COLLINS, CO USA. LOUISIANA STATE UNIV, BATON ROUGE, LA 70803 USA. TASK FORCE DESIGN & ANAL, LAWRENCEVILLE, NJ USA. AMER DENT ASSOC, CHICAGO, IL 60611 USA. FORSYTH DENT CTR, BOSTON, MA 02115 USA. RP IMREY, PB (reprint author), UNIV ILLINOIS, URBANA, IL 61801 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3484 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1992 VL 27 IS 4 BP 420 EP 424 PN 2 PG 5 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JF125 UT WOS:A1992JF12500026 ER PT J AU KENT, R AF KENT, R TI ISSUES SPECIFIC TO EVALUATION OF STUDIES OF PERIODONTITIS - DISCUSSION SO JOURNAL OF PERIODONTAL RESEARCH LA English DT Discussion DE META ANALYSIS; PUBLICATION BIAS; CLINICAL TRIALS; RANDOM EFFECTS MODELS ID RANDOMIZED CONTROL TRIALS; CLINICAL-TRIALS; QUALITY ASSESSMENT; DENTAL RESEARCH RP KENT, R (reprint author), FORSYTH DENT CTR, 140 FENWAY, BOSTON, MA 02115 USA. NR 10 TC 2 Z9 2 U1 0 U2 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0022-3484 EI 1600-0765 J9 J PERIODONTAL RES JI J. Periodont. Res. PD JUL PY 1992 VL 27 IS 4 BP 445 EP 447 DI 10.1111/j.1600-0765.1992.tb01712.x PN 2 PG 3 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JF125 UT WOS:A1992JF12500030 PM 1507034 ER PT J AU RAVICZ, ME ROSOWSKI, JJ VOIGT, HF AF RAVICZ, ME ROSOWSKI, JJ VOIGT, HF TI SOUND-POWER COLLECTION BY THE AUDITORY PERIPHERY OF THE MONGOLIAN GERBIL MERIONES-UNGUICULATUS .1. MIDDLE-EAR INPUT IMPEDANCE SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID GUINEA-PIG; TYMPANIC MEMBRANE; COCHLEA; ADMITTANCE; CAT; CHINCHILLA; FREQUENCY; EARDRUM; HAMSTER; PROBE AB This is the first paper of a series dealing with sound-power collection by the auditory periphery of the gerbil. The purpose of the series is to quantify the physiological action of the gerbil's relatively large tympanic membrane and middle-ear air cavities. To this end the middle-ear input impedance Z(T) was measured at frequencies between 10 Hz and 18 kHz before and after manipulations of the middle-ear cavity. The frequency dependence of Z(T) is consistent with that of the middle-ear transfer function computed from extant data. Comparison of the impedance and transfer function suggests a middle-ear transformer ratio of 50 at frequencies below 1 kHz, substantially smaller than the anatomical value of 90 [Lay, J. Morph. 138, 41-120 (1972)]. Below 1 kHz the data suggest a low-frequency acoustic stiffness K(T) for the middle ear of 970 Pa/mm3 and a stiffness of the middle-ear cavity of 720 Pa/mm3 (middle-ear volume V(MEC) of 195 mm3); thus the middle-ear air spaces contribute about 70% of the acoustic stiffness of the auditory periphery. Manipulations of a middle-ear model suggest that decreases in V(MEC) lead to proportionate increases in K(T) but that further increases in middle-ear cavity volume produce only limited decreases in middle-ear stiffness. The data and the model point out that the real part of the middle-ear impedance at frequencies below 100 Hz is determined primarily by losses within the middle-ear cavity. The measured impedance is comparable in magnitude and frequency dependence to the impedance in several larger mammalian species commonly used in auditory research. A comparison of low-frequency stiffness and anatomical dimensions among several species suggests that the large middle-ear cavities in gerbil act to reduce the middle-ear stiffness at low frequencies. A description of sound-power collection by the gerbil ear requires a description of the function of the external ear. C1 BOSTON UNIV,DEPT BIOMED ENGN,BOSTON,MA 02215. MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,BOSTON,MA 02114. MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. BOSTON UNIV,DEPT OTOLARYNGOL,BOSTON,MA 02215. RP RAVICZ, ME (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EATON PEABODY LAB AUDITORY PHYSIOL,243 CHARLES ST,BOSTON,MA 02114, USA. RI Voigt, Herbert/I-2068-2015 OI Voigt, Herbert/0000-0002-0476-6594 FU NIDCD NIH HHS [R01 DC000194, DC00310, DC01099, R01 DC00194] NR 74 TC 49 Z9 49 U1 0 U2 2 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD JUL PY 1992 VL 92 IS 1 BP 157 EP 177 DI 10.1121/1.404280 PG 21 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA JD134 UT WOS:A1992JD13400013 PM 1512321 ER PT J AU WILENS, TE BIEDERMAN, J BALDESSARINI, RJ PUOPOLO, PR FLOOD, JG AF WILENS, TE BIEDERMAN, J BALDESSARINI, RJ PUOPOLO, PR FLOOD, JG TI DEVELOPMENTAL-CHANGES IN SERUM CONCENTRATIONS OF DESIPRAMINE AND 2-HYDROXYDESIPRAMINE DURING TREATMENT WITH DESIPRAMINE SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE ANTIDEPRESSANTS; DESIPRAMINE; DEVELOPMENT; HYDROXYDESIPRAMINE; PEDIATRICS ID ELDERLY DEPRESSED-PATIENTS; PLASMA 10-HYDROXYNORTRIPTYLINE; TRICYCLIC ANTIDEPRESSANTS; ACTIVE METABOLITES; IMIPRAMINE; KINETICS; CHILDREN; ADOLESCENTS; ADD AB Steady-state serum concentrations of desipramine (DMI) and its metabolite, 2-hydroxydesipramine (OHDMI), were measured in 40 children, 36 adolescents, and 27 adult psychiatric patients. The authors predicted that younger patients would show more efficient elimination of DMI, with greater amounts of OHDMI. OHDMI averaged 52% lower than DMI. DMI per weight-corrected dose (ng/mL: mg/kg) rose significantly with maturation, from 50 in children and 56 in adolescents to 91 in adults. Contrary to expectation, OHDMI per DMI dose also rose with age, from 17 in children and 20 in adolescents to 26 in adults. It was concluded that: (1) similar mg/kg doses of DMI result in lower DMI and OHDMI in children; (2) children metabolize both DMI and OHDMI more rapidly than adults; and (3) children do not have high circulating concentrations of OHDMI. C1 MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,CLIN CHEM LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CONSOLIDATED DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. RP WILENS, TE (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. FU NIMH NIH HHS [MH-47370, R01MH-41314, MH-31154] NR 43 TC 28 Z9 28 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JUL PY 1992 VL 31 IS 4 BP 691 EP 698 DI 10.1097/00004583-199207000-00017 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA JD377 UT WOS:A1992JD37700017 PM 1644733 ER PT J AU DEC, GW WALDMAN, H SOUTHERN, J FALLON, JT HUTTER, AM PALACIOS, I AF DEC, GW WALDMAN, H SOUTHERN, J FALLON, JT HUTTER, AM PALACIOS, I TI VIRAL MYOCARDITIS MIMICKING ACUTE MYOCARDIAL-INFARCTION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID NORMAL CORONARY-ARTERIES; INFECTION; ONSET AB Anecdotal reports have shown that myocarditis can mimic acute myocardial infarction with chest pain, electrocardiographic (ECG) abnormalities, serum creatine kinase elevation and hemodynamic instability. Thirty-four patients with clinical signs and symptoms consistent with acute myocardial infarction underwent right ventricular endomyocardial biopsy during a 6.5-year period after angiographic identification of normal coronary anatomy. Myocarditis was found on histologic study in 11 of these 34 patients. Cardiogenic shock requiring intraaortic balloon support developed within 6 h of admission in three (27 %) of the patients with myocarditis. The mean age of the group with myocarditis was 42 +/- 5 years. A preceding viral illness had been present in six patients (54 %). The ECG abnormalities were varied and included ST segment elevation (n = 6), T wave inversions (n = 3), ST segment depression (n = 2) and pathologic Q waves (n = 2). The ECG abnormalities were typically seen in the anterior precordial leads but were diffusely evident in three patients. Left ventricular function was normal in six patients and globally decreased in the remaining five patients, whose ejection fraction ranged from 14 % to 45 %. Lymphocytic myocarditis was diagnosed in 10 patients, and giant cell myocarditis was detected in the remaining patient. Four patients with impaired left ventricular function received immunosuppressive therapy with prednisone and either azathioprine (n = 2) or cyclosporine (n = 2). All six patients whose left ventricular function was normal on admission remain alive in functional class 1. Of the five patients with impaired systolic function, ejection fraction normalized in three of the four patients who received immunosuppressive therapy within 3 months of treatment and in the one patient who received only supportive therapy. All patients who required intraaortic balloon pump support survived to discharge. One death, due to progressive heart failure, occurred at 18 months in the patient with giant cell myocarditis. Myocarditis should be clinically suspected in patients with an ischemic chest pain syndrome, particularly when ECG abnormalities are present beyond a single vascular distribution, segmental wall motion abnormalities are lacking or global left ventricular hypokinesia is present on ventriculography. The subsequent demonstration of normal coronary anatomy should prompt consideration of right ventricular endomyocardial biopsy, because those patients with myocarditis have an excellent long-term prognosis and do not require anti-ischemic therapy. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DEC, GW (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114, USA. NR 14 TC 114 Z9 124 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUL PY 1992 VL 20 IS 1 BP 85 EP 89 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JB300 UT WOS:A1992JB30000013 PM 1607543 ER PT J AU SEMIGRAN, MJ ARONEY, CN HERRMANN, HC DEC, GW BOUCHER, CA FIFER, MA AF SEMIGRAN, MJ ARONEY, CN HERRMANN, HC DEC, GW BOUCHER, CA FIFER, MA TI EFFECTS OF ATRIAL-NATRIURETIC-PEPTIDE ON MYOCARDIAL CONTRACTILE AND DIASTOLIC FUNCTION IN PATIENTS WITH HEART-FAILURE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article ID PRESSURE-VOLUME RELATIONSHIPS; CONSCIOUS DOGS; ATRIOPEPTIN-II; SODIUM-NITROPRUSSIDE; CARDIAC-OUTPUT; INFUSION; RELAXATION; HEMODYNAMICS; INDEXES; LOAD AB Atrial natriuretic peptide alters left ventricular performance in patients with heart failure. To assess the direct effects of this hormone on myocardial function, its actions were compared with those of the pure vasodilator nitroprusside in 10 patients with heart failure. Simultaneous left ventricular micromanometer pressure and radionuclide volume were obtained during a baseline period, during nitroprusside infusion, during a second baseline period and during atrial natriuretic peptide infusion. The baseline end-systolic pressure-volume relation was generated in nine patients from pressure-volume loops obtained during the two baseline periods and during afterload reduction with nitroprusside. Mean arterial pressure decreased with atrial natriuretic peptide (89 +/- 3 to 80 +/- 2 mm Hg, p < 0.05) and by a greater amount with nitroprusside (90 +/- 4 to 73 +/- 3 mm Hg, p < 0.05). Left ventricular end-diastolic pressure also decreased with atrial natriuretic peptide (24 +/- 2 to 16 +/- 3 mm Hg, p < 0.05) and by a greater amount with nitroprusside (24 +/- 2 to 13 +/- 3 mm Hg, p < 0.05). Cardiac index increased during infusion of each agent from 2.0 +/- 0.2 to 2.4 +/- 0.2 liters/min per m2 (p < 0.01). Heart rate increased slightly with nitroprusside but did not change with atrial natriuretic peptide. Peak positive first derivative of left ventricular pressure (dP/dt), ejection fraction and stroke work index were unchanged by either agent. The relation between end-systolic pressure and volume during atrial natriuretic peptide infusion was shifted slightly leftward from the baseline value in four patients, slightly rightward in four and not at all in one patient, indicating no consistent inotropic effect. Both agents shortened the time constant of isovolumetric relaxation calculated by the logarithmic method, but only nitroprusside shortened the time constant calculated by the derivative method. Peak filling rate was unchanged from baseline with either agent. Atrial natriuretic peptide did not shift the end-diastolic pressure-volume point away from the relation constructed from baseline and nitroprusside points. It is concluded that atrial natriuretic peptide has no direct effect on myocardial contractile or diastolic function in patients with heart failure. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP FIFER, MA (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,WACC 478,15 PARKMAN ST,BOSTON,MA 02114, USA. RI Aroney, Constantine/A-7672-2013 OI Aroney, Constantine/0000-0002-0908-7179 NR 49 TC 26 Z9 27 U1 0 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUL PY 1992 VL 20 IS 1 BP 98 EP 106 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JB300 UT WOS:A1992JB30000016 PM 1535081 ER PT J AU HUTTER, AM AF HUTTER, AM TI ACC INDUSTRY RELATIONS - KEEPING A BALANCE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material RP HUTTER, AM (reprint author), MASSACHUSETTS GEN HOSP,ACC BLDG,SUITE 467,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUL PY 1992 VL 20 IS 1 BP 257 EP 258 PG 2 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA JB300 UT WOS:A1992JB30000041 ER PT J AU KASINATH, BS SINGH, AK AF KASINATH, BS SINGH, AK TI DETECTION OF SIALIC-ACID ON CULTURED-CELLS BY BINDING OF A LECTIN FROM LIMAX-FLAVUS SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Note ID PODOCALYXIN; SIALOGLYCOPROTEIN; NEPHROSIS; KIDNEY C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP KASINATH, BS (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK41517, DK 35804] NR 11 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD JUL PY 1992 VL 3 IS 1 BP 113 EP 115 PG 3 WC Urology & Nephrology SC Urology & Nephrology GA JF320 UT WOS:A1992JF32000015 PM 1391703 ER PT J AU MEYER, JS KAWAMURA, J TERAYAMA, Y AF MEYER, JS KAWAMURA, J TERAYAMA, Y TI WHITE MATTER LESIONS IN THE ELDERLY SO JOURNAL OF THE NEUROLOGICAL SCIENCES LA English DT Review DE LEUKOARAIOSIS; WHITE MATTER; DEMENTIA; AGING ID CEREBROVASCULAR RISK-FACTORS; ENCEPHALOPATHY BINSWANGERS DISEASE; NUCLEAR MAGNETIC-RESONANCE; CAROTID-ARTERY DISEASE; CEREBRAL BLOOD-FLOW; SCAN LEUKO-ARAIOSIS; ALZHEIMERS-DISEASE; VASCULAR DEMENTIA; SIGNAL ABNORMALITIES; NEUROLOGIC FINDINGS AB The advent of neuroimaging has brought medical attention to the frequency of unsuspected white matter lesions in the brains of elderly people. In 1987 Hachinski suggested the term "leuko-araiosis" to identify such white matter abnormalities detected by computed tomography and magnetic resonance imaging to emphasize that their etiology and clinical relevance require clarification. Since then, leuko-araiosis has been recognized among approximately ten percent of apparently normal, elderly people over age sixtyfive. The severity and frequency of leuko-araiosis increases with advancing age, risk factors for stroke, history of strokes particularly of the lacunar type and dementia of both the vascular and Alzheimer type. Current concepts concerning the pathogenesis and neurological concomitants of leuko-araiosis are reviewed. The etiology of leuko-araiosis may be heterogeneous but is most likely ischemic in nature. However, as white matter lesions progress among the elderly they are likely to become associated with cognitive impairments and motor dyspraxias presumably resulting from cortico-subcortical disconnections, particularly involving the frontal cortex and basal ganglia and may themselves be considered a radiological "risk factor" or precursor for dementia. C1 BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. RP MEYER, JS (reprint author), DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LABS,2002 HOLCOMBE BLVD-151A,HOUSTON,TX 77030, USA. NR 55 TC 85 Z9 86 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0022-510X J9 J NEUROL SCI JI J. Neurol. Sci. PD JUL PY 1992 VL 110 IS 1-2 BP 1 EP 7 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA JD132 UT WOS:A1992JD13200001 PM 1506848 ER PT J AU HUG, EB DONNELLY, SM SHIPLEY, WU HENEY, NM KAUFMAN, DS PREFFER, FI SCHWARTZ, SM COLVIN, RB ALTHAUSEN, AF AF HUG, EB DONNELLY, SM SHIPLEY, WU HENEY, NM KAUFMAN, DS PREFFER, FI SCHWARTZ, SM COLVIN, RB ALTHAUSEN, AF TI DEOXYRIBONUCLEIC-ACID FLOW-CYTOMETRY IN INVASIVE BLADDER-CARCINOMA - A POSSIBLE PREDICTOR FOR SUCCESSFUL BLADDER PRESERVATION FOLLOWING TRANSURETHRAL SURGERY AND CHEMOTHERAPY-RADIOTHERAPY SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; DNA; FLOW CYTOMETRY; PLOIDIES ID URINARY-BLADDER; DNA CONTENT; CANCER; IRRADIATION; CISPLATIN AB Tumor deoxyribonucleic acid (DNA) ploidy was evaluated as an objective parameter that may correlate better with the responsiveness of bladder cancer to chemotherapy plus radiotherapy than do clinical features or histopathological subtypes. A total of 40 patients with localized muscle-invading bladder cancer (clinical stages T2 to T4) underwent prospective treatment on a potential bladder preserving protocol. Tumors of 37 of the 40 patients were analyzed by DNA flow cytometry of multiple paraffin embedded specimens. Transurethral resection, neoadjuvant chemotherapy and 40 Gy. radiotherapy plus cisplatin were followed by urological reevaluation of the tumor (a complete response required a negative biopsy and a negative urine cytology study). A total of 7 noncomplete response patients underwent immediate radical cystectomy whereas the full bladder sparing treatment (radiotherapy to 64.80 Gy. plus cisplatin) was given to 23 complete response patients and 7 noncomplete response patients who were unsuited for surgery. Of the tumors 22 (59%) were purely aneuploid and 10 (27%) were purely diploid. Five tumors contained aneuploid and diploid patterns in different tumor specimens (partly diploid). Current status with a 30-month median followup in surviving patients includes an 82% overall survival rate in the aneuploid group versus 47% in the diploid/partly diploid group. Of all the patients 68% are free of invasive tumor: 82% in the aneuploid group versus 47% in the diploid/partly diploid group. By multivariate analysis pure aneuploidy was significantly (p = 0.05) correlated with freedom from invasive tumor in the bladder (either as persistence or as recurrence) and approached significance (p = 0.08) in correlation with overall patient survival. A longer observation time will be required to confirm this unexpectedly good outcome for patients with pure aneuploid tumors. We hypothesize that pretreatment DNA ploidy status may become a clinically useful prognostic factor in selecting patients for successful treatment with transurethral surgery and neoadjuvant chemotherapy plus radiotherapy. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,MED SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT UROL,BOSTON,MA 02114. RP HUG, EB (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 21 TC 26 Z9 26 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD JUL PY 1992 VL 148 IS 1 BP 47 EP 51 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA JB434 UT WOS:A1992JB43400014 PM 1613879 ER PT J AU PEVEC, WC DARLING, RC LITALIEN, GJ ABBOTT, WM AF PEVEC, WC DARLING, RC LITALIEN, GJ ABBOTT, WM TI FEMOROPOPLITEAL RECONSTRUCTION WITH KNITTED, NONVELOUR DACRON VERSUS EXPANDED POLYTETRAFLUOROETHYLENE SO JOURNAL OF VASCULAR SURGERY LA English DT Article ID BYPASS GRAFTS; SAPHENOUS-VEIN; ABOVE-KNEE; FOLLOW-UP AB No ideal prosthetic conduit exists for femoropopliteal reconstruction. Expanded polytetrafluoroethylene (PTFE) has gained much greater popularity than the less expensive Dacron, despite disappointing long-term patency for each material. Few direct comparisons of results with the two materials have been performed. Thc concurrent experience of a single surgeon with femoropopliteal reconstructions of PTFE (n = 85) or knitted, nonvelour Dacron (KNVD, n = 38) was reviewed. Risk factors were comparable in the two groups. Overall patency was significantly better for KNVD than for PTFE (p = 0.0096 by log rank;p = 0.039 by Cox proportional hazards; 48% vs 27% at 5 years). Since in this series the overall performance of KNVD was significantly better than PTFE, a reassessment of the prosthetic materials used in femoropopliteal reconstruction is necessary. These results justify a prospective comparison of PTFE and KNVD. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,DIV VASC SURG,ACC 458,BOSTON,MA 02114. NR 15 TC 68 Z9 68 U1 0 U2 3 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JUL PY 1992 VL 16 IS 1 BP 60 EP 65 PG 6 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA JE392 UT WOS:A1992JE39200009 PM 1535669 ER PT J AU GRASSMANN, R BERCHTOLD, S RADANT, I ALT, M FLECKENSTEIN, B SODROSKI, JG HASELTINE, WA RAMSTEDT, U AF GRASSMANN, R BERCHTOLD, S RADANT, I ALT, M FLECKENSTEIN, B SODROSKI, JG HASELTINE, WA RAMSTEDT, U TI ROLE OF HUMAN T-CELL LEUKEMIA-VIRUS TYPE-1 X-REGION PROTEINS IN IMMORTALIZATION OF PRIMARY HUMAN-LYMPHOCYTES IN CULTURE SO JOURNAL OF VIROLOGY LA English DT Note ID TROPICAL SPASTIC PARAPARESIS; I TAX GENE; HERPESVIRUS-SAIMIRI; HTLV-I; DELETION MUTANTS; TRANSGENIC MICE; PROVIRUS GENOME; MESSENGER-RNA; ACTIVATION; TRANSFORMATION AB Human T-cell leukemia virus type 1 (HTLV-1) immortalizes human CD4+ T lymphocytes in culture. Previous studies show that in the context of a herpesvirus saimiri vector, the sequence of the X region at the 3' end of the HTLV-1 genome is also capable of immortalizing CD4+ lymphocytes in the absence of HTLV-1 structural proteins. The X region of HTLV-1 encodes two trans-acting viral proteins, the 42-kDa Tax protein and the 27-kDa Rex protein. Infection of human cord blood cells with herpesvirus saimiri recombinants which contain HTLV-1 X region sequences defective for expression of tax, rex, or both tax and rex demonstrates that tax function is necessary and sufficient for immortalization of primary human CD4+ cord blood lymphocytes in culture in the context of the herpesvirus saimiri vector. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. RP GRASSMANN, R (reprint author), UNIV ERLANGEN NURNBERG,INST KLIN & MOLEK VIROL,LOSCHGESTR 7,W-8520 ERLANGEN,GERMANY. FU NCI NIH HHS [CA 36974] NR 52 TC 265 Z9 268 U1 0 U2 5 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUL PY 1992 VL 66 IS 7 BP 4570 EP 4575 PG 6 WC Virology SC Virology GA HY086 UT WOS:A1992HY08600071 PM 1351105 ER PT J AU DYSON, N GUIDA, P MCCALL, C HARLOW, E AF DYSON, N GUIDA, P MCCALL, C HARLOW, E TI ADENOVIRUS-E1A MAKES 2 DISTINCT CONTACTS WITH THE RETINOBLASTOMA PROTEIN SO JOURNAL OF VIROLOGY LA English DT Note ID LARGE T-ANTIGEN; REGION 1A PROTEINS; GENE-PRODUCT; E1A GENE; MUTATIONAL ANALYSIS; SEPARATE DOMAINS; CELLULAR PROTEIN; PRIMARY-CELLS; 5 DNA; TRANSFORMATION AB Two regions near the amino terminus of the adenovirus E1A protein, which were first identified by sequence conservation among various adenovirus serotypes, have been shown by genetic studies to be essential for E1A-mediated transformation. These same regions are also required for interaction with a number of cellular proteins, including the retinoblastoma protein (pRB). Using synthetic peptides corresponding to portions of these conserved regions, we show that each region can bind independently to pRB. These interactions were observed in both competition and binding assays. In both types of assay, region 2 peptides (E1A amino acids 115 to 132) bound pRB with higher affinity than did region 1 peptides (E1A amino acids 37 to 54), while a peptide combining region 1 and 2 sequences consistently provided the highest-affinity interaction. Cross-blocking experiments using region 1 peptides and region 2 peptides suggested that these two regions of E1A make distinct contacts with pRB. These data support the notion that the pRB-binding domain of E1A contains at least two functional elements. C1 COLD SPRING HARBOR LAB, COLD SPRING HARBOR, NY 11724 USA. RP MASSACHUSETTS GEN HOSP, CTR CANC, BOSTON, MA 02129 USA. FU NCI NIH HHS [CA13106] NR 53 TC 90 Z9 90 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1752 N ST NW, WASHINGTON, DC 20036-2904 USA SN 0022-538X EI 1098-5514 J9 J VIROL JI J. Virol. PD JUL PY 1992 VL 66 IS 7 BP 4606 EP 4611 PG 6 WC Virology SC Virology GA HY086 UT WOS:A1992HY08600078 PM 1534854 ER PT J AU CONHAIM, RL HARMS, BA AF CONHAIM, RL HARMS, BA TI A SIMPLIFIED 2-PORE FILTRATION MODEL EXPLAINS THE EFFECTS OF HYPOPROTEINEMIA ON LUNG AND SOFT-TISSUE LYMPH FLUX IN AWAKE SHEEP SO MICROVASCULAR RESEARCH LA English DT Article ID COLLOID OSMOTIC-PRESSURE; REFLECTION COEFFICIENTS; UNANESTHETIZED SHEEP; CAPILLARY; BALANCE; TRANSPORT; PRODUCTS; EDEMA C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP CONHAIM, RL (reprint author), UNIV WISCONSIN,DEPT SURG,MADISON,WI 53705, USA. NR 26 TC 14 Z9 14 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 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD JUL PY 1992 VL 44 IS 1 BP 14 EP 26 DI 10.1016/0026-2862(92)90098-A PG 13 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA JA598 UT WOS:A1992JA59800002 PM 1640876 ER PT J AU RUTGERS, JL BELL, DA AF RUTGERS, JL BELL, DA TI IMMUNOHISTOCHEMICAL CHARACTERIZATION OF OVARIAN BORDERLINE TUMORS OF INTESTINAL AND MULLERIAN TYPES SO MODERN PATHOLOGY LA English DT Article DE BORDERLINE TUMORS; IMMUNOHISTOCHEMISTRY ID CARCINOEMBRYONIC ANTIGEN CEA; CANCER-ASSOCIATED ANTIGEN; MONOCLONAL-ANTIBODIES; ENDOMETRIAL ADENOCARCINOMA; CLINICOPATHOLOGIC ANALYSIS; PAPILLARY CYSTADENOMAS; UTERINE CERVIX; IMMUNOPEROXIDASE; LOCALIZATION; CARCINOMA AB A panel of monoclonal antibodies (MAbs) including MOv2, MOv8, anti-CA 19-9, and anti-carcinoembryonic antigen (CEA), and a polyclonal antibody against CEA, was applied to three types of ovarian borderline tumors. The tumors included 19 intestinal-type mucinous borderline tumors (IMBTs), 22 endocervical-like mucinous borderline tumors (EMBTs), and 23 mixed-epithelial borderline tumors (MEBTs); the latter two tumors are of mullerian type. Statistically significant differences in the percentage of positive IMBTs compared to the mullerian tumors were seen for anti-CEA and MOv8; strikingly different staining patterns were also seen. IMBTs were more often and more diffusely CEA-positive than were the mullerian tumors; within the mullerian tumors, only one type of cell, the indifferent eosinophilic cell, was consistently CEA positive. The MAbs MOv2, MOv8, and anti-CA 19-9 showed more extensive positivity in the mullerian tumors than in the IMBTs. This study highlights the differences in cell types between IMBTs and these two types of mullerian borderline tumors. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. RP RUTGERS, JL (reprint author), UNIV CALIF LOS ANGELES,LOS ANGELES CTY HARBOR MED CTR,DEPT PATHOL,1000 W CARSON ST,TORRANCE,CA 90509, USA. NR 39 TC 18 Z9 18 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JUL PY 1992 VL 5 IS 4 BP 367 EP 371 PG 5 WC Pathology SC Pathology GA JD534 UT WOS:A1992JD53400003 PM 1495942 ER PT J AU FOLBERG, R JAKOBIEC, FA MCLEAN, IW ZIMMERMAN, LE AF FOLBERG, R JAKOBIEC, FA MCLEAN, IW ZIMMERMAN, LE TI PRIMARY ACQUIRED MELANOSIS OF THE CONJUNCTIVA IS MELANOMA INSITU - REPLY SO MODERN PATHOLOGY LA English DT Letter ID MALIGNANT-MELANOMA; MELANOCYTIC LESIONS C1 ARMED FORCES INST PATHOL,WASHINGTON,DC 20306. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP FOLBERG, R (reprint author), UNIV IOWA,IOWA CITY,IA 52242, USA. NR 10 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD JUL PY 1992 VL 5 IS 4 BP 475 EP 475 PG 1 WC Pathology SC Pathology GA JD534 UT WOS:A1992JD53400027 ER PT J AU ZON, LI MOREAU, JF KOO, JW MATHEYPREVOT, B DANDREA, AD AF ZON, LI MOREAU, JF KOO, JW MATHEYPREVOT, B DANDREA, AD TI THE ERYTHROPOIETIN RECEPTOR TRANSMEMBRANE REGION IS NECESSARY FOR ACTIVATION BY THE FRIEND SPLEEN FOCUS-FORMING VIRUS GP55 GLYCOPROTEIN SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; ENVELOPE GENE; ENV GENE; DOMAIN; GROWTH; SUPERFAMILY; BINDING; CLONING; FAMILY; DNA AB The erythropoietin receptor (EPO-R), a member of the cytokine receptor superfamily, can be activated by binding either erythropoietin (EPO) or gp55, the Friend spleen focus-forming virus glycoprotein. The highly specific interaction between gp55 and EPO-R triggers cell proliferation and thereby causes the first stage of Friend virus-induced erythroleukemia. We have generated functional chimeric receptors containing regions of the EPO-R and the interleukin-3 receptor (AIC2A polypeptide), a related cytokine receptor which does not interact with gp55. All chimeric receptors were expressed at similar levels, had similar binding affinities for EPO, and conferred EPO-dependent cell growth. Only those chimeric receptors which contained the EPO-R transmembrane region were activated by gp55. These results demonstrate that the transmembrane region of the EPO-R is critical for activation by gp55. In addition, analysis of a soluble, secreted EPO-R and cysteine point mutants of the EPO-R show that the extracytoplasmic region of the EPO-R specifically interacts with gp55. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL02347, P01 HL32262-10] NR 38 TC 77 Z9 77 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 JUL PY 1992 VL 12 IS 7 BP 2949 EP 2957 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JA250 UT WOS:A1992JA25000006 PM 1320192 ER PT J AU GOLEMIS, EA BRENT, R AF GOLEMIS, EA BRENT, R TI FUSED PROTEIN DOMAINS INHIBIT DNA-BINDING BY LEXA SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID ESCHERICHIA-COLI; TRANSCRIPTIONAL ACTIVATION; SACCHAROMYCES-CEREVISIAE; NUCLEAR-LOCALIZATION; GEL-ELECTROPHORESIS; REGULATORY SYSTEM; TERMINAL DOMAIN; GENE-PRODUCT; FOS PROTEINS; C-MYC AB Many studies of transcription activation employ fusions of activation domains to DNA binding domains derived from the bacterial repressor LexA and the yeast activator GAL4. Such studies often implicitly assume that DNA binding by the chimeric proteins is equivalent to that of the protein donating the DNA binding moiety. To directly investigate this issue, we compared operator binding by a series of LexA-derivative proteins to operator binding by native LexA, by using both in vivo and in vitro assays. We show that operator binding by many proteins such as LexA-Myc, LexA-Fos, and LexA-Bicoid is severely impaired, while binding of other LexA-derivative proteins, such as those that carry bacterially encoded acidic sequences ("acid blobs"), is not. Our results also show that DNA binding by LexA derivatives that contain the LexA carboxy-terminal dimerization domain (amino acids 88 to 202) is considerably stronger than binding by fusions that lack it and that heterologous dimerization motifs cannot substitute for the LexA88-202 function. These results suggest the need to reevaluate some previous studies of activation that employed LexA derivatives and modifications to recent experimental approaches that use LexA and GAL4 derivatives to detect and study protein-protein interactions. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,50 BLOSSOM ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NCI NIH HHS [CA08817] NR 75 TC 147 Z9 149 U1 0 U2 2 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JUL PY 1992 VL 12 IS 7 BP 3006 EP 3014 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA JA250 UT WOS:A1992JA25000012 PM 1620111 ER PT J AU KEUTMANN, HT AF KEUTMANN, HT TI RECEPTOR-BINDING REGIONS IN HUMAN GLYCOPROTEIN HORMONES SO MOLECULAR AND CELLULAR ENDOCRINOLOGY LA English DT Note DE LUTEINIZING HORMONE; CHORIONIC GONADOTROPIN; FOLLICLE-STIMULATING HORMONE; THYROID-STIMULATING HORMONE; GONADOTROPINS; RECEPTOR BINDING; STRUCTURE-ACTIVITY RELATIONS; PEPTIDE SYNTHESIS; SITE-DIRECTED MUTAGENESIS ID HUMAN CHORIONIC-GONADOTROPIN; HUMAN LUTEINIZING-HORMONE; ALPHA-SUBUNIT PEPTIDES; BETA-SUBUNIT; PREGNANCY URINE; LUTROPIN; DETERMINANTS; INHIBITION; FRAGMENT; SEQUENCE C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KEUTMANN, HT (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,ENDOCRINE UNIT,BOSTON,MA 02114, USA. NR 37 TC 53 Z9 53 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0303-7207 J9 MOL CELL ENDOCRINOL JI Mol. Cell. Endocrinol. PD JUL PY 1992 VL 86 IS 1-2 BP C1 EP C6 DI 10.1016/0303-7207(92)90168-6 PG 6 WC Cell Biology; Endocrinology & Metabolism SC Cell Biology; Endocrinology & Metabolism GA JD033 UT WOS:A1992JD03300001 PM 1380927 ER PT J AU FINK, JS WEAVER, DR RIVKEES, SA PETERFREUND, RA POLLACK, AE ADLER, EM REPPERT, SM AF FINK, JS WEAVER, DR RIVKEES, SA PETERFREUND, RA POLLACK, AE ADLER, EM REPPERT, SM TI MOLECULAR-CLONING OF THE RAT ADENOSINE-A2 RECEPTOR - SELECTIVE COEXPRESSION WITH D2-DOPAMINE RECEPTORS IN RAT STRIATUM SO MOLECULAR BRAIN RESEARCH LA English DT Article DE ADENOSINE; ADENOSINE A2-RECEPTOR; BASAL GANGLIA; DOPAMINE; DOPAMINE D2-RECEPTOR; CDNA ID D1 DOPAMINE RECEPTOR; GENE-EXPRESSION; ADENOSINE RECEPTORS; NEURONS; BRAIN; LOCALIZATION; AGONIST; PROTEIN; A2-RECEPTORS; NEOSTRIATUM AB A cDNA fragment homologous to other G protein-coupled receptors was isolated from rat brain using the PCR method and demonstrated to be abundantly expressed in striatum. Using this fragment as a probe, a 2.1 kb full-length cDNA was isolated from a rat striatal cDNA library. This cDNA encodes a protein of 410 amino acids and is highly homologous to previously isolated adenosine receptor cDNAs. Expression of this cDNA in COS cells revealed high affinity (K(d) = 38.6 nM) and saturable binding of the A2 adenosine receptor-selective ligand [H-3]CGS 21680. Agonist displacement profile of [H-3]CGS 21680 binding was consistent with an adenosine receptor of the A2 subtype (NECA > (R)-PIA > CPA > (S)-PIA). In situ hybridization demonstrated that rat A2 adenosine receptor mRNA was co-expressed in the same striatal neurons as D2 dopamine receptor mRNA, and never co-expressed with striatal D1 dopamine receptor mRNA. Several lines of evidence have previously suggested that dopamine-induced changes in motor behavior can be modulated by adenosine analogs acting at the A2 subtype of adenosine receptor in the forebrain. The co-expression of D2 dopamine and A2 adenosine receptors in a subset of striatal cells provides an anatomical basis for dopaminergic-adenosinergic interactions on motor behavior. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEV CHRONOBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PEDIAT & ANESTHESIA,BOSTON,MA 02114. NR 43 TC 523 Z9 526 U1 1 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-328X J9 MOL BRAIN RES JI Mol. Brain Res. PD JUL PY 1992 VL 14 IS 3 BP 186 EP 195 DI 10.1016/0169-328X(92)90173-9 PG 10 WC Neurosciences SC Neurosciences & Neurology GA JD347 UT WOS:A1992JD34700004 ER PT J AU LIPTON, SA AF LIPTON, SA TI MEMANTINE PREVENTS HIV COAT PROTEIN-INDUCED NEURONAL INJURY INVITRO SO NEUROLOGY LA English DT Note ID NERVOUS-SYSTEM; NEUROTOXICITY; AIDS AB Studies with in vitro model systems suggest that at least part of the neurologic deficits of human immunodeficiency virus (HIV)-1-associated cognitive/motor complex may stem from neuronal injury mediated by the HIV-1 coat protein gp120. Concurrent activation of N-methyl-D-aspartate (NMDA) receptors is also necessary for gp120 to induce neuronal damage. We studied memantine, a drug that blocks NMDA receptor-operated ion channels, for possible protective effects from gp120-induced neuronal injury. In identified rat retinal ganglion cells in culture, we found that 2-mu-M memantine completely prevented the injury engendered by 20 pM gp120. These data suggest that memantine has therapeutic potential as an NMDA antagonist capable of ameliorating neuronal damage associated with gp120. C1 CHILDRENS HOSP MED CTR,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT NEUROL,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. FU NEI NIH HHS [EY05477, EY09024] NR 10 TC 122 Z9 126 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0028-3878 J9 NEUROLOGY JI Neurology PD JUL PY 1992 VL 42 IS 7 BP 1403 EP 1405 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA JC955 UT WOS:A1992JC95500031 PM 1620355 ER PT J AU HALLIDAY, AL CEPKO, CL AF HALLIDAY, AL CEPKO, CL TI GENERATION AND MIGRATION OF CELLS IN THE DEVELOPING STRIATUM SO NEURON LA English DT Article ID PLACENTAL ALKALINE-PHOSPHATASE; FETAL MONKEY NEOCORTEX; MEDIATED GENE-TRANSFER; RADIAL GLIAL-CELLS; CEREBRAL-CORTEX; NERVOUS-SYSTEM; BRAIN-DEVELOPMENT; PRECURSOR CELLS; MOUSE RETINA; NEURONS AB The development of the rat striatum was investigated using a combination of two histochemically distinguishable retrovirus vectors. Using this method, it was possible to identify clonal boundaries within the embryonic striatum and thus determine patterns of proliferation, migration, and some lineal relationships. Several novel aspects of striatal histogenesis were discovered. Striatal progenitor cells do not exhibit a stem cell pattern of division between embryonic day 15 (E15) and E19; a progenitor-progeny relationship appears to exist for ventricular zone and subventricular zone (SVZ) cells; striatal progenitors produce a variety of clone types; some SVZ cells migrate radially, and some migrate tangentially within the SVZ; and radial glia and presumptive neurons can occur in the same clone. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSCI,BOSTON,MA 02114. RP HALLIDAY, AL (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115, USA. FU NINDS NIH HHS [NS23021] NR 55 TC 153 Z9 154 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD JUL PY 1992 VL 9 IS 1 BP 15 EP 26 DI 10.1016/0896-6273(92)90216-Z PG 12 WC Neurosciences SC Neurosciences & Neurology GA JE756 UT WOS:A1992JE75600002 PM 1632968 ER PT J AU LIBBY, P CLINTON, SK AF LIBBY, P CLINTON, SK TI CYTOKINES AS MEDIATORS OF VASCULAR PATHOLOGY SO NOUVELLE REVUE FRANCAISE D HEMATOLOGIE LA English DT Article; Proceedings Paper CT INTERNATIONAL WORKSHOP ON CYTOKINES, LEUKOCYTES AND VASCULAR DISEASES CY APR 11-12, 1992 CL ST PAUL DE VENCE, FRANCE SP GRP ETUDE FRANCAISE ACTIVAT LEUCOCYTAIRE DE INTERLEUKIN-1; TUMOR NECROSIS FACTOR; ATHEROSCLEROSIS; VASCULITIS; INTERFERONS; PHAGOCYTES; SHOCK ID SMOOTH-MUSCLE CELLS; LOW-DENSITY-LIPOPROTEIN; HUMAN-ENDOTHELIAL-CELLS; HUMAN ATHEROSCLEROTIC PLAQUE; FACTOR GENE-EXPRESSION; FAT-FED RABBITS; GROWTH-FACTOR; CORONARY-ARTERIES; TISSUE FACTOR; INTERLEUKIN-1 AB Interactions between leukocytes and intrinsic vascular wall cells characterize many inflammatory reactions and contribute importantly to the pathogenesis of many vascular diseases. In view of this intimate involvement of leukocytes in vascular pathology it is important to understand the signals that recruit and activate leukocytes locally in regions of vascular pathology. It is also desirable to delineate. the mechanisms by which leukocytes influence the behavior of intrinsic vascular wall cells in ways which may contribute to vascular lesion formation. Mediators elaborated by leukocytes include small molecules including lipid-derived mediators such as prostanoids, leukotrienes, and platelet activating factor. Leukocytes can also produce protein mediators including those currently classified as cytokines. The cytokines, protein mediators involved in inflammation and control of the immune response, derive from all classes of leukocytes studied. Local cytokine networks may orchestrate complex programs of expression of functions of leukocytes and endothelial and smooth muscle cells involved in vascular homeostasis and pathology. Our laboratory has been interested in hyperplastic arterial diseases including atherosclerosis and restenosis following angioplasty treatment of obstructive atherosclerosis. Definitive evidence for roles of cytokines in the pathogenesis of these syndromes are lacking. However, various in vitro and in vivo studies have furnished sufficient information to permit formulation of rather detailed hypotheses or models. In hypercholesterolemic rabbits vascular cell adhesion molecule-1 (VCAM-1) may participate in initial monocyte recruitment to prelesional areas of arterial endothelium. Other adhesion molecules including Intercellular adhesion molecule-1 (ICAM-1) may also participate in monocyte adhesion to arterial endothelial cells. Components of oxidized lipoproteins or local cytokine expression elicited by such products might signal regional expression of leukocyte adhesion molecules providing the first step in monocyte recruitment to the nascent fatty lesion. Once monocytes have adhered to arterial endothelial cells they appear to insinuate processes in between viable endothelial cells and diapedese through the endothelial monolayer. One well characterized candidate chemoattractant in this context is macrophage chemoattractant peptide-l (MCP-l). Some of the same cytokines that can augment or induce expression of monocyte adhesion molecules on the endothelium can induce MCP-1 gene expression by intrinsic vascular wall cells. Mononuclear phagocytes may express a variety of functions within evolving lesions including expression of cytokines, growth factors, apolipoprotein E, enzyme inhibitors including tissue inhibitor of metalloproteinases and alpha2 macroglobulin, and production of matrix-degrading metalloproteinases themselves, small molecules including nitric oxide, a potent vasoregulatory compound, and various biologically active oxygen metabolites as well. Regulators of these various functions include monokines such as interleukin-l (II-I) or tumor necrosis factor (TNF), lymphokines such as gamma interferon or lymphotoxin, the chemoattractent molecule MCP-1 mentioned above, and various hematopoetic growth factors including monocyte-colony stimulating factor (M-CSF). This latter mediator augments apolipoprotein E gene expression by mononuclear phagocytes and induces expression of the ''scavenger receptor'', that participates in transformation of blood monocytes into foam cells. The apolipoprotein E may play an immunomodulatory role as an inhibitor of lymphocyte proliferation. In addition apolipoprotein E may associate with high density lipoprotein (HDL) particles and target them for peripheral catabolism during ''reverse cholesterol transport'', a process that may contribute to the net accumulation of lipid within evolving or regresssing arterial lesions. Modern cytochemical studies have confirmed proliferation of smooth muscle cells in injured arteries. Macrophage-derived and other locally produced or platelet-derived mitogens may be important in stimulating hyperplasia of smooth muscle cells during formation of arterial lesions. In summary, cytokines regulate four distinct aspects of mononuclear phagocyte function in relation to atherogenesis : adhesion, penetration, activation (including mediator elaboration), and division. Cytokines likely participate in the earliest stages of lesion formation, recruitment of monocytes to the nascent fatty streak. During the long clinically silent phases of lesion evolution cytokines probably contribute to the complex regulation of adaptive and pathogenic processes that lead to lesion complication. Finally, cytokines may participate in signalling the transition from chronic to acute phases of atherosclerosis, yielding the acute arterial syndromes that constitute a major and continuing challenge to modern medicine. Further understanding of the particular roles of specific cytokines at various stages of lesion initiation, evolution, and complication may reveal new targets for intervention in these processes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LIBBY, P (reprint author), BRIGHAM & WOMENS HOSP,DEPT MED,DIV CARDIOVASC,VASC MED & ATHEROSCLEROSIS UNIT,221 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 56 TC 32 Z9 33 U1 0 U2 2 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0029-4810 J9 NOUV REV FR HEMATOL JI Nouv. Rev. Fr. Hematol. PD JUL PY 1992 VL 34 SU S BP S47 EP S53 PG 7 WC Hematology SC Hematology GA LW455 UT WOS:A1992LW45500008 PM 1340529 ER PT J AU EINHORN, N SJOVALL, K KNAPP, RC HALL, P SCULLY, RE BAST, RC ZURAWSKI, VR AF EINHORN, N SJOVALL, K KNAPP, RC HALL, P SCULLY, RE BAST, RC ZURAWSKI, VR TI PROSPECTIVE EVALUATION OF SERUM CA-125 LEVELS FOR EARLY DETECTION OF OVARIAN-CANCER SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY; CARCINOMA; POPULATION; DIAGNOSIS; ANTIGEN AB Detection of ovarian cancer at an early stage should reduce the mortality associated with this disease. Through the Stockholm Population Registry, 5550 apparently healthy women were enrolled in a study designed in part to define the use of the CA 125 radioimmunoassay (RIA) as an initial test for early detection of ovarian cancer. Women whose CA 125 levels were elevated and an equal number of age-matched controls with normal levels were followed by means of pelvic examinations, transabdominal sonography, and serial CA 125 determinations. Of the 175 women with high CA 125 levels, six were found to have ovarian cancer: two each in stages IA, IIB, and IIIC. Of those with normal-range CA 125 levels, three had ovarian cancer as identified through the Swedish Cancer Registry; all three were under 50 years of age. Ovarian cancer was diagnosed on laparotomy in six of the women age 50 or over. Using thresholds of 30 and 35 U/mL, the rates of specificity for the CA 125 RIA were 97 and 98.5%, respectively, for women age 50 or older, and 91 and 94.5%, respectively, for those younger than 50 years of age. Thus, the specificity of the CA 125 RIA is adequate in postmenopausal women to undertake a larger study to determine whether screening using CA 125 influences survival of patients with ovarian cancer. C1 CENTOCOR INC,MALVERN,PA. SOPHIAHEMMET,STOCKHOLM,SWEDEN. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. DUKE UNIV,MED CTR,DURHAM,NC 27710. BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. KAROLINSKA INST,KAROLINSKA HOSP,DEPT GYNECOL ONCOL,S-10401 STOCKHOLM 60,SWEDEN. KAROLINSKA INST,KAROLINSKA HOSP,DEPT OBSTET & GYNECOL,S-10401 STOCKHOLM 60,SWEDEN. RI Bast, Robert/E-6585-2011 OI Bast, Robert/0000-0003-4621-8462 FU NCI NIH HHS [1 R44 CA 40945-02, 1 R44 CA 40945-03] NR 15 TC 206 Z9 207 U1 0 U2 2 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 JUL PY 1992 VL 80 IS 1 BP 14 EP 18 PG 5 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA JA324 UT WOS:A1992JA32400004 PM 1603484 ER PT J AU SETO, M YAMAMOTO, K IIDA, S AKAO, Y UTSUMI, KR KUBONISHI, I MIYOSHI, I OHTSUKI, T YAWATA, Y NAMBA, M MOTOKURA, T ARNOLD, A TAKAHASHI, T UEDA, R AF SETO, M YAMAMOTO, K IIDA, S AKAO, Y UTSUMI, KR KUBONISHI, I MIYOSHI, I OHTSUKI, T YAWATA, Y NAMBA, M MOTOKURA, T ARNOLD, A TAKAHASHI, T UEDA, R TI GENE REARRANGEMENT AND OVEREXPRESSION OF PRAD1 IN LYMPHOID MALIGNANCY WITH T(11/14)(Q13/Q32) TRANSLOCATION SO ONCOGENE LA English DT Article ID T(11-14) CHROMOSOME-TRANSLOCATION; MOLECULAR-CLONING; BCL-1 LOCUS; CELL-LINES; T(11-14)(Q13-Q32); AMPLIFICATION; CARCINOMAS; BREAKPOINT; TUMORS; HST AB The proto-oncogene PRAD1 (parathyroid adenoma 1) on chromosome 11q13 was found to be overexpressed in all five B-cell lines with t(11;14)(q13;q32) translocation tested. One B-cell lymphoma and four myeloma cell lines with this translocation demonstrated more than 10-fold overexpression as determined by Northern blot analysis, when compared with normal lymphoid tissues such as thymus, spleen and lymph node. Hematopoietic cell lines without the translocation were also examined, but none of these demonstrated the overexpression, confirming that overexpression of the PRAD1 gene is associated with t(11;14) translocation. A truncated form of mRNA was seen in one of five cell lines with the translocation, SP-49. Hybridization with different regions of the PRAD1 cDNA revealed that the truncated form of mRNA retained the coding region but had lost the 3' untranslated region. Southern blot analysis demonstrated a gene rearrangement in this SP-49 cell line. To study the genetic alteration responsible for the truncated form of mRNA in this cell line, the rearranged allele as well as the germline allele were cloned. The restriction map revealed that the rearranged portion was at the 3' end of the PRAD1 gene, eliminating the mRNA-destabilizing signal AUUUA. Human-rodent hybrid cell analysis demonstrated that the region introduced 3' of PRAD1 was derived from chromosome 11. suggesting that the PRAD1 gene region is deleted at the 3' end. Overexpression of the PRAD1 gene in association with t(11;14)(q13;q32) translocation suggested that in these cases the regulation of PRAD1 was altered by the juxtaposed gene, most likely the immunoglobulin heavy-chain gene from chromosome 14. C1 AICHI CANC CTR,DEPT HEMATOL & CHEMOTHERAPY,NAGOYA,AICHI 464,JAPAN. AICHI CANC CTR,ULTRASTRUCT RES LAB,NAGOYA,AICHI 464,JAPAN. KOCHI MED SCH,DEPT INTERNAL MED,NANKOKU,KOCHI 78151,JAPAN. KAWASAKI MED UNIV,DEPT INTERNAL MED,KURASHIKI,OKAYAMA 70101,JAPAN. OKAYAMA UNIV,SCH MED,INST CANC RES,DEPT PATHOL,OKAYAMA 700,JAPAN. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. AICHI CANC CTR,IMMUNOL LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. RP SETO, M (reprint author), AICHI CANC CTR,CHEMOTHERAPY LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. FU NCI NIH HHS [CA55909] NR 27 TC 223 Z9 223 U1 0 U2 2 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD JUL PY 1992 VL 7 IS 7 BP 1401 EP 1406 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HZ971 UT WOS:A1992HZ97100019 PM 1535701 ER PT J AU SCHUMAN, JS BELLOWS, AR SHINGLETON, BJ LATINA, MA ALLINGHAM, RR BELCHER, CD PULIAFITO, CA AF SCHUMAN, JS BELLOWS, AR SHINGLETON, BJ LATINA, MA ALLINGHAM, RR BELCHER, CD PULIAFITO, CA TI CONTACT TRANSSCLERAL NDYAG LASER CYCLOPHOTOCOAGULATION - MIDTERM RESULTS SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT, 1991 CL ANAHEIM, CA SP AMER ACAD OPHTHALMOL ID YAG CYCLOPHOTOCOAGULATION; SYMPATHETIC OPHTHALMIA; NEOVASCULAR GLAUCOMA; CYCLOCRYOTHERAPY; NEODYMIUM; ND; CYCLOCOAGULATION; CYCLOTHERAPY; EYES AB Background: Early reports of both contact and noncontact transscleral Nd:YAG laser cyclophotocoagulation have been encouraging; however, recent evidence indicates a significant incidence of hypotony, visual loss, and phthisis with the noncontact technique with more than 6 months of follow-up. The authors sought to determine the intermediate term effects of contact transscleral Nd:YAG laser cyclophotocoagulation (CYC). Methods: The authors followed 116 eyes of 114 patients for a minimum of 1 year after treatment of advanced glaucoma with CYC. Results: The mean preoperative intraocular pressure (IOP) of 35.0 +/- 1.0 mmHg decreased to 18.6 +/- 1.1 mmHg (P < 0.0001) during the average follow-up of 19.0 +/- 0.6 months (range, 12 to 36 months). Intraocular pressure control of 3 to 25 mmHg was achieved in 72%, 3 to 22 mmHg in 65%, and 3 to 19 mmHg in 56% of eyes. Retreatment was required in 31 of the 116 eyes (27%). Intraocular pressure decreased to less than 3 mmHg in 9 eyes and to 0 mmHg in 6 of these 9 eyes. Nineteen eyes, all with initial visual acuity of counting fingers or worse, progressed to no light perception; 17 of 36 eyes (47%) with visual acuity of 20/200 or better lost 2 or more Snellen lines. Conclusion: Midterm results of CYC continue to be encouraging but are tempered by a nearly 10% incidence of hypotony or phthisis and the progression of visual loss. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. CTR EYE RES,BOSTON,MA. OPHTHALM CONSULTANTS BOSTON,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS,BOSTON,MA 02114. RP SCHUMAN, JS (reprint author), TUFTS UNIV,NEW ENGLAND MED CTR HOSP,SCH MED,NEW ENGLAND EYE CTR,BOSTON,MA 02111, USA. RI Schuman, Joel/K-7304-2012 OI Schuman, Joel/0000-0002-8885-3766 NR 23 TC 80 Z9 82 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 JUL PY 1992 VL 99 IS 7 BP 1089 EP 1094 PG 6 WC Ophthalmology SC Ophthalmology GA JC543 UT WOS:A1992JC54300025 PM 1495788 ER PT J AU SHORE, JW RUBIN, PAD BILYK, JR AF SHORE, JW RUBIN, PAD BILYK, JR TI REPAIR OF TELECANTHUS BY ANTERIOR FIXATION OF CANTILEVERED MINIPLATES SO OPHTHALMOLOGY LA English DT Article AB Background: The accepted surgical method for telecanthus repair is transnasal wiring. This procedure requires a stable posterior lacrimal crest on the affected side and surgical manipulation of the wires as they exit the contralateral side. A method for repairing telecanthus that obviates these prerequisites is presented. Indications for use of this technique and comparison to transnasal wiring is discussed. Methods: A Y-shaped titanium rigid orbital plating system ("miniplate") was used to surgically correct traumatic telecanthus in five patients, two in the acute setting and three in late reconstruction. The miniplate was cantilevered from the lateral aspect of the nose and directed posteriorly into the orbit. This provided a stable fixation point for the medial canthal tendon. Results: Marked resolution of the telecanthus was noted in four patients. No postoperative complications have been encountered to date. Conclusions: Miniplate fixation was used successfully to repair unilateral traumatic telecanthus. Miniplate fixation of the medial canthal tendon should be considered in unilateral cases of traumatic telecanthus and in cases where poor bony support for transnasal wires is evident. RP SHORE, JW (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,CTR EYE PLAST & ORBIT,BOSTON,MA 02114, USA. NR 4 TC 8 Z9 11 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JUL PY 1992 VL 99 IS 7 BP 1133 EP 1138 PG 6 WC Ophthalmology SC Ophthalmology GA JC543 UT WOS:A1992JC54300033 PM 1495794 ER PT J AU LOCKE, JL AF LOCKE, JL TI 30 YEARS OF RESEARCH ON DEVELOPMENTAL NEUROLINGUISTICS SO PEDIATRIC NEUROLOGY LA English DT Review ID LANGUAGE-ACQUISITION; DOWNS-SYNDROME; HEMISPHERIC-SPECIALIZATION; EMOTIONAL EXPRESSION; FACIAL EXPRESSION; AUTISTIC-CHILDREN; HUMAN-FETUS; INFANT; IMPAIRMENT; BRAIN AB A body of medically important work has accumulated in the field of developmental neurolinguistics in the 30 years since Lenneberg set forth a research agenda for that field, consisting of the following: (1) the physiologic specialization or endowment for speech; (2) the genetic origin or natural history of vocalization and speech; (3) the nature of prelinguistic behavior, making possible the detection of any environmental (social) influences; (4) the development of motor-speech organization from birth; and (5) the limiting effects of deficient intelligence, hearing, and environmental stimulation. Subsequent study of these questions has established a genetic, neuroanatomic, and functional basis for such outwardly disparate disorders as dyslexia, stuttering, autism, and delayed language. Studies of emergent motor behavior suggest that babbling may index a state of neural maturation favoring expression of spoken languages. Based on studies of the congenitally deaf, mentally retarded, and other clinical populations it is now considered possible to detect early warning signs of developmental language disorders during the first year of life based on analyses of vocal turn-taking, gesturing, and utterance complexity. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LOCKE, JL (reprint author), MGH INST HLTH PROFESS,NEUROLINGUIST LAB,101 MERRIMAC ST,BOSTON,MA 02114, USA. NR 72 TC 8 Z9 8 U1 1 U2 9 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD JUL-AUG PY 1992 VL 8 IS 4 BP 245 EP 250 DI 10.1016/0887-8994(92)90359-7 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA JJ450 UT WOS:A1992JJ45000001 PM 1388411 ER PT J AU KELLY, DH RIORDAN, L SMITH, MJ AF KELLY, DH RIORDAN, L SMITH, MJ TI APNEA AND PERIODIC BREATHING IN HEALTHY FULL-TERM INFANTS, 12-18 MONTHS OF AGE SO PEDIATRIC PULMONOLOGY LA English DT Article DE APNEA DENSITY; LONGEST APNEA; BRADYCARDIA ID DEATH SYNDROME; PNEUMOGRAMS AB Many children older than 12 months of age are now on home monitors. Home pneumograms performed on normal infants have established standards, and have been used to evaluate infants during their first year. However, no standards have been described tor infants older than 12 months. We, therefore, recorded the standard pneumogram on 88 full-term healthy infants who were 12-18 months of age. We analyzed the recordings tor average respiratory and heart rates, apnea (greater-than-or-equal-to 6 seconds) density, longest apnea, periodic breathing, and bradycardia for 12 hours. We compared the values in males vs. females and in infants 12-14.9 months vs. 15.0-18.0 months of age. Since there was no difference in any parameter measured in any group, we combined the values to determine the normal values for this population. RP KELLY, DH (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PULM UNIT,BOSTON,MA 02114, USA. NR 10 TC 8 Z9 8 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD JUL PY 1992 VL 13 IS 3 BP 169 EP 171 DI 10.1002/ppul.1950130308 PG 3 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA JG033 UT WOS:A1992JG03300007 PM 1437331 ER PT J AU FRISCH, LS COPELAND, KC BOEPPLE, PA AF FRISCH, LS COPELAND, KC BOEPPLE, PA TI RECURRENT OVARIAN CYSTS IN CHILDHOOD - DIAGNOSIS OF MCCUNE-ALBRIGHT SYNDROME BY BONE-SCAN SO PEDIATRICS LA English DT Note ID PRECOCIOUS PUBERTY; FIBROUS DYSPLASIA; HORMONE C1 MASSACHUSETTS GEN HOSP,REPROD ENDOCRINE UNIT,BHX 5,FRUIT ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,PEDIAT UNIT,BOSTON,MA 02114. UNIV VERMONT,COLL MED,DEPT PEDIAT,BURLINGTON,VT 05401. FU NCRR NIH HHS [RR 01066]; NICHD NIH HHS [HD 18169] NR 12 TC 13 Z9 13 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUL PY 1992 VL 90 IS 1 BP 102 EP 104 PN 1 PG 3 WC Pediatrics SC Pediatrics GA JA854 UT WOS:A1992JA85400023 PM 1614755 ER PT J AU KLEINMAN, RE AF KLEINMAN, RE TI WE HAVE THE SOLUTION - NOW WHATS THE PROBLEM SO PEDIATRICS LA English DT Editorial Material ID ACUTE DIARRHEA; CHILDREN C1 HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. RP KLEINMAN, RE (reprint author), MASSACHUSETTS GEN HOSP,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02114, USA. NR 14 TC 5 Z9 5 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUL PY 1992 VL 90 IS 1 BP 113 EP 115 PN 1 PG 3 WC Pediatrics SC Pediatrics GA JA854 UT WOS:A1992JA85400028 PM 1614761 ER PT J AU HUNT, CE SHANNON, DC AF HUNT, CE SHANNON, DC TI SUDDEN-INFANT-DEATH-SYNDROME AND SLEEPING POSITION SO PEDIATRICS LA English DT Editorial Material ID PRESSURE; LUNG C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114. RP HUNT, CE (reprint author), MED COLL WISCONSIN,DEPT PEDIAT,POB 10008,MILWAUKEE,WI 53226, USA. NR 19 TC 59 Z9 59 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUL PY 1992 VL 90 IS 1 BP 115 EP 118 PN 1 PG 4 WC Pediatrics SC Pediatrics GA JA854 UT WOS:A1992JA85400029 PM 1614762 ER PT J AU KREBS, DE WONG, D JEVSEVAR, D RILEY, PO HODGE, WA AF KREBS, DE WONG, D JEVSEVAR, D RILEY, PO HODGE, WA TI TRUNK KINEMATICS DURING LOCOMOTOR ACTIVITIES SO PHYSICAL THERAPY LA English DT Article DE GAIT; KINEMATICS; LOCOMOTION; SPINAL MOBILITY IMPAIRMENT ID MOVEMENTS AB We investigated upper-body (ie, trunk) angular kinematics (motions) during gait, stair climbing and descending and rising from a chair in two reference frames-relative relative to the pelvis and to room coordinates Bilateral kinematic data were collected jected from 11 healthy subjects (6 female, 5 male), who were 27 to 88 years of age (XBAR = 58.9, SD = 17.9). During stair climbing, maximum trunk flexion relative to the room was at least double that during stair descending and gait. Arising from a chair required the most trunk flexion/extension range of motion (ROM) but the least abduction/adduction and medial/lateral (internal/external) rotation. Trunk ROM during gait was small (XBAR less-than-or-equal-to 12-degrees) and consistent with previous literature. ture Trunk range of motion relative to the room during stair climbing and descending scending was greater than trunk ROM during gait in all planes The pelvis and trunk rotate in the transverse plane in greater synchrony during stair descending (XBAR = 8.10, SO=5.60) than during gait (XBAR = 12.0-degrees, SD = 4.2-degrees). For all activities, trunk frontal and sagittal ROM relative to the pelvis was greater than that relative to the room coordinates. This finding suggests that trunk/pelvis coordination may be used to reduce potentially destabilizing anti-gravity trunk motions during daily activities. We conclude that upper-body kinematics relative to both pelvis and gravity during daily activities are important to locomotor control and should be considered in future studies of patient with locomotor disabilities. C1 MIT,MGH REHAB ENGN CTR,CAMBRIDGE,MA 02139. TUFTS UNIV,NEW ENGLAND MED CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,MGH BIOMOT LAB,BOSTON,MA 02114. RP KREBS, DE (reprint author), MGH INST HLTH PROFESS,15 RIVER ST,BOSTON,MA 02108, USA. RI Riley, Patrick/B-3053-2009 NR 19 TC 102 Z9 105 U1 0 U2 6 PU AMER PHYS THER ASSN PI ALEXANDRIA PA 1111 N FAIRFAX ST, ALEXANDRIA, VA 22314 SN 0031-9023 J9 PHYS THER JI Phys. Ther. PD JUL PY 1992 VL 72 IS 7 BP 505 EP 514 PG 10 WC Orthopedics; Rehabilitation SC Orthopedics; Rehabilitation GA JD361 UT WOS:A1992JD36100006 PM 1409883 ER PT J AU TAL, M WU, YJ LEISER, M SURANA, M LODISH, H FLEISCHER, N WEIR, G EFRAT, S AF TAL, M WU, YJ LEISER, M SURANA, M LODISH, H FLEISCHER, N WEIR, G EFRAT, S TI [VAL12]HRAS DOWN-REGULATES GLUT2 IN BETA-CELLS OF TRANSGENIC MICE WITHOUT AFFECTING GLUCOSE-HOMEOSTASIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MOUSE PANCREATIC-ISLETS; RAT PANCREAS; TRANSPORTER; EXPRESSION; SECRETION; LIVER AB Glucose-induced insulin release from pancreatic beta-cells depends on the beta-cell metabolism of glucose, which generates intracellular signals for secretion. The beta-cell glucose transporter isotype GLUT2 and the glucose phosphorylating enzyme glucokinase have both been implicated in coupling insulin secretion to extracellular glucose levels. Here we present evidence that a pronounced decrease in beta-cell GLUT2 has no immediate effect on glucose homeostasis. Analysis of transgenic mice overexpressing human [Val12]HRAS oncoprotein under control of the insulin promoter reveals a great reduction in plasma-membrane GLUT2 levels. These mice are nonetheless able to maintain normal fed and fasting plasma glucose and insulin levels for a period of several months. Insulin secretion studied in isolated islets and the perfused pancreas is characterized by a normal incremental response to increasing glucose concentrations. Glucose metabolism, as measured by glucose phosphorylation and oxidation in isolated islets, shows a normal dose dependence on extracellular glucose concentrations. These findings suggest that normal GLUT2 expression in beta-cells is not essential for glucose sensing. The transgenic mice provide an experimental system for studying the role of glucose phosphorylation in regulation of insulin release in the absence of GLUT2. C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,CTR DIABET RES & TRAINING,BRONX,NY 10461. WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. JOSLIN DIABET CTR,BOSTON,MA 02215. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MED,BRONX,NY 10461. YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT MOLEC PHARMACOL,BRONX,NY 10461. FU NIDDK NIH HHS [DK-35449, DK-20541] NR 23 TC 37 Z9 37 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 JUL 1 PY 1992 VL 89 IS 13 BP 5744 EP 5748 DI 10.1073/pnas.89.13.5744 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800010 PM 1631055 ER PT J AU PETERS, LL WHITE, RA BIRKENMEIER, CS BLOOM, ML LUX, SE BARKER, JE AF PETERS, LL WHITE, RA BIRKENMEIER, CS BLOOM, ML LUX, SE BARKER, JE TI CHANGING PATTERNS IN CYTOSKELETAL MESSENGER-RNA EXPRESSION AND PROTEIN-SYNTHESIS DURING MURINE ERYTHROPOIESIS INVIVO SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN ERYTHROCYTE ANKYRIN; INHERITED HEMOLYTIC-ANEMIAS; CYTOPLASMIC DOMAIN; MEMBRANE SKELETON; ALPHA-SPECTRIN; BETA-SPECTRIN; MOUSE; DIFFERENTIATION; CELLS; CDNA AB The major cytoskeletal proteins alpha-spectrin, beta-spectrin, and ankyrin are synthesized and assembled into a supportive membrane skeleton during erythroid differentiation. Information on the temporal appearance of mRNA and protein species is essential for understanding both the cytoskeletal assembly process and the function of various isoforms. We have isolated highly enriched populations of fetal erythroid cells at various stages of maturation. mRNAs for erythroid ankyrin, alpha-spectrin, and beta-spectrin were expressed at all stages but there were differences in transcript types and levels. The ratio of 9-kilobase (kb) to 7.5-kb erythroid ankyrin transcripts decreased markedly during differentiation, but there was no change in the ratio of the 10.1-kb and 9.3-kb erythroid beta-spectrin transcripts. The relative amounts of ankyrin, alpha-spectrin, and beta-spectrin mRNA increased during yolk sac cell differentiation, whereas only alpha-spectrin mRNA increased during differentiation of the fetal liver cells. The amounts of beta-spectrin mRNA exceeded the amounts of alpha-spectrin mRNA in the early precursors from both yolk sac and fetal liver; protein synthetic levels showed the same pattern. The 16-day fetal peripheral reticulocytes, on the other hand, had the adult mRNA and protein synthetic ratios with alpha/beta > 1. The data indicate that at least two mechanisms exist to meet changing erythroid membrane cytoskeletal requirements during development in utero: (i) stage-specific processing of the mRNA for the major cytoskeletal linker protein ankyrin and (ii) developmentally regulated alpha/beta-spectrin protein synthetic rates. C1 JACKSON LAB,BAR HARBOR,ME 04609. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02215. FU NHLBI NIH HHS [HL29305] NR 53 TC 21 Z9 21 U1 1 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 JUL 1 PY 1992 VL 89 IS 13 BP 5749 EP 5753 DI 10.1073/pnas.89.13.5749 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800011 PM 1385865 ER PT J AU HOPE, B KOSOFSKY, B HYMAN, SE NESTLER, EJ AF HOPE, B KOSOFSKY, B HYMAN, SE NESTLER, EJ TI REGULATION OF IMMEDIATE EARLY GENE-EXPRESSION AND AP-1 BINDING IN THE RAT NUCLEUS-ACCUMBENS BY CHRONIC COCAINE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID C-FOS; NERVOUS-SYSTEM; CYCLIC-AMP; AMPHETAMINE; PROTEIN; SEIZURE; BRAIN; JUN AB Chronic treatment of rats with cocaine leads to long-term biochemical changes in the nucleus accumbens (NAc), a brain region implicated in mediating the reinforcing effects of cocaine and other drugs of abuse. Immediate early genes (IEGs) and their protein products appear to play an important role in transducing extracellular stimuli into altered patterns of cellular gene expression and, therefore, into long-term changes in cellular functioning. We therefore examined changes in the mRNA levels for the IEGs c-fos, c-jun, fosB, junB, and zif268 in the NAc of rats treated acutely and chronically with cocaine. A single cocaine injection increased the mRNA levels of all of the IEGs examined. Following chronic cocaine treatment, however, IEG expression had returned to control levels and was not significantly increased following a further acute challenge with cocaine, suggesting desensitization in the ability of cocaine to induce these IEGs. Similarly, levels of Fos-like immunoreactivity, which are increased in the NAc by acute cocaine, were reduced to control levels in chronic cocaine-treated rats. Fos, Jun, and a number of related proteins activate or repress transcription of genes by binding to DNA response elements called AP-1 sites. As would be expected from the RNA data and immunohistochemistry, acute cocaine administration increased AP-1 binding activity in the NAc, an effect that reverted completely to control levels within 8-12 hr. In contrast, AP-1 binding activity in the NAc of animals treated chronically with cocaine remained elevated at acute levels 18 hr after the last chronic injection, a time at which c-fos and c-jun mRNA levels and Fos-like immunoreactivity had returned to control values. An additional acute cocaine challenge did not further increase AP-1 binding. The data suggest that chronic cocaine treatment leads to a persistent increase in AP-1 binding activity, which may be involved in some of the physiological and behavioral aspects of cocaine addiction. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PSYCHIAT,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. YALE UNIV,SCH MED,CONNECTICUT MENTAL HLTH CTR,DEPT PHARMACOL,NEW HAVEN,CT 06508. RP HOPE, B (reprint author), YALE UNIV,SCH MED,CONNECTICUT MENTAL HLTH CTR,DEPT PSYCHIAT,MOLEC PSYCHIAT LAB,NEW HAVEN,CT 06508, USA. RI Hope, Bruce/A-9223-2010 OI Hope, Bruce/0000-0001-5804-7061 FU NIDA NIH HHS [DA05490, DA07359]; NIMH NIH HHS [MH00892] NR 32 TC 383 Z9 389 U1 0 U2 10 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 JUL 1 PY 1992 VL 89 IS 13 BP 5764 EP 5768 DI 10.1073/pnas.89.13.5764 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800014 PM 1631058 ER PT J AU STRAUSS, EC ORKIN, SH AF STRAUSS, EC ORKIN, SH TI INVIVO PROTEIN DNA INTERACTIONS AT HYPERSENSITIVE SITE-3 OF THE HUMAN BETA-GLOBIN LOCUS-CONTROL REGION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CHROMATIN STRUCTURE; DIMETHYL SULFATE; ERYTHROLEUKEMIA CELLS; TRANSCRIPTION FACTOR GATA-1 ID DOMINANT CONTROL REGION; TRANSGENIC MICE; ERYTHROID-CELLS; GENE; EXPRESSION; ENHANCER; BINDING; DOMAIN AB The expression of beta-globin genes in developing erythroid cells is dependent on distant, upstream regulatory sequences, known as the locus control region (LCR), which are marked in chromatin by DNase I hypersensitive sites (HS-1 to HS-4). Linkage of the beta-globin gene complex LCR or fragments surrounding core regions of 200-300 base pairs to the human beta-globin gene permits consistent, high-level expression of the transgene in mice. To define the array of nuclear factors interacting with beta-LCR HS-3, we have performed in vivo dimethyl sulfate footprinting of the active HS-3 core in erythroid cells by a modified procedure that permits assessment of protein-DNA contacts at adenine, as well as guanine, residues. In vivo protein occupancy differs considerably from that predicted from previous in vitro binding analyses. In vivo foot-printing detects protein binding at four sites recognized by the erythroid transcription factor GATA-1, at two CACC/GT motifs, and at a single AP-1/NF-E2 site. The regulatory clements occupied in vivo in HS-3 appear similar to those described previously in globin gene promoters and 3' enhancers. These findings suggest that the distinctive properties of the HS-3 region may be attributable to the organization of these occupied motifs and the consequent protein interactions, rather than to the binding of unique LCR regulatory factors. C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,300 LONGWOOD AVE,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,MIT,DEPT PEDIAT,DIV HLTH SCI & TECHNOL,BOSTON,MA 02115. NR 26 TC 78 Z9 78 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 JUL 1 PY 1992 VL 89 IS 13 BP 5809 EP 5813 DI 10.1073/pnas.89.13.5809 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800023 PM 1631062 ER PT J AU HIRAYAMA, F SHIH, JP AWGULEWITSCH, A WARR, GW CLARK, SC OGAWA, M AF HIRAYAMA, F SHIH, JP AWGULEWITSCH, A WARR, GW CLARK, SC OGAWA, M TI CLONAL PROLIFERATION OF MURINE LYMPHOHEMATOPOIETIC PROGENITORS IN CULTURE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIETIC STEM CELL; GROWTH FACTOR; LYMPHOCYTE-B ID MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; COLONY-STIMULATING FACTOR; INTERLEUKIN-3-DEPENDENT PROLIFERATION; LYMPHOCYTES-T; IDENTIFICATION; DIFFERENTIATION; IMMUNOGLOBULIN; ORIGIN; REGION; IL-7 AB We have used a two-step clonal culture system to unequivocally demonstrate that individual primitive lymphohemopoietic progenitor cells have the capacity for differentiation along either the myeloid or the B-lymphoid lineage. Highly enriched murine marrow cells were plated individually in culture by micromanipulation in the presence of pokeweed mitogen-stimulated spleen cell conditioned medium, erythropoietin, steel factor (SF), and interleukin (IL) 7. Forty-five percent of the single cells formed primary colonies expressing multiple hemopoietic lineages. When aliquots from individual colonies were replated in secondary methyl cellulose culture containing SF and IL-7, 41% of the primary colonies gave rise to lymphocyte colonies. Cells of the lymphocyte colonies were blast-like and B220+, sIg-, Mac-1-, Gr-1-, Ly-1-, L3T4-, Ly-2-, and CD3-. Thirty to 70% of the cells were Thy-1+. Mu-chain mRNA was detected in most of the cells by in situ hybridization with an antisense RNA probe. When lymphocyte colonies derived from a single cell were pooled and individually injected into scid mice, donor-type IgM was measurable in the serum of mice and spleens contained donor-type B cells. We then carried out initial screening of growth factors to identify growth factors that might replace pokeweed mitogen-stimulated spleen cell conditioned medium in the primary culture. Combinations of two factors that included SF plus IL-6, IL-11, or granulocyte colony-stimulating factor were all effective in the primary culture in the maintenance of the B-lymphoid potential. Interestingly, IL-3 could neither replace nor act synergistically with SF to support the lymphoid potential of the primary cultures. Our observations demonstrate that many primitive progenitors previously believed to be myeloid-committed also possess B-lymphoid potential. This culture system should prove valuable for elucidation of the mechanisms regulating early stages of lymphohemopoiesis. C1 MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29403. MED UNIV S CAROLINA,DEPT BIOCHEM & MOLEC BIOL,CHARLESTON,SC 29403. RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC 29403. GENET INST,CAMBRIDGE,MA 02140. FU NIGMS NIH HHS [GM4334-03]; PHS HHS [DM32294] NR 22 TC 144 Z9 144 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 JUL 1 PY 1992 VL 89 IS 13 BP 5907 EP 5911 DI 10.1073/pnas.89.13.5907 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800043 PM 1631072 ER PT J AU HABER, DA TIMMERS, HTM PELLETIER, J SHARP, PA HOUSMAN, DE AF HABER, DA TIMMERS, HTM PELLETIER, J SHARP, PA HOUSMAN, DE TI A DOMINANT MUTATION IN THE WILMS-TUMOR GENE WT1 COOPERATES WITH THE VIRAL ONCOGENE E1A IN TRANSFORMATION OF PRIMARY KIDNEY-CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN CHROMOSOME-11; SUPPRESSION; EXPRESSION; DELETION; PROTEIN; LOCUS AB Wilms tumor is a pediatric kidney cancer that has been linked to the inactivation of a tumor-suppressor gene at chromosome locus 11p13. The WT1 gene, mapping to this locus, is developmentally regulated in the kidney and encodes a putative transcription factor that has been shown to be mutated in Wilms tumor specimens. We have suggested that one such altered product of the WT1 gene may be capable of trans-dominant suppression, since the mutated allele was found to be coexpressed with the wild-type allele in a sporadic Wilms tumor. We therefore tested the ability of this mutant WT1 allele, containing an in-frame deletion within the DNA-binding domain, to transform primary baby rat kidney cells. The mutant WT1 gene was found to cooperate with the adenoviral E1A gene in transforming baby rat kidney cells, as demonstrated by growth in soft agar and tumorigenicity in nude mice. The wild-type WT1 gene in all of its alternatively spliced forms neither suppressed E1A-induced focus formation nor cooperated with E1A. Our results indicate that impairment of DNA binding of the WT1 tumor-suppressor gene product can result in a dominant negative mutation. C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. RP HABER, DA (reprint author), MIT,CTR CANC RES,CAMBRIDGE,MA 02139, USA. FU NCI NIH HHS [P30-CA14051, P01-CA42063]; NIGMS NIH HHS [GM27882] NR 26 TC 50 Z9 50 U1 1 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUL 1 PY 1992 VL 89 IS 13 BP 6010 EP 6014 DI 10.1073/pnas.89.13.6010 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JC868 UT WOS:A1992JC86800064 PM 1321431 ER PT J AU KAHN, RS SIEVER, LJ GABRIEL, S AMIN, F STERN, RG DUMONT, K APTER, S DAVIDSON, M AF KAHN, RS SIEVER, LJ GABRIEL, S AMIN, F STERN, RG DUMONT, K APTER, S DAVIDSON, M TI SEROTONIN FUNCTION IN SCHIZOPHRENIA - EFFECTS OF METACHLOROPHENYLPIPERAZINE IN SCHIZOPHRENIC-PATIENTS AND HEALTHY-SUBJECTS SO PSYCHIATRY RESEARCH LA English DT Article DE PROLACTIN; ADRENOCORTICOTROPIC HORMONE; BODY TEMPERATURE; 5-HYDROXYTRYPTAMINE; PSYCHOSIS ID META-CHLOROPHENYLPIPERAZINE; FRONTAL-CORTEX; RECEPTORS; RESPONSES; MCPP; RAT; ANTAGONISM AB This study examined serotonin (5-hydroxytryptamine, 5HT) receptor responsivity in 22 chronic schizophrenic patients and 17 healthy control subjects. The 5HT agonist meta-chlorophenylpiperazine (MCPP) was used as a probe of serotonergic function. MCPP (0.35 mg/kg) or placebo was administered orally after a 3-week drug-free period in a randomized double-blind design. Hormonal (adrenocorticotropic hormone and prolactin), temperature, and behavioral responses and MCPP blood levels were assessed for 210 minutes after administration of the capsules. The schizophrenic patients had blunted temperature responses compared with those of the healthy control subjects: MCPP raised body temperature in the control subjects, but not in the patients. Behavioral responses also differed in the two groups: MCPP increased the total Brief Psychiatric Rating Scale (BPRS) score in the control subjects and tended to decrease it in the patients. In patients, MCPP decreased the BPRS psychosis subscore. Hormonal responses did not differ significantly in the two groups. These findings suggest that further exploration of 5HT function in schizophrenia is warranted. C1 BRONX VET ADM MED CTR,CLIN RES UNIT,BRONX,NY 10468. CUNY MT SINAI SCH MED,DEPT PSYCHIAT,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,NEUROENDOCRINOL LAB,NEW YORK,NY 10029. FU NIMH NIH HHS [R01 MH-46957-01] NR 37 TC 48 Z9 48 U1 1 U2 2 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-1781 J9 PSYCHIAT RES JI Psychiatry Res. PD JUL PY 1992 VL 43 IS 1 BP 1 EP 12 DI 10.1016/0165-1781(92)90136-Q PG 12 WC Psychiatry SC Psychiatry GA JK629 UT WOS:A1992JK62900001 PM 1332094 ER PT J AU GOITEIN, M AF GOITEIN, M TI 3D TREATMENT PLANNING FOR HEAVY CHARGED-PARTICLES SO RADIATION AND ENVIRONMENTAL BIOPHYSICS LA English DT Article; Proceedings Paper CT 4TH WORKSHOP ON HEAVY CHARGED PARTICLES IN BIOLOGY AND MEDICINE CY SEP 23-25, 1991 CL DARMSTADT, GERMANY SP GESELL SCHWERIONENFORSCH ID RADIATION-THERAPY; PROTON AB The comments herein describe, at a necessarily superficial level, a number of issues which must be addressed in developing plans for heavy charged particle therapy. Programs now exist which provide the needed capabilities. The challenge now is to make the planning process easier and faster- and possibly more efective. It seems likely that this will be achieved in the next few years. RP GOITEIN, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239] NR 11 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-634X J9 RADIAT ENVIRON BIOPH JI Radiat. Environ. Biophys. PD JUL PY 1992 VL 31 IS 3 BP 241 EP 245 DI 10.1007/BF01214831 PG 5 WC Biology; Biophysics; Environmental Sciences; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Environmental Sciences & Ecology; Radiology, Nuclear Medicine & Medical Imaging GA JB070 UT WOS:A1992JB07000007 PM 1502332 ER PT J AU URIE, MM AF URIE, MM TI USES OF 3D PLANNING IN ADDITION TO CREATING A GOOD TREATMENT - ONGOING STUDIES AT MGH/HCL SO RADIATION AND ENVIRONMENTAL BIOPHYSICS LA English DT Article; Proceedings Paper CT 4TH WORKSHOP ON HEAVY CHARGED PARTICLES IN BIOLOGY AND MEDICINE CY SEP 23-25, 1991 CL DARMSTADT, GERMANY SP GESELL SCHWERIONENFORSCH ID RADIATION-THERAPY; PROTON AB Ongoing studies and 3D treatment planning and its clinical impact will be described. RP URIE, MM (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA 21239] NR 17 TC 0 Z9 0 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-634X J9 RADIAT ENVIRON BIOPH JI Radiat. Environ. Biophys. PD JUL PY 1992 VL 31 IS 3 BP 247 EP 250 DI 10.1007/BF01214832 PG 4 WC Biology; Biophysics; Environmental Sciences; Radiology, Nuclear Medicine & Medical Imaging SC Life Sciences & Biomedicine - Other Topics; Biophysics; Environmental Sciences & Ecology; Radiology, Nuclear Medicine & Medical Imaging GA JB070 UT WOS:A1992JB07000008 PM 1502333 ER PT J AU LEE, MJ HAHN, PF AF LEE, MJ HAHN, PF TI STATISTICAL-ANALYSIS WITH RECEIVER OPERATING CHARACTERISTIC CURVES - REPLY SO RADIOLOGY LA English DT Article RP LEE, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD JUL PY 1992 VL 184 IS 1 BP 38 EP 38 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HZ682 UT WOS:A1992HZ68200009 ER PT J AU TOLKOFFRUBIN, NE RUBIN, RH AF TOLKOFFRUBIN, NE RUBIN, RH TI CLINICAL APPROACH TO VIRAL AND FUNGAL-INFECTIONS IN THE RENAL-TRANSPLANT PATIENT SO SEMINARS IN NEPHROLOGY LA English DT Article ID CYTOMEGALO-VIRUS INFECTION; HERPES-SIMPLEX INFECTION; NON-B-HEPATITIS; ALLOGRAFT RECIPIENTS; NON-A; DISEASE; GLOMERULOPATHY; ANTIBODY C1 MASSACHUSETTS GEN HOSP,HEMODIALYSIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CAPD UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,TRANSPLANTAT INFECT DIS UNIT,BOSTON,MA 02114. NR 47 TC 11 Z9 11 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9295 J9 SEMIN NEPHROL JI Semin. Nephrol. PD JUL PY 1992 VL 12 IS 4 BP 364 EP 375 PG 12 WC Urology & Nephrology SC Urology & Nephrology GA JC459 UT WOS:A1992JC45900009 PM 1410863 ER PT J AU MOORE, EH TEMPLETON, PA AF MOORE, EH TEMPLETON, PA TI IMAGING THE ADVANCING FRONTIER OF LUNG-CANCER OPERABILITY SO SEMINARS IN RESPIRATORY MEDICINE LA English DT Article ID CHEST-WALL INVASION; INDETERMINATE MEDIASTINAL INVASION; BRONCHIAL NEEDLE ASPIRATION; FACTORS AFFECTING SURVIVAL; SUPERIOR SULCUS TUMORS; EN BLOC RESECTION; BRONCHOGENIC-CARCINOMA; COMPUTED-TOMOGRAPHY; SLEEVE LOBECTOMY; CT EVALUATION C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV MARYLAND,SCH MED,DEPT RADIOL,BALTIMORE,MD 21201. UNIV MARYLAND HOSP,BALTIMORE,MD 21201. NR 84 TC 1 Z9 1 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0192-9755 J9 SEMIN RESPIR MED PD JUL PY 1992 VL 13 IS 4 BP 293 EP 308 DI 10.1055/s-2007-1006278 PG 16 WC Respiratory System SC Respiratory System GA JC718 UT WOS:A1992JC71800003 ER PT J AU BERKMAN, B AF BERKMAN, B TI FAMILIES AND HEALTH-CARE - PSYCHOSOCIAL PRACTICE - ELL,K, NORTHEN,H SO SOCIAL WORK LA English DT Book Review RP BERKMAN, B (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU NATL ASSOC SOCIAL WORKERS PI WASHINGTON PA 750 FIRST ST, NE, STE 700, WASHINGTON, DC 20002-4241 SN 0037-8046 J9 SOC WORK JI Soc. Work PD JUL PY 1992 VL 37 IS 4 BP 382 EP 383 PG 2 WC Social Work SC Social Work GA JG242 UT WOS:A1992JG24200022 ER PT J AU KIM, KM DEMETS, DL AF KIM, KM DEMETS, DL TI SAMPLE-SIZE DETERMINATION FOR GROUP SEQUENTIAL CLINICAL-TRIALS WITH IMMEDIATE RESPONSE SO STATISTICS IN MEDICINE LA English DT Article ID DESIGN; TESTS AB The use function approach to group sequential methods has been explored previously. Any group sequential design requires specifying the frequency and times of repeated analyses, but only the use function approach allows deviations from those specified in the design, without affecting the type I error in the analysis. This paper illustrates how the use function provides a simple and flexible design procedure and how the initially projected maximum sample size can be calculated for randomized clinical trials in which responses are known relatively soon after patient entry and for which there is an early stopping rule built into the study protocol. Also the consequence of using the proposed design procedure is investigated in terms of the operating characteristics of the subsequent group sequential analyses. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WISCONSIN,DEPT BIOSTAT,MADISON,WI 53706. RP KIM, KM (reprint author), HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,44 BINNEY ST,MAYER 4,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA-18332, CA-52733] NR 10 TC 31 Z9 31 U1 2 U2 3 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 JUL PY 1992 VL 11 IS 10 BP 1391 EP 1399 DI 10.1002/sim.4780111012 PG 9 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 JH268 UT WOS:A1992JH26800010 PM 1518999 ER PT J AU YUNIS, JJ DELGADO, MB LEELEWANDROSKI, E YUNIS, EJ BING, DH AF YUNIS, JJ DELGADO, MB LEELEWANDROSKI, E YUNIS, EJ BING, DH TI RAPID IDENTIFICATION OF HLA-DRW53-POSITIVE SAMPLES BY A GENERIC DRB-PCR AMPLIFICATION WITHOUT FURTHER ANALYSIS SO TISSUE ANTIGENS LA English DT Note DE MHC; CLASS-II; DRW53; PCR; PSEUDOGENES ID MAJOR HISTOCOMPATIBILITY COMPLEX; BETA-GENES; DNA; CHAIN; POLYMERASE C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. AMER RED CROSS BLOOD SERV,DEDHAM,MA. RP YUNIS, JJ (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02155, USA. NR 27 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 JUL PY 1992 VL 40 IS 1 BP 41 EP 44 DI 10.1111/j.1399-0039.1992.tb01956.x PG 4 WC Cell Biology; Immunology; Pathology SC Cell Biology; Immunology; Pathology GA JE108 UT WOS:A1992JE10800007 PM 1440560 ER PT J AU LEAHY, D KINK, J BYRNE, R SHAH, D PREISELSIMMONS, B LASKA, S DIENSTAG, J THOMAS, H KARAYIANNIS, P BROWN, J ARIMA, T MAEDA, E TODD, J AF LEAHY, D KINK, J BYRNE, R SHAH, D PREISELSIMMONS, B LASKA, S DIENSTAG, J THOMAS, H KARAYIANNIS, P BROWN, J ARIMA, T MAEDA, E TODD, J TI IMPROVED SEROLOGIC DETECTION OF HEPATITIS-C VIRUS WITH A PARAMAGNETIC MICROPARTICLE ASSAY USING MULTIPLE ANTIGENIC SEQUENCES SO TRANSFUSION LA English DT Article ID NON-B-HEPATITIS; NON-A-HEPATITIS; POLYMERASE CHAIN-REACTION; POSTTRANSFUSION HEPATITIS; RIBONUCLEIC-ACID; CAPSID PROTEIN; ANTIBODIES; INFECTION; AMPLIFICATION; CHIMPANZEES AB A paramagnetic microparticle (MP) assay for antibody to hepatitis C virus (anti-HCV) was developed, in which the probe for antibody consisted of synthetic peptides corresponding to HCV capsid and nonstructural c-100 regions, as well as a recombinant protein corresponding to the nonstructural c33c region. Assay performance was evaluated by testing serum from 108 geographically diverse patients with non-A, non-B hepatitis (NANBH). The frequency of anti-HCV reactivity detected with the MP assay and with an enzyme-linked immunosorbent assay (ELISA) for c-100 was 91 and 70 percent, respectively. All c-100 HCV ELISA-reactive specimens also reacted on the MP assay. In addition, anti-HCV seroconversion in three plasma donors was detected one to two blood collection dates earlier by the MP assay than by the c-100 HCV ELISA and at similar blood collection dates by the MP assay and a second-generation anti-HCV ELISA. Serologic responses to the three distinct antigenic regions of HCV in NANBH patients varied: reactivity to all three antigens was most common (49%), reactivity to both capsid and c33c (40%) was next most common, and single-antigen reactivity was rare (4%). MP assay reactivity of 825 volunteer donors was 0.1 percent. These results demonstrate both the utility of additional HCV antigens for an effective anti-HCV screening assay and the application of paramagnetic MP technology to serologic testing for HCV infection. C1 MASSACHUSETTS GEN HOSP,MED SERV,GASTROENTEROL UNIT,BOSTON,MA 02114. KAGOSHIMA UNIV,DEPT INTERNAL MED 2,KAGOSHIMA 890,JAPAN. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV LONDON IMPERIAL COLL SCI TECHNOL & MED,ST MARYS HOSP,SCH MED,DEPT MED,LONDON SW7 2AZ,ENGLAND. BAXTER DIAGNOST INC,PANDEX DIV,MUNDELEIN,IL 60060. NR 27 TC 3 Z9 3 U1 0 U2 2 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD JUL-AUG PY 1992 VL 32 IS 6 BP 548 EP 553 DI 10.1046/j.1537-2995.1992.32692367199.x PG 6 WC Hematology SC Hematology GA JJ564 UT WOS:A1992JJ56400011 PM 1323886 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI INSULINOTROPIC GLUCAGON-LIKE PEPTIDE-I(7-37)/(7-36)AMIDE - A NEW INCRETIN HORMONE SO TRENDS IN ENDOCRINOLOGY AND METABOLISM LA English DT Review ID GASTRIC-INHIBITORY POLYPEPTIDE; PERFUSED RAT PANCREAS; PEPTIDE-I; ADENYLATE-CYCLASE; GENE-EXPRESSION; RINM5F CELLS; 7-36 AMIDE; PEPTIDE-1(7-36)AMIDE; SECRETION; RECEPTORS AB Intestinal peptide hormones, released into circulation in response to a meal, are important augmentors of the postprandial insulin release stimulated by absorbed nutrients. In this "incretin concept" glucagon-like peptide I(7-37) plays a major role because it is the most powerful glucose-dependent insulin secretagogue described so far. Glucagonlike peptide 1(7-37) also stimulates proinsulin gene expression and proinsulin biosynthesis in insulinoma cells, and it may be involved in the regulation of the intracellular insulin pool of the B cell. Recent studies show elevated levels of glucagonlike peptide 1(7-37) in patients with non-insulin-dependent diabetes mellitus. The physiology and pathophysiology of the enteroinsular axis is a promising field of basic and clinical research that has a relevance to diabetes mellitus. RP FEHMANN, HC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. NR 50 TC 55 Z9 55 U1 1 U2 3 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1043-2760 J9 TRENDS ENDOCRIN MET JI Trends Endocrinol. Metab. PD JUL PY 1992 VL 3 IS 5 BP 158 EP 163 DI 10.1016/1043-2760(92)90165-W PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JB092 UT WOS:A1992JB09200002 PM 18407095 ER PT J AU PICKLES, JO COREY, DP AF PICKLES, JO COREY, DP TI MECHANOELECTRICAL TRANSDUCTION BY HAIR-CELLS SO TRENDS IN NEUROSCIENCES LA English DT Review ID GUINEA-PIG COCHLEA; INNER-EAR; CROSS-LINKS; TIP LINKS; STEREOCILIA; BUNDLE; ORGANIZATION; CHICK; SENSITIVITY; ADAPTATION AB Hair cells of the inner ear are one of nature's great success stories, appearing early in vertebrate evolution and having a similar form in all vertebrate classes. They are specialized columnar epithelial cells, with an array of modified microvilli or stereocilia on their apical surface, interconnected by a series of linkages. The mechanical stimulus causes deflection of the stereocilia, stretching linkages between them, and opening the mechanotransducer channels. On a slower timescale, hair cells adapt in order to maintain optimum sensitivity, with an adaptation motor within the stereocilia acting to keep the resting tension on channels constant. C1 MASSACHUSETTS GEN HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP PICKLES, JO (reprint author), UNIV QUEENSLAND,CTR VIS TOUCH & HEARING RES,DEPT PHYSIOL & PHARMACOL,BRISBANE,QLD 4072,AUSTRALIA. OI Corey, David/0000-0003-4497-6016 NR 47 TC 128 Z9 132 U1 1 U2 10 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, OXON, ENGLAND OX5 1GB SN 0166-2236 J9 TRENDS NEUROSCI JI Trends Neurosci. PD JUL PY 1992 VL 15 IS 7 BP 254 EP 259 DI 10.1016/0166-2236(92)90066-H PG 6 WC Neurosciences SC Neurosciences & Neurology GA HZ488 UT WOS:A1992HZ48800011 PM 1381121 ER PT J AU WARD, VK MARRIOTT, AC POLYZONI, T ELGHORR, AA ANTONIADIS, A NUTTALL, PA AF WARD, VK MARRIOTT, AC POLYZONI, T ELGHORR, AA ANTONIADIS, A NUTTALL, PA TI EXPRESSION OF THE NUCLEOCAPSID PROTEIN OF DUGBE VIRUS AND ANTIGENIC CROSS-REACTIONS WITH OTHER NAIROVIRUSES SO VIRUS RESEARCH LA English DT Article DE DUGBE VIRUS; BACULOVIRUS EXPRESSION; NAIROVIRUS CROSS-REACTIVITY ID S-RNA; BUNYAVIRIDAE; GENUS AB The small (S) RNA segment of Dugbe (DUG) virus (Nairovirus, Bunyaviridae) encodes a single protein, the nucleocapsid (N) protein, of M(r) 49.4 kDa. cDNA derived from the complete coding region for the N protein was cloned into Autographa californica nuclear polyhedrosis virus (AcNPV) under control,of the polyhedrin promoter and used to infect Spodoptera frugiperda insect cells. Western blotting analysis using monoclonal antibodies demonstrated the production of DUG N protein in the infected cells. Monoclonal and polyclonal antibodies to the N protein of Crimean-Congo haemorrhagic fever (CCHF) virus were found to cross-react weakly with the baculovirus expressed DUG N protein by Western blotting. When used in an enzyme linked immunoassay (ELISA), the DUG N protein reacted with polyclonal mouse immune ascitic fluids raised against either CCHF or Hazara viruses (both members of the CCHF serogroup of nairoviruses). Cross-reactions between DUG virus (Nairobi sheep disease serogroup) and members of other nairovirus serogroups were not detected. C1 NERC,INST VIROL & ENVIRONM MICROBIOL,MANSFIELD RD,OXFORD OX1 3SR,ENGLAND. UNIV CALIF DAVIS,DEPT ENTOMOL,DAVIS,CA 95616. ARISTOTELIAN UNIV SALONIKA,SCH MED,DEPT MICROBIOL,ARBOVIRUS NATL REFERENCE LAB,SALONIKA,GREECE. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02115. RI Nuttall, Pat/I-6142-2012 OI Nuttall, Pat/0000-0002-0385-8294 NR 11 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0168-1702 J9 VIRUS RES JI Virus Res. PD JUL PY 1992 VL 24 IS 2 BP 223 EP 229 DI 10.1016/0168-1702(92)90009-X PG 7 WC Virology SC Virology GA JD514 UT WOS:A1992JD51400009 PM 1529645 ER PT J AU BOTFIELD, MC JANCSO, A WEISS, MA AF BOTFIELD, MC JANCSO, A WEISS, MA TI BIOCHEMICAL-CHARACTERIZATION OF THE OCT-2 POU DOMAIN WITH IMPLICATIONS FOR BIPARTITE DNA RECOGNITION SO BIOCHEMISTRY LA English DT Article ID BACTERIOPHAGE-T7 RNA-POLYMERASE; OCTAMER-BINDING PROTEINS; TRANSCRIPTION FACTOR; ANTENNAPEDIA HOMEODOMAIN; STIMULATE TRANSCRIPTION; CAENORHABDITIS-ELEGANS; IMMUNOGLOBULIN GENES; PROMOTER INVITRO; HELA-CELLS; STEM-CELLS AB B-cell specific regulation of immunoglobulin gene expression provides a model for the interaction of promoter and enhancer elements with eukaryotic sequence-specific DNA binding proteins. A critical element of this system, the octamer site (5'-ATGCAAAT-3'), is recognized by the B-cell transcription factor Oct-2. Octamer recognition is mediated by the POU domain, a conserved structural motif which-like the zinc finger and leucine zipper-defines a family of related transcription factors. Homologies among POU sequences suggest a bipartite structure, consisting of an N-terminal POU-specific subdomain and C-terminal variant homeodomain connected by a linker of variable length and sequence. As a first step toward a molecular understanding of the Oct-2 POU domain and its mechanism of DNA recognition, we have overexpressed in Escherichia coli the intact POU domain and subdomains as thrombin-cleavable fusion proteins and have purified these fragments to homogeneity following digestion with thrombin. Biochemical and biophysical characterization yields the following results. (i) The intact POU domain (166 residues) is monomeric and exhibits high-affinity octamer-specific DNA-binding activity. (ii) Limited proteolytic digestion demonstrates that the POU domain contains two proteolytically stable subdomains (the POU-specific subdomain and the variant homeodomain) connected by a proteolytically sensitive linker. (iii) The isolated subdomains are each monomeric and do not interact to form noncovalent heterodimers. (iv) Unlike the intact POU domain, the isolated subdomains do not exhibit high-affinity binding to the octamer DNA site, nor is DNA binding restored by mixing the two isolated subdomains. (v) Circular dichroism studies demonstrate that the intact POU-specific region and homeodomain each contain substantial alpha-helix and exhibit cooperative folding/unfolding transitions. The alpha-helix content of the intact POU region is equal to the sum of the alpha-helix content of the two subdomains. (vi) H-1-NMR spectra of the isolated subdomains are additive to yield a spectra that is nearly identical to that of the parent POU domain. Together, these results confirm the bipartite structure of the POU domain and the existence of the POU-specific and variant homeo-subdomains as autonomous structural units. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. FU NCRR NIH HHS [1S10RR04862-01]; NIGMS NIH HHS [GM45290] NR 58 TC 38 Z9 38 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD JUN 30 PY 1992 VL 31 IS 25 BP 5841 EP 5848 DI 10.1021/bi00140a020 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JB211 UT WOS:A1992JB21100020 PM 1610826 ER PT J AU PATHAK, MA FITZPATRICK, TB AF PATHAK, MA FITZPATRICK, TB TI THE EVOLUTION OF PHOTOCHEMOTHERAPY WITH PSORALENS AND UVA (PUVA) - 2000 BC TO 1992 AD SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY LA English DT Review DE HISTORY OF PSORALENS; PUVA; PHOTOCHEMOTHERAPY; PSORIASIS; VITILIGO; RETINOIDS; PHOTOPHERESIS; PHOTOCHEMOPROTECTION ID ORAL METHOXSALEN-PHOTOCHEMOTHERAPY; T-CELL LYMPHOMA; 5-METHOXYPSORALEN BERGAPTEN; CROSS-LINKING; PSORIASIS; DNA; 8-METHOXYPSORALEN; LIGHT; PHOTOPHERESIS AB The therapeutic uses of naturally occurring psoralens in modern-day medicine (8-methoxypsoralen (8-MOP), 5-methoxypsoralen (5-MOP), 4,5',8-trimethylpsoralen, and a few other synthetic psoralens) have evolved through five stages of development. (1) In the historical period (2000 BC to 1930 AD), the pigment-stimulating properties of naturally occurring plants containing psoralens were described anecdotally. (2) The second period (1930-1960) dealing with the chemistry of psoralens involved extraction, identification of their structure, synthesis, and the relationship between chemical structure and their photoreactivity and pigment-stimulating properties. The treatment of vitiligo with oral and topical 8-MOP became popular. (3) In the third period (1960-1974), we witnessed a new beginning and the growth of basic science studies and clinical investigations into various biological properties of psoralens including action spectrum studies, mutagenesis and carcinogenesis studies, in vitro and in vivo photoreactivity studies of various psoralens with DNA, RNA, proteins, and pharinacological and toxicological studies in vitiligo patients undergoing long-term therapy for repigmentation. (4) The fourth period (1974-1988) is recognized as the period of photochemotherapy and the development of the science of photomedicine which established the therapeutic effectiveness of psoralens in combination with newly developed UV irradiation systems that emitted high-intensity UVA radiation in the treatment of severe psoriasis, mycosis fungoides, and over 16 other skin diseases. The effectiveness of PUVA (psoralen + UVA) was confirmed by well controlled clinical trials in thousands of patients, both in the USA and in European countries. Combination therapy with oral retinoids and PUVA contributed to greater effectiveness and long-term safety of psoralen photochemotherapy. (5) In the fifth period (1989 and beyond), psoralens are now emerging as photochemoprotective agents against non-melanoma skin cancers and as immunologic modifiers in the management of certain patients with disorders of circulating T-cells using new techniques of photopheresis. In the final analysis, perhaps the application of pharmacological and therapeutic concepts and principles of using psoralens in combination with UVA has contributed to the development of a new science of photomedicine in which the interaction between basic scientists, photobiologists, and physicians has produced both basic and new clinical knowledge for the care and control of human suffering. RP PATHAK, MA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [R01-CA-05003-32] NR 80 TC 131 Z9 137 U1 0 U2 17 PU ELSEVIER SCIENCE SA LAUSANNE PI LAUSANNE 1 PA PO BOX 564, 1001 LAUSANNE 1, SWITZERLAND SN 1011-1344 J9 J PHOTOCH PHOTOBIO B JI J. Photochem. Photobiol. B-Biol. PD JUN 30 PY 1992 VL 14 IS 1-2 BP 3 EP 22 PG 20 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JH316 UT WOS:A1992JH31600002 PM 1432383 ER PT J AU CARBONARE, MD PATHAK, MA AF CARBONARE, MD PATHAK, MA TI SKIN PHOTOSENSITIZING AGENTS AND THE ROLE OF REACTIVE OXYGEN SPECIES IN PHOTOAGING SO JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY LA English DT Article DE PHOTOAGING; COLLAGEN CROSS-LINKS; UV RADIATION; FREE RADICALS; SINGLET OXYGEN; SUPEROXIDE ANION; PSORALENS; PORPHYRINS; RIBOFLAVIN ID HAIRLESS MOUSE SKIN; BIOCHEMICAL-CHANGES; VISIBLE CHANGES; CROSS-LINKING; ULTRAVIOLET; RADIATION; PROTEINS; CLEAVAGE; COLLAGEN; MICE AB In this paper, the role of reactive oxygen species in photoaging is presented. Many photosensitizing agents are known to generate reactive oxygen species (singlet oxygen (O-1(2)), superoxide anion (O2.-) and .OH radicals). Although photoaging (dermatoheliosis) of human skin is caused by UVB and UVA radiation, the hypothesis tested here in the pathogenesis of photoaging of human skin is the free radical theory involving the generation of reactive oxygen species by UVA (320-400 nm) radiation and their damaging oxidative effects on cutaneous collagen and other model proteins. The UVA-generated reactive oxygen species cause cross-linking of proteins (eg. collagen), oxidation of sulfydryl groups causing disulfide cross-links, oxidative inactivation of certain enzymes causing functional impairment of cells (fibroblasts, keratinocytes, melanocytes, Langerhans cells) and liberation of proteases, collagenase and elastase. The skin-damaging effects of UVA appear to result from type II, oxygen-mediated photodynamic reactions in which UVA or near-UV radiation in the presence of certain photosensitizing chromophores (eg, riboflavin, porphyrins, nicotinamide adenine dinucleotide phosphate (NADPH), etc.) leads to the formation of reactive oxygen species (O-1(2), O2.-,.OH). Four specific observations are presented to illustrate the concept: (1) the production of O-1(2), and O2.- by UVB, UVA and UVA plus photosensitizing agents (such as riboflavin, porphyrin and 3-carbethoxypsoralens) as a function of UV exposure dose, the sensitizer concentration and the pH of the irradiated solution; (2) the formation of protein cross-links in collagen, catalase and superoxide dismutase by O-1(2) and O2.- (.OH) and the resulting denaturation of proteins and enzyme activities as a function of UVA exposure dose; (3) the protective role of selective quenchers of O-1(2) and O2.-(e.g. alpha-tocopherol acetate, beta-carotene, sodium azide, ascorbic acid, etc.) against the photoinactivation of enzymes and the prevention of the protein cross-linking reaction; (4) the possible usefulness of certain antioxidants or quenchers that interact with the UVA-induced generation of reactive oxygen species in the amelioration of the process of photoaging. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. FU NCI NIH HHS [R01-CA-05003-32] NR 41 TC 85 Z9 86 U1 1 U2 13 PU ELSEVIER SCIENCE SA LAUSANNE PI LAUSANNE 1 PA PO BOX 564, 1001 LAUSANNE 1, SWITZERLAND SN 1011-1344 J9 J PHOTOCH PHOTOBIO B JI J. Photochem. Photobiol. B-Biol. PD JUN 30 PY 1992 VL 14 IS 1-2 BP 105 EP 124 DI 10.1016/1011-1344(92)85086-A PG 20 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JH316 UT WOS:A1992JH31600008 PM 1331386 ER PT J AU BUZZI, MG DIMITRIADOU, V THEOHARIDES, TC MOSKOWITZ, MA AF BUZZI, MG DIMITRIADOU, V THEOHARIDES, TC MOSKOWITZ, MA TI 5-HYDROXYTRYPTAMINE RECEPTOR AGONISTS FOR THE ABORTIVE TREATMENT OF VASCULAR HEADACHES BLOCK MAST-CELL, ENDOTHELIAL AND PLATELET ACTIVATION WITHIN THE RAT DURA-MATER AFTER TRIGEMINAL STIMULATION SO BRAIN RESEARCH LA English DT Article DE 5-HYDROXYTRYPTAMINE; DIHYDROERGOTAMINE; MAST CELL; MIGRAINE; NEUROGENIC INFLAMMATION; SUMATRIPTAN ID NEUROGENIC PLASMA EXTRAVASATION; SUBSTANCE-P; MIGRAINE HEADACHE; ERGOT ALKALOIDS; BLOOD-VESSELS; RELEASE; NERVE; VASODILATION; NOCICEPTORS; MECHANISMS AB Antidromic stimulation of small caliber trigeminal axons causes neurogenic inflammation in the dura mater and tongue as evidenced by marked increases in mast cell activation, protein extravasation, as well as in the numbers of endothelial cytoplasmic vesicles, endothelial microvilli and platelet aggregates within ipsilateral post-capillary venules. In this report, we examined the effects of pretreatment with serotonin1 receptor agonists, dihydroergotamine (50-mu-g/kg, i.v.) and sumatriptan (100-mu-g/kg, i.v.) on the light and electron microscopic changes which develop after trigeminal ganglion stimulation. Both dihydroergotamine and sumatriptan are useful in the acute treatment of vascular headaches and bind with high affinity to 5-HT1D receptors. Both drugs decreased significantly the number of dural vessels showing endothelial or platelet changes and the numbers of activated mast cells, but did not affect the neurogenic response in the tongue. The drugs also blocked the accumulation of horseradish peroxidase reaction product within the endothelium and perivascular space on the stimulated side. The receptor is not present on trigeminovascular fibers innervating extracranial cephalic tissues. Drug mechanism probably involves inhibition of a proximal step in the pathophysiological cascade (e.g., via activation of a prejunctional receptor) because (a) receptors for sumatriptan have not been identified on mast cells whereas the inflammatory response was attenuated in mast cells as well as within platelets and the endothelium and (b) previous work indicates that sumatriptan and dihydroergotamine block neurotransmitter release. Hence, constriction of vascular smooth muscle mediated by postjunctional 5-hydroxytryptamine receptors is unlikely to explain the anti-inflammatory actions of dihydroergotamine or sumatriptan reported here. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. TUFTS UNIV,SCH MED,DEPT PHARMACOL,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Theoharides, Theoharis/E-5596-2010 FU NINDS NIH HHS [NS21558] NR 53 TC 72 Z9 75 U1 0 U2 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0006-8993 J9 BRAIN RES JI Brain Res. PD JUN 26 PY 1992 VL 583 IS 1-2 BP 137 EP 149 PG 13 WC Neurosciences SC Neurosciences & Neurology GA JD615 UT WOS:A1992JD61500014 PM 1324091 ER PT J AU HAHN, WC MENU, E BOTHWELL, ALM SIMS, PJ BIERER, BE AF HAHN, WC MENU, E BOTHWELL, ALM SIMS, PJ BIERER, BE TI OVERLAPPING BUT NONIDENTICAL BINDING-SITES ON CD2 FOR CD58 AND A 2ND LIGAND CD59 SO SCIENCE LA English DT Article ID T-CELL ACTIVATION; THYMIC EPITHELIAL-CELLS; MEMBRANE-PROTEIN; SURFACE LIGAND; RECEPTOR CD2; LFA-3; COMPLEMENT; ANTIGEN; EXPRESSION; MOLECULES AB The interaction of the T cell glycoprotein CD2 with one ligand, CD58, contributes to T cell function. We have identified CD59, a glycoprotein with complement-inhibitory function, as a second physiological ligand for CD2. Antibodies to CD59 inhibit CD2-dependent T cell activation in murine T cell hybridomas expressing human CD2. In an in vitro binding assay with purified CD58 and CD59, CD2+ cells bind not only immobilized CD58 but also CD59. With two complementary approaches, it was demonstrated that the binding sites on CD2 for CD58 and CD59 are overlapping but nonidentical. These observations suggest that direct interactions between CD2 and both CD58 and CD59 contribute to T cell activation and adhesion. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. OKLAHOMA MED RES FDN,CARDIOVASC BIOL RES PROGRAM,OKLAHOMA CITY,OK 73104. OKLAHOMA STATE UNIV,HLTH SCI CTR,DEPT MICROBIOL & IMMUNOL,OKLAHOMA CITY,OK 73104. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. YALE UNIV,SCH MED,IMMUNOBIOL SECT,NEW HAVEN,CT 06510. RI MENU, Elisabeth/B-2886-2010 OI MENU, Elisabeth/0000-0001-8844-9328 FU NHLBI NIH HHS [HL36061]; NIAID NIH HHS [AI28554] NR 37 TC 167 Z9 169 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JUN 26 PY 1992 VL 256 IS 5065 BP 1805 EP 1807 DI 10.1126/science.1377404 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JA434 UT WOS:A1992JA43400032 PM 1377404 ER PT J AU FAUSTMAN, D LI, XP LIN, HY HUANG, R GUO, J AF FAUSTMAN, D LI, XP LIN, HY HUANG, R GUO, J TI EXPRESSION OF INTRA-MHC TRANSPORTER (HAM) GENES AND CLASS-I ANTIGENS IN DIABETES-SUSCEPTIBLE NOD MICE - RESPONSE SO SCIENCE LA English DT Article C1 MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. MASSACHUSETTS GEN HOSP,MED SERV,CHARLESTON,MA 02129. RP FAUSTMAN, D (reprint author), MASSACHUSETTS GEN HOSP,DIABET UNIT,IMMUNOBIOL LAB,CHARLESTON,MA 02129, USA. NR 6 TC 16 Z9 16 U1 0 U2 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD JUN 26 PY 1992 VL 256 IS 5065 BP 1830 EP 1831 DI 10.1126/science.256.5065.1830 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JA434 UT WOS:A1992JA43400041 PM 17743036 ER PT J AU YAMADA, K GONCALVES, E KAHN, CR SHOELSON, SE AF YAMADA, K GONCALVES, E KAHN, CR SHOELSON, SE TI SUBSTITUTION OF THE INSULIN-RECEPTOR TRANSMEMBRANE DOMAIN WITH THE C-NEU/ERBB2 TRANSMEMBRANE DOMAIN CONSTITUTIVELY ACTIVATES THE INSULIN-RECEPTOR KINASE INVITRO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID GROWTH-FACTOR RECEPTOR; MIMICS LIGAND INDUCTION; FMS PROTO-ONCOGENE; POINT MUTATION; CYTOPLASMIC DOMAIN; TYROSINE KINASE; NEU ONCOGENE; MONOCLONAL-ANTIBODIES; STRUCTURAL BASIS; BETA-SUBUNIT AB To examine the role of the transmembrane domain (TM) of the insulin receptor in insulin-induced receptor kinase activation, we prepared four mutated insulin receptors: 1) a Val938 --> Asp substitution (IR/TM(V-->D)), 2) insertion of a 3-amino acid repeat (Val938-Phe939-Leu940) (IR/TM+3), or the entire TM was replaced by the corresponding domain of either the 3) platelet-derived growth factor (PDGF) receptor (IR/TM(PDGFR)) or 4) c-neu/erbB2 proto-oncogene product (IR/TM(c-neu)). Each mutant receptor was stably expressed in Chinese hamster ovary cells, assessed by fluorescence-activated cell sorting, insulin binding, and biosynthetic labeling. All mutant receptors exhibited normal affinity for insulin. Pulse-chase experiments showed that each proreceptor was processed into alpha- and beta-subunits, although the rate of IR/TM(V-->D) conversion was reduced almost-equal-to 3-fold. With IR/TM(PDGFR), IR/TM(V-->D), and IR/TM+3 basal and insulin-stimulated levels of autophosphorylation and tyrosine kinase activation were normal, both in wheat germ agglutinin (WGA)-purified receptor preparations and intact cells. By contrast, following WGA purification or isolation of crude membranes, IR/TM(c-neu) was a constitutively active autokinase and substrate kinase in vitro. However, in intact cells insulin-stimulated autophosphorylation and kinase activity appeared normal. We conclude that although there is considerable latitude in acceptable structure, residues within the insulin receptor transmembrane domain can play a functional role in regulation of insulin receptor tyrosine kinase activity. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. FU NIDDK NIH HHS [DK31036, DK36836] NR 62 TC 39 Z9 39 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 12452 EP 12461 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300015 PM 1352286 ER PT J AU METZ, SA RABAGLIA, ME PINTAR, TJ AF METZ, SA RABAGLIA, ME PINTAR, TJ TI SELECTIVE INHIBITORS OF GTP SYNTHESIS IMPEDE EXOCYTOTIC INSULIN RELEASE FROM INTACT RAT ISLETS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MOUSE PANCREATIC-ISLETS; PROTEIN-KINASE-C; GUANINE-NUCLEOTIDES; ADENYLATE-CYCLASE; MYCOPHENOLIC-ACID; LIPOXYGENASE INHIBITORS; ARACHIDONIC-ACID; MAMMALIAN-CELLS; PHOSPHOLIPASE-C; HUMAN-PLATELETS AB To investigate whether GTP concentrations can be a regulatory step in exocytotic hormone secretion, we treated isolated rat islets with mycophenolic acid (MPA) or mizoribine, two selective inhibitors of de novo GTP synthesis. When islets were cultured over-night in purine-free medium containing the drug, MPA reduced GTP levels by up to 81 +/- 1%; guanine circumvented this block via the nucleotide "salvage" pathway. MPA concomitantly inhibited glucose (16.7 mM)-induced insulin secretion in batch-type incubations (or perifusions), by up to 68% at 50-mu-g/ml. Although the inhibition of secretion occurred over a similar concentration range as the reduction in total GTP content, the two variables were not directly correlated. However, the secretory effects also were prevented by adding guanine, but not hypoxanthine or xanthine, to the culture medium. Similar results for GTP content and insulin release were seen using mizoribine. Insulin content was modestly (-18%) reduced by MPA but indices of fractional release (release/insulin content) were also markedly impaired. Although MPA also reduced ATP levels more modestly (-39%) and increased UTP (+87%), these were not the cause of the secretory defect since adenine restored ATP and UTP nearly to normal, but did not alter the reduction in GTP content or insulin secretion. MPA also inhibited secretion induced by amino acid or by a phorbol ester but had virtually no effect on release induced by a depolarizing concentration of K+, suggesting that GTP depletion does not merely impede Ca+ influx or directly block Ca2+-activated exocytosis. However, a severe reduction of GTP content did not prevent the pertussis toxin-sensitive inhibition of insulin release induced by epinephrine, suggesting that the function of heterotrimeric GTP-binding proteins is not limited by ambient GTP concentrations. Although these studies do not elucidate the exact site(s) in the exocytotic cascade which depend on intact GTP stores, they do provide the first direct evidence that GTP is required (and can be rate limiting) for insulin release. C1 UNIV WISCONSIN,ENDOCRINOL SECT,MADISON,WI 53792. UNIV WISCONSIN,DEPT MED,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. FU NIDDK NIH HHS [DK-HL07389-11, DK 37312] NR 75 TC 75 Z9 75 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 12517 EP 12527 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300025 PM 1352288 ER PT J AU CHOY, LN ROSEN, BS SPIEGELMAN, BM AF CHOY, LN ROSEN, BS SPIEGELMAN, BM TI ADIPSIN AND AN ENDOGENOUS PATHWAY OF COMPLEMENT FROM ADIPOSE-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID TUMOR-NECROSIS-FACTOR; SERINE PROTEASE HOMOLOG; FACTOR-B; ALTERNATIVE PATHWAY; GENE-EXPRESSION; HORMONAL-REGULATION; HUMAN-FIBROBLASTS; HUMAN-MONOCYTES; MESSENGER-RNA; FACTOR-ALPHA AB The alternative complement pathway is best known for its role in humoral suppression of infectious agents. We have previously shown that adipose cells synthesize adipsin, the mouse homolog of human complement factor D, and that the synthesis of this protein is reduced in several rodent models of obesity. We show here that adipose cells and adipose tissue also synthesize two other essential components of the alternative pathway of complement, factors C3 and B, and activate the proximal portion of this pathway. This activation occurs in the absence of infectious agents and without triggering the terminal, lytic part of this pathway. We demonstrate the production in vitro of several polypeptides characteristic of complement activation that are known to have potent biological activities, including the anaphylatoxin C3a. Cultured adipocytes require stimulation with cytokines to activate complement, while explanted adipose tissue has no such requirement. The adipose tissue from obese mice is deficient in this localized activation of the alternative pathway. These results indicate that complement activation occurs in a localized site, adipose tissue, in normal mice and is impaired in a state of metabolic dysfunction. This suggests a novel function for the proximal portion of this complement pathway related to adipose cell biology or energy balance. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP CHOY, LN (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 46 TC 225 Z9 230 U1 0 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 12736 EP 12741 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300055 PM 1618777 ER PT J AU VALLEJO, M MILLER, CP HABENER, JF AF VALLEJO, M MILLER, CP HABENER, JF TI SOMATOSTATIN GENE-TRANSCRIPTION REGULATED BY A BIPARTITE PANCREATIC-ISLET D-CELL-SPECIFIC ENHANCER COUPLED SYNERGETICALLY TO A CAMP RESPONSE ELEMENT SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ALPHA-SUBUNIT GENE; PROTEIN-BINDING DOMAINS; CYCLIC-AMP; PROMOTER ELEMENT; CONTROL REGION; MESSENGER-RNA; GLUCAGON GENE; MAMMALIAN-CELLS; DNA ELEMENTS; EXPRESSION AB The insulin-, glucagon-, and somatostatin-producing cells in the pancreatic islets derive from a common precursor stem cell and differentiate sequentially during embryonic development, thereby providing an informative model for the study of the transcriptional mechanisms involved in the control of cell-specific gene expression. Relative to the early expression of the glucagon and insulin genes on embryonic days 10 and 12, respectively, the expression of the somatostatin gene is delayed (day 17). The relatively late expression of the somatostatin gene indicates the involvement of both negative and positive transcriptional control mechanisms. We show that the expression of the somatostatin gene in pancreatic islet cells is accomplished by the interplay of both positive and negative cis-regulatory DNA elements. We have characterized the functional properties of one of these positive control elements, the somatostatin gene upstream enhancer element (SMS-UE). The SMS-UE is a pancreatic islet D-cell-specific transcriptional regulator that acts synergistically with the cyclic AMP response element. Mutation-expression and cell-free transcription analyses show that the SMS-UE is a bipartite element with two interdependent functional domains. Our results indicate that the SMS-UE is part of a functional unit that includes other transcriptional control elements of the somatostatin gene proximal promoter, and that they act together to regulate the D-cell-specific transcription of the somatostatin gene in the islet cells of the pancreas. RP VALLEJO, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK30834, DK30457] NR 59 TC 50 Z9 50 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 12868 EP 12875 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300073 PM 1352291 ER PT J AU VALLEJO, M PENCHUK, L HABENER, JF AF VALLEJO, M PENCHUK, L HABENER, JF TI SOMATOSTATIN GENE UPSTREAM ENHANCER ELEMENT ACTIVATED BY A PROTEIN COMPLEX CONSISTING OF CREB, ISL-1-LIKE, AND ALPHA-CBF-LIKE TRANSCRIPTION FACTORS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-SPECIFIC EXPRESSION; DNA-BINDING PROTEIN; CAMP RESPONSE ELEMENTS; CYCLIC-AMP; INSULIN GENE; PROMOTER ELEMENT; NUCLEAR FACTORS; GLUCAGON GENE; SUBUNIT GENE; SEQUENCE AB The expression of the genes encoding the hormones glucagon, insulin, somatostatin, and pancreatic polypeptide in the endocrine islets of the pancreas is regulated in a cell-specific manner, defining four distinct cellular phenotypes (A-, B-, D-, and F-cells, respectively). Binding of nuclear proteins to cognate DNA sequences within cis-acting regulatory elements mediates the transcriptional events that result in the cell-specific activation or repression of gene expression. In a parallel study, we describe the functional properties of the SMS-UE, a pancreatic islet D-cell specific enhancer element that regulates the expression of the somatostatin gene and contains two interdependent domains, A and B. In the studies described herein, we have characterized the nuclear proteins that recognize the SMS-UE. Domain A of the SMS-UE is a DNA enhancer sequence that is identical to that bound by the ubiquitously distributed CCAAT box-binding protein alpha-CBF, a transcription factor that regulates the expression of the human chorionic gonadotrophin alpha-subunit gene. The B-domain, on the other hand, binds an islet cell-specific protein with characteristics similar to those of Isl-1, a transcriptional activator protein that binds to the E2 enhancer of the rat insulin-1 gene. In addition, the SMS-UE binds transcription factor CREB but not CREM, the close homolog of CREB, on a site adjacent to, or overlapping, the 3' end of domain B. We show that the carboxyl-terminal bZIP domain of CREB binds to the cAMP response element of the somatostatin gene but is not sufficient for binding to the SMS-UE, and we present evidence suggesting that CREB.SMS-UE binding requires stabilization by a region of the protein located within the transactivation domain. RP VALLEJO, M (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK 30457] NR 73 TC 67 Z9 68 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 12876 EP 12884 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300074 PM 1352292 ER PT J AU NAGAYA, T MADISON, LD JAMESON, JL AF NAGAYA, T MADISON, LD JAMESON, JL TI THYROID-HORMONE RECEPTOR MUTANTS THAT CAUSE RESISTANCE TO THYROID-HORMONE - EVIDENCE FOR RECEPTOR COMPETITION FOR DNA-SEQUENCES IN TARGET GENES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID C-ERBA PROTOONCOGENES; RAT GROWTH-HORMONE; GLUCOCORTICOID RECEPTOR; GENERALIZED RESISTANCE; NEGATIVE REGULATION; BINDING; BETA; EXPRESSION; PROTEIN; MEDIATE AB Several distinct mutations in the ligand-binding domain of the beta-form of the thyroid hormone receptor have been reported in kindreds with the autosomal dominant syndrome of generalized resistance to thyroid hormone (GRTH). GRTH receptor mutants are functionally inactive but capable of inhibiting normal receptor function in transient expression studies. We examined the possibility that this dominant negative activity of the GRTH mutants involves competition for receptor binding to DNA. Mutations introduced into either the T3 ligand-binding domain (LBD) or into the DNA-binding domain (DBD) of the receptor eliminated the transcriptional activity of the receptor. In cotransfection experiments, the LBD mutants, but not the DBD mutants, inhibited the transcriptional activity of the normal receptor. The inhibitory activity of the LBD mutants was abolished by the introduction of an additional mutation into the DBD, suggesting that the DBD is required for dominant negative activity. A chimeric receptor, in which the DNA-binding domain of the thyroid hormone receptor was exchanged with the homologous region in the glucocorticoid receptor (GTG), was used to study thyroid hormone receptor competition for GTG interactions with thyroid receptor target sequences. In the absence of thyroid hormone, the normal thyroid hormone receptor inhibited dexamethasone stimulated transcription by GTG. The transcriptional activity of GTG was also inhibited by the LBD mutants but not by a DBD mutant of the thyroid hormone receptor. These results indicate that the thyroid hormone receptor mutations that occur in GRTH compete with normal receptors at DNA-binding sites in target genes to block normal receptor function. C1 MASSACHUSETTS GEN HOSP,THYROID UNIT,JACKSON 1021,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD 28138]; NIDDK NIH HHS [DK 42144] NR 48 TC 108 Z9 109 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 25 PY 1992 VL 267 IS 18 BP 13014 EP 13019 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ483 UT WOS:A1992HZ48300092 PM 1618799 ER PT J AU BICK, D FRANCO, B SHERINS, RJ HEYE, B PIKE, L CRAWFORD, J MADDALENA, A INCERTI, B PRAGLIOLA, A MEITINGER, T BALLABIO, A AF BICK, D FRANCO, B SHERINS, RJ HEYE, B PIKE, L CRAWFORD, J MADDALENA, A INCERTI, B PRAGLIOLA, A MEITINGER, T BALLABIO, A TI INTRAGENIC DELETION OF THE KALIG-1 GENE IN KALLMANNS SYNDROME SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Note ID ISOLATED HYPOGONADOTROPIC HYPOGONADISM; DISTAL SHORT ARM; STEROID SULFATASE; X-CHROMOSOME; ANOSMIA; IDENTIFICATION; ICHTHYOSIS; DEFICIENCY; MIGRATION; LINKAGE C1 BAYLOR COLL MED,INST MOLEC GENET,1 BAYLOR PL,HOUSTON,TX 77030. GENET & IVF INST,FAIRFAX,VA. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV MUNICH,KINDER POLIKLIN,PADIATR GENET ABT,W-8000 MUNICH 2,GERMANY. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. RI Meitinger, Thomas/O-1318-2015 FU NICHD NIH HHS [1 RO1 HD-28333-01] NR 37 TC 136 Z9 139 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 JUN 25 PY 1992 VL 326 IS 26 BP 1752 EP 1755 DI 10.1056/NEJM199206253262606 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HZ894 UT WOS:A1992HZ89400006 PM 1594017 ER PT J AU CAVINESS, VS AF CAVINESS, VS TI KALLMANNS SYNDROME - BEYOND MIGRATION SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP CAVINESS, VS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 10 TC 12 Z9 12 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD JUN 25 PY 1992 VL 326 IS 26 BP 1775 EP 1777 DI 10.1056/NEJM199206253262612 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA HZ894 UT WOS:A1992HZ89400012 PM 1594021 ER PT J AU WARSHAW, AL CASTILLO, CF AF WARSHAW, AL CASTILLO, CF TI PANCREATIC-CARCINOMA - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP WARSHAW, AL (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 6 TC 1 Z9 1 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 JUN 25 PY 1992 VL 326 IS 26 BP 1782 EP 1782 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HZ894 UT WOS:A1992HZ89400027 ER PT J AU LEE, JW MORGAN, JR TOMPKINS, RG YARMUSH, ML AF LEE, JW MORGAN, JR TOMPKINS, RG YARMUSH, ML TI THE IMPORTANCE OF PROLINE ON LONG-TERM HEPATOCYTE FUNCTION IN A COLLAGEN GEL SANDWICH CONFIGURATION - REGULATION OF PROTEIN SECRETION SO BIOTECHNOLOGY AND BIOENGINEERING LA English DT Article DE ALBUMIN; TRANSFERRIN; PROLINE; HEPATOCYTES; PRIMARY CULTURE; SERUM FREE; LONG TERM ID ISOLATED RAT HEPATOCYTES; AMINO-ACID DEPRIVATION; PRIMARY CULTURES; LIVER; ALBUMIN; MAINTENANCE; DEGRADATION; EXPRESSION; TOXICITY; HORMONES AB A serum-free culture system for primary hepatocytes which maintains stable high-level hepatocyte function for prolonged periods in culture has been developed. Isolated rat primary hepatocytes were cultured in serum-free media between two layers of gelled collagen in a sandwich configuration which reinstates the cellular polarity necessary for long-term function in vitro. These serum-free hepatocyte cultures maintained near physiological rates of albumin and transferrin secretion for a minimum of 26 days in culture. L-Proline was shown to be critical for both the approach to steady state and maximal level of protein secretion. Analysis of dose-response data gave K(m) values of 2.9 and 17-mu-g/mL for albumin and transferrin secretion, respectively. C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,SURG SERV,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. OI Morgan, Jeffrey/0000-0002-7546-3443 NR 35 TC 22 Z9 22 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0006-3592 J9 BIOTECHNOL BIOENG JI Biotechnol. Bioeng. PD JUN 20 PY 1992 VL 40 IS 2 BP 298 EP 305 DI 10.1002/bit.260400214 PG 8 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HX275 UT WOS:A1992HX27500013 PM 18601116 ER PT J AU JASANOFF, A KOCHOYAN, M FRAENKEL, E LEE, JP WEISS, MA AF JASANOFF, A KOCHOYAN, M FRAENKEL, E LEE, JP WEISS, MA TI AROMATIC AROMATIC INTERACTIONS IN THE ZINC FINGER MOTIF - ANALYSIS OF THE 2-DIMENSIONAL NUCLEAR-MAGNETIC-RESONANCE STRUCTURE OF A MUTANT DOMAIN SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE PROTEIN FOLDING; PROTEIN STABILITY; PROTEIN DNA INTERACTIONS ID TRANSCRIPTION FACTOR-IIIA; PROTEIN ZFY; XENOPUS; CHAINS; MODEL; GENE C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. BIOP POLYTECH,CNRS,URA 32,F-91128 PALAISEAU,FRANCE. NR 30 TC 21 Z9 21 U1 2 U2 2 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0022-2836 J9 J MOL BIOL JI J. Mol. Biol. PD JUN 20 PY 1992 VL 225 IS 4 BP 1035 EP 1047 DI 10.1016/0022-2836(92)90103-Q PG 13 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA JA437 UT WOS:A1992JA43700012 PM 1613788 ER PT J AU HU, H CHRISTIANI, D AF HU, H CHRISTIANI, D TI REACTIVE AIRWAYS DYSFUNCTION AFTER EXPOSURE TO TEARGAS SO LANCET LA English DT Letter ID LEVEL IRRITANT EXPOSURES; PERSISTENT C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. RP HU, H (reprint author), BRIGHAM & WOMENS HOSP,CHANNING LAB,BOSTON,MA 02115, USA. OI Hu, Howard/0000-0002-3676-2707 NR 5 TC 25 Z9 25 U1 0 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD JUN 20 PY 1992 VL 339 IS 8808 BP 1535 EP 1535 DI 10.1016/0140-6736(92)91296-K PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HZ175 UT WOS:A1992HZ17500026 PM 1351200 ER PT J AU DEVEREAUX, R PEARLMAN, A KING, D WEYMAN, A GARDIN, J AF DEVEREAUX, R PEARLMAN, A KING, D WEYMAN, A GARDIN, J TI 3-DIMENSIONAL RECONSTRUCTION - DISCUSSION-VI SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Discussion C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 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 JUN 18 PY 1992 VL 69 IS 20 BP H131 EP H134 PG 4 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HZ517 UT WOS:A1992HZ51700019 ER PT J AU LEVINE, RA WEYMAN, AE HANDSCHUMACHER, MD AF LEVINE, RA WEYMAN, AE HANDSCHUMACHER, MD TI 3-DIMENSIONAL ECHOCARDIOGRAPHY - TECHNIQUES AND APPLICATIONS SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article; Proceedings Paper CT SYMP ON ADVANCES IN ECHOCARDIOGRAPHY : A VIEW TOWARD THE YEAR 2000 CY SEP 12-14, 1991 CL WILLIAMSBURG, VA SP MALLINCKRODT MED ID MITRAL-VALVE PROLAPSE; TWO-DIMENSIONAL ECHOCARDIOGRAPHY; CROSS-SECTIONAL ECHOCARDIOGRAPHY; LEFT-VENTRICULAR VOLUMES; RECONSTRUCTION; DIAGNOSIS; VALIDATION; CHILDREN; ANNULUS; MOTION AB Current echocardiographic devices provide only 2-dimensional views of the heart. To appreciate 3-dimensional structural relations, therefore, requires mental reconstruction of 2-dimensional views by an experienced observer. Our ability to answer new questions about the heart could be increased if 2-dimensional images could be combined to display 3-dimensional relations. Such 3-dimensional reconstruction would permit analysis of structures of unknown or complex shape and the noninvasive quantification of cardiac chamber size and function without making geometric assumptions. To overcome previous limitations, mechanisms have been developed for automated integration of images and positional data during routine echocardiographic scanning, thereby greatly enhancing the efficiency and application of image reconstruction. Refining the diagnosis of mitral valve prolapse has presented a uniquely 3-dimensional problem requiring information previously unavailable from the 2-dimensional technique. To date, 3-dimensional studies have demonstrated that the mitral valve is saddle-shaped in systole, so that apparent superior leaflet displacement in the mediolateral 4-chamber view, often seen in otherwise normal individuals, lies entirely within the bounds defined by the mitral annulus and occurs without leaflet distortion or actual displacement above the entire mitral valve. Other applications of 3-dimensional image reconstruction include calculation of ventricular volume and ejection fraction by transthoracic or transesophageal scanning without geometric assumptions; improving the standardization and accuracy of 2-dimensional measurements by improving spatial appreciation; and 3-dimensional reconstruction of vascular walls to guide interventions. In the future, systems for acquiring multiple views more rapidly by parallel processing and improving endocardial border extraction should allow more routine application of 3-dimensional methods as the next stage in the evolution of cardiac ultrasound, thereby expanding the range of questions that can be answered. Achieving these goals will depend, in large measure, on persistence in developing the necessary technology. RP LEVINE, RA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,CARDIAC ULTRASOUND LAB,FOUNDERS HOUSE 8,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-38176, HL-07535] NR 45 TC 36 Z9 36 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 JUN 18 PY 1992 VL 69 IS 20 BP H121 EP H130 DI 10.1016/0002-9149(92)90656-J PG 10 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HZ517 UT WOS:A1992HZ51700018 PM 1605116 ER PT J AU LAMKIN, JC AZAR, DT MEAD, MD VOLPE, NJ AF LAMKIN, JC AZAR, DT MEAD, MD VOLPE, NJ TI SIMULTANEOUS CORNEAL LACERATION REPAIR, CATARACT REMOVAL, AND POSTERIOR CHAMBER INTRAOCULAR-LENS IMPLANTATION SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID CORNEOSCLERAL LACERATIONS; CHILDREN; INJURY; EYE AB Frequently, patients with lens laceration or traumatic cataract coincident with corneal laceration, or both, must undergo two separate procedures-primary repair of the corneal laceration and secondary lens removal with or without intraocular lens implantation. We performed simultaneous corneal laceration repair, extracapsular cataract extraction, and posterior chamber lens implantation in seven patients with lacerating ocular injuries who met inclusion criteria for this procedure. With average follow-up of 10 1/2 months, all seven patients achieved visual acuity of 20/40 or better with spectacle correction. YAG posterior capsulotomy was the only additional procedure. One patient had macular pigmentation consistent with either traumatic or photic maculopathy. There were no other complications attributable to the surgical procedures. We believe that certain lacerating injuries of the anterior segment are particularly amenable to cataract extraction and lens implantation at the time of primary laceration repair. This approach obviates additional operative and anesthetic risks, while affording more timely visual rehabilitation. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 22 TC 23 Z9 24 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JUN 15 PY 1992 VL 113 IS 6 BP 626 EP 631 PG 6 WC Ophthalmology SC Ophthalmology GA HX952 UT WOS:A1992HX95200002 PM 1598952 ER PT J AU GUYER, DR DAMICO, DJ SMITH, CW AF GUYER, DR DAMICO, DJ SMITH, CW TI SUBRETINAL FIBROSIS AFTER LASER PHOTOCOAGULATION FOR DIABETIC MACULAR EDEMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID FOCAL ARGON-LASER; PHOTO-COAGULATION; NEOVASCULARIZATION AB Seven eyes had subretinal fibrosis after grid laser photocoagulation for diabetic macular edema. The fibrosis caused persistent loss in visual acuity, and in six of the seven eyes, was not associated with detectable laser-induced Bruch's membrane rupture or subretinal hemorrhage. Choroidal neovascularization was detected in only one patient, who was notably younger (27 years) than the median age of 70 years in this series. The median preoperative visual acuity was 20/80 (range, 20/40 to 20/400); the median postoperative visual acuity was 20/400 (range, 20/80 to counting fingers). The subretinal fibrosis was detected at a median of three months (range, 14 days to 4 1/2 months) after laser therapy. In one of five bilaterally treated patients (20%), subretinal fibrosis developed in both eyes. Subretinal fibrosis may be caused by undetected choroidal neovascularization or by excessive proliferation after stimulation of an aged retinal pigment epithelium. Subretinal fibrosis may be a potential cause of loss in visual acuity after laser treatment for diabetic macular edema. C1 MASSACHUSETTS EYE & EAR INFIRM,SERV RETINA,DIABET RETINOPATHY UNIT,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. NR 12 TC 61 Z9 70 U1 0 U2 1 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JUN 15 PY 1992 VL 113 IS 6 BP 652 EP 656 PG 5 WC Ophthalmology SC Ophthalmology GA HX952 UT WOS:A1992HX95200006 PM 1376019 ER PT J AU TINGEY, DP OZMENT, RR SCHROEDER, A EPSTEIN, DL AF TINGEY, DP OZMENT, RR SCHROEDER, A EPSTEIN, DL TI THE EFFECT OF INTRACAMERAL ETHACRYNIC-ACID ON THE INTRAOCULAR-PRESSURE OF LIVING MONKEYS SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article ID AQUEOUS-HUMOR; OUTFLOW AB Previous studies have shown that the sulfhydryl-reactive ethacrynic acid increases outflow facility in living monkeys when perfused via the anterior chamber. To study its potential clinical use further, living monkeys were intracamerally injected with 10-mu-l of ethacrynic acid, with concentrations ranging from 0.5 to 7.5 mmol/l. The fellow control eye was injected with 10-mu-l of diluent. The status of the anterior segment was monitored by slit-lamp biomicroscopy and the intraocular pressure was measured by pneumatonometry with the monkeys anesthetized with ketamine. The anterior segment of living monkeys tolerated injections up to 3.0-mmol/l ethacrynic acid without marked adverse effects. One of 13 monkey eyes injected with 3.0-mmol/l ethacrynic acid demonstrated mild reversible segmental corneal edema. The greatest mean intraocular pressure reduction in the 3.0- to 3.75-mmol/1 group occurred at six hours, with the experimental intraocular pressure decreasing 2.9 mm Hg compared to a mean intraocular pressure increase of 0.1 mm Hg in the control group (n = 19). Concentrations of ethacrynic acid less than 3.0 mmol/1 did not provide reliable reduction of intraocular pressure, whereas concentrations greater than 3.75 mmol/l caused a greater incidence and severity of corneal edema. We believe that the intracameral injection of ethacrynic acid can reliably and safely reduce intraocular pressure in living monkey eyes, and that this drug deserves further investigation as a potential antiglaucomatous agent. C1 UNIV CALIF SAN FRANCISCO,SCH MED,DEPT OPHTHALMOL,10 KIRKHAM ST,K-301,SAN FRANCISCO,CA 94143. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY01894] NR 16 TC 16 Z9 16 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD JUN 15 PY 1992 VL 113 IS 6 BP 706 EP 711 PG 6 WC Ophthalmology SC Ophthalmology GA HX952 UT WOS:A1992HX95200016 PM 1598964 ER PT J AU GELBER, RD LENDERKING, WR COTTON, DJ COLE, BF FISCHL, MA GOLDHIRSCH, A TESTA, MA AF GELBER, RD LENDERKING, WR COTTON, DJ COLE, BF FISCHL, MA GOLDHIRSCH, A TESTA, MA TI QUALITY-OF-LIFE EVALUATION IN A CLINICAL-TRIAL OF ZIDOVUDINE THERAPY IN PATIENTS WITH MILDLY SYMPTOMATIC HIV-INFECTION SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE QUALITY OF LIFE; ZIDOVUDINE; ACQUIRED IMMUNODEFICIENCY SYNDROME; DOSE-RESPONSE RELATIONSHIP, DRUG; HUMAN IMMUNODEFICIENCY VIRUS ID PLACEBO-CONTROLLED TRIAL; ADJUSTED SURVIVAL ANALYSIS; AIDS-RELATED COMPLEX; ADJUVANT THERAPY; BREAST-CANCER; DOUBLE-BLIND; AZT AB Objective: To evaluate the effects of zidovudine therapy in patients with mildly symptomatic HIV infection using Q-TWiST (quality-adjusted: Time Without Symptoms and Toxicity). Design: Analysis of a previously reported multi-center, randomized, placebo-controlled clinical trial. Setting: Thirty-two AIDS Clinical Trial units. Patients: A total of 351 patients with mildly symptomatic HIV infection were assigned to placebo, and 360 patients were assigned to zidovudine, 1200 mg/d. Measurements: A modified Q-TWiST method for comparing treatments based on time spent without severe symptomatic adverse events and without disease progression. Zidovudine and placebo were compared in a threshold utility analysis considering reduction in quality of life associated with adverse events and disease progression. Adverse events defined by laboratory findings were distinguished from findings representing symptomatic events. Results: The incidence of severe symptomatic adverse events was 22.8% for the zidovudine group and 15.1% for the placebo group (P = 0.01), but, as previously reported, zidovudine improved progression-free survival relative to placebo (at 18 months, 91% compared with 81%; P = 0.001). In an 18 month period, patients receiving zidovudine went an average of 14.5 months without disease progression or a severe symptomatic adverse event compared with 14.7 months for placebo. The zidovudine group gained 0.9 months without disease progression but lost 1.1 months due to adverse events. Within the 18-month observation period, treatment provided more Q-TWiST than placebo if the quality of life after HIV disease progression was assumed to be 10% to 20% worse than the quality of life after a severe symptomatic adverse event. Conclusions: The Q-TWiST analysis projects that quality-of-life reductions due to severe symptomatic adverse events might be balanced by the quality-of-life benefits of delayed HIV disease progression for patients who receive zidovudine for mildly symptomatic HIV infection. At currently recommended doses (500 to 600 mg/d half the dose used in this study) zidovudine therapy is likely to yield a more favorable results. C1 HARVARD UNIV,SCH PUBL HLTH,CTR STAT & DATA ANAL,BOSTON,MA 02115. OSPED CIV,DEPT ONCOL,LUGANO,SWITZERLAND. UNIV MIAMI,JACKSON MEM HOSP,SCH MED,DEPT MED,MIAMI,FL 33101. RP GELBER, RD (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,MAYER 432,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [N0-AI-95030] NR 13 TC 76 Z9 76 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 JUN 15 PY 1992 VL 116 IS 12 BP 961 EP 966 PN 1 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HY793 UT WOS:A1992HY79300001 PM 1586104 ER PT J AU POTTS, JT AF POTTS, JT TI RECRUITMENT OF MINORITY PHYSICIANS INTO CAREERS IN INTERNAL-MEDICINE SO ANNALS OF INTERNAL MEDICINE LA English DT Article ID SCHOOLS AB Despite some initial success in the early 1970s, the important goal of increasing the numbers of under-represented minorities in medical school and on medical faculties has stalled short of proportionate representation. To further the current efforts of the Association of Professors in Medicine (APM) and other national medical groups that are devoted to improving the numbers of minorities in medicine, ideas and program information must be shared among institutions. In this spirit, we review our experience at Massachusetts General Hospital. We found that the first step toward this goal must be an institutional commitment based on increased awareness and on special effort focused on housestaff recruitment. Once the numbers of minorities increase, the department chairperson, training program directors, and other involved faculty can work with younger minority physicians; the cooperative relationship thus created can guide the development of a strong minority recruitment program without requiring an undue time commitment from minority trainees and faculty. The APM has a combined goal: to achieve early practical results in individual departments, to play a catalytic role with the community and other national medical organizations, and to increase the number of minorities entering medical school and careers in medicine generally. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP POTTS, JT (reprint author), MASSACHUSETTS GEN HOSP,FRUIT ST,BOSTON,MA 02114, USA. NR 5 TC 6 Z9 6 U1 0 U2 2 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD JUN 15 PY 1992 VL 116 IS 12 BP 1099 EP 1102 PN 2 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA HY794 UT WOS:A1992HY79400016 PM 1586126 ER PT J AU TOWLE, CA WEISSBACH, L TREADWELL, BV AF TOWLE, CA WEISSBACH, L TREADWELL, BV TI ALTERNATIVELY SPLICED ANNEXIN-XI TRANSCRIPTS ENCODE PROTEINS THAT DIFFER NEAR THE AMINO-TERMINUS SO BIOCHIMICA ET BIOPHYSICA ACTA LA English DT Note DE ANNEXIN; CALCIUM PHOSPHOLIPID BINDING PROTEIN; LIPOCORTIN; ALTERNATIVE SPLICING ID SEQUENCES AB Annexins are a family of structurally related calcium-dependent phospholipid binding proteins. We recently described a new member of this family, bovine annexin XI [1]. Two kinds of cDNAs were identified corresponding to annexin XI mRNA variants A and B, which are generated by alternative splicing of identical primary transcripts. Annexin XI isoforms are predicted to differ at the amino-terminus, suggesting that they may have distinct biological roles. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP TOWLE, CA (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED RES LABS,FRUIT ST,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [2 RO1 AR16265-17A3] NR 11 TC 21 Z9 22 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 JUN 15 PY 1992 VL 1131 IS 2 BP 223 EP 226 DI 10.1016/0167-4781(92)90084-D PG 4 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA JC041 UT WOS:A1992JC04100019 PM 1535225 ER PT J AU CHUNG, CK ANTONIADES, HN AF CHUNG, CK ANTONIADES, HN TI EXPRESSION OF C-SIS/PLATELET-DERIVED GROWTH FACTOR-B, INSULIN-LIKE GROWTH FACTOR-I, AND TRANSFORMING GROWTH FACTOR-ALPHA MESSENGER-RNAS AND THEIR RESPECTIVE RECEPTOR MESSENGER-RNAS IN PRIMARY HUMAN GASTRIC CARCINOMAS - INVIVO STUDIES WITH INSITU HYBRIDIZATION AND IMMUNOCYTOCHEMISTRY SO CANCER RESEARCH LA English DT Article ID CELL-LINES; TRANSCRIPTS; SECRETION; DEFINE; GENES; CHAIN; BETA; EGF AB In situ hybridization and immunocytochemistry have been applied to investigate the expression of c-sis/platelet-derived growth factor (PDGF)-B, insulin-like growth factor (IGF)-I, and transforming growth factor-alpha mRNAs and their respective receptor mRNAs in three primary human gastric carcinomas and in their adjacent nonmalignant mucosas. Expression of c-sis/PDGF-B mRNA and PDGF-receptor-beta mRNA was seen in the tumor cells of the three gastric cancer specimens but not in their adjacent nonmalignant mucosa. The mRNA expression was accompanied by the expression of their respective protein products. IGF-I, IGF-I receptor, and epidermal growth factor receptor mRNAs were seen in both the tumor cells of the gastric cancer specimens and in nonmalignant mucosa. Transforming growth factor-alpha mRNA was expressed in gastric tumor cells but not in nonmalignant mucosa. The coexpression of a potent "competence" growth factor, PDGF, and "progression" growth factors, IGF-I and transforming growth factor-alpha, in the tumor cells of gastric carcinomas may contribute to their growth and maintenance. C1 CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. FU NCI NIH HHS [CA30101]; NHLBI NIH HHS [HL29583] NR 27 TC 44 Z9 45 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 JUN 15 PY 1992 VL 52 IS 12 BP 3453 EP 3459 PG 7 WC Oncology SC Oncology GA HY054 UT WOS:A1992HY05400033 PM 1317752 ER PT J AU TSUKAMOTO, T TAKAHASHI, T UEDA, R HIBI, K SAITO, H TAKAHASHI, T AF TSUKAMOTO, T TAKAHASHI, T UEDA, R HIBI, K SAITO, H TAKAHASHI, T TI MOLECULAR ANALYSIS OF THE PROTEIN TYROSINE PHOSPHATASE-GAMMA GENE IN HUMAN LUNG-CANCER CELL-LINES SO CANCER RESEARCH LA English DT Article ID POINT MUTATIONS; P53; HETEROZYGOSITY; ABNORMALITIES; CHROMOSOME-3; INACTIVATION; EXPRESSION; CARCINOMA; FREQUENT; DELETION AB The protein tyrosine phosphatase-gamma (PTP-gamma) gene has recently been suggested as a candidate tumor suppressor gene involved in the oncogenesis of human lung and renal cancers, although no direct evidence for PTP-gamma mutations has been demonstrated thus far. We explored the status of PTP-gamma in 31 human lung cancer cell lines as well as in various other types of human tumor cell lines. Northern blot analysis revealed that two independent cell lines expressed PTP-gamma mRNAs with sizes distinct from those in human fetal and adult normal lung. However, our extensive search for mutations in the PTP-gamma gene failed to identify any abnormalities in the cytoplasmic region, which contains two protein tyrosine phosphatase-like domains. These results warrant further examination of genetic alterations in the extracellular and transmembrane domains of PTP-gamma, which had not been cloned at the time of the present study. C1 AICHI CANC CTR,RES INST,IMMUNOL LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. AICHI CANC CTR,RES INST,CHEMOTHERAPY LAB,CHIKUSA KU,NAGOYA,AICHI 464,JAPAN. NAGOYA UNIV,SCH MED,DEPT SURG 2,SHOWA KU,NAGOYA,AICHI 466,JAPAN. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RI Takahashi, Takashi/I-7262-2014 NR 20 TC 47 Z9 47 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 JUN 15 PY 1992 VL 52 IS 12 BP 3506 EP 3509 PG 4 WC Oncology SC Oncology GA HY054 UT WOS:A1992HY05400044 PM 1596910 ER PT J AU OUELLETTE, AJ MILLER, SI HENSCHEN, AH SELSTED, ME AF OUELLETTE, AJ MILLER, SI HENSCHEN, AH SELSTED, ME TI PURIFICATION AND PRIMARY STRUCTURE OF MURINE CRYPTDIN-1, A PANETH CELL DEFENSIN SO FEBS LETTERS LA English DT Article DE ANTIMICROBIAL PEPTIDE; SALMONELLA; CATION-EXCHANGE CHROMATOGRAPHY; HIGH PERFORMANCE LIQUID CHROMATOGRAPHY (HPLC); PEPTIDE SEQUENCING ID SALMONELLA-TYPHIMURIUM; SMALL-INTESTINE; PEPTIDES; RESISTANCE; VIRULENCE; PROTEINS; LOCUS AB We have purified and determined the amino acid sequence of cryptdin-1, a murine Paneth cell defensin. The peptide corresponds to a previously characterized mRNA that accumulates to high abundance during postnatal ontogeny of the small bowel. Acid-extracted intestinal protein was fractionated by cation-exchange chromatography and fractions were assayed for antimicrobial activity. One peak of anti-Salmonella activity contained a putative defensin, based on its predicted electrophoretic migration in acid-urea PAGE. The peptide was purified to homogeneity by RP-HPLC and sequenced. These studies demonstrate defensin expression in non-myeloid tissue. The N-terminal extension of cryptdin-1 is a unique structural feature of this novel epithelial defensin. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. UNIV CALIF IRVINE,SCH MED,DEPT MOLEC BIOL & BIOCHEM,IRVINE,CA 92717. UNIV CALIF IRVINE,SCH MED,DEPT PATHOL,IRVINE,CA 92717. RP OUELLETTE, AJ (reprint author), SHRINERS BURN INST,RES CTR,CELL BIOL UNIT,BLDG 1400,1 KENDALL SQ,CAMBRIDGE,MA 02142, USA. FU NIAID NIH HHS [AI00917, AI22931, AI30479] NR 20 TC 69 Z9 71 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0014-5793 J9 FEBS LETT JI FEBS Lett. PD JUN 15 PY 1992 VL 304 IS 2-3 BP 146 EP 148 DI 10.1016/0014-5793(92)80606-H PG 3 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA JA748 UT WOS:A1992JA74800009 PM 1618314 ER PT J AU ENG, C AF ENG, C TI THORACIC ADENOPATHY - METASTATIC SEMINOMA OR SARCOID SO HOSPITAL PRACTICE LA English DT Article RP ENG, C (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MCGRAW HILL HEALTHCARE PUBLICATIONS PI MINNEAPOLIS PA 4530 WEST 77TH ST, MINNEAPOLIS, MN 55435-5000 SN 8750-2836 J9 HOSP PRACT JI Hosp. Pract. PD JUN 15 PY 1992 VL 27 IS 6 BP 208 EP & PG 0 WC Medicine, General & Internal SC General & Internal Medicine GA HZ444 UT WOS:A1992HZ44400016 PM 1597494 ER PT J AU YANG, Y FRUH, K CHAMBERS, J WATERS, JB WU, L SPIES, T PETERSON, PA AF YANG, Y FRUH, K CHAMBERS, J WATERS, JB WU, L SPIES, T PETERSON, PA TI MAJOR HISTOCOMPATIBILITY COMPLEX (MHC)-ENCODED HAM2 IS NECESSARY FOR ANTIGENIC PEPTIDE LOADING ONTO CLASS-I MHC MOLECULES SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID H-2-DEFICIENT LYMPHOMA VARIANTS; MULTICATALYTIC PROTEINASE; REGION; TRANSPORTERS; PATHWAY; CELLS; GENE AB The mutant murine lymphoma cell line RMA-S is unable to present endogenous antigens due to its inability to efficiently assemble class I major histocompatibility complex molecules and antigenic peptides. Therefore, it has been suggested that RMA-S cells are defective either in peptide generation or in peptide transport into the endoplasmic reticulum, where class I major histocompatibility complex molecule assembly is believed to occur. As proteasomes and the putative peptide transporters HAM1 and HAM2 have been implicated in class I antigen processing, we have investigated their expression in RMA-S and its wild-type counterpart RMA. Both proteasomes and HAM1 proteins are expressed at similar levels and show identical subcellular distributions in the two cell lines. However, only one copy of the HAM2 gene is present in RMA-S cells, and it contains a point mutation that leads to a premature stop codon. Thus, the HAM2 protein is absent from RMA-S cells. These data demonstrate that HAM2 is essential for peptide loading onto class I molecules. C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR VIROL, BOSTON, MA 02115 USA. RP YANG, Y (reprint author), SCRIPPS RES INST, DEPT IMMUNOL, LA JOLLA, CA 92037 USA. NR 29 TC 111 Z9 113 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1992 VL 267 IS 17 BP 11669 EP 11672 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HY947 UT WOS:A1992HY94700003 PM 1339432 ER PT J AU MORRISON, BW LEDER, P AF MORRISON, BW LEDER, P TI A RECEPTOR-BINDING DOMAIN OF MOUSE INTERLEUKIN-4 DEFINED BY A SOLID-PHASE BINDING ASSAY AND INVITRO MUTAGENESIS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID STIMULATORY FACTOR-I; EXPRESSES B-CELL; T-CELL; CDNA CLONE; PROTEINS; IL-4; SEQUENCE; INVIVO; LIGAND; MUTANT AB Interleukin 4 (IL-4) is a Potent, pleiotropic lymphokine that affects a variety of cells, especially those of hematopoietic origin. Although murine and human IL-4 are homologous proteins, they display a species specificity in which murine IL-4 acts only upon mouse cells, and human IL-4 only upon human cells. We have used a mutagenesis strategy to define both the structural determinants of this specificity and a receptor binding domain of murine IL-4. To do this, we developed convenient solid-phase binding assays for mouse and for human IL-4, each utilizing receptor-immunoglobulin fusion proteins and alkaline phosphatase-tagged ligands. These were employed to assess the receptor binding activities of wild type and mutant forms of IL-4. In a separate biological assay, we measured the ability of each version of IL-4 to induce proliferation of a cultured mouse T-cell line. By replacing regions of mouse IL-4 with homologous segments of human IL-4, we found that the amino-terminal 16 residues and the carboxyl-terminal 20 residues of murine IL-4 are required for species-specific receptor binding as well as for T-cell proliferation. A major portion of the amino acid sequence between these regions can be substituted between mouse and human without loss of receptor binding or biological activity. Further, alanine-scanning mutagenesis revealed specific residues in the amino- and carboxyl-terminal regions (Glu-12, Ile-14, Leu-104, Asp-106, Phe-107, and Leu-111) that bear side chains critical for function. An analysis of the carboxyl-terminal region of murine IL-4 and its comparison with carboxyl-terminal regions of other related cytokines suggest an evolutionary conservation of structural and functional features. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA 09172] NR 39 TC 50 Z9 50 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 15 PY 1992 VL 267 IS 17 BP 11957 EP 11963 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HY947 UT WOS:A1992HY94700047 PM 1601864 ER PT J AU KUCHROO, VK SOBEL, RA LANING, JC MARTIN, CA GREENFIELD, E DORF, ME LEES, MB AF KUCHROO, VK SOBEL, RA LANING, JC MARTIN, CA GREENFIELD, E DORF, ME LEES, MB TI EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS MEDIATED BY CLONED T-CELLS SPECIFIC FOR A SYNTHETIC PEPTIDE OF MYELIN PROTEOLIPID PROTEIN - FINE SPECIFICITY AND T-CELL RECEPTOR V-BETA USAGE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; BASIC-PROTEIN; ENCEPHALITOGENIC DETERMINANT; APOPROTEIN; LINES; SJL/J; MICE; IDENTIFICATION; RECOGNITION; MOLECULE AB Proteolipid protein (PLP) is the major protein of central nervous system myelin. SJL (H-2s) mice immunized with a synthetic peptide corresponding to PLP residues 139-151 develop acute EAE. In this study, 6 IA(s)-restricted, CD4+, TCR alpha/beta-bearing T cell clones were derived from SJL/J mice after immunization with this synthetic peptide. The clones responded in in vitro proliferative assays to the whole PLP molecule and to PLP peptide 139-151, but not to irrelevant Ag. They also responded to truncated and overlapping forms of the peptide but five distinct reactivity patterns were observed using these peptides. A panel of anti-TCR V-beta mAb and TCR V-beta-specific cDNA probes were used to determine the TCR V-beta usage of the clones. Five clones were found to use four different V-beta (V-beta-2, V-beta-6, V-beta-10, or V-beta-17a), whereas the V-beta on the sixth clone could not be identified. Five of the clones induced EAE of varying severity upon adoptive transfer into naive syngeneic mice or mice pretreated with irradiation and pertussis and one clone was nonencephalitogenic. The Ag-specific proliferative response of all but the nonencephalitogenic clone could be blocked by an anti-CD4 mAb. Thus, the clones showed differences in their fine specifity, TCR V-beta usage, sensitivity to antibody blocking, and encephalitogenic potency. These data demonstrate that the T cell response to the encephalitogenic PLP peptide 139-151 is heterogeneous. C1 HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. EK SHRIVER CTR,DEPT BIOCHEM,WALTHAM,MA 02254. RP KUCHROO, VK (reprint author), HARVARD UNIV,SCH MED,DEPT PATHOL,BLDG D-2,ROOM 5408,200 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 39790]; NINDS NIH HHS [NS 26773, NS 16945] NR 46 TC 136 Z9 136 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD JUN 15 PY 1992 VL 148 IS 12 BP 3776 EP 3782 PG 7 WC Immunology SC Immunology GA HY056 UT WOS:A1992HY05600013 PM 1376341 ER PT J AU KALLIONIEMI, OP KALLIONIEMI, A KURISU, W THOR, A CHEN, LC SMITH, HS WALDMAN, FM PINKEL, D GRAY, JW AF KALLIONIEMI, OP KALLIONIEMI, A KURISU, W THOR, A CHEN, LC SMITH, HS WALDMAN, FM PINKEL, D GRAY, JW TI ERBB2 AMPLIFICATION IN BREAST-CANCER ANALYZED BY FLUORESCENCE INSITU HYBRIDIZATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HER-2 NEU ONCOGENE; GENE AMPLIFICATION; PROTEIN OVEREXPRESSION; C-ERBB-2 ONCOGENE; CELLS; MECHANISMS; DNA; CARCINOMAS; SURVIVAL; TUMORS AB We illustrate the use of fluorescence in situ hybridization (FISH) for analysis of ERBB2 oncogene copy number, the level of amplification (here defined as the ratio of ERBB2 copy number to copy number of chromosome 17 centromeres), and the distribution of amplified genes in breast cancer cell lines and uncultured primary breast carcinomas. The relative ERBB2 copy number determined by FISH in 10 breast cancer cell lines correlated strongly with Southern blot results (r = 0.98) when probes for an identical reference locus were used in the two methods. Metaphase analysis of cell lines showed that amplified ERBB2 copies always occurred in intrachromosomal clusters but that the number and chromosomal location of these clusters varied among the cell lines. In interphase nuclei of primary tumors showing ERBB2 amplification (10/44), ERBB2 copies were seen as one to four clusters, also suggesting intrachromosomal localization. Regardless of the average level of amplification, all these tumors contained highly amplified cell subpopulations with at least 25, and sometimes more than 100, ERBB2 copies per cell. Tumors that did not show amplification by FISH (34/44) had an average of one to five ERBB2 copies scattered randomly in the nuclei and completely lacked cells with high copy levels. FISH results on primary tumors were concordant with slot blot results on amplification and with immunohistochemical detection of over-expression. Quantitative analysis of ERBB2 amplification by FISH may improve prognostic assessments based on the pattern of amplification and detection of heavily amplified tumor cell subpopulations. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. GERALDINE BRUSH CANC RES INST,SAN FRANCISCO,CA 94115. RP KALLIONIEMI, OP (reprint author), UNIV CALIF SAN FRANCISCO,DEPT LAB MED,DIV MOLEC CYTOMETRY,MCB 230,SAN FRANCISCO,CA 94143, USA. RI Kallioniemi, Olli/H-5111-2011; Kallioniemi, Olli/H-4738-2012; OI Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Olli/0000-0002-3231-0332; Kallioniemi, Anne/0000-0003-3552-8158 FU NCI NIH HHS [CA 45919, CA 44768] NR 34 TC 408 Z9 416 U1 0 U2 11 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 JUN 15 PY 1992 VL 89 IS 12 BP 5321 EP 5325 DI 10.1073/pnas.89.12.5321 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HY053 UT WOS:A1992HY05300025 PM 1351679 ER PT J AU ANTONIADES, HN NEVILLEGOLDEN, J GALANOPOULOS, T KRADIN, RL VALENTE, AJ GRAVES, DT AF ANTONIADES, HN NEVILLEGOLDEN, J GALANOPOULOS, T KRADIN, RL VALENTE, AJ GRAVES, DT TI EXPRESSION OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 MESSENGER-RNA IN HUMAN IDIOPATHIC PULMONARY FIBROSIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE INFLAMMATION; MACROPHAGE; MONOCYTE CHEMOTAXIS ID HUMAN ENDOTHELIAL-CELLS; SMOOTH-MUSCLE CELLS; GROWTH-FACTOR; ALVEOLAR MACROPHAGES; SPONTANEOUS RELEASE; GENE JE; SECRETION; PRODUCTS; CLONING AB Macrophages are thought to play an important role in the pathologic changes associated with idiopathic pulmonary fibrosis (IPF). The mechanisms for increased monocyte/macrophage recruitment in IPF are unknown. Monocyte chemoattractant protein 1 (MCP-1) is the predominant monocyte chemoattractant secreted by a variety of different cell types in culture. We examined the expression of MCP-1 mRNA and its protein product in vivo in IPF and non-IPF lung specimens by in situ hybridization and immunocytochemistry. The cell types expressing MCP-1 in vivo were identified by immunostaining with specific antibodies. We demonstrated the expression of MCP-1 mRNA in pulmonary epithelial cells, in monocytes/macrophages, and in vascular endothelial and smooth muscle cells. Lung epithelial cells in patients with IPF strongly expressed MCP-1 mRNA and its protein product. In contrast, epithelial cells in non-IPF specimens did not express MCP-1 mRNA. Macrophages and vascular endothelial and smooth muscle cells were shown to express MCP-1 in both IPF and non-IPF lung specimens. These findings provide a basis for the understanding of the in vivo physiologic processes that mediate monocyte/macrophage recruitment and infiltration in the lung interstitium and the pathologic state contributing to an increased alveolar monocyte/macrophage population and inflammation in IPF. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PULM IMMUNOL & MOLEC BIOL LAB,BOSTON,MA 02114. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. BOSTON UNIV,MED CTR,DEPT ORAL BIOL,BOSTON,MA 02118. RP ANTONIADES, HN (reprint author), HARVARD UNIV,SCH PUBL HLTH,CTR BLOOD RES,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA30101]; NHLBI NIH HHS [HL29583]; NIDCR NIH HHS [DE07559] NR 27 TC 226 Z9 229 U1 1 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 JUN 15 PY 1992 VL 89 IS 12 BP 5371 EP 5375 DI 10.1073/pnas.89.12.5371 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HY053 UT WOS:A1992HY05300035 PM 1608944 ER PT J AU ROSEN, KM MCCORMACK, MA VILLAKOMAROFF, L MOWER, GD AF ROSEN, KM MCCORMACK, MA VILLAKOMAROFF, L MOWER, GD TI BRIEF VISUAL EXPERIENCE INDUCES IMMEDIATE EARLY GENE-EXPRESSION IN THE CAT VISUAL-CORTEX SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID TRANSCRIPTION FACTOR AP-1; OCULAR DOMINANCE COLUMNS; C-FOS; ORIENTATIONAL PROPERTIES; MONOCULAR DEPRIVATION; NERVOUS-SYSTEM; PLASTICITY; PROTEIN; JUN; KITTENS AB Brief visual experience causes rapid physiological changes in the visual cortex during early postnatal development. A possible mediator of these effects is the immediate early genes whose protein products are involved in the rapid response of neurons to transsynaptic stimulation. Here we report evidence that the levels of immediate early gene mRNAs in the visual cortex can be altered by manipulating the visual environment. Specifically, we find that brief (1 h) visual experience in dark-reared cats causes dramatic transient inductions of egr1, c-fos, and junB mRNAs in the visual cortex but not in the frontal cortex. Levels of c-jun and c-myc mRNAs are unaffected. These results suggest that select combinatorial interactions of immediate early gene proteins are an important step in the cascade of events through which visually elicited activity controls visual cortical development. C1 UNIV LOUISVILLE,HLTH SCI CTR,SCH MED,DEPT ANAT SCI & NEUROBIOL,LOUISVILLE,KY 40292. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR NEUROSCI,DEPT NEUROBIOL,BOSTON,MA 02129. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. FU NICHD NIH HHS [P30-HD18655]; NINDS NIH HHS [NS25216, NS27832] NR 40 TC 106 Z9 108 U1 1 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD JUN 15 PY 1992 VL 89 IS 12 BP 5437 EP 5441 DI 10.1073/pnas.89.12.5437 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HY053 UT WOS:A1992HY05300049 PM 1376920 ER PT J AU REMOLDODONNELL, E CHIN, J ALBERTS, M AF REMOLDODONNELL, E CHIN, J ALBERTS, M TI SEQUENCE AND MOLECULAR CHARACTERIZATION OF HUMAN MONOCYTE NEUTROPHIL ELASTASE INHIBITOR SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE CDNA CLONING; INFLAMMATION; SERPINS; OVALBUMIN FAMILY ID AMINO-ACID-SEQUENCE; PLASMINOGEN-ACTIVATOR INHIBITOR-2; ANTI-THROMBIN-III; MESSENGER-RNA; CATHEPSIN-G; LEUKOCYTE ELASTASE; CHICKEN OVALBUMIN; CDNA; GENE; ALPHA-1-ANTITRYPSIN AB cDNA encoding human monocyte/neutrophil elastase inhibitor (EI), a M(r) almost-equal-to 42,000 protein with serpin-like functional properties, has been sequenced. The 1316-base-pair sequence was obtained from overlapping clones and amplified DNA from libraries of monocyte-like and neutrophil-like cells. Hybridization with EI cDNA identified three EI MRNA species of 1.5, 1.9, and 2.6 kilobases in U937 monocyte-like cells and no hybridizing mRNA in lymphoblastoid cells lacking detectable EI. The CDNA open reading frame encodes a 379-amino acid protein, of which 167 residues were confirmed by tryptic peptides. Although EI may function extracellularly as well as intracellularly, its deduced sequence lacks a typical cleavable N-terminal signal sequence. Sequence analysis established that EI is a member of the serpin superfamily. El has greatest homology (50.1% identity of amino acids) with plasminogen activator inhibitor 2, also a monocyte protein, and ovalbumin and gene Y, which were previously grouped as an ancient branch of the serpin superfamily. The extent of EI identity with the functionally related serpin al antitrypsin is only 30.1%. Sequence alignment indicates that the reactive center P1 residue is Cys-344, consistent with abrogation of elastase inhibitory activity by iodoacetamide and making EI a naturally occurring Cys-serpin. The cleavable bond, Cys-Met, suggests an oxidation-sensitive molecule capable of inhibiting more than one serine protease. Oxidation sensitivity would limit the place of action of EI to the immediate vicinity of carrier cells. The molecular structure will help clarify the likely role of EI in regulating protease action and preventing tissue damage by phagocytic cells. RP REMOLDODONNELL, E (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL41579] NR 46 TC 112 Z9 113 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 JUN 15 PY 1992 VL 89 IS 12 BP 5635 EP 5639 DI 10.1073/pnas.89.12.5635 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HY053 UT WOS:A1992HY05300089 PM 1376927 ER PT J AU KWONG, KK BELLIVEAU, JW CHESLER, DA GOLDBERG, IE WEISSKOFF, RM PONCELET, BP KENNEDY, DN HOPPEL, BE COHEN, MS TURNER, R CHENG, HM BRADY, TJ ROSEN, BR AF KWONG, KK BELLIVEAU, JW CHESLER, DA GOLDBERG, IE WEISSKOFF, RM PONCELET, BP KENNEDY, DN HOPPEL, BE COHEN, MS TURNER, R CHENG, HM BRADY, TJ ROSEN, BR TI DYNAMIC MAGNETIC-RESONANCE-IMAGING OF HUMAN BRAIN ACTIVITY DURING PRIMARY SENSORY STIMULATION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID POSITRON-EMISSION TOMOGRAPHY; CEREBRAL BLOOD-FLOW; HUMAN VISUAL-CORTEX; FUNCTIONAL ARCHITECTURE; INTRINSIC SIGNALS; STRIATE CORTEX; DEPENDENCE; CONTRAST; FIELDS; INVIVO AB Neuronal activity causes local changes in cerebral blood flow, blood volume, and blood oxygenation. Magnetic resonance imaging (MRI) techniques sensitive to changes in cerebral blood flow and blood oxygenation were developed by high-speed echo planar imaging. These techniques were used to obtain completely noninvasive tomographic maps of human brain activity, by using visual and motor stimulus paradigms. Changes in blood oxygenation were detected by using a gradient echo (GE) imaging sequence sensitive to the paramagnetic state of deoxygenated hemoglobin. Blood flow changes were evaluated by a spin-echo inversion recovery (IR), tissue relaxation parameter T1-sensitive pulse sequence. A series of images were acquired continuously with the same imaging pulse sequence (either GE or IR) during task activation. Cine display of subtraction images (activated minus baseline) directly demonstrates activity-induced changes in brain MR signal observed at a temporal resolution of seconds. During 8-Hz patterned-flash photic stimulation, a significant increase in signal intensity (paired t test; P < 0.001) of 1.8% +/- 0.8% (GE) and 1.8% +/- 0.9% (IR) was observed in the primary visual cortex (V1) of seven normal volunteers. The mean rise-time constant of the signal change was 4.4 +/- 2.2 s for the GE images and 8.9 +/- 2.8 s for the IR images. The stimulation frequency dependence of visual activation agrees with previous positron emission tomography observations, with the largest MR signal response occurring at 8 Hz. Similar signal changes were observed within the human primary motor cortex (Ml) during a hand squeezing task and in animal models of increased blood flow by hypercapnia. By using intrinsic blood-tissue contrast, functional MRI opens a spatial-temporal window onto individual brain physiology. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. NHLBI,CARDIAC ENERGET LAB,BETHESDA,MD 20892. MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP KWONG, KK (reprint author), MASSACHUSETTS GEN HOSP,CTR MGH NMR,DEPT RADIOL,BOSTON,MA 02114, USA. RI Turner, Robert/C-1820-2008; Kennedy, David/H-3627-2012; Li, Chong/F-4265-2015; Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [5PO1CA48729-02, R01-CA40303]; NHLBI NIH HHS [R01-HL39810] NR 38 TC 2711 Z9 2774 U1 19 U2 169 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 JUN 15 PY 1992 VL 89 IS 12 BP 5675 EP 5679 DI 10.1073/pnas.89.12.5675 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HY053 UT WOS:A1992HY05300097 PM 1608978 ER PT J AU AXELROD, L VICKERY, AL HAHN, PF CRYNS, VL BLAND, EF AF AXELROD, L VICKERY, AL HAHN, PF CRYNS, VL BLAND, EF TI A 52-YEAR-OLD MAN WITH HYPERTENSION, HYPOKALEMIA, AND AN ADRENAL MASS - ALDOSTERONE-PRODUCING ADENOMA OF LEFT ADRENAL-GLAND SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP AXELROD, L (reprint author), MASSACHUSETTS GEN HOSP,JAMES HOWARD MEANS FIRM,BOSTON,MA 02114, USA. NR 19 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 JUN 11 PY 1992 VL 326 IS 24 BP 1617 EP 1623 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HX633 UT WOS:A1992HX63300007 ER PT J AU LAMPERTI, ED KITTELBERGER, JM SMITH, TF VILLAKOMAROFF, L AF LAMPERTI, ED KITTELBERGER, JM SMITH, TF VILLAKOMAROFF, L TI CORRUPTION OF GENOMIC DATABASES WITH ANOMALOUS SEQUENCE SO NUCLEIC ACIDS RESEARCH LA English DT Article ID COMPLETE NUCLEOTIDE-SEQUENCE; SALIVARY AMYLASE GENE; STRUCTURAL ORGANIZATION; MOLECULAR-CLONING; ESCHERICHIA-COLI; BETA-SUBUNIT; HUMAN DNA; PROTEIN; IDENTIFICATION; REGION AB We describe evidence that DNA sequences from vectors used for cloning and sequencing have been incorporated accidentally into eukaryotic entries in the GenBank database. These incorporations were not restricted to one type of vector or to a single mechanism. Many minor instances may have been the result of simple editing errors, but some entries contained large blocks of vector sequence that had been incorporated by contamination or other accidents during cloning. Some cases involved unusual rearrangements and areas of vector distant from the normal insertion sites. Matches to vector were found in 0.23% of 20,000 sequences analyzed in GenBank Release 63. Although the possibility of anomalous sequence incorporation has been recognized since the inception of GenBank and should be easy to avoid, recent evidence suggests that this problem is increasing more quickly than the database itself. The presence of anomalous sequence may have serious consequences for the interpretation and use of database entries, and will have an impact on issues of database management. The incorporated vector fragments described here may also be useful for a crude estimate of the fidelity of sequence information in the database. In alignments with well-defined ends, the matching sequences showed 96.8% identity to vector; when poorer matches with arbitrary limits were included, the aggregate identity to vector sequence was 94.8%. C1 HARVARD UNIV, CHILDRENS HOSP,SCH MED,DEPT NEUROL,ENDERS 250, 300 LONGWOOD AVE, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, DANA FARBER CANC INST, BOSTON, MA 02115 USA. FU NICHD NIH HHS [HD 18655]; NINDS NIH HHS [NS27832] NR 67 TC 21 Z9 21 U1 0 U2 0 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0305-1048 EI 1362-4962 J9 NUCLEIC ACIDS RES JI Nucleic Acids Res. PD JUN 11 PY 1992 VL 20 IS 11 BP 2741 EP 2747 DI 10.1093/nar/20.11.2741 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HZ673 UT WOS:A1992HZ67300016 PM 1614861 ER PT J AU GRESSENS, P KOSOFSKY, BE EVRARD, P AF GRESSENS, P KOSOFSKY, BE EVRARD, P TI COCAINE-INDUCED DISTURBANCES OF CORTICOGENESIS IN THE DEVELOPING MURINE BRAIN SO NEUROSCIENCE LETTERS LA English DT Article DE COCAINE; GLIOGENESIS; MOUSE; NEOPALLIUM; NEUROGENESIS ID CENTRAL NERVOUS-SYSTEM; REELER MICE; GESTATION; RAT AB Exposure of fetuses to cocaine can induce behavioral disturbances and structural modifications of the CNS. Cocaine was injected into pregnant mice from the eighth day of gestation until term and the brains of their offspring were examined at the light and EM levels. Cocaine severely disturbs neocortical architecture, disrupting horizontal and vertical lamination, and inducing abnormal array of the axonal-dendritic bundles. Cocaine also alters several steps of gliogenesis. The severity of the malformations is variable, but evident in all exposed animals. C1 CATHOLIC UNIV LOUVAIN,SCH MED,NEUROL DEV LAB,AV HIPPOCRATE 10-1303,B-1200 BRUSSELS,BELGIUM. MASSACHUSETTS GEN HOSP,DEPT PEDIAT NEUROL,BOSTON,MA 02114. NR 15 TC 105 Z9 106 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 JUN 8 PY 1992 VL 140 IS 1 BP 113 EP 116 DI 10.1016/0304-3940(92)90694-3 PG 4 WC Neurosciences SC Neurosciences & Neurology GA HZ798 UT WOS:A1992HZ79800028 PM 1407688 ER PT J AU JIN, YJ BURAKOFF, SJ BIERER, BE AF JIN, YJ BURAKOFF, SJ BIERER, BE TI MOLECULAR-CLONING OF A 25-KDA HIGH-AFFINITY RAPAMYCIN BINDING-PROTEIN, FKBP25 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID PEPTIDYL-PROLYL ISOMERASE; CIS-TRANS ISOMERASE; T-CELL ACTIVATION; IMMUNOSUPPRESSANT FK506; FK506-BINDING PROTEIN; MACROLIDES FK-506; DISTINCT; CYCLOPHILIN; IMMUNOPHILIN; CYCLOSPORINE AB Two FK506 binding proteins of molecular mass 12 kDa (FKBP12) and 13 kDa (FKBP13) have been identified as common cellular receptors of the immunosuppressants FK506 and rapamycin. Here we report the molecular cloning and overexpression of a 25-kDa rapamycin and FK506 binding protein (termed FKBP25) with peptidylprolyl cis-trans-isomerase (PPIase) activity. The amino acid sequence, predicted from the FKBP25 cDNA, shares identity with FKBP12 (44%) and FKBP13 (47%) in the C-terminal 97 amino acids. Unlike either FKBP12 or FKBP13, the nucleotide sequence of FKBP25 contains a number of putative nuclear localization sequences. The PPIase activity of recombinant FKBP25 was comparable with that of FKBP12. The PPIase activity of FKBP25 was far more sensitive to inhibition by rapamycin (IC50 = 50 nM) than FK506 (IC50 = 400 nM). PPIase activity of 100 nM FKBP25 was almost completely inhibited by 150 nm rapamycin while only 90% inhibition was achieved by 4-mu-M FK506. These data demonstrate that FKBP25 has a higher affinity for rapamycin than for FK506 and suggest that this cellular receptor may be an important target molecule for immunosuppression by rapamycin. C1 BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP JIN, YJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115, USA. NR 29 TC 74 Z9 76 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD JUN 5 PY 1992 VL 267 IS 16 BP 10942 EP 10945 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX169 UT WOS:A1992HX16900004 PM 1375932 ER PT J AU RABOUILLE, C SPIRO, RG AF RABOUILLE, C SPIRO, RG TI NONSELECTIVE UTILIZATION OF THE ENDOMANNOSIDASE PATHWAY FOR PROCESSING GLYCOPROTEINS BY HUMAN HEPATOMA (HEPG2) CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID N-LINKED OLIGOSACCHARIDES; ALPHA-D-MANNOSIDASE; ROUGH ENDOPLASMIC-RETICULUM; ALPHA-1-PROTEINASE INHIBITOR; SECRETORY GLYCOPROTEINS; GOLGI-COMPLEX; RAT-LIVER; CASTANOSPERMINE; PROTEINS; 1-DEOXYNOJIRIMYCIN AB Endo-alpha-D-mannosidase, a Golgi-situated processing enzyme, provides a glucosidase-independent pathway for the formation of complex N-linked oligosaccharides of glycoproteins (Moore, S. E. H., and Spiro, R. G. (1990) J. Biol. Chem. 265, 13104-13112). The present report demonstrates that at least five distinct glycoproteins secreted by HepG2 cells (alpha-1-antitrypsin, transferrin, alpha-1-acid glycoprotein, alpha-1-antichymotrypsin, and alpha-fetoprotein) as well as cell surface components can effectively utilize this alternate processing route. During a castanospermine (CST)-imposed glucosidase blockade, these glycoproteins apparently were produced with their usual complement of complex carbohydrate units, and upon addition of the mannosidase I inhibitor, 1-deoxymannojirimycin (DMJ), to prevent further processing of deglucosylated N-linked oligosaccharides, Man6-8GlcNAc, but not Man9GlcNAc, were identified; the Man8GlcNAc component occurred as the characteristic isomer generated by endomannosidase cleavage. Although the endomannosidase-mediated deglucosylation pathway appeared to be nonselective, a differential inhibitory effect on the secretion of the various glycoproteins was noted in the presence of CST which was directly related to the number of their N-linked oligosaccharides, ranging from minimal in alpha-fetoprotein to substantial (approximately-65%) in alpha-1-acid glycoprotein. Addition of DMJ to CST-incubated cells did not further decrease secretion of the glycoproteins, although processing was now arrested at the polymannose stage, and a portion of the oligosaccharides were still in the glucosylated form. These latter findings indicate that complex carbohydrate units are not required for secretion of these glycoproteins and that any effect which glucose residues exert on their intracellular transit would be related to movement from the endoplasmic reticulum to 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 35 TC 46 Z9 46 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 JUN 5 PY 1992 VL 267 IS 16 BP 11573 EP 11578 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HX169 UT WOS:A1992HX16900097 PM 1317871 ER PT J AU BURGLIN, TR BARNES, TM AF BURGLIN, TR BARNES, TM TI INTRONS IN SEQUENCE TAGS SO NATURE LA English DT Letter C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT GENET,BOSTON,MA 02114. RP BURGLIN, TR (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,WELLMAN 8,BOSTON,MA 02114, USA. NR 6 TC 8 Z9 8 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 JUN 4 PY 1992 VL 357 IS 6377 BP 367 EP 367 DI 10.1038/357367a0 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX172 UT WOS:A1992HX17200035 PM 1350660 ER PT J AU GOLDBERG, AL ROCK, KL AF GOLDBERG, AL ROCK, KL TI PROTEOLYSIS, PROTEASOMES AND ANTIGEN PRESENTATION SO NATURE LA English DT Review ID MAJOR HISTOCOMPATIBILITY COMPLEX; MOLECULAR-WEIGHT PROTEASE; MULTICATALYTIC PROTEINASE COMPLEX; RAT-LIVER; SKELETAL-MUSCLE; DEPENDENT PROTEOLYSIS; RABBIT RETICULOCYTES; 26S COMPLEX; T-CELLS; UBIQUITIN AB Proteins presented to the immune system must first be cleaved to small peptides by intracellular proteinases. Proteasomes are proteolytic complexes that degrade cytosolic and nuclear proteins. These particles have been implicated in ATP-ubiquitin-dependent proteolysis and in the processing of intracellular antigens for cytolytic immune responses. C1 HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. RP GOLDBERG, AL (reprint author), HARVARD UNIV, SCH MED, DEPT CELLULAR & MOLEC PHYSIOL, BOSTON, MA 02115 USA. NR 90 TC 540 Z9 543 U1 4 U2 8 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD JUN 4 PY 1992 VL 357 IS 6377 BP 375 EP 379 DI 10.1038/357375a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX172 UT WOS:A1992HX17200052 PM 1317508 ER PT J AU STIEGMANN, GV GOFF, JS MICHALETZONODY, PA KORULA, J LIEBERMAN, D SAEED, ZA REVEILLE, RM SUN, JH LOWENSTEIN, SR AF STIEGMANN, GV GOFF, JS MICHALETZONODY, PA KORULA, J LIEBERMAN, D SAEED, ZA REVEILLE, RM SUN, JH LOWENSTEIN, SR TI ENDOSCOPIC SCLEROTHERAPY AS COMPARED WITH ENDOSCOPIC LIGATION FOR BLEEDING ESOPHAGEAL-VARICES SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID RANDOMIZED CONTROLLED TRIAL; CONTROLLED CLINICAL-TRIAL; DISTAL SPLENORENAL SHUNT; LONG-TERM MANAGEMENT; INJECTION SCLEROTHERAPY; COMPLICATIONS; SURVIVAL AB Background. Endoscopic sclerotherapy is an accepted treatment for bleeding esophageal varices, but it is associated with substantial local and systemic complications. Endoscopic ligation, a new form of endoscopic treatment for bleeding varices, may be safer. We compared the effectiveness and safety of the two techniques. Methods. In this randomized trial we compared endoscopic sclerotherapy and endoscopic ligation in 129 patients with cirrhosis who had proved bleeding from esophageal varices. Sixty-five patients were treated with sclerotherapy, and 64 with ligation. Initial treatment for acute bleeding was followed by elective retreatment to eradicate varices. The patients were followed for a mean of 10 months, during which we determined the incidence of complications and recurrences of bleeding, the number of treatments needed to eradicate varices, and survival. Results. Active bleeding at the first treatment was controlled by sclerotherapy in 10 of 13 patients (77 percent) and by ligation in 12 of 14 patients (86 percent). Slightly more sclerotherapy-treated patients had recurrent hemorrhage during the study (48 percent vs. 36 percent for the ligation-treated patients, P = 0.072). The eradication of varices required a lower mean (+/- SD) number of treatments with ligation (4 +/- 2 vs. 5 +/- 2, P = 0.056) than with sclerotherapy. The mortality rate was significantly higher in the sclerotherapy group (45 percent vs. 28 percent, P = 0.041), as was the rate of complications (22 percent vs. 2 percent, P < 0.001). The complications of sclerotherapy were predominantly esophageal strictures, pneumonias, and other infections. Conclusions. Patients with cirrhosis who have bleeding esophageal varices have fewer treatment-related complications and better survival rates when they are treated by esophageal ligation than when they are treated by sclerotherapy. C1 UNIV COLORADO,DEPT MED,DENVER,CO 80202. UNIV COLORADO,EMERGENCY MED RES CTR,DENVER,CO 80202. DENVER VET AFFAIRS HOSP,DENVER,CO. BAYLOR COLL MED,DEPT MED,HOUSTON,TX 77030. HOUSTON VET AFFAIRS HOSP,HOUSTON,TX. UNIV SO CALIF,SCH MED,LIVER UNIT,DOWNEY,CA 90242. OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. PORTLAND VET AFFAIRS HOSP,PORTLAND,OR. RP STIEGMANN, GV (reprint author), UNIV COLORADO,HLTH SCI CTR,DEPT SURG,C-313,4200 E 9TH AVE,DENVER,CO 80262, USA. NR 24 TC 457 Z9 463 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 JUN 4 PY 1992 VL 326 IS 23 BP 1527 EP 1532 DI 10.1056/NEJM199206043262304 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HW972 UT WOS:A1992HW97200004 PM 1579136 ER PT J AU THOR, AD MOORE, DH EDGERTON, SM KAWASAKI, ES REIHSAUS, E LYNCH, HT MARCUS, JN SCHWARTZ, L CHEN, LC MAYALL, BH SMITH, HS AF THOR, AD MOORE, DH EDGERTON, SM KAWASAKI, ES REIHSAUS, E LYNCH, HT MARCUS, JN SCHWARTZ, L CHEN, LC MAYALL, BH SMITH, HS TI ACCUMULATION OF P53 TUMOR SUPPRESSOR GENE PROTEIN - AN INDEPENDENT MARKER OF PROGNOSIS IN BREAST CANCERS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Article ID MUTATIONS; EXPRESSION; TRANSFORMATION; ANTIBODIES; SARCOMAS; ONCOGENE; ANTIGEN; 17P13 AB Background: Mutations of the tumor suppressor gene p53 have been identified in breast cancer cell fines, and some breast carcinomas are detectable by immunohistochemical assay because of p53 protein accumulation. Purpose: This study was designed to determine whether p53 protein accumulation in breast cancers correlates with p53 gene mutation, with survival, and with five pathobiologic factors associated with prognosis. Methods: IgG1 monoclonal antibody to human p53 protein (PAb 1801) and immunohistochemical methods were used to detect p53 protein accumulation in archival formalin-fixed, paraffin-embedded, randomly selected carcinomas. We studied 295 invasive ductal carcinomas from the Massachusetts General Hospital; 151 were determined to be sporadic (not hereditary). We also studied 97 invasive ductal carcinomas-21 sporadic and 76 familial (hereditary)-from Creighton University. In addition, we examined 31 archival in situ carcinomas, 15 snap-frozen invasive ductal carcinomas, primary cell cultures from three benign breast tissue samples, and breast carcinoma cell lines MDA-MB-231 and MDA-MB-468. Results: Nuclear p53 protein was observed in 16% of the 31 in situ carcinomas, 22% of the 172 sporadic carcinomas, 34% of the 50 tumors from patients with familial breast cancer, 52% of the 23 tumors from patients with the familial breast and ovarian cancer syndrome, and all three tumors from two patients with the Li-Fraumeni syndrome. There was complete concordance between p53 gene mutation and p53 protein accumulation in the 15 snap-frozen carcinomas and in both breast carcinoma cell lines. Statistically significant associations of p53 protein accumulation with estrogen receptor negativity and with high nuclear grade were found. There were statistically significant associations, independent of other prognostic factors, between p53 protein accumulation and metastasis-free and overall survival, for randomly accrued and for both sporadic and familial tumors. Conclusions: Immunohistochemically detected p53 protein accumulation was an independent marker of shortened survival and was seen more often in familial than in sporadic carcinomas. Our findings also suggest a correlation between p53 protein accumulation and p53 gene mutation. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. LAWRENCE LIVERMORE NATL LAB,DIV BIOMED SCI,LIVERMORE,CA 94550. CETUS CORP,DEPT HUMAN GENET,EMERYVILLE,CA 94608. CREIGHTON UNIV,DEPT PREVENT MED & PATHOL,OMAHA,NE 68178. CALIF PACIFIC MED CTR,GERALDINE BRUSH CANC RES INST,SAN FRANCISCO,CA. UNIV CALIF SAN FRANCISCO,DEPT LAB MED,SAN FRANCISCO,CA 94143. RP THOR, AD (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,WARREN 2,FRUIT ST,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-44768, CA-48802] NR 49 TC 785 Z9 791 U1 3 U2 16 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD JUN 3 PY 1992 VL 84 IS 11 BP 845 EP 855 DI 10.1093/jnci/84.11.845 PG 11 WC Oncology SC Oncology GA HW636 UT WOS:A1992HW63600009 PM 1317462 ER PT J AU SELAND, JH CHYLACK, LT WOLFE, JK AF SELAND, JH CHYLACK, LT WOLFE, JK TI INDIRECT SPECTRAL TRANSMISSION RATIO MEASUREMENTS OF THE AGING CRYSTALLINE LENS NUCLEUS SO ACTA OPHTHALMOLOGICA LA English DT Article DE CRYSTALLINE LENS; LENS NUCLEUS; LENS COLOR; ABSORPTION; TRANSMISSION RATIO ID CLASSIFICATION AB A new objective approach to characterize color and opalescence in the lens nucleus, using wavelength indexed transmission ratios (TR) is described. Transmission ratios, i.e. the transmissivity per unit lens thickness, for the whole visible spectral range (390-720 nm) were calculated using fast scanning spectral colorimetry (FSSC). The lowest transmission ratios values were obtained in the blue part of the spectrum in general and at 450 nm in particular. They inversely followed the subjectively determined LOCS II color grading. The difference between transmission ratios at the absorbed part of the spectrum (<500 nm) and the non-absorbed part (>550 nm) also reflects the LOCS II color grading. The overall mean transmission ratios for all wavelengths in the spectrum gives an index that closely followed the nuclear opalescence grading of the LOCS II system. The transmission ratios are theoretically independent of the spectral characteristics of the incident light as long as it contains suprathreshold energies in the whole measured spectral range. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,CTR CLIN CATARACT RES,BOSTON,MA 02115. UNIV BERGEN,DEPT OPHTHALMOL,N-5014 BERGEN,NORWAY. NR 25 TC 3 Z9 3 U1 0 U2 0 PU ARHUS UNIV HOSPITAL PI AARHUS PA DEPT OHPTHALMOLOGY, DK-8000 AARHUS, DENMARK SN 0001-639X J9 ACTA OPHTHALMOL PD JUN PY 1992 VL 70 IS 3 BP 376 EP 382 PG 7 WC Ophthalmology SC Ophthalmology GA JB793 UT WOS:A1992JB79300018 PM 1636402 ER PT J AU RUPRECHT, RM KOCH, JA SHARMA, PL ARMANY, RS AF RUPRECHT, RM KOCH, JA SHARMA, PL ARMANY, RS TI DEVELOPMENT OF ANTIVIRAL TREATMENT STRATEGIES IN MURINE MODELS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Review ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; LONG TERMINAL REPEAT; AIDS-RELATED COMPLEX; PLACEBO-CONTROLLED TRIAL; MOLONEY LEUKEMIA-VIRUS; TRANSGENIC MICE; ANTIRETROVIRAL THERAPY; INTERFERON-ALPHA; RETROVIRAL DISEASE; ANIMAL-MODEL AB Murine models with type C murine leukemia viruses have been used to develop major new prophylactic and therapeutic strategies in vaccination, drug therapy of acute virus exposure and chronic viremia, combination therapy, prevention of maternal transmission, and therapy targeted to the central nervous system. Transgenic mice expressing either the whole human immunodeficiency virus type 1 (HIV-1) provirus or subgenomic sequences allow the in vivo analysis of selected HIV-1 functions. The full replicative cycle of HIV-1 can be studied in human/mouse chimerae which were created by transplanting human hematolymphoid cells into SCID mice. The chimeric SCID mouse models have been used successfully to evaluate anti-HIV-1 drugs. The role of the various murine retrovirus systems in the development of anti-HIV-1 and anti-AIDS therapies is summarized. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOCHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP RUPRECHT, RM (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [24O1AI24845, N01-AI-72664, R01-AI-25715] NR 124 TC 12 Z9 12 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD JUN PY 1992 VL 8 IS 6 BP 997 EP 1011 DI 10.1089/aid.1992.8.997 PG 15 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JG873 UT WOS:A1992JG87300003 PM 1323985 ER PT J AU ZIMMER, W DELUCA, SA AF ZIMMER, W DELUCA, SA TI PRIMARY TRACHEAL NEOPLASMS - RECOGNITION, DIAGNOSIS AND EVALUATION SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Primary neoplasms of the trachea are much less common than malignancies of the larynx and lungs. Tracheal neoplasms account for less than 0.1 percent of all neoplasms. Their importance lies in the fact that they may initially be misdiagnosed, resulting in a delay in diagnosis ranging from months to years. The most common benign tracheal neoplasms are hemangiomas, squamous papillomas and fibromas. The most common tracheal malignancy is squamous cell carcinoma. Symptoms of these lesions are usually related to airway obstruction and include wheezing, dyspnea and cough. RP ZIMMER, W (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 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 JUN PY 1992 VL 45 IS 6 BP 2650 EP 2657 PG 8 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA HY084 UT WOS:A1992HY08400019 ER PT J AU RODRIGUEZ, L MONTERROSO, VH ABASCAL, VM KING, ME OSHEA, JP PALACIOS, IF WEYMAN, AE AF RODRIGUEZ, L MONTERROSO, VH ABASCAL, VM KING, ME OSHEA, JP PALACIOS, IF WEYMAN, AE TI DOES ASYMMETRIC MITRAL-VALVE DISEASE PREDICT AN ADVERSE OUTCOME AFTER PERCUTANEOUS BALLOON MITRAL VALVOTOMY - AN ECHOCARDIOGRAPHIC STUDY SO AMERICAN HEART JOURNAL LA English DT Note ID VALVULOPLASTY; MECHANISMS; INCREASE; STENOSIS; DOPPLER; ADULTS; AREA C1 MASSACHUSETTS GEN HOSP,CARDIAC ULTRASOUND LAB,PHILLIPS HOUSE LEVEL 8,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 8 TC 9 Z9 9 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0002-8703 J9 AM HEART J JI Am. Heart J. PD JUN PY 1992 VL 123 IS 6 BP 1678 EP 1682 DI 10.1016/0002-8703(92)90821-C PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HX943 UT WOS:A1992HX94300030 PM 1595546 ER PT J AU LEAF, A AF LEAF, A TI AGING - NUTRITION AND THE QUALITY-OF-LIFE - PROCEEDINGS OF A CONFERENCE HELD IN MARBELLA, SPAIN, NOVEMBER 12-14, 1990 - SUMMARY AND CONCLUDING REMARKS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Editorial Material C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, BOSTON, MA 02114 USA. NR 2 TC 3 Z9 3 U1 1 U2 1 PU AMER SOC NUTRITION-ASN PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0002-9165 EI 1938-3207 J9 AM J CLIN NUTR JI Am. J. Clin. Nutr. PD JUN PY 1992 VL 55 IS 6 SU S BP 1271 EP 1273 PG 3 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HX761 UT WOS:A1992HX76100018 ER PT J AU LEAF, A AF LEAF, A TI AGING - NUTRITION AND THE QUALITY-OF-LIFE - PROCEEDINGS OF A CONFERENCE HELD IN MARBELLA, SPAIN, NOVEMBER 12-14, 1990 - PREFACE SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Editorial Material RP LEAF, A (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 1 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 JUN PY 1992 VL 55 IS 6 SU S BP R11 EP R11 PG 1 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HX761 UT WOS:A1992HX76100001 ER PT J AU GARDNER, SF GREEN, JA BEDNARCZYK, EM FARNETT, L MIRALDI, F AF GARDNER, SF GREEN, JA BEDNARCZYK, EM FARNETT, L MIRALDI, F TI PRINCIPLES AND CLINICAL-APPLICATIONS OF POSITRON EMISSION TOMOGRAPHY SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Article DE COSTS; PHARMACISTS; RADIOPHARMACEUTICALS; SPECIALTIES; TOMOGRAPHY ID CEREBRAL GLUCOSE-METABOLISM; MYOCARDIAL BLOOD-FLOW; COMPUTED-TOMOGRAPHY; F-18 FLUORODEOXYGLUCOSE; PARTIAL SEIZURES; N-13 AMMONIA; HUMAN-BRAIN; INVIVO; QUANTIFICATION; ABNORMALITIES AB The basics of positron emission tomography (PET) are presented, including the physics, instrumentation, and radiopharmaceuticals involved; the clinical and research applications; and the cost. In PET, organic molecules labeled with positron-emitting radionuclides are injected or inhaled, and the high-energy photons produced by annihilation events are detected by paired, integrated crystal detectors. A computer uses the lines of origin of these photons to reconstruct a three-dimensional map of a functioning organ system. The positron-emitting radionuclides most often used are carbon 11, oxygen 15, nitrogen 13, fluorine 18, and rubidium 82. PET imaging centers usually consist of a cyclotron facility, a radiochemistry facility, a PET scanner, and computers for image reconstruction. Radiopharmaceuticals used in PET may be divided into blood flow-imaging agents, metabolic imaging agents, and drug receptor-imaging agents. Although PET is still primarily a research tool, it has shown diagnostic potential in neurology, cardiology, and oncology. It has also shown promise as a tool for pharmacologic assessment, as in studies of the effects of the fluorinated quinolones on cerebral blood flow and glucose metabolism. PET may become important in drug development because it yields specific information relatively noninvasively. A single study carries an average break-even price tag of $1500-$2000; rigorous cost-benefit analyses should be conducted before society is asked to subsidize such costs. Positron emission tomography is a frontier technology for which valuable clinical applications are being discovered. Pharmacists can contribute enormously to PET applications and at the same time establish a unique subspecialty for the profession. C1 CASE WESTERN RESERVE UNIV,ENGN,CLEVELAND,OH 44106. AUDIE L MURPHY MEM VET ADM MED CTR,MED & RADIOL,SAN ANTONIO,TX 78284. CASE WESTERN RESERVE UNIV,RADIOL,CLEVELAND,OH 44106. RP GARDNER, SF (reprint author), UNIV ARKANSAS MED SCI HOSP,DEPT PHARM PRACTICE,SLOT 522,4301 W MARKHAM ST,LITTLE ROCK,AR 72205, USA. NR 35 TC 9 Z9 10 U1 0 U2 2 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD JUN PY 1992 VL 49 IS 6 BP 1499 EP 1506 PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HX214 UT WOS:A1992HX21400037 PM 1530002 ER PT J AU BRAZY, PC PIRSCH, JD BELZER, FO AF BRAZY, PC PIRSCH, JD BELZER, FO TI FACTORS AFFECTING RENAL-ALLOGRAFT FUNCTION IN LONG-TERM RECIPIENTS SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE CREATININE CLEARANCES; CADAVERIC DONORS; LIVING-RELATED DONORS; HYPERTENSION; DIABETES-MELLITUS; HYPERCHOLESTEROLEMIA ID DIABETIC NEPHROPATHY; SERUM CREATININE; BLOOD-PRESSURE; PROGRESSION; KIDNEY; TRANSPLANTATION; COMPLICATIONS; CYCLOSPORINE; NEPHRECTOMY; REJECTION C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,DEPT MED,MADISON,WI 53706. UNIV WISCONSIN,DEPT SURG,MADISON,WI 53706. NR 29 TC 45 Z9 45 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD JUN PY 1992 VL 19 IS 6 BP 558 EP 566 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA HX178 UT WOS:A1992HX17800009 PM 1595705 ER PT J AU RANKIN, AC BROOKS, R RUSKIN, JN MCGOVERN, BA AF RANKIN, AC BROOKS, R RUSKIN, JN MCGOVERN, BA TI ADENOSINE AND THE TREATMENT OF SUPRAVENTRICULAR TACHYCARDIA SO AMERICAN JOURNAL OF MEDICINE LA English DT Review ID ATRIOVENTRICULAR NODAL CONDUCTION; SUPRA-VENTRICULAR TACHYCARDIA; PARKINSON-WHITE SYNDROME; INTRAVENOUS ADENOSINE; JUNCTIONAL TACHYCARDIA; ACUTE MANAGEMENT; THERAPEUTIC USE; CLINICAL USE; CYCLIC-AMP; REENTRANT TACHYCARDIA AB Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. This is of therapeutic value in the conversion to sinus rhythm of the majority of paroxysmal supraventricular tachycardias, which involve the atrioventricular node in a re-entrant circuit. The mean success rate was 93% from over 600 reported episodes. Compared with other antiarrhythmic agents, adenosine is remarkable for its rapid metabolism and brevity of action, with a half-life of a few seconds. It commonly produces subjective symptoms, particularly chest discomfort, dyspnea, and flushing, which are of short duration only. No serious adverse effect has been reported. Arrhythmias may recur within minutes in a minority of patients. Comparative studies have shown that adenosine is as effective as verapamil in the treatment of supraventricular tachycardia, and has less potential for adverse effects. Patients with supraventricular tachycardia should initially be treated using vagotonic physical maneuvers. Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present. C1 MASSACHUSETTS GEN HOSP,CARDIAC ARRHYTHMIA SERV,BOSTON,MA 02114. NR 92 TC 65 Z9 66 U1 0 U2 1 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD JUN PY 1992 VL 92 IS 6 BP 655 EP 664 DI 10.1016/0002-9343(92)90784-9 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA HY439 UT WOS:A1992HY43900012 PM 1605147 ER PT J AU HORVATH, CJ SIMON, MA BERGSAGEL, DJ PAULEY, DR KING, NW GARCEA, RL RINGLER, DJ AF HORVATH, CJ SIMON, MA BERGSAGEL, DJ PAULEY, DR KING, NW GARCEA, RL RINGLER, DJ TI SIMIAN-VIRUS 40-INDUCED DISEASE IN RHESUS-MONKEYS WITH SIMIAN ACQUIRED-IMMUNODEFICIENCY-SYNDROME SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY; DEFICIENCY SYNDROME AIDS; JC VIRUS; BK-VIRUS; CELLULAR-LOCALIZATION; INSITU HYBRIDIZATION; LYMPHOID-TISSUES; BRAIN-TISSUE; PAPOVAVIRUS; DNA AB Simian virus 40 (SV40) disease was diagnosed in four rhesus monkeys that died with SIV-induced acquired immunodeficiency syndrome (AIDS). One juvenile monkey seroconverted for SV40 6 months after inoculation with SIV and developed severe bilateral tubulointerstitial nephritis. In contrast, progressive multifocal leukoencephalopathy (PML) occurred in two adult monkeys that were seropositive for SV40 before SIV inoculation, as well as a third adult that was naturally infected with SIV and seropositive for SV40 5 years before death. Large intranuclear inclusions containing abundant polyomavirus particles were limited to either renal tubular epithelial cells or oligodendrocytes. In situ DNA hybridization for SV40 large T antigen further demonstrated that SV40 nucleic acid was localized to either kidney or brain tissue. By immunohistochemical analysis, areas of central nervous system inflammation and demyelination were shown to contain CD68+ macrophages (gitter cells), aggregates of CD8+ T lymphocytes, and numerous gemistocytic astrocytes that labeled for glial fibrillary acidic protein These observations indicate that rhesus monkeys with SIV-induced AIDS are predisposed to polyomaviral disease, in which SV40 nucleic acid is observed in renal tissue in primary infections and brain tissue after viral reactivation. Furthermore, this organ-specific replication suggests that tissue-tropic strains of SV40 may develop in immunodeficient monkeys. C1 HARVARD UNIV,SCH MED,NEW ENGLAND REG PRIMATE RES CTR,SOUTHBOROUGH,MA 01772. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. FU NCRR NIH HHS [RR 00168]; NIAID NIH HHS [AI 29855, AI 25644] NR 52 TC 75 Z9 77 U1 0 U2 3 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD JUN PY 1992 VL 140 IS 6 BP 1431 EP 1440 PG 10 WC Pathology SC Pathology GA HY135 UT WOS:A1992HY13500017 PM 1376560 ER PT J AU FORCE, T BONVENTRE, JV FLANNERY, MR GORN, AH YAMIN, M GOLDRING, SR AF FORCE, T BONVENTRE, JV FLANNERY, MR GORN, AH YAMIN, M GOLDRING, SR TI A CLONED PORCINE RENAL CALCITONIN RECEPTOR COUPLES TO ADENYLYL CYCLASE AND PHOSPHOLIPASE-C SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Note DE CALCITONIN GENE-RELATED PEPTIDE; SIGNAL TRANSDUCTION; CALCIUM; INOSITOL PHOSPHOLIPIDS; INOSITOL PHOSPHATES ID CYCLIC-AMP; PHOSPHOINOSITIDE TURNOVER; INOSITOL TRISPHOSPHATE; SIGNAL-TRANSDUCTION; CELLS; INCREASES; HORMONE; PHOSPHATES; PATHWAYS; SYSTEMS AB The signal transduction pathways of the recently cloned porcine kidney calcitonin (CT) receptor were evaluated. This receptor, when stably transfected into MC-3T3 cells, avidly bound salmon CT (SCT) [dissociation constant (K(d)) = 4 nM]. Incubation with SCT resulted in a dose-dependent accumulation of adenosine 3',5'-cyclic monophosphate (cAMP) [50% effective concentration (EC50) = 0.02 nM] in transfected cells (referred to as PC-1 cells). Binding kinetics and cAMP dose response relationships were similar to those of the native receptor in LLC-PK1 cells. PC-1 cells also responded to calcitonin generelated peptide (CGRP), but the EC50 value for cAMP accumulation was more than three orders of magnitude higher than for SCT. Exposure of PC-1 cells to SCT (5 nM to 1-mu-M) produced a dose-dependent rise in cytosolic free Ca2+ concentration ([Ca2+]i), whereas CGRP did not. The initial rise in [Ca2+]i was not dependent on extracellular Ca2+, suggesting that SCT induced release of Ca2+ from intracellular stores. SCT also increased inositol trisphosphate production in PC-1 cells. In conclusion, the cloned, transfected porcine CT receptor functionally couples to and activates both adenylyl cyclase and phospholipase C. This dual coupling is also a characteristic of the parathyroid hormone receptor, which has significant homology in amino acid sequence with the CT receptor. C1 MASSACHUSETTS GEN HOSP,ARTHRIT UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. NEW ENGLAND DEACONESS HOSP,ARTHRIT UNIT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP FORCE, T (reprint author), MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BULLFINCH 457,BOSTON,MA 02114, USA. NR 29 TC 118 Z9 118 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 JUN PY 1992 VL 262 IS 6 BP F1110 EP F1115 PN 2 PG 6 WC Physiology SC Physiology GA JC377 UT WOS:A1992JC37700106 ER PT J AU FOSTER, CD HILL, WAG HONEYMAN, TW SCHEID, CR AF FOSTER, CD HILL, WAG HONEYMAN, TW SCHEID, CR TI CHARACTERIZATION OF NA+-H+ EXCHANGE IN SEGMENTS OF RAT MESENTERIC-ARTERY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE INTACT ARTERIAL SEGMENTS; KINETICS ID INTRACELLULAR PH REGULATION; VASCULAR SMOOTH-MUSCLE; CYTOPLASMIC PH; BUFFERING POWER; ANGIOTENSIN-II; GROWTH-FACTORS; ACINAR-CELLS; ANTIPORT; FIBROBLASTS; ACTIVATION AB To develop a technique for measuring Na+-H+ exchange activity and intracellular pH (pH(i)) "on line" in resistance vessels, we utilized strips of rat mesenteric arteries loaded with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Strips were held at a fixed length within a 3-ml cuvette, and fluorescence emission was monitored at 530 nm. The spectrofluorimeter was monitored in the ratio mode, and the excitation wavelength was alternated between 440 and 505 nm. Tissues were maintained by perfusing with N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid containing buffers. The introduction of ammonium chloride produced a rapid alkalinization. Washout of ammonium caused rapid acidification. Restoration of pH(i) was Na+ dependent and inhibited by dimethyl amiloride (concentration that produces half-maximal inhibition, K0.5 = 30-mu-M), features characteristic of Na+-H+ exchange. Further studies assessed the transport rate of the exchanger, which averaged 0.19 +/- 0.02 pH U/min (means +/- SE, n = 8). An estimate of the dependence of Na+-H+ exchange on external Na+ gave an apparent Michaelis constant for external Na+ of 10 mM and an apparent maximal velocity of 0.1 mM H+/s. Intracellular H+ was found to have a cooperative effect (Hill coefficient = 4) on Na+-H+ exchange. C1 UNIV MASSACHUSETTS,SCH MED,DEPT PHYSIOL,55 LAKE AVE N,WORCESTER,MA 01655. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 30 TC 15 Z9 15 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 JUN PY 1992 VL 262 IS 6 BP H1651 EP H1656 PN 2 PG 6 WC Physiology SC Physiology GA JC377 UT WOS:A1992JC37700005 ER PT J AU FREEMAN, GL COLSTON, JT AF FREEMAN, GL COLSTON, JT TI SIMPLE CIRCUIT FOR PACING HEARTS OF EXPERIMENTAL-ANIMALS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE BRADYCARDIA; TACHYCARDIA HEART FAILURE; RABBITS AB In this paper we describe a simple pacing circuit which can be used to drive the heart over a wide range of rates. The circuit is an astable multivibrator, based on an LM555 integrated circuit. It is powered by a 9-V battery and is small enough for use in rabbits. The circuit is easily constructed and inexpensive, making it attractive for numerous applications in cardiovascular research. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RP FREEMAN, GL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV CARDIOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. NR 6 TC 8 Z9 9 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 JUN PY 1992 VL 262 IS 6 BP H1939 EP H1940 PN 2 PG 2 WC Physiology SC Physiology GA JC377 UT WOS:A1992JC37700043 ER PT J AU SCHNEEBERGER, EE LYNCH, RD AF SCHNEEBERGER, EE LYNCH, RD TI STRUCTURE, FUNCTION, AND REGULATION OF CELLULAR TIGHT JUNCTIONS SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Review DE ZONULA-OCCLUDENS; JUNCTIONAL COMPLEX; CALCIUM; PERMEABILITY ID CANINE KIDNEY-CELLS; ADHESION MOLECULE UVOMORULIN; PROTEIN KINASE-C; ALVEOLAR EPITHELIAL MONOLAYERS; PLASMA-MEMBRANE; OCCLUDING JUNCTIONS; INTERCELLULAR-JUNCTIONS; MDCK CELLS; BIOELECTRIC PROPERTIES; FETAL LAMB AB The tight junction (TJ) is a dynamic structure that is controlled, in part, by the activity of the cytoskeleton. It has become abundantly clear that, in the presence of Ca2+, assembly of the TJ is the result of cellular interactions that trigger a complex cascade of biochemical events that ultimately lead to the formation of an organized network of TJ elements, the composition of which remains unknown. The TJ functions both as a barrier between two fluid compartments and, to a lesser extent, as a fence between apical and basolateral membrane domains. To meet the many physiological and pathological challenges to which epithelia and endothelia are subjected, the TJ must be capable of a rapid and coordinated response, which depends on complex regulatory mechanisms. The precise characterization of the mechanisms involved in the assembly and regulation of the TJ is an area of current active investigation. However, until the biochemical composition of this structure has been defined and its gene identified, the TJ will continue to be an elusive yet tantalizing challenge to the cell biologist. C1 UNIV MASSACHUSETTS,DEPT BIOL SCI,LOWELL,MA 01854. RP SCHNEEBERGER, EE (reprint author), MASSACHUSETTS GEN HOSP,DEPT PATHOL,COX BLDG 5,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL-25822] NR 145 TC 257 Z9 260 U1 1 U2 11 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 JUN PY 1992 VL 262 IS 6 BP L647 EP L661 PN 1 PG 15 WC Physiology SC Physiology GA JC376 UT WOS:A1992JC37600083 PM 1616050 ER PT J AU RICCIARDI, JN BAER, L JENIKE, MA FISCHER, SC SHOLTZ, D BUTTOLPH, ML AF RICCIARDI, JN BAER, L JENIKE, MA FISCHER, SC SHOLTZ, D BUTTOLPH, ML TI CHANGES IN DSM-III-R AXIS-II DIAGNOSES FOLLOWING TREATMENT OF OBSESSIVE-COMPULSIVE DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PERSONALITY-DISORDERS AB Seventeen patients with obsessive-compulsive disorder and concomitant personality disorders were treated with pharmacologic and/or behavioral therapy and reassessed after 4 months. Nine of the 10 patients who responded to treatment for obsessive-compulsive disorder no longer met criteria for a personality disorder. Of the seven nonresponders, five continued to meet criteria for a personality disorder. C1 MASSACHUSETTS SCH PROFESS PSYCHOL,DEDHAM,MA. RP RICCIARDI, JN (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,OBSESS COMPULS DISORDERS CLIN & RES UNIT,BOSTON,MA 02129, USA. NR 10 TC 65 Z9 71 U1 0 U2 3 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 JUN PY 1992 VL 149 IS 6 BP 829 EP 831 PG 3 WC Psychiatry SC Psychiatry GA HW163 UT WOS:A1992HW16300016 PM 1590503 ER PT J AU SORENSEN, G MORRIS, DM HUNT, MK HEBERT, JR HARRIS, DR STODDARD, A OCKENE, JK AF SORENSEN, G MORRIS, DM HUNT, MK HEBERT, JR HARRIS, DR STODDARD, A OCKENE, JK TI WORK-SITE NUTRITION INTERVENTION AND EMPLOYEES DIETARY HABITS - THE TREATWELL PROGRAM SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Note AB In a randomized, controlled study of the Treatwell work-site nutrition intervention program, which focused on promoting eating patterns low in fat and high in fiber, 16 work sites from Massachusetts and Rhode Island were recruited to participate and randomly assigned to either an intervention or a control condition. The intervention included direct education and environmental programming tailored to each work site; control work sites received no intervention. A cohort of workers randomly sampled from each site was surveyed both prior to and following the intervention. Dietary pattens were assessed using a semiquantitative food frequency questionnaire. Adjusting for work site, the decrease in mean dietary fat intake was 1.1% of total calories more in intervention sites than in control sites (P < .005). Mean changes in dietary fiber intake between intervention and control sites did not differ. This study provides evidence that a work-site nutrition intervention program can effectively influence the dietary habits of workers. C1 UNIV MASSACHUSETTS,SCH MED,DIV PREVENT & BEHAV MED,WORCESTER,MA 01605. UNIV MASSACHUSETTS,SCH MED,SCH PUBL HLTH,WORCESTER,MA 01605. MAINSTREAM NUTR,WINNIPEG,MANITOBA,CANADA. RP SORENSEN, G (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC EPIDEMIOL & CONTROL,44 BINNEY ST,BOSTON,MA 02115, USA. OI Harris, Donald/0000-0002-8262-3716 FU NCI NIH HHS [5R01 CA46028] NR 7 TC 68 Z9 68 U1 0 U2 0 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD JUN PY 1992 VL 82 IS 6 BP 877 EP 880 DI 10.2105/AJPH.82.6.877 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA HW165 UT WOS:A1992HW16500021 PM 1316722 ER PT J AU CRUMP, JW GEIST, LJ AURON, PE WEBB, AC STINSKI, MF HUNNINGHAKE, GW AF CRUMP, JW GEIST, LJ AURON, PE WEBB, AC STINSKI, MF HUNNINGHAKE, GW TI THE IMMEDIATE EARLY GENES OF HUMAN CYTOMEGALOVIRUS REQUIRE ONLY PROXIMAL PROMOTER ELEMENTS TO UP-REGULATE EXPRESSION OF INTERLEUKIN-1-BETA SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID HUMAN PROINTERLEUKIN-1-BETA; VIRUS INFECTION; TRANSCRIPTION; SEQUENCE; PRODUCTS; ENHANCER; REPEAT; CELLS AB Human cytomegalovirus (HCMV) can infect monocytes and macrophages. The immediate early one (IE1) gene product of HCMV positively regulates its own expression, as well as the expression of the interleukin-1-beta (IL-1) gene. This study describes the IL-1 promoter proximal region required for upregulation of IL-1 gene expression by the HCMV IE1 or IE1 plus IE2 gene products. An IL-1 chloramphenicol acetyltransferase (CAT) construct containing the IL-1 genomic upstream sequence from position -1097 to +14 and four additional IL-1CAT plasmids containing progressive deletions of the -1097 to -131 sequence were used to evaluate the effect of the HCMV IE gene products on IL-1 gene expression. IL-1CAT plasmids were transfected into a monocytic cell line, THP-1, with plasmids containing either the IE promoter-regulatory region upstream of the bona fide IE1 (pIE1), IE2 (pIE2), or IE1+2 genes (pIE1+2) or a control plasmid containing the IE promoter-regulatory region alone (pLink760). In the presence of pIE1+2, there was an approximate 15-fold increase in CAT activity compared with-the control, pLink760, in cells with CAT plasmids containing the -1097 to +14 IL-1 sequence. Plasmids with progressive deletions of this sequence, including the plasmid containing the shortest upstream segment (-131 to +14) also had an approximate 15-fold increase in CAT activity. The upregulation of IL-1 expression,was mediated, primarily, by IE1 and not by IE2. This effect was promoter specific because an IL-1CAT plasmid with a complete deletion of the proximal promoter elements (-234 to +146) did not respond to the HCMV IE gene products. These studies indicate that HCMV IE gene products require only proximal promoter elements from -131 to +14 to upregulate IL-1 gene expression. C1 UNIV IOWA, COLL MED, DEPT INTERNAL MED, DIV PULM DIS, C33, GH, IOWA CITY, IA 52242 USA. UNIV IOWA, COLL MED, DEPT VET AFFAIRS, IOWA CITY, IA 52242 USA. UNIV IOWA, COLL MED, DEPT MICROBIOL, IOWA CITY, IA 52242 USA. WELLESLEY COLL, DEPT BIOL SCI, WELLESLEY, MA 02181 USA. MASSACHUSETTS GEN HOSP, LOVETT RES FACIL MARTIN LABS, BOSTON, MA USA. FU NHLBI NIH HHS [HL37121]; NIAID NIH HHS [AI 13562, AI 27850] NR 25 TC 36 Z9 37 U1 0 U2 1 PU AMER THORACIC SOC PI NEW YORK PA 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD JUN PY 1992 VL 6 IS 6 BP 674 EP 677 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA HY984 UT WOS:A1992HY98400016 PM 1317194 ER PT J AU CRENSHAW, WB CHEW, FS AF CRENSHAW, WB CHEW, FS TI RATHKE CLEFT CYST SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 4 TC 4 Z9 4 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUN PY 1992 VL 158 IS 6 BP 1312 EP 1312 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV273 UT WOS:A1992HV27300029 PM 1590132 ER PT J AU YODER, IC HALL, DA AF YODER, IC HALL, DA TI HYSTEROSALPINGOGRAPHY IN ENGLAND - REPLY SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Letter RP YODER, IC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD JUN PY 1992 VL 158 IS 6 BP 1410 EP 1411 PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV273 UT WOS:A1992HV27300073 ER PT J AU CLEMENT, PB YOUNG, RH AF CLEMENT, PB YOUNG, RH TI ENDOCERVICOSIS OF THE URINARY-BLADDER - A REPORT OF 6 CASES OF A BENIGN MULLERIAN LESION THAT MAY MIMIC ADENOCARCINOMA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE URINARY BLADDER; ENDOCERVICOSIS; ENDOMETRIOSIS; MULLERIAN TUMORS ID UTERINE CERVIX; CLINICOPATHOLOGIC ANALYSIS; OVARIAN-TUMORS; ENDOMETRIOSIS; EPITHELIUM; METAPLASIA; CARCINOMAS AB Six tumor-like glandular lesions characterized by a prominent component of endocervical-type epithelium involved the wall of the urinary bladder in women of reproductive age (31 to 44 years; mean, 37). All of the lesions posed problems in histologic diagnosis; indeed, a diagnosis of adenocarcinoma was initially rendered in three cases. Five patients presented with bladder symptoms, including-alone or in combination-surprapubic pain, dysuria, frequency, and hematuria. There was catamenial exacerbation of the symptoms in one case. The sixth patient-the only one with documented pelvic endometriosis-presented with dysmenorrhea, dysparenunia, and lower abdominal tenderness. In each patient, a mass that ranged from 2 to 5 cm in maximum dimension was typically located in the posterior wall or posterior dome of the urinary bladder. A partial cystectomy (five cases) or transurethral resection (one case) was performed. In one patient, extravesical pelvic soft tissue was involved, precluding complete resection of the lesion. Microscopic examination revealed extensive involvement of the bladder wall by irregularly disposed, benign-appearing, or mildly atypical endocervical-type glands, some of which were cystically dilated. Other findings included occasional ciliated cells, typically interspersed with the endocervical-type cells (four cases), a minor component of endometrioid glands (three cases), and glands lined by nonspecific cuboidal or flattened cells with eosinophilic cytoplasm (all cases). Some of the glands were surrounded only by the smooth muscle of the muscularis propria, but in other areas, the periglandular tissue was fibrous or edematous. In three cases, rare glands were surrounded by thin rims of endometriotic stroma. Gland rupture resulted in stromal extravasation of mucin in all cases and was a prominent feature in one. All patients had unevenful postoperative follow-up periods ranging from 1.5 to 14 years. The findings indicate that these bladder lesions are mullerian in nature and represent examples of endocervicosis, the mucinous analogue of endometriosis. Awareness of the lesion, which with one possible exception is hitherto undescribed in the bladder, and attention to its typical histologic features should facilitate its crucial distinction from adenocarcinoma. C1 UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP CLEMENT, PB (reprint author), VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. NR 34 TC 74 Z9 76 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 JUN PY 1992 VL 16 IS 6 BP 533 EP 542 DI 10.1097/00000478-199206000-00001 PG 10 WC Pathology; Surgery SC Pathology; Surgery GA HV505 UT WOS:A1992HV50500001 PM 1318002 ER PT J AU COTE, CJ AF COTE, CJ TI NEONATAL POSTOPERATIVE APNEA - UNEXPLAINED - REPLY SO ANESTHESIOLOGY LA English DT Letter C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP COTE, CJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD JUN PY 1992 VL 76 IS 6 BP 1072 EP 1072 PG 1 WC Anesthesiology SC Anesthesiology GA HY137 UT WOS:A1992HY13700052 ER PT J AU GOFF, BA BAMBERG, M HASAN, T AF GOFF, BA BAMBERG, M HASAN, T TI EXPERIMENTAL PHOTODYNAMIC TREATMENT OF OVARIAN-CARCINOMA CELLS WITH IMMUNOCONJUGATES SO ANTIBODY IMMUNOCONJUGATES AND RADIOPHARMACEUTICALS LA English DT Article ID ANTIBODY-TARGETED PHOTOLYSIS; MONOCLONAL-ANTIBODY; CANCER; CA-125; TUMOR; PHOTOSENSITIZERS; HEMATOPORPHYRIN; THERAPY; DISEASE; BENIGN AB Photodynamic therapy (PDT) is a relatively new and selective approach to the treatment of malignant neoplasms. In PDT, nontoxic photoactivatable compounds (photosensitizers) are accumulated preferentially in malignant tissues. Activation with light produces a phototoxic effect by the production of active molecular species. The only photosensitizer aproved for experimental clinical application is Photofrin, a mixture of porphyrins. The therapeutic efficacy of Photofrin is limited due to a significant non-specific accumulation in the skin, leading to prolonged cutaneous phototoxicity for up to 8-10 weeks. Therefore new photosensitizers with improved specificity are being investigated. Specificity may also be improved by linking photosensitizers with monoclonal antibodies (Mab). Because of the double selectivity inherent in PDT, the requirements for Mab specificity are not as stringent as for other immunoconjugates. We have conjugated the photosensitizer, a chlorin derivative (CMA), via polyglutamic acid (PGA) to OC125, an antibody directed against an antigen, CA125 on human ovarian cancer (CA) cells. Phototoxic efficacy of these conjugates was tested against a human ovarian carcinoma cell line, NIH:OVCAR3 (target cells), and a human keratinocyte cell line (non-target cells). Cells were incubated with the immunoconjugate for 1 hour. They were then washed and irradiated at 654 nm (lambda(max)CMA) with an argon-ion-pumped dye laser or 25 J/cm2. NIH:OVCAR3 cells showed only a 2% +/- 2 survival compared with untreated controls, while under identical conditions keratinocytes showed a 65% +/- 5 survival compared with untreated controls. Treatment with light or immunoconjugate alone resulted in no cytotoxicity to any of these cells. These results demonstrate that photochemical destruction with high levels of antigen selectivity can be achieved with photoimmunotargeting. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,VINCENT GYNECOL SERV,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 24 TC 10 Z9 11 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0892-7049 J9 ANTIBODY IMMUNOCONJ JI Antib. Immunoconjug. Radiopharm. PD SUM PY 1992 VL 5 IS 2 BP 191 EP 199 PG 9 WC Immunology; Radiology, Nuclear Medicine & Medical Imaging SC Immunology; Radiology, Nuclear Medicine & Medical Imaging GA JA791 UT WOS:A1992JA79100004 ER PT J AU ASHLAND, JE HO, M AF ASHLAND, JE HO, M TI PHONETICS FOR SPEECH PATHOLOGY - BALL,MJ SO APPLIED PSYCHOLINGUISTICS LA English DT Book Review RP ASHLAND, JE (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 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 JUN PY 1992 VL 13 IS 2 BP 249 EP 251 DI 10.1017/S0142716400005609 PG 3 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA JK784 UT WOS:A1992JK78400009 ER PT J AU JETMALANI, SN RICH, P WHITE, CR AF JETMALANI, SN RICH, P WHITE, CR TI PAINFUL SOLITARY SUBUNGUAL NODULE - SUBUNGUAL EXOSTOSIS (SE) SO ARCHIVES OF DERMATOLOGY LA English DT Note C1 PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP JETMALANI, SN (reprint author), OREGON HLTH SCI UNIV,PORTLAND,OR 97201, USA. NR 7 TC 2 Z9 2 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 JUN PY 1992 VL 128 IS 6 BP 847 EP & PG 0 WC Dermatology SC Dermatology GA HY066 UT WOS:A1992HY06600023 ER PT J AU DENBESTEN, PK HEFFERNAN, LM FEATHERSTONE, JDB SHIELDS, CP AF DENBESTEN, PK HEFFERNAN, LM FEATHERSTONE, JDB SHIELDS, CP TI FLUORIDE BINDING BY MATRIX PROTEINS IN RAT MINERALIZING TISSUE SO ARCHIVES OF ORAL BIOLOGY LA English DT Article DE FLUORIDE; ENAMEL; BONE ID FORMING ENAMEL; AMELOGENESIS AB Chronic fluoride exposure in vivo results in alterations iri the formation of mineralizing tissues One possible mechanism for the formation of fluorosed tooth enamel and bone is a binding of fluoride to matrix proteins, resulting in an alteration in their structure and function. Studies were designed to investigate fluoride binding to matrix proteins in vivo and their possible role in fluorosis. Rats were given either 0 or 100 parts/10(6) fluoride in drinking water for 6 weeks to allow the formation of fluorotic mineralizing tissues. The animals were killed by CO2 inhalation, and the enamel and bone were analysed for fluoride and calcium. Matrix binding by fluoride in enamel was determined after extraction of proteins from undemineralized matrix. In bone, the matrix was demineralized and F, Ca and P were determined in both ashed and unashed samples, The studies showed ionic binding of fluoride to the matrix in both enamel and bone, possibly associated with calcium binding by the matrix. There was no difference in the amount of matrix-bound fluoride in control as compared to fluorosed bone or maturation-stage enamel. This indicates that although matrix proteins can bind fluoride, it is not likely that this mechanism is important in the formation of fluorosed mineralizing tissues. C1 EASTMAN DENT CTR,ROCHESTER,NY 14620. RP DENBESTEN, PK (reprint author), FORSYTH DENT CTR,140 FENWAY,BOSTON,MA 02115, USA. FU NIDCR NIH HHS [DE07384] NR 16 TC 5 Z9 5 U1 0 U2 0 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 JUN PY 1992 VL 37 IS 6 BP 459 EP 462 DI 10.1016/0003-9969(92)90100-M PG 4 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA JF334 UT WOS:A1992JF33400005 PM 1637261 ER PT J AU SALE, GE ANDERSON, P BROWNE, M MYERSON, D AF SALE, GE ANDERSON, P BROWNE, M MYERSON, D TI EVIDENCE OF CYTOTOXIC T-CELL DESTRUCTION OF EPIDERMAL-CELLS IN HUMAN GRAFT-VS-HOST DISEASE - IMMUNOHISTOLOGY WITH MONOCLONAL-ANTIBODY TIA-1 SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID CYTO-TOXIC LYMPHOCYTES; SKIN; DIAGNOSIS; TARGETS; BIOPSY AB A newly described mouse monoclonal IgG1 antibody, TIA-1, binds serine esterase-positive granule membranes of cytotoxic human T cells and is a candidate for an effector molecule involved in T-cell cytolytic mechanisms analogous to those of the perforin system. We performed immunohistologic studies on frozen human skin (n = 5) and lip (n = 21) sections as well as on control frozen sections of tonsils, purified cytolytic T (CD8) cells, and B cells using an indirect immunoperoxidase system. We found a strong association of TIA-1+ cells with CD8+ cells invading the epidermis in lip and skin lesions of graft-vs-host disease in human marrow allograft recipients, as well as a sharp geographic association of TIA+ lymphocytes with CD8+ regions in human tonsil sections. Double staining of CD8 and TIA-1 antigens with fluorescein isothiocyanate and Texas red confirmed that 80% to 90% of the CD8 cells were TIA-1+ in the epidermal infiltrates. Leu-7 activity (natural killer cell) was minimal and found in only three of 17 lip biopsy specimens. These data provide new evidence that direct cytolytic attack by donor T lymphocytes is the mechanism of epithelial target cell killing in human graft-vs-host disease. C1 UNIV WASHINGTON,DEPT PATHOL,SEATTLE,WA 98195. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP SALE, GE (reprint author), FRED HUTCHINSON CANC RES CTR,DEPT PATHOL,DIV CLIN RES,SC111,1124 COLUMBIA,SEATTLE,WA 98104, USA. FU NCI NIH HHS [CA 18029, CA 15704]; NHLBI NIH HHS [HL 36444] NR 24 TC 29 Z9 29 U1 0 U2 1 PU COLLEGE AMER PATHOLOGISTS PI NORTHFIELD PA C/O KIMBERLY GACKI, 325 WAUKEGAN RD, NORTHFIELD, IL 60093-2750 SN 0003-9985 J9 ARCH PATHOL LAB MED JI Arch. Pathol. Lab. Med. PD JUN PY 1992 VL 116 IS 6 BP 622 EP 625 PG 4 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA HX009 UT WOS:A1992HX00900019 PM 1616423 ER PT J AU NISSEN, SJ NEWMAN, WP AF NISSEN, SJ NEWMAN, WP TI FACTORS INFLUENCING REINTEGRATION TO NORMAL LIVING AFTER AMPUTATION SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Article DE AMPUTATION; QUALITY OF LIFE; REHABILITATION ID STAGE RENAL-DISEASE; QUALITY; LIFE AB This study identified factors affecting reintegration to normal living (RNL) after lower extremity amputation. A questionnaire was used to evaluate RNL at a veterans' medical center and private rehabilitation clinic. The patients were 42 elderly individuals (68 +/- 1.5 years). Eighty-eight percent were men and 76% had additional health problems. Unilateral below-knee amputations, unilateral above-knee amputations, and bilateral amputations accounted for 38%, 36%, and 26% of subjects, respectively. Eleven questions were asked to evaluate mobility, self-care, work, recreation, social activities (daily functioning), relationships, social self, and life events (perception of self). The median overall RNL, score was 16 of 22 (range, 5 to 22). Poor reintegration occurred in community mobility, work, and recreation. Perception of self questions showed satisfactory reintegration. Examination of variables impacting reintegration showed only additional illness significantly reducing the RNL score. It was concluded that current rehabilitative efforts regarding home mobility and psychological adjustment are satisfactory. More attention to community mobility, recreation, and additional illnesses would improve RNL after amputation. C1 UNIV N DAKOTA,CTR MED EDUC,SCH MED,DEPT MED,GRAND FORKS,ND 58201. US DEPT VET AFFAIRS,DIV ENDOCRINOL,FARGO,ND. NR 13 TC 51 Z9 52 U1 1 U2 5 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD JUN PY 1992 VL 73 IS 6 BP 548 EP 551 PG 4 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA HX739 UT WOS:A1992HX73900006 PM 1622303 ER PT J AU HASHIMOTO, N ZHANG, WR GOLDSTEIN, BJ AF HASHIMOTO, N ZHANG, WR GOLDSTEIN, BJ TI INSULIN-RECEPTOR AND EPIDERMAL GROWTH-FACTOR RECEPTOR DEPHOSPHORYLATION BY 3 MAJOR RAT-LIVER PROTEIN-TYROSINE PHOSPHATASES EXPRESSED IN A RECOMBINANT BACTERIAL SYSTEM SO BIOCHEMICAL JOURNAL LA English DT Article ID MESSENGER-RNA; CDNA AB Protein-tyrosine phosphatases (PTPases) play an essential role in thc regulation of signal transduction mediated by reversible protein-tyrosine phosphorylation. In order to characterize individual rat hepatic PTPases that might have specificity for autophosphorylated receptor tyrosine kinases, we isolated cDNA segments encoding three PTPases (PTPase 1B, LAR and LRP) that are expressed in insulin-sensitive liver and skeletal muscle tissue. and evaluated their catalytic activity in vitro. The intrinsic PTPase activities of the full-length PTPase 1 B protein and the cytoplasmic domains of LAR and LRP were studied by expression of recombinant cDNA constructs in the inducible bacterial vector pKK233-2 using extracts of a host strain of Escherichia coli that lacks endogenous PTPase activity. Each of the cloned cDNAs dephosphorylated a cognate phosphopeptide derived from the regulatory region of the insulin receptor. Despite having only 30-39% sequence identity in their catalytic domains, LAR and PTPase 1 B had similar relative activities between the peptide substrate and intact insulin receptors, and also displayed similar initial rates of simultaneous dephosphorylation of insulin and epidermal growth factor (EGF) receptors. In contrast, LRP exhibited a higher rate of dephosphorylation of both intact receptors relative to the peptide substrate, and also dephosphorylated EGF receptors more rapidly than insulin receptors. These studies indicate that three PTPases with markedly divergent structures have the catalytic potential to dephosphorylate both insulin and EGF receptors in intact cells and that redundant PTPase activity may occur in vivo. For these PTPases to have specific physiological actions in intact cells, they must be influenced by steric effects of the additional protein segments of the native transmembrane enzymes, cellular compartmentalization and/or interactions with regulatory proteins. C1 JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36836, DK43396] NR 19 TC 65 Z9 67 U1 0 U2 0 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD JUN 1 PY 1992 VL 284 BP 569 EP 576 PN 2 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HY203 UT WOS:A1992HY20300041 PM 1599438 ER PT J AU TSUJI, K LYMAN, SD SUDO, T CLARK, SC OGAWA, M AF TSUJI, K LYMAN, SD SUDO, T CLARK, SC OGAWA, M TI ENHANCEMENT OF MURINE HEMATOPOIESIS BY SYNERGISTIC INTERACTIONS BETWEEN STEEL FACTOR (LIGAND FOR C-KIT), INTERLEUKIN-11, AND OTHER EARLY ACTING FACTORS IN CULTURE SO BLOOD LA English DT Article ID COLONY-STIMULATING FACTOR; FACTOR-I; INTERLEUKIN-3-DEPENDENT PROLIFERATION; MOLECULAR-CLONING; GROWTH-FACTOR; W-LOCUS; PROGENITORS; RECEPTOR; CELLS; IDENTIFICATION C1 RALPH H JOHNSON VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29403. IMMUNEX CORP,SEATTLE,WA. BIOMAT RES INST CO LTD,YOKOHAMA,JAPAN. GENET INST,CAMBRIDGE,MA. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. FU NIDDK NIH HHS [DK32294] NR 29 TC 160 Z9 160 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 1 PY 1992 VL 79 IS 11 BP 2855 EP 2860 PG 6 WC Hematology SC Hematology GA JA203 UT WOS:A1992JA20300007 PM 1375116 ER PT J AU OKUDA, K SANGHERA, JS PELECH, SL KANAKURA, Y HALLEK, M GRIFFIN, JD DRUKER, BJ AF OKUDA, K SANGHERA, JS PELECH, SL KANAKURA, Y HALLEK, M GRIFFIN, JD DRUKER, BJ TI GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR, INTERLEUKIN-3, AND STEEL FACTOR INDUCE RAPID TYROSINE PHOSPHORYLATION OF P42 AND P44 MAP KINASE SO BLOOD LA English DT Article ID SERINE-THREONINE KINASE; PROTEIN-KINASE; SIGNAL TRANSDUCTION; CELL-LINES; ACTIVATION; GROWTH; FIBROBLASTS; EXPRESSION; MATURATION; RECEPTOR C1 HARVARD UNIV, SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL, 44 BINNEY ST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02115 USA. UNIV BRITISH COLUMBIA, DEPT MED, VANCOUVER V6T 1W5, BC, CANADA. UNIV BRITISH COLUMBIA, BIOMED RES CTR, VANCOUVER V6T 1W5, BC, CANADA. FU NCI NIH HHS [CA 34183, CA 36167] NR 36 TC 234 Z9 235 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 2021 L ST NW, SUITE 900, WASHINGTON, DC 20036 USA SN 0006-4971 EI 1528-0020 J9 BLOOD JI Blood PD JUN 1 PY 1992 VL 79 IS 11 BP 2880 EP 2887 PG 8 WC Hematology SC Hematology GA JA203 UT WOS:A1992JA20300011 PM 1375118 ER PT J AU EMANUEL, PD EAVES, CJ BROUDY, VC PAPAYANNOPOULOU, T MOORE, MR DANDREA, AD PRCHAL, JF EAVES, AC PRCHAL, JT AF EMANUEL, PD EAVES, CJ BROUDY, VC PAPAYANNOPOULOU, T MOORE, MR DANDREA, AD PRCHAL, JF EAVES, AC PRCHAL, JT TI FAMILIAL AND CONGENITAL POLYCYTHEMIA IN 3 UNRELATED FAMILIES SO BLOOD LA English DT Article ID HUMAN ERYTHROPOIETIN RECEPTOR; ERYTHROID COLONY FORMATION; HUMAN MARROW; PURE ERYTHROCYTOSIS; CELL-GROWTH; VERA; INVITRO; BINDING; EXPRESSION; GENE C1 UNIV ALABAMA,DEPT MED,DIV HEMATOL ONCOL,CTR COMPREHENS CANC,513 TINSLEY HARRISON TOWERS,BIRMINGHAM,AL 35294. UNIV BRITISH COLUMBIA,VANCOUVER V6T 1W5,BC,CANADA. UNIV WASHINGTON,DIV HEMATOL,SEATTLE,WA 98195. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,DIV HEMATOL ONCOL,BOSTON,MA 02115. MCGILL UNIV,DIV HEMATOL,MONTREAL H3A 2T5,QUEBEC,CANADA. BRITISH COLUMBIA CANC AGCY,TERRY FOX LAB,VANCOUVER,BC,CANADA. WILLIS KNIGHTON MED CTR,SHREVEPORT,LA. OI Emanuel, Peter/0000-0002-9764-2434 FU NIDDK NIH HHS [DK07488, DK31232] NR 81 TC 60 Z9 61 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD JUN 1 PY 1992 VL 79 IS 11 BP 3019 EP 3030 PG 12 WC Hematology SC Hematology GA JA203 UT WOS:A1992JA20300029 PM 1316790 ER PT J AU ELIAS, AD AYASH, L ANDERSON, KC HUNT, M WHEELER, C SCHWARTZ, G TEPLER, I MAZANET, R LYNCH, C PAP, S PELAEZ, J REICH, E CRITCHLOW, J DEMETRI, G BIBBO, J SCHNIPPER, L GRIFFIN, JD FREI, E ANTMAN, KH AF ELIAS, AD AYASH, L ANDERSON, KC HUNT, M WHEELER, C SCHWARTZ, G TEPLER, I MAZANET, R LYNCH, C PAP, S PELAEZ, J REICH, E CRITCHLOW, J DEMETRI, G BIBBO, J SCHNIPPER, L GRIFFIN, JD FREI, E ANTMAN, KH TI MOBILIZATION OF PERIPHERAL-BLOOD PROGENITOR CELLS BY CHEMOTHERAPY AND GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR FOR HEMATOLOGIC SUPPORT AFTER HIGH-DOSE INTENSIFICATION FOR BREAST-CANCER SO BLOOD LA English DT Article ID BONE-MARROW TRANSPLANTATION; HEMATOPOIETIC STEM-CELLS; NON-LYMPHOBLASTIC LEUKEMIA; NON-HODGKINS-LYMPHOMA; AUTOLOGOUS TRANSPLANTATION; EARLY REMISSION; CYCLOPHOSPHAMIDE C1 HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT MED, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT BIOSTAT, BOSTON, MA 02115 USA. HARVARD UNIV, BETH ISRAEL HOSP, SCH MED, DEPT MED & SURG, BOSTON, MA 02215 USA. FU NCI NIH HHS [P01CA-38493] NR 50 TC 283 Z9 283 U1 0 U2 0 PU AMER SOC HEMATOLOGY PI WASHINGTON PA 1900 M STREET. NW SUITE 200, WASHINGTON, DC 20036 USA SN 0006-4971 J9 BLOOD JI Blood PD JUN 1 PY 1992 VL 79 IS 11 BP 3036 EP 3044 PG 9 WC Hematology SC Hematology GA JA203 UT WOS:A1992JA20300031 PM 1350229 ER PT J AU NOZAKI, K MOSKOWITZ, MA BOCCALINI, P AF NOZAKI, K MOSKOWITZ, MA BOCCALINI, P TI CP-93,129, SUMATRIPTAN, DIHYDROERGOTAMINE BLOCK C-FOS EXPRESSION WITHIN RAT TRIGEMINAL NUCLEUS CAUDALIS CAUSED BY CHEMICAL-STIMULATION OF THE MENINGES SO BRITISH JOURNAL OF PHARMACOLOGY LA English DT Article DE SUMATRIPTAN; CP-93,129; DIHYDROERGOTAMINE; TRIGEMINOVASCULAR SYSTEM; SUBARACHNOID HEMORRHAGE; C-FOS EXPRESSION; 5-HT(1B/D) RECEPTOR AGONISTS; HEADACHE ID SUBARACHNOID HEMORRHAGE; SPINAL-CORD; DURA MATER; PROTEIN; PHARMACOLOGY; ARTERIOLES; GR43175; AGONIST; BRAIN AB 1 The effects of intravenously administered 5-HT1B receptor agonists were examined on c-fos-like immunoreactivity, an indicator of neuronal activation, within the brain stem. C-fos was induced by injecting an analgesic, vasoconstrictor substance (0.3 ml of autologous blood) or a pro-inflammatory molecule, carrageenin (I mg in 0.1 ml saline) into the cisterna magna of pentobarbitone-anaesthetized Sprague-Dawley rats and was visualized in serial sections (50-mu-m) by use of a polyclonal antiserum. 2 As previously reported, the injection of blood caused significant labelling within laminae I, II(o) of the trigeminal nucleus caudalis, a major nociceptive brain stem nucleus, as well as within nucleus of the solitary tract and area postrema. A similar pattern of expression with fewer cells per section was detected after carrageenin instillation. The number of expressing cells was reduced by 54% in trigeminal nucleus caudalis but not within the nucleus of the solitary tract or area postrema when blood was injected in adult rats after neonatal capsaicin treatment. 3 Pretreatment with 5-HT1 agonists with some selectivity for the 5-HT1B receptor, CP-93,129 (460 nmol kg-1 x 2, i.v.), sumatriptan (720 nmol kg-1 x 2, i.v.) or dihydroergotamine (86 nmol kg-1 x 2, i.v.) reduced positive cells by 39%, 31%, and 33% respectively in trigeminal nucleus caudalis but not in nucleus of the solitary tract or area postrema after blood instillation. Pretreatment with the analgesic morphine (15-mu-mol kg-1, s.c.) also decreased the number of positive cells by 63% in trigeminal nucleus caudalis. 4 CP-93,129 (460 nmol kg-1 x 2, i.v.) reduced the number of c-fos labelled cells by 47% within lamina I, II(o) after carrageenin instillation. 5 Drug-induced blockade appeared to be tissue-dependent. Pretreatment with sumatriptan (720 nmol kg-1 x 2, i.v.) did not block,c-fos expression in trigeminal nucleus caudalis following formalin application to the nasal mucosa. 6 Drug-induced blockade may be mediated by an action on primary afferent (trigeminovascular) fibres in as much as CP-93,129 (460 nmol kg-1 x 2, i.v.) did not reduce the number of expressing cells within the trigeminal nucleus caudalis following blood instillation in rats treated as neonates with capsaicin. 7 We infer from these results that the analgesic actions of agonists at 5-HT1B receptors (the receptor subtype analogous to 5-HT1D in man) need not depend upon the presence of vasodilatation and, that 5-HT1D receptor-mediated blockade of neurotransmission contributes significantly to the analgesic effects of these drugs in headache. 8 Based on the demonstrated effects of 5-HT1B/D agonists against the actions of two chemically-unrelated meningeal stimulants, we suggest that treatment with 5-HT1D agonists may be useful for the alleviation of pain in other headache conditions associated with meningeal irritation. Bacterial, viral (including AIDS meningovascular inflammation) and other forms of chemical meningitis merit further investigation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,BOSTON,MA 02114. NR 29 TC 120 Z9 120 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0007-1188 J9 BRIT J PHARMACOL JI Br. J. Pharmacol. PD JUN PY 1992 VL 106 IS 2 BP 409 EP 415 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HX274 UT WOS:A1992HX27400030 PM 1327382 ER PT J AU DRINKA, PJ DESMET, AA BAUWENS, SF ROGOT, A AF DRINKA, PJ DESMET, AA BAUWENS, SF ROGOT, A TI THE EFFECT OF OVERLYING CALCIFICATION ON LUMBAR BONE DENSITOMETRY SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE BONE DENSITOMETRY; MALES; FACET SCLEROSIS; AORTIC CALCIFICATION ID ABSORPTIOMETRY AB We studied bone mineral density (BMD) of the spine using dual photon absorptiometry, as well as standard anterior-posterior and lateral lumbar spine X-ray film in 113 ambulatory elderly male volunteers with a mean age of 72 years (range 66-91 years). Each subject had three measurements taken for lumbar vertebrae 1 through 4: BMD, length of aortic calcification (AC), and degenerative facet sclerosis grated 0-3. A separate statistical model was fit to BMD for each vertebra using analysis of covariance. AC did not contribute significantly to BMD. BMD was increased by 0.28-0.03 g/cm-2 (L1-L4) with a sclerosis score of 2, and by 0.47-0.25 g/cm-2 with a sclerosis score of 3, P < 0.001. The association between increased BMD and overlying facet sclerosis may be related to the bone density within the sclerosis itself or to an association between degenerative joint disease and a generalized increase in subchondral bone. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,CTR MED BIOSTAT,MADISON,WI 53706. MANAGED CARE RESOURCES INC,CHESAPEAKE,VA. RP DRINKA, PJ (reprint author), WISCONSIN VET HOME,KING,WI 54946, USA. NR 10 TC 79 Z9 82 U1 0 U2 0 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 JUN PY 1992 VL 50 IS 6 BP 507 EP 510 DI 10.1007/BF00582163 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HU648 UT WOS:A1992HU64800005 PM 1525705 ER PT J AU SCHWARTZ, SS HAY, DI SCHLUCKEBIER, SK AF SCHWARTZ, SS HAY, DI SCHLUCKEBIER, SK TI INHIBITION OF CALCIUM-PHOSPHATE PRECIPITATION BY HUMAN SALIVARY STATHERIN - STRUCTURE-ACTIVITY-RELATIONSHIPS SO CALCIFIED TISSUE INTERNATIONAL LA English DT Article DE SALIVARY PROTEINS; PRECIPITATION INHIBITORS; CALCIUM PHOSPHATE ID PROLINE-RICH PROTEINS; HUMAN-PAROTID SALIVA; COMPLETE COVALENT STRUCTURE; CRYSTAL-GROWTH; HYDROXYAPATITE FORMATION; OXALATE MONOHYDRATE; ACIDIC PEPTIDE; ORGANIC MATRIX; PLAQUE FLUID; PHOSPHOPROTEINS AB Previous studies of human statherin showed the active region for inhibition of secondary calcium phosphate precipitation (crystal growth) to reside in the highly charged amino-terminal one-third of this molecule, and the neutral tyrosine-, glutamine- and proline-rich carboxy-terminal two-thirds of the molecule is required for maximal inhibition of primary (spontaneous) precipitation. The purpose of the present study was to define more clearly the activities of these different molecular segments of statherin with respect to the two kinds of inhibitory activities. Peptides from statherin were prepared by specific proteolysis using trypsin, endoproteinase Arg-C, and activated factor X to produce the amino-terminal hexa-, nona- and decapeptides, respectively, and carboxypeptidase-A was used to obtain a peptide extending from residue 1 to about residues 32-37. The peptides were purified by anion exchange and gel filtration chromatography, and characterized and quantified by amino-acid analysis. Serially diluted samples of statherin and derived peptides were assayed to determine the concentrations, giving a standard 50% inhibition of precipitation (C50%) in assay systems designed for this purpose using polyaspartate as a standard. Results are expressed as (C50% statherin)/(C50% peptide). For inhibition of primary precipitation, these values were peptide(1-6), 0.20; peptide(1-9), 0.15; peptide(1-31/35), 0.24. For inhibition of secondary precipitation, the values were peptide(1-6), 3.8; peptide(1-9), 2.8; peptide(1-10), 1.9; peptide(1-32/37), 1.5. These quantitative findings show that maximum inhibition of primary precipitation by statherin requires the entire molecule. Thus, removal of a relatively small segment of its carboxy-terminal region results in a substantial reduction in inhibitory activity. Inhibition of secondary precipitation is associated only with the amino-terminal portion of the molecule; this activity increased with decreasing molecular size and increasing net negative charge, and is probably related to more efficient adsorption of the inhibitory peptide onto crystal growth sites. C1 FORSYTH DENT CTR,DEPT BIOCHEM,BOSTON,MA 02115. HARVARD UNIV,SCH DENT MED,CAMBRIDGE,MA 02138. FU NIDCR NIH HHS [DE 3915, DE 7008] NR 44 TC 51 Z9 51 U1 1 U2 13 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 JUN PY 1992 VL 50 IS 6 BP 511 EP 517 DI 10.1007/BF00582164 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HU648 UT WOS:A1992HU64800006 PM 1525706 ER PT J AU BRANDWEIN, MS HUVOS, AG PATIL, J JAGIRDAR, J AF BRANDWEIN, MS HUVOS, AG PATIL, J JAGIRDAR, J TI TUMOR-ASSOCIATED GLYCOPROTEIN DISTRIBUTION DETECTED BY MONOCLONAL-ANTIBODY B72.3 IN SALIVARY NEOPLASIA SO CANCER LA English DT Article ID MALIGNANT MIXED TUMORS; PLEOMORPHIC ADENOMA; CARCINOMA; TAG-72; ADENOCARCINOMA; ANTIGEN; BENIGN; MESOTHELIOMA; DIAGNOSIS; SERUM AB The expression of tumor-associated glycoprotein (TAG-72), an oncofetal mucin-like tumor-associated glycoprotein derived from membrane-enriched fractions of metastatic breast carcinoma, has been detected by monoclonal antibody (MoAb) B72.3 in adenocarcinomas of breast, colon, lung, endometrium, pancreas, and ovary. The authors reported the scope of TAG-72 expression detected by MoAb B72.3 in salivary neoplasia. They examined 96 salivary lesions (53 malignant and 37 benign primary tumors, 2 metastatic carcinomas, and 4 other benign lesions) and 17 normal tissues from parotid glands and found: diffuse TAG-72 expression in 29 of 55 (53%) malignant tumors and 6 of 36 (17%) benign tumors and in no normal tissue; focal TAG-72 expression in 10 of 55 (17%) malignant salivary tumors, 10 of 37 (25%) benign salivary tumors (all benign mixed tumors), and 1 of 17 (6%) histologically normal parotid gland ducts. Any expression of TAG-72, whether diffuse or focal, was found to have a 71% sensitivity for detecting salivary malignant tumors, but an unacceptably low specificity for malignant lesions (57%). Alternatively, if only diffuse TAG-72 expression was regarded as indicative of malignancy, the specificity of diffuse TAG-72 expression was 86%, but sensitivity of detection decreased to 53%. The authors studied a subset of benign and malignant mixed tumors (BMT and MMT) and found that 12 of 15 (80%) MMT diffusely and strongly expressed TAG-72, 2 of 15 MMT (13%) expressed TAG-72 focally, and 1 MMT (7%) was nonreactive. By contrast, most BMT did not express TAG-72; only sparse, focal TAG-72 expression was seen in 10 of 27 (37%) BMT. If diffuse TAG-72 expression is considered indicative of malignancy, its sensitivity and specificity for malignant mixed tumors is 80% and 100%, respectively. The authors suggest that diffuse TAG-72 expression may resolve conflicts in determining whether or not a mixed tumor is malignant. C1 MEM SLOAN KETTERING CANC CTR,DEPT PATHOL,1275 YORK AVE,NEW YORK,NY 10021. BRONX VET AFFAIRS MED CTR,BRONX,NY. NR 28 TC 15 Z9 15 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD JUN 1 PY 1992 VL 69 IS 11 BP 2623 EP 2630 DI 10.1002/1097-0142(19920601)69:11<2623::AID-CNCR2820691102>3.0.CO;2-N PG 8 WC Oncology SC Oncology GA HV177 UT WOS:A1992HV17700001 PM 1315205 ER PT J AU HUNCHAREK, M AF HUNCHAREK, M TI CHANGING RISK GROUPS FOR MALIGNANT MESOTHELIOMA SO CANCER LA English DT Article ID SHEET-METAL WORKERS; PLEURAL MESOTHELIOMA; AMPHIBOLE ASBESTOSES; PARTICLE DIMENSION; FIBROUS MINERALS; UNITED-STATES; EXPOSURE; CARCINOGENICITY; RAILROAD; DISEASE AB Although malignant mesothelioma is a relatively rare tumor, its incidence is rising. Much of the increase is attributable to widespread exposure to asbestos in past decades in asbestos-related industries. In recent years, it has become increasingly clear that mesothelioma risk is no longer confined to workers in the asbestos industry. This article reports a variety of recently identified "risk groups" and highlights the need for increased surveillance of these groups to document the occurrence of asbestos-related malignancy and the institution of measures for disease prevention. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. RP HUNCHAREK, M (reprint author), INST CANC EPIDEMIOL,SUITE 2513,ONE DEVONSHIRE PL,BOSTON,MA 02109, USA. NR 37 TC 32 Z9 33 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 JUN 1 PY 1992 VL 69 IS 11 BP 2704 EP 2711 DI 10.1002/1097-0142(19920601)69:11<2704::AID-CNCR2820691113>3.0.CO;2-F PG 8 WC Oncology SC Oncology GA HV177 UT WOS:A1992HV17700012 PM 1571901 ER PT J AU BARNARD, GF STANIUNAS, RJ BAO, S MAFUNE, KI STEELE, GD GOLLAN, JL CHEN, LB AF BARNARD, GF STANIUNAS, RJ BAO, S MAFUNE, KI STEELE, GD GOLLAN, JL CHEN, LB TI INCREASED EXPRESSION OF HUMAN RIBOSOMAL PHOSPHOPROTEIN P0 MESSENGER-RNA IN HEPATOCELLULAR-CARCINOMA AND COLON-CARCINOMA SO CANCER RESEARCH LA English DT Article ID CDNA CLONES; PROTEIN; METASTASIS; CLONING; DNA; PROGRESSION; ANTIBODIES; HEPATITIS; ENCODES; VIRUS AB To search for differentially expressed gene products in selected cancers of endodermal origin, cDNA libraries derived from mRNA in human hepatocellular carcinoma and adjacent grossly normal tissue were generated. From these parent libraries, subtracted cDNA libraries of tumor minus normal and normal minus tumor tissues were constructed. After screening these subtracted libraries by +/- hybridization, a cDNA clone that is overexpressed in hepatocellular carcinoma and encodes the human acidic ribosomal phosphoprotein P0 (P0) was identified. We then evaluated the expression of this phosphoprotein P0 in human colon carcinoma samples. Surgical specimens of primary tumors and liver metastases were examined by Northern hybridization of total RNA with one of 2 P-32-labeled P0 probes. The mRNA level of the P0 was greater in primary colon carcinoma than in paired adjacent normal colonic epithelium in 36 of 38 cases; the mean tumor/normal ratio was 2.7 (range, up to 13). The tumor/normal ratio, when plotted against the Dukes' stage of disease, gave evidence for increasing P0 expression with increasing stage of colon carcinoma (P = 0.02). In all 8 cases of paired colon carcinoma metastatic to liver and 2 cases of paired primary hepatocellular carcinoma, the PO mRNA level was greater in tumor than in adjacent normal liver tissue. The mean tumor/normal ratio was 4.0 (range, up to 11) for the colon cancers metastatic to liver and 4.2 for the primary hepatocellular carcinoma samples. These findings support a common increased expression of selected gene products in different tumors of endodermal origin and suggest that increased P0 expression, in line with certain other ribosomal proteins, may be associated with human colorectal cancer progression and biological aggressiveness. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,MAYER 840,44 BINNEY ST,BOSTON,MA 02115. NEW ENGLAND DEACONESS HOSP,DEPT SURG,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV GASTROENTEROL,BOSTON,MA 02115. FU NCI NIH HHS [CA44704, 1F32 CA-0900]; NIDDK NIH HHS [DK07533] NR 34 TC 93 Z9 97 U1 2 U2 3 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 JUN 1 PY 1992 VL 52 IS 11 BP 3067 EP 3072 PG 6 WC Oncology SC Oncology GA HW134 UT WOS:A1992HW13400012 PM 1350508 ER PT J AU BORRESEN, AL ANDERSEN, TI GARBER, J BARBIERPIRAUX, N THORLACIUS, S EYFJORD, J OTTESTAD, L SMITHSORENSEN, B HOVIG, E MALKIN, D FRIEND, SH AF BORRESEN, AL ANDERSEN, TI GARBER, J BARBIERPIRAUX, N THORLACIUS, S EYFJORD, J OTTESTAD, L SMITHSORENSEN, B HOVIG, E MALKIN, D FRIEND, SH TI SCREENING FOR GERM LINE TP53 MUTATIONS IN BREAST-CANCER PATIENTS SO CANCER RESEARCH LA English DT Article ID FAMILY AB The constant denaturant gel electrophoresis technique was used to screen for TP53 germ line mutations in 237 women with breast carcinoma (167 unselected patients, 30 patients with at least one first-degree relative with breast cancer, and 40 women diagnosed with breast cancer before age 35). A germ line mutation at codon 181 was noted in one of the unselected patients and a codon 245 mutation in one of the early-onset patients. Both had a family history of breast cancer and other malignancies suggestive of Li-Fraumeni syndrome. The codon 245 mutation was also present in this patient's affected mother. C1 NORWEGIAN RADIUM HOSP,DEPT ONCOL,OSLO 3,NORWAY. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. ICELAND CANC SOC,REYKJAVIK,ICELAND. RP BORRESEN, AL (reprint author), NORWEGIAN RADIUM HOSP,INST CANC RES,DEPT GENET,MONTEBELLO,N-0310 OSLO 3,NORWAY. RI Hovig, Eivind/H-2474-2011 OI Hovig, Eivind/0000-0002-9103-1077 NR 21 TC 164 Z9 166 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD JUN 1 PY 1992 VL 52 IS 11 BP 3234 EP 3236 PG 3 WC Oncology SC Oncology GA HW134 UT WOS:A1992HW13400038 PM 1591732 ER PT J AU LEE, I BOUCHER, Y JAIN, RK AF LEE, I BOUCHER, Y JAIN, RK TI NICOTINAMIDE CAN LOWER TUMOR INTERSTITIAL FLUID PRESSURE - MECHANISTIC AND THERAPEUTIC IMPLICATIONS SO CANCER RESEARCH LA English DT Article ID BLOOD-FLOW; SOLID TUMORS; HETEROGENEITY; RESISTANCE; DELIVERY AB Several investigators have shown that nicotinamide (NA) may increase the tumor blood flow and/or alleviate temporal fluctuations in tumor blood flow and, consequently, increase pO2. However, the mechanisms of these changes in tumor blood flow are not understood, especially because NA lowers the mean arterial blood pressure in mice. Our hypothesis is that NA may decrease flow resistance in tumors, which would lower vascular pressure and tumor interstitial fluid pressure (TIFP). To test this hypothesis, we measured the physiological parameters: mean arterial blood pressure, TIFP, tumor water content, and hematocrit in C3H mice bearing FSaII tumors, before and after treatment with 500 mg/kg of NA. In control animals, TIFP increased with tumor growth up to 400 MM3 , reached a plateau, and then decreased when the tumor size was above 1000 mm3 (n = 135). Tumor water content correlated significantly with TIFT (for tumors < 500 mm3) (n = 26). NA caused approximately a 15% decrease in mean arterial blood pressure (P < 0.05) and a 35% decrease in TIFP (P < 0.001) at 2 h postinjection, without any change in hematocrit. The change in TIFP was found to be tumor size dependent. Specifically, NA decreased the TIFP by 47% (P < 0.001) and 39% (P < 0.001) in medium (200 to 500 mm3) and large (500 to 800 mm3) tumors, respectively. The decrease in TIFP in small (< 200 mm3) and very large (> 800 mm3) tumors was not statistically significant (P > 0.1). Our results may explain the size-dependent enhancement in PO2 and radiation response reported by I. Lee and C. W. Song (Radiat. Res., 130: 65-71, 1992) for this tumor line. If our results could be confirmed in human tumors in situ, they would have significant implications in noninvasive measurements of TIFP using NMR and in cancer treatment using radiation, chemotherapy, and immunotherapy. RP LEE, I (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. FU NCI NIH HHS [CA-13311, CA-37239, CA-49792] NR 22 TC 98 Z9 100 U1 0 U2 3 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 JUN 1 PY 1992 VL 52 IS 11 BP 3237 EP 3240 PG 4 WC Oncology SC Oncology GA HW134 UT WOS:A1992HW13400039 PM 1534273 ER PT J AU LIVINGSTON, D MIHICH, E AF LIVINGSTON, D MIHICH, E TI 3RD ANNUAL PEZCOLLER SYMPOSIUM - TUMOR SUPPRESSOR GENES SO CANCER RESEARCH LA English DT Article C1 ROSWELL PK CANC INST,BUFFALO,NY. RP LIVINGSTON, D (reprint author), DANA FARBER CANC CTR,BOSTON,MA 02115, USA. NR 0 TC 3 Z9 3 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 JUN 1 PY 1992 VL 52 IS 11 BP 3246 EP 3249 PG 4 WC Oncology SC Oncology GA HW134 UT WOS:A1992HW13400041 PM 1591734 ER PT J AU YAMADA, A KANEYUKI, T HARA, A ROTHSTEIN, DM YOKOYAMA, MM AF YAMADA, A KANEYUKI, T HARA, A ROTHSTEIN, DM YOKOYAMA, MM TI CD45 ISOFORM EXPRESSION ON HUMAN NEONATAL T-CELLS - EXPRESSION AND TURNOVER OF CD45 ISOFORMS ON NEONATAL VERSUS ADULT T-CELLS AFTER ACTIVATION SO CELLULAR IMMUNOLOGY LA English DT Article ID LEUKOCYTE-COMMON ANTIGEN; PROTEIN TYROSINE PHOSPHATASE; HELPER-INDUCER; MONOCLONAL-ANTIBODY; LYMPHOCYTES-T; SUBSETS; MEMORY; UCHL1; DIFFERENTIATION; SUBPOPULATIONS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP YAMADA, A (reprint author), KURUME UNIV,SCH MED,DEPT IMMUNOL,KURUME,FUKUOKA 830,JAPAN. NR 39 TC 22 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JUN PY 1992 VL 142 IS 1 BP 114 EP 124 DI 10.1016/0008-8749(92)90273-R PG 11 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HZ071 UT WOS:A1992HZ07100010 PM 1534035 ER PT J AU YAMADA, A KANEYUKI, T TORIMOTO, Y DALEY, JF PRADO, CM YOKOYAMA, MM AF YAMADA, A KANEYUKI, T TORIMOTO, Y DALEY, JF PRADO, CM YOKOYAMA, MM TI SIGNALING FROM LFA-1 CONTRIBUTES SIGNAL TRANSDUCTION THROUGH CD2 ALTERNATIVE PATHWAY IN T-CELL ACTIVATION SO CELLULAR IMMUNOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; HUMAN-LYMPHOCYTES; MONOCLONAL-ANTIBODIES; RECEPTOR COMPLEX; MOLECULES; PROLIFERATION; FIBRONECTIN; VLA-5; MESSENGER; ADHESION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP YAMADA, A (reprint author), KURUME UNIV,SCH MED,DEPT IMMUNOL,KURUME,FUKUOKA 830,JAPAN. NR 36 TC 14 Z9 14 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD JUN PY 1992 VL 142 IS 1 BP 145 EP 158 DI 10.1016/0008-8749(92)90276-U PG 14 WC Cell Biology; Immunology SC Cell Biology; Immunology GA HZ071 UT WOS:A1992HZ07100013 PM 1375131 ER PT J AU BUSH, RK AF BUSH, RK TI THE ROLE OF ALLERGENS IN ASTHMA SO CHEST LA English DT Article ID HOUSE-DUST MITE; CHILDHOOD ASTHMA; GRASS-POLLEN; EXPOSURE; RESPONSIVENESS; EPIDEMIOLOGY; SENSITIVITY; ASSOCIATION; DISEASES; SEVERITY C1 UNIV WISCONSIN,DEPT MED,ALLERGY & IMMUNOL SECT,MADISON,WI 53706. RP BUSH, RK (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,MED SERV,ALLERGY SECT,2300 OVERLOOK TERRACE,MADISON,WI 53705, USA. RI Osborne, Nicholas/N-4915-2015 OI Osborne, Nicholas/0000-0002-6700-2284 NR 26 TC 4 Z9 4 U1 0 U2 1 PU AMER COLL CHEST PHYSICIANS PI NORTHBROOK PA 3300 DUNDEE ROAD, NORTHBROOK, IL 60062-2348 SN 0012-3692 J9 CHEST JI Chest PD JUN PY 1992 VL 101 IS 6 SU S BP S378 EP S380 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA JA186 UT WOS:A1992JA18600007 PM 1591935 ER PT J AU NI, C KUO, PK DRYJA, TP AF NI, C KUO, PK DRYJA, TP TI HISTOPATHOLOGICAL CLASSIFICATION OF 272 PRIMARY EPITHELIAL TUMORS OF THE LACRIMAL GLAND SO CHINESE MEDICAL JOURNAL LA English DT Article AB 272 primary epithelial gland tumors were classified pathologically. These tumors were sampled from 70% of 390 lacrimal fossa lesions out of 1530 orbital tumors from one hospital. Benign mixed tumors ranked the first in frequency (52%) to be followed by adenocystic carcinomas (25%) and malignant mixed tumors (9%). From the other less common tumor types, we identified, for the first time 3 polymorphous low-grade adenocarcinomas, 2 spindle celled myoepitheliomas and one carcinosarcoma of the lacrimal gland. The diagnosis and differential diagnosis of polymorphous low-grade adenocarcinoma and spindle cell myoepithelioma were discussed. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP NI, C (reprint author), SHANGHAI MED UNIV,EYE ENT HOSP,SHANGHAI 200031,PEOPLES R CHINA. NR 15 TC 23 Z9 23 U1 0 U2 0 PU CHINESE MEDICAL ASSOCIATION PI BEIJING PA 42 DONGSI XIDAJIE, BEIJING 100710, PEOPLES R CHINA SN 0366-6999 J9 CHINESE MED J-PEKING JI Chin. Med. J. PD JUN PY 1992 VL 105 IS 6 BP 481 EP 485 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA JK197 UT WOS:A1992JK19700009 PM 1333391 ER PT J AU STERN, EH SCHWEITZER, P AF STERN, EH SCHWEITZER, P TI POLYMORPHOUS VENTRICULAR-TACHYCARDIA ASSOCIATED WITH ACUTE MYOCARDIAL-INFARCTION SO CIRCULATION LA English DT Letter C1 CUNY MT SINAI SCH MED,MED,NEW YORK,NY 10029. CUNY MT SINAI SCH MED,CARDIOL SECT,NEW YORK,NY 10029. RP STERN, EH (reprint author), BRONX VET AFFAIRS MED CTR,CARDIOL SECT,BRONX,NY, USA. NR 4 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD JUN PY 1992 VL 85 IS 6 BP 2333 EP 2334 PG 2 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HX707 UT WOS:A1992HX70700047 PM 1591853 ER PT J AU WEI, EP MOSKOWITZ, MA BOCCALINI, P KONTOS, HA AF WEI, EP MOSKOWITZ, MA BOCCALINI, P KONTOS, HA TI CALCITONIN GENE-RELATED PEPTIDE MEDIATES NITROGLYCERIN AND SODIUM NITROPRUSSIDE-INDUCED VASODILATION IN FELINE CEREBRAL ARTERIOLES SO CIRCULATION RESEARCH LA English DT Article DE CALCITONIN GENE-RELATED PEPTIDE; NITROGLYCERIN; SODIUM NITROPRUSSIDE; VASODILATION; TRIGEMINOVASCULAR SYSTEM ID SUBSTANCE-P; TRANSCRANIAL DOPPLER; TRIGEMINAL ORIGIN; NERVE-STIMULATION; FUNCTIONAL-ROLE; BLOOD-VESSELS; NITRIC-OXIDE; MECHANISMS; MUSCLE; RAT AB The cerebral vasodilator response induced by topical nitroglycerin and nitroprusside was examined in cats equipped with cranial windows for the observation of the cerebral microcirculation. In cats subjected to chronic unilateral trigeminal ganglionectomy, the vasodilator responses to nitroprusside and nitroglycerin were markedly depressed on the denervated side. Application of a selective calcitonin gene-related peptide (CGRP) antagonist [CGRP(8-37)] on the innervated side reduced the response to nitrodilators to the same extent as seen on the denervated side. The vasodilator response to acetylcholine was unaffected by trigeminal ganglionectomy. CGRP(8-37) almost abolished the vasodilator response to nitroglycerin and sodium nitroprusside and to CGRP, but did not affect the response to adenosine or to adenosine diphosphate. Pretreatment with LY83583, a drug that lowers cyclic GMP levels, diminished the vasodilation to CGRP and to nitroprusside but not to adenosine. We conclude that the nitrovasodilators activate sensory fibers to release CGRP, which in turn relaxes cerebral vascular smooth muscle by activating guanylate cyclase. Hence, nitrovasodilators possess a novel mechanism of action within the cephalic circulation which may explain both the occurrence of vasodilation and headache. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,DEPT MED,RICHMOND,VA 23298. FU NHLBI NIH HHS [HL-21851]; NINDS NIH HHS [NS-26361, NS-19316] NR 40 TC 216 Z9 224 U1 1 U2 3 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD JUN PY 1992 VL 70 IS 6 BP 1313 EP 1319 PG 7 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA HV923 UT WOS:A1992HV92300026 PM 1576743 ER PT J AU OPPENHEIM, DS BIKKAL, H CROWLEY, WF KLIBANSKI, A AF OPPENHEIM, DS BIKKAL, H CROWLEY, WF KLIBANSKI, A TI EFFECTS OF CHRONIC GNRH ANALOG ADMINISTRATION ON GONADOTROPIN AND ALPHA-SUBUNIT SECRETION IN POSTMENOPAUSAL WOMEN SO CLINICAL ENDOCRINOLOGY LA English DT Article ID LUTEINIZING-HORMONE ALPHA; PITUITARY-TUMORS; BETA-SUBUNITS; AGONIST; MEN; LH; DESENSITIZATION; SUPPRESSION; STIMULATION; INHIBITION AB OBJECTIVE To investigate in detail the regulation of LH, FSH, and alpha-subunit secretion by a GnRH agonist analogue under physiological conditions of gonadotrophin elevation. SUBJECTS Six normal healthy post-menopausal women. DESIGN Subjects were given D-Trp6-Pro9-Net-GnRH (GnRHa), 32-mu-g/kg, subcutaneously, daily for 24 days. On days 1, 2, 3, 4, 7, 11, 14, 17, 21, and 24, blood samples before and after GnRHa injection were taken. Sampling was continued off GnRHa twice a week for 4 weeks and then on days 66, 76, and 98. GnRH tests (100-mu-g i.v.) were performed on days 0, 24, and 98. MEASUREMENTS All serum samples were analysed for LH, FSH, and alpha-subunit levels. RESULTS LH and FSH levels reached a maximum on day 2 after which there was a steady decline to day 24. LH did not begin to rise again until day 44 (20 days off GnRHa), then rose steadily. FSH began to rise earlier, on day 34 (10 days off GnRHa). Alpha-subunit levels also showed maximum elevation on day 2 but remained equally elevated throughout the period of GnRHa administration and then fell rapidly to baseline by day 34. LH, FSH, and alpha-subunit responses to i.v. GnRH were absent on day 24 and were equivalent to baseline on day 98. CONCLUSIONS We conclude that there is a striking dissociation in the regulation of gonadotrophin and alpha-subunit secretion in response to GnRHa in normal post-menopausal women. Gonadotrophin secretion is profoundly suppressed during GnRHa administration and recovers only after a long delay post-treatment, while alpha-subunit is markedly stimulated and recovers rapidly. The difference between this pattern and that seen in patients with pituitary tumours could be useful for diagnosis. C1 MASSACHUSETTS GEN HOSP,NEUROENDOCRINE UNIT,JACKSON 10,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,REPROD ENDOCRINE UNIT,BOSTON,MA 02114. FU NCRR NIH HHS [RR-01066]; NICHD NIH HHS [HD-15080, U54 HD029164]; NIDDK NIH HHS [DK-40947] NR 30 TC 14 Z9 14 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 JUN PY 1992 VL 36 IS 6 BP 559 EP 564 DI 10.1111/j.1365-2265.1992.tb02265.x PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HW984 UT WOS:A1992HW98400006 PM 1385024 ER PT J AU RUBIN, RH BEAM, TR STAMM, WE AF RUBIN, RH BEAM, TR STAMM, WE TI AN APPROACH TO EVALUATING ANTIBACTERIAL AGENTS IN THE TREATMENT OF URINARY-TRACT INFECTION SO CLINICAL INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT CONF ON THE EVALUATION OF NEW ORAL ANTIMICROBIAL AGENTS AND THE EXPERIENCE WITH CEFPROZIL - A BROAD-SPECTRUM ORAL CEPHALOSPORIN CY SEP 26-29, 1991 CL AMELIA ISLAND, FL ID TRIMETHOPRIM-SULFAMETHOXAZOLE; RANDOMIZED TRIAL; WOMEN; BACTERIURIA; MANAGEMENT; DIAGNOSIS; CHILDREN; INFANTS; CULTURE AB The evaluation of antibacterial therapy for urinary tract infection (UTI) is based on the results of randomized, controlled comparative studies (preferably double-blinded) in which sufficient numbers of patients are entered into both arms to ensure statistical validity. Since the term UTI encompasses a broad array of clinical syndromes (acute uncomplicated UTI; acute uncomplicated pyelonephritis; complicated UTI; and asymptomatic bacteriuria), the design of clinical studies should include a careful definition of the clinical syndromes being studied, the course of therapy prescribed, and the microbiological characterization necessary for evaluability. End points to be considered in the evaluation of new therapies include the effect of therapy on clinical symptoms; the ability of the therapy to eradicate the original infecting organism; the incidence of reinfection posttherapy; the number of instances of primary drug resistance of the infecting inoculum; and the incidence of adverse effects with a particular regimen. C1 MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. VET ADM MED CTR,DEPT MED,INFECT DIS SERV,BUFFALO,NY 14215. SUNY BUFFALO,SCH MED,DEPT MED,BUFFALO,NY 14214. UNIV WASHINGTON,HARBORVIEW MED CTR,DEPT MED,INFECT DIS UNIT,SEATTLE,WA 98104. UNIV WASHINGTON,SCH MED,SEATTLE,WA 98195. RP RUBIN, RH (reprint author), MASSACHUSETTS GEN HOSP,MED SERV,CLIN INVEST PROGRAM,25 FRUIT ST,BOSTON,MA 02114, USA. FU AHRQ HHS [HHS 223-88-1301] NR 20 TC 20 Z9 20 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 JUN PY 1992 VL 14 SU 2 BP S246 EP S251 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HW746 UT WOS:A1992HW74600011 PM 1617045 ER PT J AU WILLIAMS, ME LEWIS, D AF WILLIAMS, ME LEWIS, D TI HYPERURICEMIC ACUTE-RENAL-FAILURE ASSOCIATED WITH FK506 NEPHROTOXICITY SO CLINICAL TRANSPLANTATION LA English DT Article DE HYPERURICEMIA; FK506; NEPHROTOXICITY AB Acute renal failure due to severe hyperuricemia is reported in a liver transplant recipient undergoing rescue therapy with FK506. Earlier treatment with cyclosporine had been complicated by gout and uric acid nephrolithiasis. Transplant recipients with symptomatic hyperuricemia on cyclosporine may be at particular risk for marked hyperuricemia when conversion to FK506 results in FK506 toxicity. RP WILLIAMS, ME (reprint author), JOSLIN DIABET CTR,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0063 J9 CLIN TRANSPLANT JI Clin. Transplant. PD JUN PY 1992 VL 6 IS 3 BP 194 EP 195 PN 1 PG 2 WC Surgery; Transplantation SC Surgery; Transplantation GA JB849 UT WOS:A1992JB84900010 ER PT J AU HIBBERD, PL RUBIN, RH AF HIBBERD, PL RUBIN, RH TI ANTIVIRAL THERAPY - AN ANTIMALIGNANCY STRATEGY FOR TRANSPLANT RECIPIENTS SO CLINICAL TRANSPLANTATION LA English DT Article; Proceedings Paper CT SYMP ON IMMUNOSUPPRESSION AND LYMPHOPROLIFERATIVE DISORDERS CY JUN 07, 1991 CL CINCINNATI, OH DE POSTTRANSPLANTATION LYMPHOPROLIFERATIVE DISORDER; TRANSPLANTATION, IMMUNOSUPPRESSION, EPSTEIN-BARR VIRUS; PREVENTION; PREEMPTIVE THERAPY; ANTILYMPHOCYTE GLOBULIN; MUROMONAB-CD3 (OKT3) AB The post-transplantation lymphoproliferative disorder (PTLD), a well-recognized complication of immunosuppression, has been linked to the interaction between the Epstein-Barr virus (EBV) and the exogenous immunosuppressive therapy that is administered to the transplant recipient. Although the specific risk factors for the development of the disorder have not been well characterized, the risk appears to be increased in patients in whom the "net state of immunosuppression" is likely to be the greatest, such as cardiac transplant recipients receiving OKT3 in addition to conventional immunosuppressive regimens, or renal transplant recipients treated with high-dose cyclosporine. Two potential strategies that may decrease the incidence of PTLD include: 1) reduction of the doses of concomitant immunosuppression during therapy with antibody preparations, such as murine mAb CD3 (OKT3) and anti-lymphocyte globulin (ALG); and 2) the use of "preemptive" antiviral therapy, with agents such as acyclovir and ganciclovir, during periods of maximal immunosuppression, i.e. during the administration of antibody preparations. RP HIBBERD, PL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0902-0063 J9 CLIN TRANSPLANT JI Clin. Transplant. PD JUN PY 1992 VL 6 IS 3 BP 240 EP 245 PN 2 PG 6 WC Surgery; Transplantation SC Surgery; Transplantation GA JB851 UT WOS:A1992JB85100007 ER PT J AU CIMINO, JJ ELKIN, PL BARNETT, GO AF CIMINO, JJ ELKIN, PL BARNETT, GO TI AS WE MAY THINK - THE CONCEPT SPACE AND MEDICAL HYPERTEXT SO COMPUTERS AND BIOMEDICAL RESEARCH LA English DT Article ID INFORMATION; RETRIEVAL; MANAGEMENT; COMPUTER C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,COMP SCI LAB,BOSTON,MA 02114. RP CIMINO, JJ (reprint author), COLUMBIA UNIV,CTR MED INFORMAT,NEW YORK,NY 10027, USA. OI Cimino, James/0000-0003-4101-1622 NR 43 TC 17 Z9 18 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0010-4809 J9 COMPUT BIOMED RES JI Comput. Biomed. Res. PD JUN PY 1992 VL 25 IS 3 BP 238 EP 263 DI 10.1016/0010-4809(92)90041-8 PG 26 WC Computer Science, Interdisciplinary Applications; Medical Informatics SC Computer Science; Medical Informatics GA HX264 UT WOS:A1992HX26400004 PM 1611890 ER PT J AU JOHNSON, LS AF JOHNSON, LS TI SELF-HYPNOSIS - THE CHICAGO PARADIGM - FROMM,E, KAHN,S SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review C1 MONTANA STATE UNIV,CTR COUNSELING,BOZEMAN,MT 59717. RP JOHNSON, LS (reprint author), MONTANA DEACONESS MED CTR,CLIN PSYCHOL,GREAT FALLS,MT, USA. NR 8 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD JUN PY 1992 VL 37 IS 6 BP 551 EP 552 PG 2 WC Psychology, Multidisciplinary SC Psychology GA HY155 UT WOS:A1992HY15500021 ER PT J AU SALADINO, R BALDWIN, G ALPERT, G PARSONNET, J GILLIS, Z THOMPSON, C SIBER, G FLEISHER, G AF SALADINO, R BALDWIN, G ALPERT, G PARSONNET, J GILLIS, Z THOMPSON, C SIBER, G FLEISHER, G TI EFFECT OF A HUMAN-IMMUNOGLOBULIN PREPARATION FOR INTRAVENOUS USE IN A RABBIT MODEL OF MENINGOCOCCAL ENDOTOXIN-INDUCED SHOCK SO CRITICAL CARE MEDICINE LA English DT Article DE IMMUNOGLOBULIN; ENDOTOXIN; LIPOPOLYSACCHARIDE; LIPOOLIGOSACCHARIDE; TUMOR NECROSIS FACTOR; SHOCK; SEPSIS; MENINGOCOCCUS; ANIMAL MODEL; INFECTION ID TUMOR-NECROSIS-FACTOR; LOCAL SHWARTZMAN REACTION; ESCHERICHIA-COLI; BACTERIAL LIPOPOLYSACCHARIDES; SEPTIC SHOCK; MONOCLONAL-ANTIBODIES; PASSIVE-IMMUNIZATION; SALMONELLA-MINNESOTA; HUMAN ANTISERUM; IGG ANTIBODY AB Background and Methods: Endotoxin shock is mediated by various cytokines, including tumor necrosis factor. Treatment of patients with iv immunoglobulin has been shown to reduce the concentration of circulating cytokines. The purpose of this study was to determine the protective effects of immunoglobulin for iv use on meningococcal endotoxin-induced shock in a rabbit model. Experimental animals were challenged with iv meningococcal endotoxin (lipooligosaccharide) 10-mu-g/kg, and treated with either a 2-hr iv immunoglobulin infusion (400 mg/kg) or a similar saline infusion that was initiated 30 mins before endotoxin challenge. Control animals were challenged with saline alone. Results: Compared with untreated control animals, pulse rate increased (p < .007) and mean arterial pressure and serum bicarbonate concentrations decreased (p < .02) in both experimental groups, but did not differ between immunoglobulin-treated and saline-treated animals (p > .05) at any time after the endotoxin challenge. Geometric mean serum endotoxin concentrations were significantly (p < .03) lower in the immunoglobulin-treated animals at 60, 120, 180, 240, 300, and 360 mins after the endotoxin challenge. The geometric mean serum tumor necrosis factor level at 1 hr after the endotoxin challenge in the immunoglobulin-treated experimental animals was lower than in saline-treated animals (5.53 vs. 8.47 tumor necrosis factor enzyme-linked immunosorbent assay U/mL), but not significantly so (p > .05). Mortality rate was similar in both experimental groups; eight (67%) of 12 saline-treated experimental rabbits and seven (70%) of ten immunoglobulin-treated rabbits died. All untreated control animals survived 24 hrs. Conclusions: In this model of circulatory shock in rabbits, iv immunoglobulin: a) does not significantly alter the physiologic responses to endotoxin challenge; b) significantly reduces endotoxin concentrations; c) reduces tumor necrosis factor concentrations, but not significantly; and d) does not improve survival rate. C1 HARVARD UNIV,SCH MED,CHILDRENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02115. RP SALADINO, R (reprint author), HARVARD UNIV,SCH MED,CHILDRENS HOSP,DIV EMERGENCY MED,300 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 37 TC 6 Z9 7 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 JUN PY 1992 VL 20 IS 6 BP 816 EP 822 DI 10.1097/00003246-199206000-00020 PG 7 WC Critical Care Medicine SC General & Internal Medicine GA HX520 UT WOS:A1992HX52000020 PM 1597037 ER PT J AU LIEBER, CS AF LIEBER, CS TI ALCOHOLIC LIVER-INJURY SO CURRENT OPINION IN GASTROENTEROLOGY LA English DT Article AB A considerable wealth of new information was gained on the metabolism and hepatotoxicity of ethanol during 1991. Much progress has been made on the elucidation of pathways of ethanol metabolism, including gastric alcohol dehydrogenase and associated alcohol-drug interactions, as well as genetic determinants of hepatic alcohol metabolism and associated changes of relevance to alcoholic liver injury. Significant, though less impressive, advances have been made in the field of prevention and treatment. RP LIEBER, CS (reprint author), BRONX VET AFFAIRS MED CTR,LIVER DIS SECT,130 W KINGSBRIDGE RD,BRONX,NY 10468, 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 0267-1379 J9 CURR OPIN GASTROEN JI Curr. Opin. Gastroenterol. PD JUN PY 1992 VL 8 IS 3 BP 449 EP 457 DI 10.1097/00001574-199206000-00013 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HV460 UT WOS:A1992HV46000013 ER PT J AU EZZELL, RM LEUNG, J COLLINS, K CHAFEL, MM CARDOZO, TJ MATSUDAIRA, PT AF EZZELL, RM LEUNG, J COLLINS, K CHAFEL, MM CARDOZO, TJ MATSUDAIRA, PT TI EXPRESSION AND LOCALIZATION OF VILLIN, FIMBRIN, AND MYOSIN-I IN DIFFERENTIATING MOUSE F9 TERATOCARCINOMA CELLS SO DEVELOPMENTAL BIOLOGY LA English DT Article ID EMBRYONAL CARCINOMA-CELLS; MICROVILLAR CORE PROTEINS; INTESTINAL BRUSH-BORDER; VISCERAL ENDODERM; CALMODULIN; BINDING; DOMAINS; REDISTRIBUTION; CYTOSKELETON; ORGANIZATION C1 MIT,DEPT BIOL,CAMBRIDGE,MA 02142. MIT,WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142. HARVARD UNIV,SCH MED,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. RP EZZELL, RM (reprint author), MASSACHUSETTS GEN HOSP,SURG SERV,SURG RES LAB,149 13TH ST,BOSTON,MA 02129, USA. RI Matsudaira, Paul/H-1475-2012 OI Matsudaira, Paul/0000-0002-8399-3276 FU NCI NIH HHS [CA44704] NR 43 TC 22 Z9 23 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD JUN PY 1992 VL 151 IS 2 BP 575 EP 585 DI 10.1016/0012-1606(92)90195-M PG 11 WC Developmental Biology SC Developmental Biology GA HY740 UT WOS:A1992HY74000023 PM 1601186 ER PT J AU PARK, EC SZOSTAK, JW AF PARK, EC SZOSTAK, JW TI ARD1 AND NAT1 PROTEINS FORM A COMPLEX THAT HAS N-TERMINAL ACETYLTRANSFERASE ACTIVITY SO EMBO JOURNAL LA English DT Article DE PROTEIN MODIFICATION; PROTEIN PROTEIN INTERACTIONS; YEAST ID SACCHAROMYCES-CEREVISIAE; ALPHA-ACETYLTRANSFERASE; YEAST; GENE; PURIFICATION; PRODUCT; LOCUS; SITE; HML AB Two yeast genes, ARD1 and NAT1, are required for the expression of an N-terminal protein acetyltransferase. This activity is required for full repression of the silent mating type locus HML, for sporulation, and for entry into G0. While the NAT1 gene product is thought to be the catalytic subunit of the enzyme, the role of the ARD1 protein has remained unclear. We have used epitope tagged derivatives of ARD1 and NAT1 to provide biochemical evidence for the formation of an ARD1-NAT1 complex, and to show that both proteins are required for the N-terminal acetyltransferase activity. We also present evidence for the formation of ARD1-ARD1 homodimers. Deletion analysis suggests that the C-terminal region of ARD1 may be involved in the formation of both ARD1-ARD1 and ARD1-NAT1 complexes. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. RP PARK, EC (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. NR 17 TC 119 Z9 124 U1 2 U2 4 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 JUN PY 1992 VL 11 IS 6 BP 2087 EP 2093 PG 7 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HX081 UT WOS:A1992HX08100011 PM 1600941 ER PT J AU SUDO, Y VALENZUELA, D BECKSICKINGER, AG FISHMAN, MC STRITTMATTER, SM AF SUDO, Y VALENZUELA, D BECKSICKINGER, AG FISHMAN, MC STRITTMATTER, SM TI PALMITOYLATION ALTERS PROTEIN-ACTIVITY - BLOCKADE OF G0 STIMULATION BY GAP-43 SO EMBO JOURNAL LA English DT Article DE GAP-43; GROWTH CONE; GTP BINDING PROTEIN; PALMITOYLATION ID GROWTH-ASSOCIATED PROTEIN; DYNAMIC FATTY ACYLATION; COVALENT MODIFICATION; NUCLEOTIDE BINDING; ADENYLATE-CYCLASE; EUKARYOTIC CELLS; CONE PROTEIN; MEMBRANE; RECEPTOR; ACID AB The addition of palmitate to cysteine residues enhances the hydrophobicity of proteins, and consequently their membrane association. Here we have investigated whether this type of fatty acylation also regulates protein-protein interactions. GAP-43 is a neuronal protein that increases guanine nucleotide exchange by heterotrimeric G proteins. Two cysteine residues near the N-terminus of GAP-43 are subject to palmitoylation, and are necessary for membrane binding as well as for G(o) activation. N-terminal peptides, which include these cysteines, stimulate G(o). Monopalmitoylation reduces, and dipalmitoylation abolishes the activity of the peptides. The activity of GAP-43 protein purified from brain also is reversibly blocked by palmitoylation. This suggests that palmitoylation controls a cycle of GAP-43 between an acylated, membrane-bound reservoir of inactive GAP-43, and a depalmitoylated, active pool of protein. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02129. UNIV TUBINGEN,INST ORGAN CHEM,W-7400 TUBINGEN 1,GERMANY. RP SUDO, Y (reprint author), MASSACHUSETTS GEN HOSP,DEV BIOL LAB,149 13TH ST,BOSTON,MA 02129, USA. OI Strittmatter, Stephen/0000-0001-8188-3092 NR 50 TC 106 Z9 108 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 JUN PY 1992 VL 11 IS 6 BP 2095 EP 2102 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HX081 UT WOS:A1992HX08100012 PM 1534749 ER PT J AU NATHAN, DM AF NATHAN, DM TI THE RATIONALE FOR GLUCOSE CONTROL IN DIABETES-MELLITUS SO ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA LA English DT Article ID SUBCUTANEOUS INSULIN INFUSION; CORONARY HEART-DISEASE; NEWLY DIAGNOSED DIABETICS; RISK-FACTORS; GLYCEMIC CONTROL; NERVE-CONDUCTION; NATURAL-HISTORY; PLASMA-GLUCOSE; METABOLIC CONTROL; BLOOD-PRESSURE C1 MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. NR 95 TC 14 Z9 14 U1 0 U2 0 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0889-8529 EI 1558-4410 J9 ENDOCRIN METAB CLIN JI Endocrinol. Metabol. Clin. North Amer. PD JUN PY 1992 VL 21 IS 2 BP 221 EP 235 PG 15 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA LA541 UT WOS:A1992LA54100003 PM 1612066 ER PT J AU HASS, R AF HASS, R TI RETRODIFFERENTIATION - AN ALTERNATIVE BIOLOGICAL PATHWAY IN HUMAN LEUKEMIA-CELLS SO EUROPEAN JOURNAL OF CELL BIOLOGY LA English DT Review DE DIFFERENTIATION; RETRODIFFERENTIATION; CELL DEATH; CELL CYCLE; LEUKEMIC CELLS; PHORBOL ESTER; PROTEIN KINASE-C; TRANSCRIPTION FACTORS; INTERMEDIATE FILAMENTS; GLYCOPROTEINS; LECTINS; CELLULAR LIPIDS ID PROTEIN-KINASE-C; TUMOR NECROSIS FACTOR; NF-KAPPA-B; VIMENTIN INTERMEDIATE FILAMENTS; CLONED PLACENTAL CDNA; DNA-BINDING PROTEIN; GENE-EXPRESSION; GLUCOCORTICOID RECEPTOR; PHORBOL ESTERS; MONOCYTIC DIFFERENTIATION AB Human myeloid leukemia cells (i. e., HL-60, U937, THP-1) which are induced to differentiate along the monocytic pathway by 12-O-tetradecanoylphorbol-13-acetate (TPA), revert back to the undifferentiated phenotype after 3 to 4 weeks. During this differentiation and retrodifferentiation process the cells obviously establish a distinct sequence of biological processes which is integrally regulated to simultaneously control differentiation and cell growth. Thus, induction of monocytic markers by TPA is associated with a down-regulation of cell cycle genes and cessation of proliferation. In particular, crosstalk between the TPA-induced translocation of protein kinase C (PKC) and the activation of transcription factors, especially AP-1, enhances the expression of genes associated with the monocytic phenotype. This is accompanied by induction of intermediate filament proteins, surface glycoproteins, changes in membrane properties and intracellular metabolism. In parallel, the cells cease to divide, and genes associated with cell cycle progression including cdc2, cyclins, cdc25, and histones are down-regulated. Although signals responsible for arrested cell growth remain unclear, there are several control mechanisms regarding cell cycle genes and differentiation parameters (for a review, see Nigg, E. A., Seminars in Cell Biol., 2, 262-270, 1991). For example, activated p34cdc2 kinase is involved in lamina disassembly by direct phosphorylation of lamina proteins which may contribute to nuclear envelope breakdown during mitosis (Enoch, T., M. Peter, P. Nurse, J. Cell Biol. 112, 797-807 (1991)). Moreover, endomembrane traffic is arrested by a cdc2-like kinase probably via phosphorylation of members of the rab protein family which contributes to vesiculation and membrane transport by hydrolyzing GTP (Tuomikoski, T., et al., Nature 342, 942-945 (1989)). Although there are several reports on a possible feedback control between differentiation and cell cycle, including phosphorylation of cyclins and activation of a ubiquitin-dependent proteolytic degradation, signaling pathways and possible mechanisms for retrodifferentiation and reentry into the cell cycle remain unclear. While some terminally differentiated cells are committed to die, the major part of the differentiated monocytic population undergoes retrodifferentiation. All cellular signals characterized so far are reverted during retrodifferentiation: Redistribution of PKC and down-regulation of c-fos and c-jun contribute to an interruption of the differentiation-associated transsignaling cascade. Thus, down-regulation of markers associated with monocytic differentiation in combination with metabolic changes restore the original cell phenotype. At the same time cell cycle genes are up-regulated, and the cells regain proliferative capacity. Finally, retrodifferentiated and untreated control cells demonstrate indistinguishable properties. RP HASS, R (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT CLIN PHARMACOL, 44 BINNEY ST, BOSTON, MA 02115 USA. RI Hass, Ralf/F-3197-2012 OI Hass, Ralf/0000-0002-2481-7547 NR 121 TC 38 Z9 38 U1 0 U2 1 PU WISSENSCHAFTLICHE VERLAG MBH PI STUTTGART PA BIRKENWALDSTRASSE 44, POSTFACH 10 10 61, 70009 STUTTGART, GERMANY SN 0171-9335 J9 EUR J CELL BIOL JI Eur. J. Cell Biol. PD JUN PY 1992 VL 58 IS 1 BP 1 EP 11 PG 11 WC Cell Biology SC Cell Biology GA JB396 UT WOS:A1992JB39600001 PM 1644056 ER PT J AU TORCHILIN, VP KLIBANOV, AL HUANG, L ODONNELL, S NOSSIFF, ND KHAW, BA AF TORCHILIN, VP KLIBANOV, AL HUANG, L ODONNELL, S NOSSIFF, ND KHAW, BA TI TARGETED ACCUMULATION OF POLYETHYLENE GLYCOL-COATED IMMUNOLIPOSOMES IN INFARCTED RABBIT MYOCARDIUM SO FASEB JOURNAL LA English DT Note DE IMMUNOLIPOSOME; POLYETHYLENEGLYCOL; TARGETED DRUG DELIVERY; INFARCTED MYOCARDIUM ID LIPOSOMES; ANTIBODY AB The less than optimal accumulation of immunoliposome-associated reagents at target sites has often been attributed to the rapid in vivo clearance of immunoliposomes from the blood. In an attempt to overcome the drawback of rapid clearance and use the targeting potential of immunoliposomes, we have prepared long-circulating, In-111-labeled immunoliposomes. Targeting properties and enhanced circulation times were demonstrated in a rabbit model of acute experimental myocardial infarct. The specificity of liposomes for newly exposed intracellular cardiac myosin at the necrotic sites was achieved by incorporating monoclonal antimyosin antibody. Extended circulation times were achieved by cocoating the antimyosin-liposomes with polyethylene glycol (PEG). The half-life of the immunoliposomes was 40 min, which increased to 200 min with 4% mol PEG and to approximately 1000 min with 10% mol PEG. The degree of binding of modified immunoliposomes at the target sites was also dependent on the concentration of PEG incorporated at the liposome surface. This study demonstrates the accumulation of long-circulating targeted liposomes at the area of acute rabbit experimental myocardial infarction. C1 MASSACHUSETTS GEN HOSP,DEPT NUCL MED,BOSTON,MA 02129. UNIV TENNESSEE,DEPT BIOCHEM,KNOXVILLE,TN 37996. RP TORCHILIN, VP (reprint author), MASSACHUSETTS GEN HOSP E,CTR IMAGING & PHARMACEUT RES,DEPT RADIOL,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 10 TC 148 Z9 150 U1 1 U2 7 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0892-6638 J9 FASEB J JI Faseb J. PD JUN PY 1992 VL 6 IS 9 BP 2716 EP 2719 PG 4 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA HZ481 UT WOS:A1992HZ48100013 PM 1612296 ER PT J AU CHEN, J COMPTON, C CHENG, E FROMOWITZ, F VIOLA, MV AF CHEN, J COMPTON, C CHENG, E FROMOWITZ, F VIOLA, MV TI C-KI-RAS MUTATIONS IN DYSPLASTIC FIELDS AND CANCERS IN ULCERATIVE-COLITIS SO GASTROENTEROLOGY LA English DT Article ID FLOW-CYTOMETRIC DNA; CARCINOMA; COLON; ANEUPLOIDY; ONCOGENES C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 29 TC 56 Z9 56 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 JUN PY 1992 VL 102 IS 6 BP 1983 EP 1987 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HW356 UT WOS:A1992HW35600021 PM 1350261 ER PT J AU WERSHIL, BK WALKER, WA AF WERSHIL, BK WALKER, WA TI THE MUCOSAL BARRIER, IGE-MEDIATED GASTROINTESTINAL EVENTS, AND EOSINOPHILIC GASTROENTERITIS SO GASTROENTEROLOGY CLINICS OF NORTH AMERICA LA English DT Article ID RAT SMALL-INTESTINE; FEEDING PROTEIN ANTIGENS; I-125 FIBRIN DEPOSITION; MAJOR BASIC-PROTEIN; SUPPRESSOR T-CELLS; COWS MILK ALLERGY; FOOD ALLERGY; MAST-CELL; EPITHELIAL-CELLS; HISTAMINE-RELEASE C1 CHILDRENS HOSP MED CTR,COMBINED PROGRAM PEDIAT GASTROENTEROL & NUTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP WERSHIL, BK (reprint author), BETH ISRAEL HOSP,DEPT PATHOL,DIV EXPTL PATHOL,RES E,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NICHD NIH HHS [HD12437]; NIDDK NIH HHS [DK33506, DK01543] NR 92 TC 11 Z9 11 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0889-8553 J9 GASTROENTEROL CLIN N JI Gastroenterol. Clin. North Am. PD JUN PY 1992 VL 21 IS 2 BP 387 EP 404 PG 18 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HW327 UT WOS:A1992HW32700008 PM 1512048 ER PT J AU BOVA, JG SCHWESINGER, WH KURTIN, WE AF BOVA, JG SCHWESINGER, WH KURTIN, WE TI INVIVO ANALYSIS OF GALLSTONE COMPOSITION BY COMPUTED-TOMOGRAPHY SO GASTROINTESTINAL RADIOLOGY LA English DT Article DE GALLSTONES, CT-DIAGNOSIS; GALLBLADDER, CALCIFICATIONS ID INVITRO; CT; DISSOLUTION AB In vivo computed tomography (CT) of the gallbladder was performed in 39 patients with known cholelithiasis and subsequently correlated with the chemical composition of the retrieved gallstones. Six CT patterns were identified: pattern 1, negative defect within the bile; pattern 2, nonvisualization of calculi; pattern 3, faint homogeneous central calcification; pattern 4A, thin rim of calcification; pattern 4B, thick rim of calcification; pattern 5, dense homogeneous central calcification. These CT patterns correlated well with cholesterol (p = 0.05) and calcium bilirubinate (p = 0.01) contents and CT attenuation values (p < 0.001). The most common pattern was CT pattern 2 (56.5%). The authors conclude that there is good correlation of the CT pattern with gallstone composition. This simple approach can be used to help identify patients for therapy with chemical dissolution and/or lithotripsy. C1 UNIV TEXAS,HLTH SCI CTR,DEPT RADIOL,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT SURG,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. TRINITY UNIV,DEPT CHEM,SAN ANTONIO,TX 78284. NR 13 TC 5 Z9 6 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 SUM PY 1992 VL 17 IS 3 BP 253 EP 256 DI 10.1007/BF01888561 PG 4 WC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical Imaging SC Gastroenterology & Hepatology; Radiology, Nuclear Medicine & Medical Imaging GA HQ609 UT WOS:A1992HQ60900018 PM 1612311 ER PT J AU QIN, XQ CHITTENDEN, T LIVINGSTON, DM KAELIN, WG AF QIN, XQ CHITTENDEN, T LIVINGSTON, DM KAELIN, WG TI IDENTIFICATION OF A GROWTH SUPPRESSION DOMAIN WITHIN THE RETINOBLASTOMA GENE-PRODUCT SO GENES & DEVELOPMENT LA English DT Article DE RB; T/E1A-BINDING DOMAIN; GROWTH SUPPRESSION; E2F; PHOSPHORYLATION ID LARGE-T-ANTIGEN; SV40 LARGE-T; E2F TRANSCRIPTION FACTOR; SUSCEPTIBILITY GENE; CELL-CYCLE; RB GENE; BINDING; PROTEIN; INACTIVATION; EXPRESSION AB To date, all naturally occurring retinoblastoma 'susceptibility gene (RB) mutations known to be compatible with stable protein expression map to the T/E1A and cellular protein-binding region (the "pocket" domain). This domain extends from residue 379 to 792. When full-length RB and certain truncated forms were synthesized in human RB -/- cells, we found that the minimal region necessary for overt growth suppression extended from residue 379 to 928. A functional pocket domain and sequences extending from the carboxy-terminal boundary of the pocket to the carboxyl terminus of the protein were both necessary for growth suppression. Both sets of sequences were also required for E2F binding; hence, the two functions may be linked. RP QIN, XQ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115, USA. NR 57 TC 403 Z9 407 U1 0 U2 1 PU COLD SPRING HARBOR LAB PRESS PI PLAINVIEW PA 1 BUNGTOWN RD, PLAINVIEW, NY 11724 SN 0890-9369 J9 GENE DEV JI Genes Dev. PD JUN PY 1992 VL 6 IS 6 BP 953 EP 964 DI 10.1101/gad.6.6.953 PG 12 WC Cell Biology; Developmental Biology; Genetics & Heredity SC Cell Biology; Developmental Biology; Genetics & Heredity GA HY624 UT WOS:A1992HY62400005 PM 1534305 ER PT J AU FLETCHER, EC LESSKE, J WEI, Q MILLER, CC UNGER, T AF FLETCHER, EC LESSKE, J WEI, Q MILLER, CC UNGER, T TI REPETITIVE, EPISODIC HYPOXIA CAUSES DIURNAL ELEVATION OF BLOOD-PRESSURE IN RATS SO HYPERTENSION LA English DT Article DE APNEA; SLEEP APNEA SYNDROMES; ANOXIA; ANOXEMIA; BLOOD PRESSURE; ESSENTIAL HYPERTENSION ID SPONTANEOUSLY HYPERTENSIVE RATS; SLEEP-APNEA SYNDROME; CONSCIOUS DOGS; ARTERIAL-PRESSURE; HYPOBARIC HYPOXIA; ACUTE HYPOXEMIA; RESPONSES; HYPERSOMNIA; HYPERCAPNIA; NERVE AB An association between chronic high blood pressure and obstructive sleep apnea has been described. We hypothesized that repetitive episodic hypoxia patterned after the hypoxia seen in sleep apnea could contribute to diurnal elevation of blood pressure. Using 12-second infusions of nitrogen into daytime sleeping chambers, four groups of male rats (250-375 g) were subjected to intermittent hypoxia (3-5% nadir ambient oxygen) every 30 seconds, 7 hours per day for up to 35 days. In one group, blood pressure was measured weekly by the tail-cuff method in conscious animals during 5 weeks of episodic hypoxia. In the other three groups, blood pressure was measured in conscious animals via femoral artery catheters at baseline and after 20, 30, or 35 days of exposure. Additional groups served as controls: two sham groups housed in identical "hypoxia" chambers received compressed air instead of nitrogen (35 days) while two other groups remained unhandled in their usual cages (35 days). Both groups challenged with 35 days episodic hypoxia showed significant increases in blood pressure compared with controls: the tail-cuff rats showed a 21 mm Hg increase in systolic pressure (p<0.05) and the intra-arterially measured rats a 13.7 mm Hg increase in mean arterial pressure (p<0.05). The 30-day exposed rats also showed a 5.7 mm Hg increase in mean pressure over baseline (p<0.05). Blood pressure did not change significantly from baseline in the control groups. Left ventricle-to-body weight ratio was higher in both 35-day exposed groups than in unhandled or sham controls. This duration-of-exposure-related blood pressure response to hypoxia along with increased left ventricular size after 35 days indicates that chronic intermittent hypoxia could be a mechanism directly contributing to diurnal arterial blood pressure elevation. C1 UNIV HEIDELBERG,INST HIGH BLOOD PRESSURE RES,W-6900 HEIDELBERG,GERMANY. UNIV HEIDELBERG,DEPT PHARMACOL,W-6900 HEIDELBERG,GERMANY. BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,PULMONARY DIS SECT,HOUSTON,TX 77030. NR 39 TC 298 Z9 320 U1 1 U2 9 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD JUN PY 1992 VL 19 IS 6 BP 555 EP 561 PN 1 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HX022 UT WOS:A1992HX02200008 PM 1592450 ER PT J AU LAFUSE, WP LANNING, D SPIES, T DAVID, CS AF LAFUSE, WP LANNING, D SPIES, T DAVID, CS TI PFGE MAPPING AND RFLP ANALYSIS OF THE S/D REGION OF THE MOUSE H-2-COMPLEX SO IMMUNOGENETICS LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; EXPERIMENTAL ALLERGIC ORCHITIS; LENGTH-POLYMORPHISM ANALYSIS; MURINE-S-REGION; I-REGION; MOLECULAR MAP; E-ALPHA; E-BETA; CROSSOVER SITES; CLEFT-PALATE AB We have constructed a long range restriction map of the SID segment of the mouse H-2 complex by pulsed field gel electrophoresis and hybridization with mouse cDNA probes to Bf and Tnfa genes and human cDNA probes to BAT-2, BAT3, BAT4, BAT5, and BAT6 genes which have recently been mapped to the human HLA complex between C2 and HLA-B. The distance between the mouse C2 and Tnfa genes was found to be approximately 350 kilobases. The position of the mouse Bat genes in this map were found to be comparable to the position of the BAT genes in the human HLA complex. A panel of recombinant mouse strains was also examined by restriction fragment analysis with probes detecting the Hsp70, Bat5, and Tnfa genes. The results indicate that recombination in this segment is not random. No recombinants were found with crossovers between the C2 and Hsp70 genes and only one recombinant was found with a crossover between Tnfa and H-2D. In contrast, the crossover sites of 16 recombinants were mapped between the Hsp70 and Tnfa genes. Seven of these recombinants were found to have crossovers between Hsp70 and Bat5 and three recombinants were found to have crossover sites between Bat5 and Tnfa. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. MAYO CLIN & MAYO FDN,DEPT IMMUNOL,ROCHESTER,MN 55905. RP LAFUSE, WP (reprint author), OHIO STATE UNIV,DEPT MED MICROBIOL & IMMUNOL,333 W 10TH AVE,COLUMBUS,OH 43210, USA. FU NIGMS NIH HHS [GM41786] NR 45 TC 35 Z9 35 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0093-7711 J9 IMMUNOGENETICS JI Immunogenetics PD JUN PY 1992 VL 36 IS 2 BP 110 EP 116 DI 10.1007/BF00215287 PG 7 WC Genetics & Heredity; Immunology SC Genetics & Heredity; Immunology GA HX432 UT WOS:A1992HX43200006 PM 1351875 ER PT J AU WARREN, HS GLENNON, ML WAINWRIGHT, N AMATO, SF BLACK, KM KIRSCH, SJ RIVEAU, GR WHYTE, RI ZAPOL, WM NOVITSKY, TJ AF WARREN, HS GLENNON, ML WAINWRIGHT, N AMATO, SF BLACK, KM KIRSCH, SJ RIVEAU, GR WHYTE, RI ZAPOL, WM NOVITSKY, TJ TI BINDING AND NEUTRALIZATION OF ENDOTOXIN BY LIMULUS ANTILIPOPOLYSACCHARIDE FACTOR SO INFECTION AND IMMUNITY LA English DT Article ID POLYMYXIN-B SULFATE; SALMONELLA-TYPHIMURIUM LIPOPOLYSACCHARIDES; ANTI-LPS FACTOR; MONOCLONAL-ANTIBODIES; BACTERIAL LIPOPOLYSACCHARIDE; INTRAVASCULAR COAGULATION; LIPOPROTEIN-BINDING; ESCHERICHIA-COLI; HORSESHOE-CRAB; O-ANTIGENS AB In order to examine the ability of Limulus antilipopolysaccharide factor (LALF) to bind lipopolysaccharide (LPS), we purified LALF to homogeneity from Limulus amoebocyte lysate and coupled it covalently to agarose beads. LALF-coupled beads captured more tritiated LPS from rough and smooth strains of gram-negative bacteria than did control human serum albumin-coupled beads. Unlabeled homologous and heterologous LPS competed for the binding of H-3-LPS to LALF-coupled beads. LALF bound LPS in a dose-dependent manner as assessed by the precipitation of LPS-LALF complexes with 50% saturated ammonium sulfate. We also studied the ability of LALF to neutralize LPS. LPS preincubated with LALF was less mitogenic for murine splenocytes, was less pyrogenic in the rabbit fever assay, was less lethal in mice which had been sensitized to LPS with actinomycin D, and induced less fever, neutropenia, and pulmonary hypertension when infused into sheep. Our findings extend prior studies which suggested that LALF binds to and neutralizes LPS from multiple strains of gram-negative bacteria. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02129. SHRINERS BURN INST,DEPT PEDIAT,BOSTON,MA 02114. UNIV S FLORIDA,DEPT PHARMACOL,TAMPA,FL 33620. ASSOCIATES CAPE COD INC,FALMOUTH,MA 02540. RP WARREN, HS (reprint author), MASSACHUSETTS GEN HOSP,DEPT PEDIAT,BOSTON,MA 02114, USA. FU NIAID NIH HHS [R29AI28943-01] NR 50 TC 75 Z9 77 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0019-9567 J9 INFECT IMMUN JI Infect. Immun. PD JUN PY 1992 VL 60 IS 6 BP 2506 EP 2513 PG 8 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HX421 UT WOS:A1992HX42100054 PM 1587618 ER PT J AU COTE, CJ AF COTE, CJ TI PEDIATRIC BREATHING CIRCUITS AND ANESTHESIA MACHINES SO INTERNATIONAL ANESTHESIOLOGY CLINICS LA English DT Article ID PULSE OXIMETRY; NEWBORN-INFANTS; EDUCATED HAND; OZONE-LAYER; CHILDREN; VENTILATION; ACCURACY; DISEASE; DISTAL RP COTE, CJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,FRUIT ST,BOSTON,MA 02114, USA. NR 45 TC 6 Z9 6 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-5907 J9 INT ANESTHESIOL CLIN JI Int. Anesthesiol. Clin. PD SUM PY 1992 VL 30 IS 3 BP 51 EP 61 PG 11 WC Anesthesiology SC Anesthesiology GA JH658 UT WOS:A1992JH65800004 PM 1516973 ER PT J AU POWERS, SM SMITH, ST MACARUSO, P AF POWERS, SM SMITH, ST MACARUSO, P TI SYNTACTIC ABILITIES IN LANGUAGE-IMPAIRED DYSLEXICS SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NEUROLINGUIST LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE, EAST SUSSEX, ENGLAND BN3 2FA SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 1992 VL 27 IS 3-4 BP 76 EP 77 PG 2 WC Psychology, Multidisciplinary SC Psychology GA JF420 UT WOS:A1992JF42000393 ER PT J AU LEVIN, LA RUBIN, PAD AF LEVIN, LA RUBIN, PAD TI ADVANCES IN ORBITAL IMAGING SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP LEVIN, LA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,OCULOPLAST SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 5 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 1 EP 25 PG 25 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200002 PM 1639593 ER PT J AU LAMKIN, JC RAIZMAN, MB AF LAMKIN, JC RAIZMAN, MB TI UPDATE ON LABORATORY TESTS FOR DIAGNOSIS OF ORBITAL DISEASE SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP LAMKIN, JC (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, 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 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 27 EP 44 DI 10.1097/00004397-199203230-00004 PG 18 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200003 PM 1639600 ER PT J AU BILYK, JR DALLOW, RL OJEMANN, RG LINGGOOD, RM SHORE, JW AF BILYK, JR DALLOW, RL OJEMANN, RG LINGGOOD, RM SHORE, JW TI MANAGEMENT OF LESIONS AT THE CRANIOORBITAL JUNCTION SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP BILYK, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 73 EP 93 DI 10.1097/00004397-199203230-00007 PG 21 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200006 PM 1639603 ER PT J AU BILYK, JR ADAMIS, AP MULLIKEN, JB AF BILYK, JR ADAMIS, AP MULLIKEN, JB TI TREATMENT OPTIONS FOR PERIORBITAL HEMANGIOMA OF INFANCY SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP BILYK, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 95 EP 109 DI 10.1097/00004397-199203230-00008 PG 15 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200007 PM 1639604 ER PT J AU OKADA, AA SHORE, JW RUBIN, PAD AF OKADA, AA SHORE, JW RUBIN, PAD TI PERIORBITAL INTRAOSSEOUS HEMANGIOMAS SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP OKADA, AA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 12 Z9 12 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 111 EP 121 DI 10.1097/00004397-199203230-00009 PG 11 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200008 PM 1639594 ER PT J AU MCKEOWN, CA AF MCKEOWN, CA TI OCULAR MOTILITY DISORDERS AND ORBITAL TRAUMA SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP MCKEOWN, CA (reprint author), MASSACHUSETTS EYE & EAR INFIRM,243 CHARLES ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 123 EP 149 DI 10.1097/00004397-199203230-00010 PG 27 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200009 PM 1639595 ER PT J AU BILYK, JR RUBIN, PAD SHORE, JW AF BILYK, JR RUBIN, PAD SHORE, JW TI CORRECTION OF ENOPHTHALMOS WITH POROUS POLYETHYLENE IMPLANTS SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Article RP BILYK, JR (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, USA. NR 0 TC 22 Z9 23 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP 151 EP 156 DI 10.1097/00004397-199203230-00011 PG 6 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200010 PM 1639596 ER PT J AU SHORE, JW AF SHORE, JW TI ORBITAL DISEASE - PREFACE SO INTERNATIONAL OPHTHALMOLOGY CLINICS LA English DT Editorial Material RP SHORE, JW (reprint author), MASSACHUSETTS EYE & EAR INFIRM,CTR EYE PLAST & ORBIT,50 STANIFORD ST,3RD FLOOR,BOSTON,MA 02114, 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 0020-8167 J9 INT OPHTHALMOL CLIN JI Int. Ophthalmol. Clin. PD SUM PY 1992 VL 32 IS 3 BP R13 EP R13 PG 1 WC Ophthalmology SC Ophthalmology GA JG722 UT WOS:A1992JG72200001 ER PT J AU THALI, M FURMAN, C WAHREN, B POSNER, M HO, DD ROBINSON, J SODROSKI, J AF THALI, M FURMAN, C WAHREN, B POSNER, M HO, DD ROBINSON, J SODROSKI, J TI COOPERATIVITY OF NEUTRALIZING ANTIBODIES DIRECTED AGAINST THE V3 AND CD4 BINDING REGIONS OF THE HUMAN IMMUNODEFICIENCY VIRUS-GP120 ENVELOPE GLYCOPROTEIN SO JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES AND HUMAN RETROVIROLOGY LA English DT Article DE GP120 GLYCOPROTEIN; NEUTRALIZING ANTIBODIES; V3 LOOP; CD4 BINDING REGION ID VIRUS TYPE-III; MONOCLONAL-ANTIBODIES; HTLV-III; 3-DIMENSIONAL STRUCTURE; RECEPTOR-BINDING; GP120 BINDING; HIV-1 GP120; AIDS; ANTIGEN; COMPLEX AB Human immunodeficiency virus type 1 (HIV-1) infection elicits neutralizing antibodies directed against two discrete regions of the gp120 exterior envelope glycoprotein: the third variable (V3) loop and the CD4 binding region. Monoclonal antibodies directed against these two regions demonstrated additive or, in some cases, weakly synergistic neutralization of HIV-1 infection. Cooperativity in virus neutralization was also observed for some gp120 mutants that, in the absence of anti-V3 loop antibodies, were relatively resistant to neutralization by antibodies directed against the CD4 binding region. Although the binding of some anti-V3 region monoclonal antibodies increased the recognition of the multimeric envelope glycoproteins by anti-CD4 binding antibodies, this enhanced binding was not predictive of the degree of cooperativity observed in virus neutralization. These results suggest that elicitation of both types of neutralizing antibodies should increase the efficacy of vaccine preparations. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,JF707,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NATL BACTERIOL LAB,S-10521 STOCKHOLM,SWEDEN. NEW ENGLAND DEACONESS HOSP,DEPT MED,BOSTON,MA 02215. NYU,SCH MED,AARON DIAMOND AIDS RES CTR,NEW YORK,NY 10003. LOUISIANA STATE UNIV,MED CTR,DEPT PEDIAT,NEW ORLEANS,LA 70112. FU NIAID NIH HHS [AI2696, AI 25541, AI 31783] NR 55 TC 55 Z9 55 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1077-9450 J9 J ACQ IMMUN DEF SYND JI J. Acquir. Immune Defic. Syndr. Hum. Retrovirol. PD JUN PY 1992 VL 5 IS 6 BP 591 EP 599 PG 9 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA HV368 UT WOS:A1992HV36800009 PM 1588493 ER PT J AU DAVIES, JP HARRIS, WH AF DAVIES, JP HARRIS, WH TI THE EFFECT OF THE ADDITION OF METHYLENE-BLUE ON THE FATIGUE-STRENGTH OF SIMPLEX-P BONE-CEMENT SO JOURNAL OF APPLIED BIOMATERIALS LA English DT Article AB To aid in cement removal during revision arthroplasty, it has been proposed to add methylene blue to bone cement to provide contrast between the cement and bone. However, it is essential that the fatigue strength of the cement not be reduced by the addition of the methylene blue. The effect of adding 1 mL of an aqueous 1% solution of methylene blue to one pack of Simplex P prepared in the standard fashion (uncentrifuged) was studied. We also measured the fatigue properties of centrifuged Simplex P with three different methylene blue preparations. We studied adding 1 mL of an aqueous 1% solution of methylene blue, 0.5 g of methylene blue powder, and 0.1 mL of a 10% solution of methylene blue per pack of Simplex P bone cement. Adding 1 mL of a 1% methylene blue solution to 40 g of Simplex P without centrifuging the cement after mixing produced a cement with a mean fatigue life comparable to the uncentrifuged Simplex P without the methylene blue. However, the fatigue data scatter was higher for the uncentrifuged methylene blue preparation. The optimum methylene blue impregnated cement preparation was produced by adding 1 mL of a 1% methylene blue solution to 40 g of Simplex P powder, mixing with chilled monomer, and centrifuging for 60 s. Sterile 1 mL vials of 1% methylene blue solution are available in the operating room. Thus the experienced surgeon can use a cement containing color to facilitate distinguishing cement from bone in cases needing revisions without weakening the cement. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 7 TC 19 Z9 19 U1 1 U2 1 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 1045-4861 J9 J APPL BIOMATER JI J. Appl. Biomater. PD SUM PY 1992 VL 3 IS 2 BP 81 EP 85 DI 10.1002/jab.770030203 PG 5 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA HT988 UT WOS:A1992HT98800002 PM 10147706 ER PT J AU BUTTERTON, JR STOEBNER, JA PAYNE, SM CALDERWOOD, SB AF BUTTERTON, JR STOEBNER, JA PAYNE, SM CALDERWOOD, SB TI CLONING, SEQUENCING, AND TRANSCRIPTIONAL REGULATION OF VIUA, THE GENE ENCODING THE FERRIC VIBRIOBACTIN RECEPTOR OF VIBRIO-CHOLERAE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID MEDIATED IRON-TRANSPORT; OUTER-MEMBRANE PROTEINS; ESCHERICHIA-COLI; NUCLEOTIDE-SEQUENCE; UPTAKE SYSTEM; VIRULENCE; PROMOTER; ANGUILLARUM; SIDEROPHORE; PLASMID AB A 74-kDa iron-regulated outer membrane protein of Vibrio cholerae acts as the receptor for the V. cholerae iron-siderophore complex, ferric vibriobactin. MBG14, a mutant of V. cholerae 0395 containing a TnphoA insertion in a gene designated viuA, lacks this 74-kDa outer membrane protein and is unable to bind or utilize exogenous ferric vibriobactin. Introduction of a plasmid containing the complete viuA coding sequence and 513 bp of upstream DNA into MBG14 restored ferric vibriobactin utilization to the mutant. The DNA insert in this plasmid was sequenced, revealing a single open reading frame of 2,061 bp, encoding a deduced protein of 687 amino acids with a predicted molecular mass of 76,417 Da and a predicted initial signal sequence of 37 amino acids. ViuA showed only weak homology to two iron-regulated outer membrane proteins in Escherichia coli, IutA and FecA. Construction of viuA::TnphoA gene fusions allowed study of the regulation of viuA expression by iron. This regulation in E. coli was dependent on the fur gene. Northern (RNA) blot analysis of RNA from wild-type V. cholerae grown in high- and low-iron media revealed a monocistronic viuA message that was negatively regulated by iron at the transcriptional level. Primer extension analysis identified a single transcriptional start site, located 243 bp above the translational start site. The promoter region of viuA contained two interrupted dyad symmetric nucleotide sequences, overlapping the -10 and -35 boxes, each similar to the E. coli Fur binding consensus sequence. Another iron-regulated gene in V. cholerae that is negatively regulated by fur, irgA, requires a positive transcriptional activator (irgB) for expression. However, a strain of V. cholerae mutant in irgB was unaffected in viuA expression. These studies suggest that there is conserved, global coordinate iron regulation in V. cholerae by fur; additional regulatory factors, superimposed upon the fur system, may provide more precise control of individual iron-regulated genes. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. UNIV TEXAS,DEPT MICROBIOL,AUSTIN,TX 78712. HARVARD UNIV,SCH MED,DEPT MICROBIOL & GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI 27329]; NIGMS NIH HHS [N01-GM-7-2110] NR 46 TC 59 Z9 60 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD JUN PY 1992 VL 174 IS 11 BP 3729 EP 3738 PG 10 WC Microbiology SC Microbiology GA HX278 UT WOS:A1992HX27800042 PM 1317381 ER PT J AU HODGSON, JM JONES, C AF HODGSON, JM JONES, C TI PHONOLOGICAL DYSLEXIA IN THE PRESENCE OF METAPHONOLOGICAL SKILLS - A CASE-REPORT SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 1 PU SWETS ZEITLINGER PUBLISHERS PI LISSE PA P O BOX 825, 2160 SZ LISSE, NETHERLANDS SN 1380-3395 J9 J CLIN EXP NEUROPSYC JI J. Clin. Exp. Neuropsychol. PD JUN PY 1992 VL 14 IS 3 BP 389 EP 389 PG 1 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA HZ771 UT WOS:A1992HZ77100094 ER PT J AU SLUSS, PM SCHNEYER, AL AF SLUSS, PM SCHNEYER, AL TI LOW-MOLECULAR-WEIGHT FOLLICLE-STIMULATING-HORMONE RECEPTOR-BINDING INHIBITOR IN SERA FROM PREMATURE OVARIAN FAILURE PATIENTS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID CELL AROMATASE BIOASSAY; FLUID CONTAINS; PURIFICATION; PREGNANCY; SUBUNIT; ASSAY; FSH AB Ovarian insensitivity to FSH, as observed in some patients suffering premature ovarian failure (POF), could conceivably involve abnormal regulation of local factors that modulate FSH action. Low molecular weight FSH receptor-binding inhibitor (FRBI) has been identified in ovarian follicular fluid and shown to be an antagonist of FSH action. Thus, we undertook these studies to test the hypothesis that elevated FRBI can account for the high serum levels of FSH as measured by RRA relative to RIA values in some POF patients. In order to accomplish this, 2 POF patients were selected from a group of 27 from whom serum FSH had been measured by RIA and RRA. Using a recently developed and validated RRA, FSH was 430 IU (second IRP-78/549)/L and 182 IU/L for serum from patients 1 and 2, respectively. FSH quantitated by RIA was 96 and 136 IU/L in these same serum samples. Thus, the RRA/RIA values for these patients were 4.48 and 1.34. These ratios are: 1) higher than observed for normal cycling women (0.62); 2) higher than observed for normal, postmenopausal women (0.65); and 3) at least 2 SD higher than the mean RRA/RIA ratio of the 27 patients screened. FRBI was separated from FSH in serum from both these patients. FRBI accounted for most of the elevated FSH measured in serum by RRA. The HPLC chromatographic behavior and binding inhibitory activity of FRBI isolated from a large volume of serum from patient 2 were virtually identical to previously observed characteristics of FRBI isolated from porcine follicular fluid. These observations demonstrate that FRBI can account for elevated FSH measured by RRA relative to that measured by RIA. Furthermore, the inhibitor can be biochemically separated from FSH and quantitated by RRA in order to study its postulated relationship to POF. Expanded studies to identify causal relationships between FRBI and ovarian insensitivity to FSH seem warranted at this time. C1 MASSACHUSETTS GEN HOSP, REPROD ENDOCRINE UNIT, BOSTON, MA 02114 USA. UNIV ROCHESTER, MED CTR, DEPT UROL, ROCHESTER, NY 14642 USA. FU NICHD NIH HHS [HD-19302, HD-25941] NR 24 TC 19 Z9 19 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 EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1992 VL 74 IS 6 BP 1242 EP 1246 DI 10.1210/jc.74.6.1242 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX258 UT WOS:A1992HX25800005 PM 1592865 ER PT J AU SCHNEYER, AL ONEIL, DA CROWLEY, WF AF SCHNEYER, AL ONEIL, DA CROWLEY, WF TI ACTIVIN-BINDING PROTEINS IN HUMAN SERUM AND FOLLICULAR-FLUID SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID INHIBIN; RADIOIMMUNOASSAY; FOLLISTATIN AB Binding proteins that transport and/or modify the biological action of peptide hormones and growth factors have been identified for an increasing number of endocrinologically important substances. Since these binding proteins can mask epitopes critical for recognition in immunoassays and can neutralize the bioactivity of their targets, elucidation of hormonal physiology can be intricately tied to analysis of binding protein structure and function. Therefore, we investigated whether circulating activin- and inhibin-binding proteins exist in human serum by incubating purified recombinant human I-125-activin with serum samples. After gel permeation chromatography, radioactive activin was identified in three peaks, a high molecular wt (mol wt) binding protein peak (230 kDa), a lower mol wt binding protein peak (60 kDa), and free activin (22.5 kDa). Bound activin was displaced from the lower mol wt binding protein with either activin or inhibin, but was not displaced from the high mol wt peak with a 10-fold greater concentration of activin. Since an activin-binding protein, follistatin, has been identified in ovarian and pituitary extracts, these same analytical techniques were applied to analysis of human follicular fluid as well. A large, 60 kDa binding protein peak eluting in a position similar to the lower mol wt peak in serum was observed, consistent with this protein being follistatin. These results demonstrate the presence of at least two activin-binding proteins, distinguishable by size, in human serum that may interfere with attempts to assay activin levels in circulation without prior extraction, and may also be involved in regulating the biological actions of activin. RP SCHNEYER, AL (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, REPROD ENDOCRINOL UNIT, BHX 5, BOSTON, MA 02114 USA. FU NICHD NIH HHS [U54 HD028138, HD 15788, HD 25941, P30 HD028138, HD 15080] NR 20 TC 58 Z9 58 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 EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1992 VL 74 IS 6 BP 1320 EP 1324 DI 10.1210/jc.74.6.1320 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX258 UT WOS:A1992HX25800018 PM 1592877 ER PT J AU KATZNELSON, L ALEXANDER, JM BIKKAL, HA JAMESON, JL HSU, DW KLIBANSKI, A AF KATZNELSON, L ALEXANDER, JM BIKKAL, HA JAMESON, JL HSU, DW KLIBANSKI, A TI IMBALANCED FOLLICLE-STIMULATING-HORMONE BETA-SUBUNIT HORMONE BIOSYNTHESIS IN HUMAN PITUITARY-ADENOMAS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID GONADOTROPIN-RELEASING-HORMONE; HUMAN CHORIONIC-GONADOTROPIN; FREE ALPHA-SUBUNIT; LUTEINIZING-HORMONE; CELL ADENOMAS; SECRETION; THYROTROPIN; EXPRESSION; TUMORS; BROMOCRIPTINE AB Clinically nonfunctioning pituitary adenomas represent approximately 25% of all pituitary tumors. Recent studies using a number of in vitro techniques show that the majority of such tumors produce gonadotropins. Hypersecretion of uncombined gonadotropin subunits by these tumors has also been identified raising the possibility that gonadotropin biosynthetic alterations may occur in neoplastic pituitary tissue. To determine whether underlying intracellular biosynthetic alterations lead to imbalanced secretion of the gonadotropin subunits by such tumors, we investigated 1) steady state gonadotropin-subunit messenger ribonucleic acid (mRNA) levels in tumor tissue from 49 patients with clinically nonfunctioning adenomas, 2) secretion of gonadotropins in dispersed pituitary tumor cultures, and 3) serum concentrations of gonadotropins and free subunits. Northern blots of RNA extracted from surgically obtained pituitary tumor tissue were hybridized with complementary DNA probes for FSH-beta, LH-beta, and alpha-subunit, and quantitative analysis was done to compare alpha- and beta-subunit biosynthesis in individual tumors. Of these tumors, 47 contained sufficient RNA for Northern analysis and 77% of these tumors contained one or more of the gonadotropin-subunit mRNAs. Steady state alpha-subunit mRNA was detected in 57% of tumors, FSH-beta mRNA in 49%, and LH-beta in 1 (2%). We found FSH-beta mRNA in excess of alpha-subunit mRNA in one-third of tumors, including 9 tumors where alpha-subunit mRNA was undetectable. In cultured cells, FSH-beta was secreted in excess of alpha-subunit in 41% of tumors. For those tumors in which both mRNA and culture data were available, FSH-beta mRNA and secreted subunit levels were in excess of alpha-subunit in 64% of tumors. We conclude that clinically nonfunctioning pituitary adenomas frequently synthesize excess FSH-beta subunit relative to alpha-subunit. This finding is in contrast to previous data in normal pituitary or placental tissue where alpha-subunit is present in excess of beta-subunits at both the mRNA and protein levels. The free-beta-subunit hypersecretion identified in pituitary adenomas may be due to biosynthetic abnormalities intrinsic to neoplastic gonadotrophs. C1 MASSACHUSETTS GEN HOSP, NEUROENDOCRINE UNIT, FRUIT ST, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, THYROID UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROPATHOL, BOSTON, MA 02114 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD 23519]; NIDDK NIH HHS [DK40947, DK07028] NR 36 TC 39 Z9 39 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 EI 1945-7197 J9 J CLIN ENDOCR METAB JI J. Clin. Endocrinol. Metab. PD JUN PY 1992 VL 74 IS 6 BP 1343 EP 1351 DI 10.1210/jc.74.6.1343 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HX258 UT WOS:A1992HX25800022 PM 1375599 ER PT J AU PEDERSEN, O KAHN, CR KAHN, BB AF PEDERSEN, O KAHN, CR KAHN, BB TI DIVERGENT REGULATION OF THE GLUT-1 AND GLUT-4 GLUCOSE TRANSPORTERS IN ISOLATED ADIPOCYTES FROM ZUCKER RATS SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE AGING; OBESITY; DIABETES; INSULIN RESISTANCE; LIPOGENESIS ID ADIPOSE-CELLS; MESSENGER-RNA; OBESE RATS; FATTY RAT; INSULIN; METABOLISM; PROTEIN; HYPERINSULINEMIA; EXPRESSION; STIMULATION AB We have studied the relationship between glucose uptake rate and Glut 1 and Glut 4 protein and mRNA levels per fat cell in lean (FA/FA) and obese (fa/fa) Zucker rats at 5, 10, and 20 wk of age, and after induction of acute diabetes with streptozotocin. 5 wk obese rats exhibit insulin hyperresponsive glucose uptake, whereas 20 wk obese rats show insulin resistant glucose uptake. The relative abundance of Glut 1 and Glut 4 mRNA and protein per equal amount of total RNA and total membrane protein, respectively, is lower in adipocytes from obese rats. However, at all ages the enlargement of fat cells from obese rats is accompanied by a severalfold increase in total RNA and total membrane protein per cell. Thus, on a cellular basis, mRNA and protein levels of Glut 4 increases in young obese rats and gradually declines as a function of age. Basal glucose uptake is increased severalfold in fat cells from obese rats, and in parallel Glut 1 expression per cell in obese rats is two- to threefold increased over lean rats at all ages. Acute diabetes in 20 wk obese rats causes a profound downregulation of glucose uptake and a concomitant reduction of both Glut 1 and Glut 4 protein levels. Thus, changes in Glut 4 expression are a major cause of alteration in insulin-stimulated glucose uptake of adipocytes during evolution of obesity and diabetes in Zucker rats. C1 JOSLIN DIABET CTR,RES LAB,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BETH ISRAEL HOSP,THORNDIKE LAB,BOSTON,MA 02215. BETH ISRAEL HOSP,CHARLES A DANA RES INST,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT MED,BOSTON,MA 02215. RP PEDERSEN, O (reprint author), STENO DIABET CTR,NIELS STEENSENS VEJ 2,DK-2820 COPENHAGEN,DENMARK. FU NIA NIH HHS [AG-00294]; NIDDK NIH HHS [DK-33201, DK-36836] NR 40 TC 63 Z9 63 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 JUN PY 1992 VL 89 IS 6 BP 1964 EP 1973 DI 10.1172/JCI115804 PG 10 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400035 PM 1534819 ER PT J AU SCHWABER, J MALONE, B AF SCHWABER, J MALONE, B TI GERM LINE TRANSCRIPTION OF THE IMMUNOGLOBULIN HEAVY-CHAIN LOCUS DIRECTS PRODUCTION OF MU-CHAIN WITHOUT VDJ SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IMMUNOGLOBULIN; RECOMBINATION; LYMPHOCYTES-B; LEADER SEQUENCE; PRE-B CELLS ID VARIABLE REGION GENE; PRE-B-CELLS; X-LINKED AGAMMAGLOBULINEMIA; C-MU; SEGMENTS; REARRANGEMENT; RECEPTOR; DNA; VH; EXPRESSION AB Immunoglobulin VDJ recombination is associated with transcriptional activation of the Ig variable region elements. We have previously described a novel Ig mu-chain protein and mRNA produced by pre-B cell hybrids from normal and X-linked agammaglobulinemic bone marrow. We have now characterized the mRNA encoding this protein and find that it is composed of a 5' leader sequence spliced to C-mu (LS-C-mu), lacking the variable (V), diversity (D), and joining (J) gene sequences. The leader sequence is encoded by a novel exon 16 kb upstream of the J(H) locus. Transcription of the germ line heavy chain locus from this LS exon results in transcriptional activation of the J(H) locus, apparently the initial step in commitment to B lymphoid development. Polymerase chain reaction amplification of normal bone marrow shows that these germ line LS-C-mu transcripts are a product of bone marrow pre-B cells. Production of LS-C-mu commences a sequential process of transcriptional activation, with concordant translation of Ig rearrangement intermediates, in the process of creating a productive VDJ rearrangement. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,CTR BLOOD RES,SCH MED,BOSTON,MA 02115. RP SCHWABER, J (reprint author), HAHNEMANN UNIV,DEPT PATHOL,MS 435,BROAD & VINE,PHILADELPHIA,PA 19102, USA. FU NIAID NIH HHS [AI21163, AI21165] NR 38 TC 6 Z9 6 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 JUN PY 1992 VL 89 IS 6 BP 2046 EP 2052 DI 10.1172/JCI115816 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400047 PM 1602010 ER PT J AU SCHWABER, J AF SCHWABER, J TI EVIDENCE FOR FAILURE OF V(D)J RECOMBINATION IN BONE-MARROW PRE-B CELLS FROM X-LINKED AGAMMAGLOBULINEMIA SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE IMMUNOGLOBULIN; LYMPHOCYTES-B; TRANSCRIPTIONAL ACTIVATION; ANTIBODY DEFICIENCY; POLYMERASE CHAIN REACTION ID VARIABLE REGION GENE; CARRIER DETECTION; ANTIGEN RECEPTOR; SEGMENTS; REARRANGEMENT; VH; ANTIBODY; DNA; IDENTIFICATION; TRANSCRIPTION AB X-linked agammaglobulinemia (XLA) results from a failure of B lymphoid development. We have previously examined pre-B cell hybrids from three patients with XLA and found them to be limited to production of a novel germ line transcript of the Ig H chain locus composed of a leader sequence (LS) spliced to the constant region of mu-chain (C-mu) as mRNA and polypeptide. These transcripts result from transcriptional activation of the germ line heavy chain locus from an LS exon upstream of the embryonic J(H) locus. Germ line LS-C-mu transcripts are produced by pre-B cells from normal bone marrow and fetal liver, indicating that they are products of normal pre-B cell development, as part of the process of transcriptional activation to provide access for the recombinase. Bone marrow from three patients with XLA has been examined directly by polymerase chain reaction amplification to determine whether the exclusive production of LS-C-mu by XLA pre-B cell hybrids is representative of XLA pre-B cells. I report that LS-C-mu is the predominant Ig molecule produced by XLA pre-B cells, with limited production of the D-mu product of DJ(H) intermediate stage of V(D)J recombination. Mature V(H)DJ(H) recombinations were not detected with a variety of primers that amplify V(H) sequences. I conclude that XLA is associated with a limitation in V(D)J recombination that may cause the failure of pre-B cell development. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,CTR BLOOD RES,SCH MED,BOSTON,MA 02115. RP SCHWABER, J (reprint author), HAHNEMANN UNIV,DEPT PATHOL,MS 435,BROAD & VINE,PHILADELPHIA,PA 19102, USA. FU NIAID NIH HHS [AI21165, AI21163] NR 31 TC 6 Z9 6 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 JUN PY 1992 VL 89 IS 6 BP 2053 EP 2059 DI 10.1172/JCI115817 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA HX974 UT WOS:A1992HX97400048 PM 1602011 ER PT J AU BRATOEVA, MP JOHN, JF BARG, NL AF BRATOEVA, MP JOHN, JF BARG, NL TI MOLECULAR EPIDEMIOLOGY OF TRIMETHOPRIM-RESISTANT SHIGELLA-BOYDII SEROTYPE-2 STRAINS FROM BULGARIA SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID SONNEI AB In 1990 an increased number of strains of Shigella boydii serotype 2 were isolated from different regions of Bulgaria. Strains were reported as sporadic, although they showed identical phenotypic characteristics, including resistance to ampicillin, carbenicillin, streptomycin, sulfonamide, tetracycline, ticarcillin, and trimethoprim. The objective of this study was to determine the genetic relatedness of the strains and the mechanism of their antimicrobial resistance. Plasmid fingerprinting showed an identical pattern for 23 of 25 of the selected strains. All 25 strains tested transferred their resistances en bloc to an Escherichia coli recipient. Transconjugants contained a 112-kb R plasmid which carried all the resistance genes, including that conferring type I dihydrofolate reductase-mediated trimethoprim resistance (MIC > 2,000-mu-g/ml). Riboprobe analysis showed identical restriction length fragment polymorphisms, suggesting a highly conserved genome. All findings indicate that strains of S. boydii serotype 2 isolated in 1990 from different regions of Bulgaria were highly related genetically and can be considered representatives of a single bacterial clone. The presence of an R plasmid and selection pressure because of the usage of antimicrobial agents, particularly trimethoprim, have likely facilitated the spread of the clone throughout the country. C1 MED UNIV S CAROLINA,RALPH H JOHNSON VET AFFAIRS MED CTR,CHARLESTON,SC 29425. ACAD MED SOFIA,INFECT & PARASIT DIS RES INST,SOFIA,BULGARIA. VANDERBILT UNIV,ST THOMAS HOSP,SCH MED,DEPT MED,NASHVILLE,TN 37203. NR 24 TC 6 Z9 6 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0095-1137 J9 J CLIN MICROBIOL JI J. Clin. Microbiol. PD JUN PY 1992 VL 30 IS 6 BP 1428 EP 1431 PG 4 WC Microbiology SC Microbiology GA HU603 UT WOS:A1992HU60300011 PM 1624559 ER PT J AU DELAPAZ, MA CHUNG, SM MCCRARY, JA AF DELAPAZ, MA CHUNG, SM MCCRARY, JA TI BILATERAL INTERNUCLEAR OPHTHALMOPLEGIA IN A PATIENT WITH WERNICKES ENCEPHALOPATHY SO JOURNAL OF CLINICAL NEURO-OPHTHALMOLOGY LA English DT Article DE INTERNUCLEAR OPHTHALMOPLEGIA; WERNICKES ENCEPHALOPATHY; ALCOHOLISM ID MULTIPLE-SCLEROSIS; KORSAKOFF-SYNDROME; MR; NYSTAGMUS; DIAGNOSIS AB The most common cause of bilateral internuclear ophthalmoplegia is multiple sclerosis. Wernicke's encephalopathy has been reported as a cause of unilateral internuclear ophthalmoplegia but not of bilateral internuclear ophthalmoplegia. In this report, we present the case of a patient with a history of alcohol abuse and acute onset of bilateral internuclear ophthalmoplegia whose clinical course and diagnostic studies are most consistent with a diagnosis of Wernicke's encephalopathy. C1 ST LOUIS UNIV, MED CTR, BETHESDA EYE INST, 3655 VISTA AVE, ST LOUIS, MO 63110 USA. BAYLOR COLL MED, HOUSTON, TX 77030 USA. MASSACHUSETTS EYE & EAR INFIRM, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. NR 32 TC 4 Z9 4 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 USA SN 0272-846X J9 J CLIN NEURO-OPHTHAL PD JUN PY 1992 VL 12 IS 2 BP 116 EP 120 PG 5 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA HY010 UT WOS:A1992HY01000010 PM 1629372 ER PT J AU BORODIC, GE FERRANTE, R AF BORODIC, GE FERRANTE, R TI EFFECTS OF REPEATED BOTULINUM TOXIN INJECTIONS ON ORBICULARIS OCULI MUSCLE SO JOURNAL OF CLINICAL NEURO-OPHTHALMOLOGY LA English DT Article DE BLEPHAROSPASM; MEIGES SYNDROME, BOTULINUM-A TOXIN; DYSTONIA; ACETYLCHOLINESTERASE; HEMI-FACIAL SPASM ID SPASMODIC TORTICOLLIS; DOUBLE-BLIND; CHOLINESTERASE; BLEPHAROSPASM; DYSTONIA AB Histologic evaluation was conducted on 12 orbicularis oculi specimens from 11 patients with essential blepharospasm and Meige's disease who had received an average f 11.3 injections of botulinum A toxin over 3.5 years. Denervation was demonstrated by the spread of acetylcholinesterase staining on muscle fibers when specimens were evaluated within 11 weeks of the last injection. When specimens were taken after 12 weeks spread of acetylcholinesterase was confined to the neuromuscular junctions, with little fiber size variability resembling normal muscle. Fibrosis seen in three specimens could be correlated to prior surgery. Repeated injections of botulinum toxin into human muscle do not appear to cause irreversible muscle atrophy or other degenerative changes. Denervation changes (fiber size variability, acetylcholinesterase spread) appear to correlate to the time interval since the last injection. C1 MASSACHUSETTS GEN HOSP,NEUROPATHOL UNIT,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. NR 18 TC 59 Z9 61 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0272-846X J9 J CLIN NEURO-OPHTHAL PD JUN PY 1992 VL 12 IS 2 BP 121 EP 127 PG 7 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA HY010 UT WOS:A1992HY01000011 PM 1385821 ER PT J AU ANDERSEN, JW HARRINGTON, D AF ANDERSEN, JW HARRINGTON, D TI META-ANALYSES NEED NEW PUBLICATION STANDARDS SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Editorial Material RP ANDERSEN, JW (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN PY 1992 VL 10 IS 6 BP 878 EP 880 PG 3 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400002 PM 1588369 ER PT J AU WEISDORF, DJ ANDERSEN, JW GLICK, JH OKEN, MM AF WEISDORF, DJ ANDERSEN, JW GLICK, JH OKEN, MM TI SURVIVAL AFTER RELAPSE OF LOW-GRADE NON-HODGKINS-LYMPHOMA - IMPLICATIONS FOR MARROW TRANSPLANTATION SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID POORLY DIFFERENTIATED LYMPHOMA; PROGNOSTIC FACTORS; REGRESSION-MODELS; LONG-TERM; CHEMOTHERAPY; VALIDATION; MODERATE; CELL C1 UNIV MINNESOTA,VIRGINIA PIPER INST,MINNEAPOLIS,MN 55455. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. FU NCI NIH HHS [CA20365, CA15488, CA23318] NR 26 TC 76 Z9 76 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN PY 1992 VL 10 IS 6 BP 942 EP 947 PG 6 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400011 PM 1588373 ER PT J AU RUBIN, EH ANDERSEN, JW BERG, DT SCHIFFER, CA MAYER, RJ STONE, RM AF RUBIN, EH ANDERSEN, JW BERG, DT SCHIFFER, CA MAYER, RJ STONE, RM TI RISK-FACTORS FOR HIGH-DOSE CYTARABINE NEUROTOXICITY - AN ANALYSIS OF A CANCER AND LEUKEMIA GROUP-B TRIAL IN PATIENTS WITH ACUTE MYELOID-LEUKEMIA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID CENTRAL NERVOUS-SYSTEM; ACUTE NONLYMPHOCYTIC LEUKEMIA; CYTOSINE-ARABINOSIDE; ARA-C; REFRACTORY LEUKEMIA; CEREBELLAR TOXICITY; PHARMACOKINETICS; THERAPY; 1-BETA-D-ARABINOFURANOSYLCYTOSINE; CHEMOTHERAPY C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. UNIV MARYLAND,CTR CANC,COLLEGE PK,MD 20742. CANC & LUKEMIA GRP B,LEBANON,NH. FU NCI NIH HHS [5 U10 CA-31946-10, CA-06516, P01 CA-34183-08] NR 33 TC 59 Z9 62 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 JUN PY 1992 VL 10 IS 6 BP 948 EP 953 PG 6 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400012 PM 1588374 ER PT J AU AYASH, LJ WRIGHT, JE TRETYAKOV, O GONIN, R ELIAS, A WHEELER, C EDER, JP ROSOWSKY, A ANTMAN, K FREI, E AF AYASH, LJ WRIGHT, JE TRETYAKOV, O GONIN, R ELIAS, A WHEELER, C EDER, JP ROSOWSKY, A ANTMAN, K FREI, E TI CYCLOPHOSPHAMIDE PHARMACOKINETICS - CORRELATION WITH CARDIAC TOXICITY AND TUMOR RESPONSE SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID BONE-MARROW TRANSPLANTATION; INDUCED CARDIOMYOPATHY; CHEMOTHERAPY; PHARMACOLOGY; THERAPY C1 HARVARD UNIV,BETH ISRAEL HOSP,DANA FARBER CANC INST,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02215. HARVARD UNIV,BETH ISRAEL HOSP,DANA FARBER CANC INST,SCH MED,DEPT BIOSTAT,BOSTON,MA 02215. RP AYASH, LJ (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,DANA FARBER CANC INST,SCH MED,DEPT MED,44 BINNEY ST,BOSTON,MA 02215, USA. FU NCI NIH HHS [P01-CA-38493] NR 22 TC 163 Z9 165 U1 0 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 JUN PY 1992 VL 10 IS 6 BP 995 EP 1000 PG 6 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400019 PM 1588381 ER PT J AU ANTMAN, K AYASH, L ELIAS, A WHEELER, C FREI, E AF ANTMAN, K AYASH, L ELIAS, A WHEELER, C FREI, E TI BREAST-CANCER - EVALUATING TRIAL RESULTS - REPLY SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Letter RP ANTMAN, K (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. NR 4 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 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD JUN PY 1992 VL 10 IS 6 BP 1025 EP 1026 PG 2 WC Oncology SC Oncology GA HW164 UT WOS:A1992HW16400024 ER PT J AU ROSS, DS DANIELS, GH AF ROSS, DS DANIELS, GH TI RIEDELS THYROIDITIS ASSOCIATED WITH HASHIMOTO THYROIDITIS SO JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION LA English DT Letter RP ROSS, DS (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 2 TC 11 Z9 11 U1 0 U2 0 PU EDITRICE KURTIS S R L PI MILANO PA VIA LUIGI ZOJA, 30-20153 MILANO, ITALY SN 0391-4097 J9 J ENDOCRINOL INVEST JI J. Endocrinol. Invest. PD JUN PY 1992 VL 15 IS 6 BP 479 EP 479 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA JF346 UT WOS:A1992JF34600011 PM 1401750 ER PT J AU VONDERHEIDE, RH SPRINGER, TA AF VONDERHEIDE, RH SPRINGER, TA TI LYMPHOCYTE ADHESION THROUGH VERY LATE ANTIGEN-4 - EVIDENCE FOR A NOVEL BINDING-SITE IN THE ALTERNATIVELY SPLICED DOMAIN OF VASCULAR CELL-ADHESION MOLECULE-1 AND AN ADDITIONAL ALPHA-4 INTEGRIN COUNTER-RECEPTOR ON STIMULATED ENDOTHELIUM SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID TUMOR-NECROSIS-FACTOR; IMMUNE-SYSTEM; T-CELLS; LFA-1; ICAM-1; CLONING; IDENTIFICATION; EXPRESSION; FIBRONECTIN; ADHERENCE AB Recent studies demonstrate that alternative splicing of mRNA from a single gene can produce two forms of vascular cell adhesion molecule 1 (VCAM-1): a six-immunoglobulin (Ig) domain form (VCAM-6D) and a seven-Ig domain form (VCAM-7D). Using a COS cell transient expression assay, we investigated whether VCAM-6D and VCAM-7D differ functionally in adhesion to the integrin VLA-4 (CD49d/CD29) on lymphoid cells. Binding of lymphoid cell lines and peripheral blood lymphocytes was completely blocked by VLA-4 monoclonal antibody (mAb) and one VCAM-1 mAb (4B9) to both VCAM-6D and VCAM-7D, whereas one VCAM-1 mAb (E1/6) completely blocked binding to VCAM-6D but only partially inhibited binding to VCAM-7D. We conclude that there is one VLA-4 binding site in the six Ig domains shared between VCAM-6D and VCAM-7D, and that the alternatively spliced domain 4 present in VCAM-7D provides a second VLA-4 binding site that is blocked by 4B9 but not the E1/6 mAb. We compared the inhibitory effects of anti-VCAM-1 and anti-VLA-4 mAbs on lymphoid cell adhesion to cultured human umbilical vein endothelial cells (HUVEC). The anti-VCAM-1 mAb 4B9 blocked the binding of PBL and lymphoid tumor cells to stimulated HUVEC better than the anti-VCAM-1 mAb E1/6. Because VCAM-7D is the predominant form of VCAM-1 expressed by stimulated endothelial cells, this difference in VCAM-1 mAb inhibition is attributed to lymphoid cell binding to VCAM-7D on stimulated HUVEC. Although the anti-VLA-4 mAb and anti-VCAM-1 mAb 4B9 equally inhibited PBL binding to stimulated HUVEC, mAb 4B9 inhibited the binding of two lymphoid cell lines significantly less than anti-VLA-4 mAb. Combination of 4B9 mAb with function-blocking antiserum to human fibronectin, a second known ligand for VLA-4, also failed to inhibit as much as anti-VLA-4 mAb. These findings suggest that adhesion of lymphoid cell lines through VLA-4 or other alpha-4 integrins may involve inducible counter-receptor(s) on endothelium distinct from either VCAM-1 or fibronectin. Time course experiments indicate that the fraction of alpha-4 integrin-dependent binding that can be blocked by anti-VCAM-1 mAb E1/6 rises and peaks within 2 h of tumor necrosis factor (TNF) stimulation. We suggest that the binding site shared between VCAM-6D and -7D is important soon after TNF stimulation, but that domain 4 of VCAM-7D or potentially other non-VCAM-1 counter-receptors are sufficient to mediate most lymphoid cell adhesion at later time points. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD MIT DIV HLTH SCI & TECHNOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-31798] NR 51 TC 144 Z9 144 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 JUN 1 PY 1992 VL 175 IS 6 BP 1433 EP 1442 DI 10.1084/jem.175.6.1433 PG 10 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600003 PM 1375259 ER PT J AU NALEFSKI, EA KASIBHATLA, S RAO, A AF NALEFSKI, EA KASIBHATLA, S RAO, A TI FUNCTIONAL-ANALYSIS OF THE ANTIGEN-BINDING SITE ON THE T-CELL RECEPTOR ALPHA-CHAIN SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Article ID HYPERVARIABLE REGIONS; RECOGNITION; SPECIFICITY; ARSONATE; PROTEINS; CLONES; AZOBENZENEARSONATE; POLYPEPTIDE; MUTAGENESIS; FEATURES AB We have identified residues on a T cell receptor (TCR) alpha-chain that are important for interaction with antigen/major histocompatibility complex (MHC). Using site-directed mutagenesis, we modified DNA encoding the postulated antigen/MHC binding loops on the TCR alpha-chain expressed by the T cell clone D5, which recognizes p-azobenzenearsonate-conjugated antigens presented by cells bearing I-A(d). These variant TCR alpha-chains were expressed in conjunction with the wild-type D5 TCR beta-chain on the surface of hybridoma cells, and were tested for the ability to recognize hapten-conjugated antigens presented by I-A(d). Individual amino acid substitutions in each of the three antigen binding loops (alpha-1, alpha-2, alpha-3) of the D5 TCR alpha-chain affected antigen recognition, demonstrating that all three loops are important in recognition of antigen/MHC. A subset of the single amino acid substitutions completely eliminated antigen recognition, thus identifying the residues that are particularly important in the recognition of antigenic peptide/MHC by the D5 TCR. Because the wild-type D5 TCR recognizes arsonate and certain structural analogues of arsonate conjugated to a variety of protein antigens, we were able to test whether the TCR substitutions affected the specificity of the D5 TCR for hapten or carrier antigen. One substitution introduced into antigen binding loop alpha-3 markedly altered the pattern of carrier recognition. Together, these results verify the Ig model for the TCR and are consistent with the proposition that residues forming the first and second antigen binding loops of the TCR contact the MHC, while those forming the third loop contact mainly antigenic peptides. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,ROOM 613,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. FU NIAID NIH HHS [AI-22900]; NIGMS NIH HHS [5 T32 GM-07226] NR 40 TC 41 Z9 41 U1 0 U2 3 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1992 VL 175 IS 6 BP 1553 EP 1563 DI 10.1084/jem.175.6.1553 PG 11 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600017 PM 1588281 ER PT J AU SPERTINI, O LUSCINSKAS, FW GIMBRONE, MA TEDDER, TF AF SPERTINI, O LUSCINSKAS, FW GIMBRONE, MA TEDDER, TF TI MONOCYTE ATTACHMENT TO ACTIVATED HUMAN VASCULAR ENDOTHELIUM INVITRO IS MEDIATED BY LEUKOCYTE ADHESION MOLECULE-1 (L-SELECTIN) UNDER NONSTATIC CONDITIONS SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note AB The receptors that mediate monocyte adhesion to cytokine-stimulated endothelial monolayers were assessed using a nonstatic (rotating) cell-attachment assay. In this system, leukocyte adhesion molecule-1 (LAM-1) (L-selectin) mediated a major portion (87 +/- 15% at 37-degrees-C) of monocyte attachment to activated endothelium. mAb blocking of endothelial leukocyte adhesion molecule-1 (41% inhibition), CD18 (36%), and vascular cell adhesion molecule-1 (25%) function had lesser effects on attachment. These results suggest that LAM-1 may serve an important role in monocyte attachment to endothelium at sites of inflammation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV VASC RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [CA-36167, CA-34183]; NIAID NIH HHS [AI-26872] NR 16 TC 151 Z9 151 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 1114 FIRST AVE, 4TH FL, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD JUN 1 PY 1992 VL 175 IS 6 BP 1789 EP 1792 DI 10.1084/jem.175.6.1789 PG 4 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA HV676 UT WOS:A1992HV67600041 PM 1375271 ER PT J AU DUFFY, FJ SEILER, JG HERGRUETER, CA KANDEL, J GELBERMAN, RH AF DUFFY, FJ SEILER, JG HERGRUETER, CA KANDEL, J GELBERMAN, RH TI INTRINSIC MITOGENIC POTENTIAL OF CANINE FLEXOR TENDONS SO JOURNAL OF HAND SURGERY-BRITISH AND EUROPEAN VOLUME LA English DT Article AB Recent studies have demonstrated an intrinsic neovascular response in intrasynovial healing tendons, introducing the possibility of mitogenic and/or angiogenic capability of intrasynovial tendon. To explore this hypothesis, healing canine flexor tendons were treated with early passive mobilization and the repair sites analysed at three, ten and 17 days. Specimens were mechanically digested and subjected to a standard BALB/c 3T3 mitogenic assay, which measures the capacity of tissue extracts to induce DNA synthesis and cell division in fibroblasts. Results revealed that both control and repaired flexor tendons possessed mitogenic activity, with the greatest activity observed in control specimens. Decreasing activity was noted as the time between repair and analysis increased. These data provide increasing evidence for the flexor tendon's active role in the healing process, and support the concept that mitogenic or growth-promoting factors are associated with flexor tendons and may be released following injury, during the early stages of healing. C1 MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC 527,BOSTON,MA 02114. FU NIAMS NIH HHS [AR33097] NR 0 TC 13 Z9 14 U1 0 U2 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH, MIDLOTHIAN, SCOTLAND EH1 3AF SN 0266-7681 J9 J HAND SURG-BRIT EUR JI J. Hand Surg.-Br. Eur. Vol. PD JUN PY 1992 VL 17B IS 3 BP 275 EP 277 DI 10.1016/0266-7681(92)90114-H PG 3 WC Orthopedics; Surgery SC Orthopedics; Surgery GA JB712 UT WOS:A1992JB71200009 PM 1624859 ER PT J AU GLEZEN, WP ENGLUND, JA SIBER, GR SIX, HR TURNER, C SHRIVER, D HINKLEY, CM FALCAO, O AF GLEZEN, WP ENGLUND, JA SIBER, GR SIX, HR TURNER, C SHRIVER, D HINKLEY, CM FALCAO, O TI MATERNAL IMMUNIZATION WITH THE CAPSULAR POLYSACCHARIDE VACCINE FOR HAEMOPHILUS-INFLUENZAE TYPE-B SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT CONF ON EPIDEMIOLOGY, PATHOGENESIS, AND PREVENTION OF HAEMOPHILUS INFLUENZAE DISEASE CY SEP 24-28, 1990 CL VELDHOVEN, NETHERLANDS SP MERCK SHARP & DOHME, PRAXIS BIOLOGICS, CONNAUGHT LABS, PASTEUR MERIEUX SERUMS & VACCINS, HOECHST ROUSSEL PHARM, MENINGITIS TRUST GREAT BRITAIN, UPJOHN, BAYER PHARM, GLAXO PHARM, ELI LILLY ID BACTERIAL-MENINGITIS; UNITED-STATES; CHILDREN; EPIDEMIOLOGY; INFECTIONS; INFANTS; ADULTS AB Maternal immunization with the capsular polysaccharide (PRP) vaccine of Haemophilus influenzae type b has been shown to extend the time that protective levels of maternal antibody are detected in infants. In a randomized, blinded trial, PRP or placebo was administered uneventfully to 213 women in the third trimester of pregnancy. Infants born to PRP recipients had significantly higher levels of antibody to PRP than did infants born to placebo recipients: 2.73-mu-g/ml compared with 0.33-mu-g/ml. It was estimated that infants of mothers who received the PRP vaccine would be protected for an average of 4 months compared to an average of only 2 months for those of mothers who received placebo. Infants were followed for invasive H. influenzae type b disease through the first year of life; none was detected. C1 BAYLOR COLL MED,DEPT PEDIAT,HOUSTON,TX 77030. BAYLOR COLL MED,DEPT OBSTET & GYNECOL,HOUSTON,TX 77030. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115. RP GLEZEN, WP (reprint author), BAYLOR COLL MED,DEPT MICROBIOL & IMMUNOL,1 BAYLOR PLAZA,HOUSTON,TX 77030, USA. FU NCRR NIH HHS [RR-00350]; NIAID NIH HHS [AI-72629] NR 12 TC 25 Z9 25 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1992 VL 165 SU 1 BP S134 EP S136 PG 3 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HW745 UT WOS:A1992HW74500045 PM 1588147 ER PT J AU SANTOSHAM, M RIVIN, B WOLFF, M REID, R NEWCOMER, W LETSON, GW ALMEIDOHILL, J THOMPSON, C SIBER, GR AF SANTOSHAM, M RIVIN, B WOLFF, M REID, R NEWCOMER, W LETSON, GW ALMEIDOHILL, J THOMPSON, C SIBER, GR TI PREVENTION OF HAEMOPHILUS-INFLUENZAE TYPE-B INFECTIONS IN APACHE AND NAVAJO CHILDREN SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT CONF ON EPIDEMIOLOGY, PATHOGENESIS, AND PREVENTION OF HAEMOPHILUS INFLUENZAE DISEASE CY SEP 24-28, 1990 CL VELDHOVEN, NETHERLANDS SP MERCK SHARP & DOHME, PRAXIS BIOLOGICS, CONNAUGHT LABS, PASTEUR MERIEUX SERUMS & VACCINS, HOECHST ROUSSEL PHARM, MENINGITIS TRUST GREAT BRITAIN, UPJOHN, BAYER PHARM, GLAXO PHARM, ELI LILLY ID CONJUGATE VACCINE; BACTERIAL-MENINGITIS; UNITED-STATES; POLYSACCHARIDE; DISEASE; EPIDEMIOLOGY; INFANTS; EFFICACY; IMMUNOGENICITY; IMMUNIZATION AB Prospective surveillance of Haemophilus influenzae type b (Hib) disease has been done since 1981 in two high-risk populations, White Mountain Apaches and Navajos. The attack rate in children <5 years of age is 5-10 times higher than in the general US population. Three vaccines were evaluated. Unconjugated Hib capsular polysaccharide produced lower antibody responses in 18- and 24-month-old Apache infants than in white infants. HbOC (Hib oligosaccharide covalently linked to the nontoxic mutant diphtheria toxin CRM197) produced low antibody responses in Navajo infants after one or two doses but induced responses similar to those in whites after three doses. The responses of 18-month-old Navajos to HbOC were lower than those of whites, but most achieved protective levels. PRP-OMP (Hib capsular polysaccharide linked to the outer membrane protein complex of Neisseria meningitidis) produced good immune responses in 2-month-old Navajo and Apache infants after a single dose. This vaccine was >90% efficacious in protecting Navajo infants from Hib disease when given at 2 and 4 months of age. Even a single dose achieved a high protective efficacy. C1 JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT PEDIAT,DIV PEDIAT INFECT DIS,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS PUBL HLTH BIOL LABS,BOSTON,MA. RP SANTOSHAM, M (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT INT HLTH,CTR AMER INDIAN & ALASKAN NAT HLTH,BALTIMORE,MD 21205, USA. FU NIAID NIH HHS [AI-20738, AI-18125] NR 23 TC 38 Z9 38 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1992 VL 165 SU 1 BP S144 EP S151 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HW745 UT WOS:A1992HW74500048 PM 1588150 ER PT J AU SIBER, GR THOMPSON, C REID, GR ALMEIDOHILL, J ZACHER, B WOLFF, M SANTOSHAM, M AF SIBER, GR THOMPSON, C REID, GR ALMEIDOHILL, J ZACHER, B WOLFF, M SANTOSHAM, M TI EVALUATION OF BACTERIAL POLYSACCHARIDE IMMUNE GLOBULIN FOR THE TREATMENT OR PREVENTION OF HAEMOPHILUS-INFLUENZAE TYPE-B AND PNEUMOCOCCAL DISEASE SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article; Proceedings Paper CT CONF ON EPIDEMIOLOGY, PATHOGENESIS, AND PREVENTION OF HAEMOPHILUS INFLUENZAE DISEASE CY SEP 24-28, 1990 CL VELDHOVEN, NETHERLANDS SP MERCK SHARP & DOHME, PRAXIS BIOLOGICS, CONNAUGHT LABS, PASTEUR MERIEUX SERUMS & VACCINS, HOECHST ROUSSEL PHARM, MENINGITIS TRUST GREAT BRITAIN, UPJOHN, BAYER PHARM, GLAXO PHARM, ELI LILLY ID HUMAN HYPERIMMUNE GLOBULIN; CAPSULAR POLYSACCHARIDE; ANTIBODY-RESPONSE; INFANT RATS; IMMUNIZATION; CHILDREN; INFECTIONS; VACCINES AB A human hyperimmune globulin termed bacterial polysaccharide immune globulin (BPIG) has been prepared from plasma donors immunized with Haemophilus influenzae type b (Hib), pneumococcal, and meningococcal vaccines. At a dose of 0.5 ml/kg, BPIG increased levels of antibody to Hib by >0.15-mu-g/ml within 4-6 h and by 2-4-mu-g/ml at 72 h. Thereafter, antibody declined, with a mean half-life of 27 days. BPIG treatment of Apache infants did not impair their active antibody responses to concurrently administered diphtheria-tetanus-pertussis or Hib oligosaccharide-diphtheria CRM197 conjugate vaccines. In high-risk Apache infants, BPIG given at 2, 6, and 10 months of age provided significant protection from invasive Hib infection during infancy. Thus, BPIG may have utility in the prevention of Hib infections in high-risk patients who cannot be immunized adequately with Hib conjugate vaccines. C1 MASSACHUSETTS PUBL HLTH BIOL LABS,BOSTON,MA. JOHNS HOPKINS UNIV,DEPT INT HLTH,CTR AMER INDIAN & ALASKAN NAT HLTH,BALTIMORE,MD 21218. RP SIBER, GR (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-18125, AI-20738, AI-24996] NR 21 TC 30 Z9 31 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0022-1899 J9 J INFECT DIS JI J. Infect. Dis. PD JUN PY 1992 VL 165 SU 1 BP S129 EP S133 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HW745 UT WOS:A1992HW74500044 PM 1588146 ER PT J AU CHUNG, RY SEIZINGER, BR AF CHUNG, RY SEIZINGER, BR TI MOLECULAR-GENETICS OF NEUROLOGICAL TUMORS SO JOURNAL OF MEDICAL GENETICS LA English DT Review ID GROWTH-FACTOR RECEPTOR; HUMAN-MALIGNANT ASTROCYTOMA; N-RAS ONCOGENE; HUMAN GLIOBLASTOMA; C-MYC; BRAIN-TUMORS; DNA-BINDING; CELL-LINES; T-ANTIGEN; TRANSCRIPTIONAL ACTIVATION C1 MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02129. RP CHUNG, RY (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BLDG 149,6TH FLOOR W,BOSTON,MA 02129, USA. NR 86 TC 12 Z9 12 U1 0 U2 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD JUN PY 1992 VL 29 IS 6 BP 361 EP 367 DI 10.1136/jmg.29.6.361 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA HX075 UT WOS:A1992HX07500001 PM 1320124 ER PT J AU MIRALBELL, R LINGGOOD, RM DELAMONTE, S CONVERY, K MUNZENRIDER, JE MIRIMANOFF, RO AF MIRALBELL, R LINGGOOD, RM DELAMONTE, S CONVERY, K MUNZENRIDER, JE MIRIMANOFF, RO TI THE ROLE OF RADIOTHERAPY IN THE TREATMENT OF SUBTOTALLY RESECTED BENIGN MENINGIOMAS SO JOURNAL OF NEURO-ONCOLOGY LA English DT Article DE BENIGN MENINGIOMA; IRRADIATION; TREATMENT PLANNING; DOSE AND OUTCOME ID INTRACRANIAL MENINGIOMAS; RADIATION-THERAPY; RECURRENCE; SURGERY AB Thirty-six patients with benign meningioma were treated for primary or recurrent disease by subtotal resection and external beam irradiation from 1968-1986 at Massachusetts General Hospital. Comparison is made with 79 patients treated by subtotal surgery alone from 1962-1980. Progression-free survival for 17 patients irradiated after initial incomplete surgeery was 88% at 8 years compared with 48% for similar patients treated by surgery alone (p = 0.057). 16 patients incompletely resected at time of first recurrence were irradiated and 78% were progression-free at 8 years while 11% of a similar group treated by surgery alone were progression free (p = 0.001). Long term overall survival was high and similar in both control and study groups. Two patients were irradiated at second recurrence and 1 patient at third recurrence. Twenty-five patients were treated with photons alone and have a median follow-up of 57 months, 6 patients have recurred at doses 45-60 Gy. Eleven patients were treated with combined 10 MV photons and 160 MV protons utilizing 3-D treatment planning. These patients have been followed for a median of 53 months and none have failed to date. Eight of 11 received 54-60.4 Gy and 3/11> 64.48 Gy. Sex, age, pathology grade and score, surgery and timing of radiation therapy were not associated with significant differences in failure patterns within the irradiated study group (p<0.1). Complications have been seen in 6 irradiated patients. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP MIRALBELL, R (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 19 TC 114 Z9 116 U1 0 U2 1 PU KLUWER ACADEMIC PUBL PI DORDRECHT PA SPUIBOULEVARD 50, PO BOX 17, 3300 AA DORDRECHT, NETHERLANDS SN 0167-594X J9 J NEURO-ONCOL JI J. Neuro-Oncol. PD JUN PY 1992 VL 13 IS 2 BP 157 EP 164 PG 8 WC Oncology; Clinical Neurology SC Oncology; Neurosciences & Neurology GA HZ030 UT WOS:A1992HZ03000007 PM 1432033 ER PT J AU HANDELSMAN, L HORVATH, T ARONSON, M SCHROEDER, M JACOBSON, J WIENER, J PETERSON, A HOLLOWAY, K NESS, R HERMAN, S MAURER, G AF HANDELSMAN, L HORVATH, T ARONSON, M SCHROEDER, M JACOBSON, J WIENER, J PETERSON, A HOLLOWAY, K NESS, R HERMAN, S MAURER, G TI AUDITORY EVENT-RELATED POTENTIALS IN HIV-1 INFECTION - A STUDY IN THE DRUG-USER RISK GROUP SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; AIDS DEMENTIA COMPLEX; CEREBROSPINAL-FLUID; ENVELOPE PROTEIN; HOMOSEXUAL MEN; ABNORMALITIES; NEUROPATHOLOGY; INDIVIDUALS AB Features of event-related potentials (ERPs) may be sensitive and clinically useful markers of central nervous system infection by the human immunodeficiency virus (HIV-1); however, this application has not been studied in the risk group of intravenous drug users. Auditory ERPs generated by an "oddball" paradigm were analyzed for 39 male drug abusers as part of a multimodal assessment Stage of HIV-1 infection was associated with prolongations of P1, N1, and P3 components of the ERP waveform. Only patients with full acquired immunodeficiency syndrome showed statistically significant increases in waveform prolongations. Specific neuropsychological deficits were not related to waveform latency prolongations. C1 BRONX VET AFFAIRS MED CTR,PSYCHOL SERV,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,NEUROL SERV,BRONX,NY 10468. BRONX VET AFFAIRS MED CTR,INFECT DIS SERV,BRONX,NY 10468. RP HANDELSMAN, L (reprint author), BRONX VET AFFAIRS MED CTR,PSYCHIAT SERV 116A,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 41 TC 11 Z9 12 U1 1 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD SUM PY 1992 VL 4 IS 3 BP 294 EP 302 PG 9 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JG128 UT WOS:A1992JG12800008 PM 1498581 ER PT J AU ROSOFF, ML BURGLIN, TR LI, C AF ROSOFF, ML BURGLIN, TR LI, C TI ALTERNATIVELY SPLICED TRANSCRIPTS OF THE FLP-1 GENE ENCODE DISTINCT FMRFAMIDE-LIKE PEPTIDES IN CAENORHABDITIS-ELEGANS SO JOURNAL OF NEUROSCIENCE LA English DT Article ID PHE-MET-ARG-PHE-NH2 FMRFAMIDE; SYMPATHETIC NEURONS; NEUROPEPTIDE GENE; NERVOUS-SYSTEM; EXPRESSION; SUBSTANCES; LEECH; ORGANIZATION; PURIFICATION; PLASTICITY AB We have isolated and characterized several cDNAs and the corresponding genomic region of a gene encoding multiple FMRFamide-like neuropeptides from the nematode Caenorhabditis elegans. The gene, named flp-1, consists of six exons of which four encode FMRFamide-like peptides. The cDNA and genomic sequences revealed that two distinct transcripts are generated by the use of an alternative 3' splice acceptor site between exons 3 and 4. This alternative splice results in the substitution of AGSDPNFLRFG for one of the copies of SADPNFLRFG found in the other translation product. Based on PCR analysis of RNA from mixed-stage animals, both transcripts are expressed. This gene is the first example of a distinct FMRFamide-like peptide being derived from alternative splicing, suggesting a unique role for the substituted peptide in the animal. C1 BOSTON UNIV,DEPT BIOL,2 CUMMINGTON ST,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. FU NICHD NIH HHS [HD25212] NR 43 TC 95 Z9 99 U1 0 U2 1 PU SOC NEUROSCIENCE PI WASHINGTON PA 11 DUPONT CIRCLE, NW, STE 500, WASHINGTON, DC 20036 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD JUN PY 1992 VL 12 IS 6 BP 2356 EP 2361 PG 6 WC Neurosciences SC Neurosciences & Neurology GA HY156 UT WOS:A1992HY15600032 PM 1607945 ER PT J AU HORVATH, KA GRANSTEIN, RD AF HORVATH, KA GRANSTEIN, RD TI PUVA AUGMENTS CYCLOSPORINE A-MEDIATED RAT CARDIAC ALLOGRAFT SURVIVAL SO JOURNAL OF SURGICAL RESEARCH LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE ASSOC FOR ACADEMIC SURGERY CY NOV 20-23, 1991 CL COLORADO SPRINGS, CO SP ASSOC ACAD SURG ID UROCANIC ACID; ULTRAVIOLET-IRRADIATION; SKIN-CANCER; FOLLOW-UP; TRANSPLANTATION; GRAFT; CELLS; 8-METHOXYPSORALEN; PROLONGATION; THERAPY C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. RP HORVATH, KA (reprint author), BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115, USA. NR 33 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD JUN PY 1992 VL 52 IS 6 BP 565 EP 570 DI 10.1016/0022-4804(92)90130-R PG 6 WC Surgery SC Surgery GA JN405 UT WOS:A1992JN40500006 PM 1528032 ER PT J AU DEMARIA, AN HUTTER, AM HATLIE, MJ SCHIFFER, HM YERKES, L AF DEMARIA, AN HUTTER, AM HATLIE, MJ SCHIFFER, HM YERKES, L TI TASK-FORCE-4 - INFLUENCE OF PRIVATE-SECTOR PARTIES ON ACCESS TO CARDIOVASCULAR CARE SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article; Proceedings Paper CT 23RD BETHESDA CONF : ACCESS TO CARDIOVASCULAR CARE CY NOV 21-22, 1991 CL BETHESDA, MD SP AMER COLL CARDIOL C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. AMER MED ASSOC,DEPT PROFESS LIABIL INSURANCE,CHICAGO,IL 60610. CIGNA CORP,FED AFFAIRS,WASHINGTON,DC 20006. MARION MERRELL DOW INC,EDUC & SCI COMMUN,KANSAS CITY,MO 64137. RP DEMARIA, AN (reprint author), UNIV KENTUCKY,COLL MED,DIV CARDIOL,ROOM MN 670,800 ROSE ST,LEXINGTON,KY 40536, USA. NR 15 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN PY 1992 VL 19 IS 7 BP 1469 EP 1477 PG 9 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HX985 UT WOS:A1992HX98500015 PM 1593041 ER PT J AU CONTI, CR BERENSON, R CLUFF, LE LEWIN, ME AF CONTI, CR BERENSON, R CLUFF, LE LEWIN, ME TI TASK-FORCE-6 - PROPOSED ACCESS TO CARE PROGRAMS IN THE UNITED-STATES SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Article; Proceedings Paper CT 23RD BETHESDA CONF : ACCESS TO CARDIOVASCULAR CARE CY NOV 21-22, 1991 CL BETHESDA, MD SP AMER COLL CARDIOL C1 US DEPT VET AFFAIRS,VET AFFAIRS MED CTR,GAINESVILLE,FL 32608. INST MED,WASHINGTON,DC 20418. RP CONTI, CR (reprint author), UNIV FLORIDA,DIV CARDIOVASC MED,POB 100277,1600 ARCHER RD,ROOM M401,GAINESVILLE,FL 32610, USA. NR 2 TC 1 Z9 1 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN PY 1992 VL 19 IS 7 BP 1486 EP 1492 PG 7 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HX985 UT WOS:A1992HX98500017 PM 1593043 ER PT J AU BETRIU, A HERAS, M COHEN, M FUSTER, V AF BETRIU, A HERAS, M COHEN, M FUSTER, V TI UNSTABLE ANGINA - OUTCOME ACCORDING TO CLINICAL PRESENTATION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Review ID LONG-TERM PROGNOSIS; CORONARY-ARTERY DISEASE; VARIANT ANGINA; MYOCARDIAL-INFARCTION; NATURAL-HISTORY; SILENT ISCHEMIA; ONSET ANGINA; PECTORIS; ASPIRIN; HEPARIN AB Unstable angina is a broad clinical diagnosis that includes patients at different levels of risk for an unfavorable outcome. Although, as in other categories of coronary artery disease, the state of left ventricular function and the extent of coronary artery disease will determine long-term prognosis, recognition of clinical markers of an early unfavorable course may be of value in defining management strategies. This review focuses on the relevance of baseline clinical characteristics and noninvasive data in assessing the prognostic significance of unstable angina in light of its presenting features. Recurrence of chest pain within 48 h after admission carries a reduction in likelihood of survival of about 20% in patients with progressive or prolonged angina. Similarly, ECG changes on admission have a negative prognostic implication, particularly in rest angina, as they predict recurrence of ischemia, myocardial infarction or need for revascularization in 80% of the patients. In variant angina, determinants of prognosis are level of disease activity, as judged by recurrence of pain, ECG changes and use of calcium channel antagonists. Patients with angina after a myocardial infarction who have more than one episode of either angina or silent ischemia in 24 h have a 10% reduction in probability of survival during the 1st year compared with that of asymptomatic patients. An abrupt course, or the rapidity with which symptoms develop, is the main determinant of prognosis in new onset angina. Thus, recurrent angina and ECG changes appear to be relevant prognostic markers in the patient subsets considered; if these are present, early coronary angiography must be performed and revascularization procedures should be considered without delay. C1 HAHNEMANN UNIV,PHILADELPHIA,PA 19102. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. RP BETRIU, A (reprint author), UNIV BARCELONA,HOSP CLIN,DEPT CARDIOL,VILLARROEL 170,E-08036 BARCELONA,SPAIN. RI Fuster, Valentin/H-4319-2015 OI Fuster, Valentin/0000-0002-9043-9986 NR 33 TC 74 Z9 74 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD JUN PY 1992 VL 19 IS 7 BP 1659 EP 1663 PG 5 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HX985 UT WOS:A1992HX98500042 PM 1593063 ER PT J AU MOON, TD AF MOON, TD TI PROSTATE-CANCER SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID CARCINOMA; ADENOCARCINOMA AB Clinically, prostate cancer (prostatic adenocarcinoma) is now the most frequently diagnosed cancer in males and the second leading cause of mortality due to cancer in the United States. However, because 75% of histologic prostate cancers remain functionally benign (will not metasiasize and kill the patient), mass screening of the male population for the disease has become a hotly debated issue among urologists. The real challenge in the upcoming decade for geriatricians, though, will be to diagnose earlier in their course the prostate cancers which, if not treated, will metastasize and kill the patient and thus allow this subgroup of patients the opportunity to be treated more effectively. This review briefly discusses the etiology of prostate cancer, ways the disease may present, current treatments, depending on disease stage, screening in the diagnosis of prostate cancer, and quality of life issues important to patients confronted with the disease. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. RP MOON, TD (reprint author), UNIV WISCONSIN HOSP & CLIN,CTR CLIN SCI G5 341,DEPT SURG,DIV UROL,600 HIGHLAND AVE,MADISON,WI 53792, USA. NR 17 TC 7 Z9 7 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 JUN PY 1992 VL 40 IS 6 BP 622 EP 627 PG 6 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HX649 UT WOS:A1992HX64900016 PM 1587984 ER PT J AU TOLKOFFRUBIN, NE RUBIN, RH AF TOLKOFFRUBIN, NE RUBIN, RH TI OPPORTUNISTIC FUNGAL AND BACTERIAL-INFECTION IN THE RENAL-TRANSPLANT RECIPIENT SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article; Proceedings Paper CT 2ND WORKSHOP OF THE NORTH AMERICAN PEDIATRIC RENAL TRANSPLANT COOPERATIVE STUDY : CLINICAL CHALLENGES IN PEDIATRIC RENAL TRANSPLANTATION CY APR 17-18, 1991 CL MINNEAPOLIS, MN SP N AMER PEDIAT RENAL TRANSPLANT COOPERAT STUDY DE FUNGAL INFECTION; BACTERIAL INFECTION; RENAL TRANSPLANT AB The risk of opportunistic infection in the renal transplant recipient is determined by the interaction between two factors: the epidemiologic exposures the individual encounters within the community and the hospital and a complex function termed the net state of immunosuppression. There are two general categories of opportunistic fungal infection in this patient population: (1) disseminated primary or reactivation infection with one of the geographically restricted systemic mycoses (histoplasmosis, coccidioidomycosis, blastomycosis, and paracoccidioidomycosis) and (2) opportunistic infection with fungal species that rarely cause invasive infection in the normal host (Aspergillus species, Candida species, Cryptococcus neoformans, and the Mucoraceae), with these last usually being acquired within the hospital environment. Newly available azole compounds, fluconazole and itraconazole, are exciting new alternatives to amphotericin in the treatment of at least some of these infections. The three most important forms of opportunistic bacterial infections are those due to Listeria monocytogenes, Nocardia asteroides, and a variety of mycobacterial species. Clinical diseases with these first two are effectively prevented by low-dose trimethoprim-sulfamethoxazole prophylaxis. There are two cardinal therapeutic rules to be followed by clinicians in dealing with these infections: prevention is better than treatment; when treatment is required, however, the major determinant of the success of therapy is the rapidity with which the diagnosis is made and effective therapy is initiated. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CAPD UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CLIN INVEST PROGRAM,BOSTON,MA 02114. RP TOLKOFFRUBIN, NE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HEMODIALYSIS UNIT,BOSTON,MA 02114, USA. NR 16 TC 30 Z9 31 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 JUN PY 1992 VL 2 IS 12 SU S BP S264 EP S269 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA JD409 UT WOS:A1992JD40900011 PM 1498286 ER PT J AU BAGLIVO, J OLIVIER, D PAGANO, M AF BAGLIVO, J OLIVIER, D PAGANO, M TI METHODS FOR EXACT GOODNESS-OF-FIT TESTS SO JOURNAL OF THE AMERICAN STATISTICAL ASSOCIATION LA English DT Article DE CONDITIONAL TESTS; CONTINGENCY TABLES; DISCRETE FOURIER TRANSFORM; LIKELIHOOD RATIO STATISTIC; MULTINOMIAL GOODNESS-OF-FIT; PARALLELIZABLE ALGORITHMS; PEARSON X2 STATISTIC; POWER DIVERGENCE STATISTIC ID RXC CONTINGENCY-TABLES; FISHER EXACT TEST; EXACT DISTRIBUTIONS; CELL COUNTS; STATISTICS; ALGORITHM; X2 AB Numerous goodness-of-fit tests with asymptotic chi-squared distributions have been proposed for discrete multivariate data, and there has been much discussion about using asymptotic results for computing critical values when there are small expected cell values. Although exact methods would be preferred in these situations, it generally is believed that such methods are computationally intractable. We propose methods for calculating exact distributions and significance levels for goodness-of-fit statistics that are computationally feasible over a wide range of models. In particular, the distribution for a simple multinomial model can be evaluated in polynomial time. For composite null hypotheses, we calculate the distribution conditional on the sufficient statistics for the nuisance parameters. We calculate the characteristic function of a distribution and invert the characteristic function using the fast Fourier transform (FFT). Our approach emphasizes the relationship between exact methods and probability formulas. Our technique, transforming the domain of the problem, is interesting for two reasons: First, algorithms that use the FFT and the convolution theorem are efficient for calculating the distribution of sums of independent statistics; and second, less storage is needed when working in the frequency domain than in the probability domain. The algorithms can be applied to general goodness-of-fit statistics and are parallelizable. C1 HARVARD UNIV,SCH PUBL HLTH,INSTRUCT COMP FACIL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOCHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BAGLIVO, J (reprint author), BOSTON COLL,DEPT MATH,CHESTNUT HILL,MA 02167, USA. NR 32 TC 26 Z9 26 U1 1 U2 4 PU AMER STATISTICAL ASSOC PI ALEXANDRIA PA 1429 DUKE ST, ALEXANDRIA, VA 22314 SN 0162-1459 J9 J AM STAT ASSOC JI J. Am. Stat. Assoc. PD JUN PY 1992 VL 87 IS 418 BP 464 EP 469 DI 10.2307/2290278 PG 6 WC Statistics & Probability SC Mathematics GA HW622 UT WOS:A1992HW62200023 ER PT J AU YUCEL, EK EGGLIN, TK WALTMAN, AC AF YUCEL, EK EGGLIN, TK WALTMAN, AC TI EXTENSION OF SAPHENOUS THROMBOPHLEBITIS INTO THE FEMORAL VEIN - DEMONSTRATION BY COLOR FLOW COMPRESSION SONOGRAPHY SO JOURNAL OF ULTRASOUND IN MEDICINE LA English DT Article DE VENOUS THROMBOSIS; SUPERFICIAL THROMBOPHLEBITIS; COLOR DOPPLER ID DEEP VENOUS THROMBOSIS; LOWER-EXTREMITY; DIAGNOSIS; ULTRASOUND AB Five cases are presented in which compression and color flow sonography were used to diagnose extension of superficial saphenous thrombophlebitis into the deep system at the saphenofemoral junction. In one case thrombus originated in the calf, demonstrating an unusual mode of propagation into the deep venous system above the knee. Color Doppler imaging is especially helpful in diagnosing this complication of superficial thrombophlebitis. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. YALE NEW HAVEN MED CTR,NEW HAVEN,CT 06504. NR 15 TC 12 Z9 12 U1 0 U2 0 PU AMER INST ULTRASOUND MEDICINE PI LAUREL PA SUBSCRIPTION DEPT, 14750 SWEITZER LANE, STE 100, LAUREL, MD 20707-5906 SN 0278-4297 J9 J ULTRAS MED JI J. Ultrasound Med. PD JUN PY 1992 VL 11 IS 6 BP 285 EP 287 PG 3 WC Acoustics; Radiology, Nuclear Medicine & Medical Imaging SC Acoustics; Radiology, Nuclear Medicine & Medical Imaging GA KY021 UT WOS:A1992KY02100008 PM 1608090 ER PT J AU ZELT, DT LAMURAGLIA, GM LITALIEN, GJ MEGERMAN, J KUNG, RTV STEWART, RB ABBOTT, WM ROHRER, M AF ZELT, DT LAMURAGLIA, GM LITALIEN, GJ MEGERMAN, J KUNG, RTV STEWART, RB ABBOTT, WM ROHRER, M TI ARTERIAL LASER-WELDING WITH A 1.9 MICROMETER RAMAN-SHIFTED LASER SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 18TH ANNUAL MEETING OF THE NEW ENGLAND SOC FOR VASCULAR SURGERY CY SEP 26-27, 1991 CL QUEBEC, CANADA SP NEW ENGLAND SOC VASC SURG ID VASCULAR ANASTOMOSES; PATENCY; ANGIOPLASTY; FUSION AB A new 1.9-mu-m Raman-shifted neodymium: yttrium aluminum garnet (Nd:YAG) laser was used for small vessel welding. Bursting pressures and stresses of sutured and laser-welded arteriotomies created in the rat femoral artery and aorta were measured. Sutured arteriotomies had a significantly higher burst stress than laser-welded arteriotomies. Although there were no significant differences in burst stress at the various laser powers tested, an optimal power was identified. The laser was also used to weld transected rat aortas. The average power delivered was 200 mW for 30 seconds per anastomosis. The average time for completing an anastomosis was 6 minutes compared with 18 minutes when sutures were used. In relation to proximal aortic diameter, there was a 7.9% decrease at the anastomosis immediately (n = 4), and a 6.6% and 4.9% increase occurred at 24 hours (n = 4) and 10 weeks (n = 5), respectively. Acute anastomotic compliance, and compliance at 24 hours and 10 weeks were decreased by 47.2%, 39.5%, and 47.8%, respectively, and were similar to sutured anastomoses. Histology showed little thermal denaturation of the aorta within 0.6 mm of the anastomosis, approximately 1 mm of medial cell death, and nearly normal clastic fiber alignment. One focal false aneurysm was noted at 10 weeks. Although the sutured and laser-welded anastomoses share similar compliance changes, the laser-welded anastomoses are more isodiametric. This preliminary experience with the 1.9-mu-m laser shows the distinct advantages of a handheld fiber, no requirement for cooling irrigation, speed, and no difference in compliance from sutured anastomoses. C1 MASSACHUSETTS GEN HOSP,GEN SURG SERV,DIV VASC SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. ABIOMED INC,DANVERS,MA. FU NHLBI NIH HHS [K-08HL02583-01, R43-HL45390] NR 24 TC 10 Z9 10 U1 1 U2 2 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JUN PY 1992 VL 15 IS 6 BP 1025 EP 1031 PG 7 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA HZ268 UT WOS:A1992HZ26800010 PM 1597884 ER PT J AU LAMURAGLIA, GM FABIAN, RL BREWSTER, DC PILESPELLMAN, J DARLING, RC CAMBRIA, RP ABBOTT, WM DREZNER, AD ODONNELL, T PILCHER, DB DONOVAN, TJ AF LAMURAGLIA, GM FABIAN, RL BREWSTER, DC PILESPELLMAN, J DARLING, RC CAMBRIA, RP ABBOTT, WM DREZNER, AD ODONNELL, T PILCHER, DB DONOVAN, TJ TI THE CURRENT SURGICAL-MANAGEMENT OF CAROTID-BODY PARAGANGLIOMAS SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 18TH ANNUAL MEETING OF THE NEW ENGLAND SOC FOR VASCULAR SURGERY CY SEP 26-27, 1991 CL QUEBEC, CANADA SP NEW ENGLAND SOC VASC SURG ID PREOPERATIVE EMBOLIZATION; CERVICAL PARAGANGLIOMAS; TUMORS; EXPERIENCE; NECK AB To determine if recent trends in evaluation and therapy have contributed to the successful surgical management of carotid body paragangliomas, we reviewed our experience over the past decade. Nineteen carotid body paragangliomas were identified in 17 patients. Eleven patients underwent complete, preoperative embolization of their afferent arteries with one complication. Calculated carotid body paragangliomas surface areas did not differ between the embolized 64.6 +/- 43.3 cm2 and nonembolized 63.0 +/- 57.9 cm2 lesions. Intraoperative blood loss was lower (p = 0.02) in the patients treated with embolization (372 +/- 213 ml) compared with their cohorts (609 +/- 564 ml). However, the operative times were equivalent 4.1 hours versus 4.5 hours in both groups. Intraoperative electroencephalographic (EEG) monitoring was used in 10 patients; in one patient the EEG indicated intraoperative thrombosis of the carotid artery, which was successfully treated by thrombectomy without complications. Two patients required carotid bifurcation resection and vascular reconstruction to remove the entire tumor; a late stroke manifested by contralateral hand weakness developed in one of these patients. The incidence of cranial nerve injury was tow at 16%, with one transient ramus mandibularis paresis and two instances of vocal cord dysfunction. Two additional patients had a postoperative Horner's syndrome. We conclude that by diminishing intraoperative blood loss through complete and careful preoperative embolization and use of intraoperative EEG monitoring along with careful surgical technique, the complications associated with this challenging operation are facilitated and diminished. C1 MASSACHUSETTS GEN HOSP,DIV VASC SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,GEN SURG SERV,HEAD & NECK SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02115. NR 21 TC 72 Z9 76 U1 0 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD JUN PY 1992 VL 15 IS 6 BP 1038 EP 1045 PG 8 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA HZ268 UT WOS:A1992HZ26800012 PM 1597886 ER PT J AU GABUZDA, DH LEVER, A TERWILLIGER, E SODROSKI, J AF GABUZDA, DH LEVER, A TERWILLIGER, E SODROSKI, J TI EFFECTS OF DELETIONS IN THE CYTOPLASMIC DOMAIN ON BIOLOGICAL FUNCTIONS OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEINS SO JOURNAL OF VIROLOGY LA English DT Article ID TRANSMEMBRANE PROTEIN; AIDS VIRUS; HTLV-III/LAV; T4 MOLECULE; CELL-LINES; MEMBRANE; HIV-1; RETROVIRUS; SEQUENCE; MUTANTS AB The role of the cytoplasmic domain of the human immunodeficiency virus type 1 (HIV-1) envelope glycoproteins in virus replication was investigated. Deletion of residues 840 to 856 at the carboxyl terminus of gp41 reduced the efficiency of virus entry during an early step in the virus life cycle between CD4 binding and formation of the DNA provirus without affecting envelope glycoprotein synthesis, processing, or syncytium-forming ability. Deletion of residues amino terminal to residue 846 was associated with decreased stability of envelope glycoproteins made in COS-1 cells, but this phenotype was cell type dependent. The cytoplasmic domain of gp41 was not required for the incorporation of the HIV-1 envelope glycoproteins into virions. These results suggest that the carboxyl terminus of the gp41 cytoplasmic domain plays a role in HIV-1 entry other than receptor binding or membrane fusion. The cytoplasmic domain of gp41 also affects the stability of the envelope glycoprotein in some cell types. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. FU NIAID NIH HHS [AI24755, AI01017, AI28193] NR 42 TC 174 Z9 174 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD JUN PY 1992 VL 66 IS 6 BP 3306 EP 3315 PG 10 WC Virology SC Virology GA HU599 UT WOS:A1992HU59900005 PM 1583717 ER PT J AU NAYAK, RC ATTAWIA, MA CAHILL, CJ KING, GL OHASHI, H MOROMISATO, R AF NAYAK, RC ATTAWIA, MA CAHILL, CJ KING, GL OHASHI, H MOROMISATO, R TI EXPRESSION OF A MONOCLONAL-ANTIBODY (3G5) DEFINED GANGLIOSIDE ANTIGEN IN THE RENAL-CORTEX SO KIDNEY INTERNATIONAL LA English DT Article ID GLOMERULAR CELLS; MESANGIAL CELLS; RAT; IDENTIFICATION; LOCALIZATION; POLYANION; KIDNEY AB The monoclonal antibody (mAb) 3G5 was found, by indirect immunofluorescence, to bind to renal cortical structures in frozen sections of human, rat and calf kidneys. Double indirect immunofluorescence studies on frozen sections of rat kidneys showed that 3G5 stained only the glomerulus and the distribution of the 3G5 antigen on the glomerulus was more extensive than the staining observed with antibodies to Factor VIII antigen. 3G5 stained the proximal convoluted tubules and collecting tubules in bovine renal sections but glomeruli did not stain with 3G5. The 3G5 mAb did not stain tissue cultured bovine glomerular endothelial cells or mesangial cells, but did stain bovine glomerular epithelial cell cultures. 3G5 did not stain MDCK cell cultures. The binding of mAb 3G5 to glomeruli was investigated by immunoelectron microscopy of rat renal tissue. In contrast to the podocyte specificity on bovine glomerular cells in vitro, it was found that the specificity of 3G5 expression on rat glomerular cells in vivo was broader. No binding of mAb 3G5 was found outside the glomerulus in the rat renal cortex. Podocytes, endothelial cells and capsular epithelial cells expressed the 3G5 antigen most strongly. A lesser amount of binding was found in the glomerular basement membrane. The mesangium showed a little binding of mAb 3G5 and no binding at all was found to other cortical structures. The 3G5 antigen in rat renal tissue was found to be a glycolipid that migrated between the ganglioside markers GM2 and GM1 by immunostaining of thin layer chromatograms. The 3G5 mAb has previously been shown to react with microvascular pericytes, resting T-lymphocytes and cells of the brain, thyroid gland and adrenal gland as well as various malignancies. The significance of the tissue specific patterns of expression remains unclear and will be understood only when the function of this ganglioside is elucidated. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP NAYAK, RC (reprint author), JOSLIN DIABET CTR,DIV RES,IMMUNOL SECT,1 JOSLIN PL,BOSTON,MA 02215, USA. FU NEI NIH HHS [EY 05110]; NIDDK NIH HHS [DK 36836]; PHS HHS [R01-39783-03] NR 27 TC 16 Z9 16 U1 0 U2 1 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD JUN PY 1992 VL 41 IS 6 BP 1638 EP 1645 DI 10.1038/ki.1992.236 PG 8 WC Urology & Nephrology SC Urology & Nephrology GA HW904 UT WOS:A1992HW90400020 PM 1501420 ER PT J AU METSON, R AF METSON, R TI ENDOSCOPIC TREATMENT OF FRONTAL SINUSITIS SO LARYNGOSCOPE LA English DT Note RP METSON, R (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,0 EMERSON PL,BOSTON,MA 02114, USA. NR 7 TC 34 Z9 39 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0023-852X J9 LARYNGOSCOPE JI Laryngoscope PD JUN PY 1992 VL 102 IS 6 BP 712 EP 716 DI 10.1288/00005537-199206000-00020 PG 5 WC Medicine, Research & Experimental; Otorhinolaryngology SC Research & Experimental Medicine; Otorhinolaryngology GA HY301 UT WOS:A1992HY30100020 PM 1602922 ER PT J AU HAHN, PF SAINI, S COHEN, MS GOLDBERG, M REIMER, P MUELLER, PR AF HAHN, PF SAINI, S COHEN, MS GOLDBERG, M REIMER, P MUELLER, PR TI AN AQUEOUS GASTROINTESTINAL CONTRAST AGENT FOR USE IN ECHO-PLANAR MR IMAGING SO MAGNETIC RESONANCE IN MEDICINE LA English DT Note C1 MASSACHUSETTS GEN HOSP,CTR NUCL MAGNET RESONANCE,BOSTON,MA 02114. RP HAHN, PF (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,DIV GASTROINTESTINAL RADIOL,BOSTON,MA 02114, USA. RI Cohen, Mark/C-6610-2011 OI Cohen, Mark/0000-0001-6731-4053 FU NCI NIH HHS [CA P01 48279] NR 6 TC 11 Z9 11 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD JUN PY 1992 VL 25 IS 2 BP 380 EP 383 DI 10.1002/mrm.1910250218 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HX356 UT WOS:A1992HX35600017 PM 1614323 ER PT J AU WOHLGEMUTH, A DUBEY, DP AF WOHLGEMUTH, A DUBEY, DP TI THE EFFECTS OF SYMBOLIC BIAS IN THE SCIENCE OF IMMUNOGENETICS - PREDICTION AND CONFIRMATION IN ALTERNATIVE MODELS SO MATHEMATICAL AND COMPUTER MODELLING LA English DT Article ID DNA POLYMORPHISM; HLA; IMPACT; GENES AB Immunogenetics uses symbols to identify antigens and alleles, as well as antibodies. The imagined structure of immununogenetic systems is influenced by the convention of using the same symbol to denote both a genetic factor and the serological reagent used to identify the factor. This convention forces a conceptual one-to-one correspondence between genetic factors and the antibodies or reagents used to define them. The notation oversimplifies things immunologically, and may produce a false, or artifactual, genetic complexity. There are apparent laws of the system which either disappear or are radically simplified when the system is described with different symbolism. By allowing a general relation, not constrained to be one-to-one, between genetic factors and their defining reagents, alternative serological definitions can be made that, in turn, lead to alternative genetic descriptions for some systems. When an alternative symbolization, which allows for cross-reactivity, is used, all linkage disequilibrium in the common human Ag bloodgroups disappears, as does the cis-trans effect seen in the Rh blood group system. The new notation describes straightforward systems with codominant alleles. Our results on HLA suggest that the C locus may itself be only a symbolic artifact. Current work in cloning genes associated with immunogenetic systems will not automatically rectify the problems. The reason is that (the wrong) serological definitions are used to identify the genes being cloned. Our work predicts that when the allele/antibody relation is identified for certain systems by molecular means, there will not be a simple one-to-one correspondence between alleles and the reagents used to identify them. This will contradict the very notation in which the immunogenetic systems are described. Serology will, therefore, have to be reinterpreted in terms of a more general notation, which will allow for cross-reactivity. C1 UNIV MAINE,DEPT MATH,ORONO,ME 04469. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV IMMUNOGENET,BOSTON,MA 02115. RP WOHLGEMUTH, A (reprint author), FDN BLOOD RES,SCARBOROUGH,ME 04074, USA. NR 18 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-7177 J9 MATH COMPUT MODEL JI Math. Comput. Model. PD JUN-JUL PY 1992 VL 16 IS 6-7 BP 225 EP 236 DI 10.1016/0895-7177(92)90164-G PG 12 WC Computer Science, Interdisciplinary Applications; Computer Science, Software Engineering; Mathematics, Applied SC Computer Science; Mathematics GA JA602 UT WOS:A1992JA60200018 ER PT J AU BLOCK, NE MILLER, JB AF BLOCK, NE MILLER, JB TI EXPRESSION OF MRF4, A MYOGENIC HELIX-LOOP-HELIX PROTEIN, PRODUCES MULTIPLE CHANGES IN THE MYOGENIC PROGRAM OF BC3H-1 CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID FIBROBLAST GROWTH-FACTOR; HEAVY-CHAIN ISOFORMS; CLONAL ANALYSIS; MOUSE MUSCLE; VERTEBRATE MYOGENESIS; SKELETAL MYOBLASTS; GENE FAMILY; SLOW MYOSIN; MYOD1; DIFFERENTIATION AB Expression of MRF4, a myogenic regulatory factor of the basic helix-loop-helix type, produced multiple changes in the myogenic program of the BC3H-1 cell line. BC3H-1 cells that stably expressed exogenous MRF4 were prepared and termed BR cell lines. Upon differentiation, the BR cells were found to have three muscle-specific properties (endogenous MyoD expression, myoblast fusion, and fast myosin light-chain 1 expression) that the parent BC3H-1 cells did not have. Of the four known myogenic regulatory factors (MyoD, myogenin, Myf-5, and MRF4), only MRF4 was capable of activating expression of the endogenous BC3H-1 myoD gene. In addition, the pattern of Myf-5 expression in BR cells was the opposite of that in BC3H-1 cells. Myf-5 expression was low in BR myoblasts and showed a small increase upon myotube formation, whereas Myf-5 expression was high in BC3H-1 myoblasts and decreased upon differentiation. Though the MRF4-transfected BR cells fused to form large myotubes and expressed fast myosin light-chain 1, the pattern of myosin heavy-chain isoform expression was the same in the BR and the nonfusing parent BC3H-1 cells, suggesting that factors in addition to the MyoD family members regulate myosin heavy-chain isoform expression patterns in BC3H-1 cells. In contrast to the changes produced by MRF4 expression, overexpression of Myf-5 did not alter BC3H-1 myogenesis. The results suggest that differential expression of the myogenic regulatory factors of the MyoD family may be one mechanism for generating cells with diverse myogenic phenotypes. C1 MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,149 13TH ST,BOSTON,MA 02129. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. FU NIAMS NIH HHS [F32 AR08176]; NICHD NIH HHS [HD25394] NR 55 TC 29 Z9 29 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD JUN PY 1992 VL 12 IS 6 BP 2484 EP 2492 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HV309 UT WOS:A1992HV30900004 PM 1588952 ER PT J AU REPPERT, SM WEAVER, DR STEHLE, JH RIVKEES, SA GRABBE, S GRANSTEIN, RD AF REPPERT, SM WEAVER, DR STEHLE, JH RIVKEES, SA GRABBE, S GRANSTEIN, RD TI MOLECULAR-CLONING OF A G-PROTEIN-COUPLED RECEPTOR THAT IS HIGHLY EXPRESSED IN LYMPHOCYTES AND PROLIFERATIVE AREAS OF DEVELOPING BRAIN SO MOLECULAR AND CELLULAR NEUROSCIENCE LA English DT Article ID BETA-ADRENERGIC-RECEPTOR; CDNA; FAMILY; TRANSDUCERS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02114. RP REPPERT, SM (reprint author), MASSACHUSETTS GEN HOSP,DEV CHRONOBIOL LAB,BOSTON,MA 02114, USA. NR 25 TC 8 Z9 8 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 1044-7431 J9 MOL CELL NEUROSCI JI Mol. Cell Neurosci. PD JUN PY 1992 VL 3 IS 3 BP 206 EP 214 DI 10.1016/1044-7431(92)90040-9 PG 9 WC Neurosciences SC Neurosciences & Neurology GA HV947 UT WOS:A1992HV94700005 PM 19912862 ER PT J AU CONWAY, B BECHTEL, LJ ADLER, KA DAQUILA, RT KAPLAN, JC HIRSCH, MS AF CONWAY, B BECHTEL, LJ ADLER, KA DAQUILA, RT KAPLAN, JC HIRSCH, MS TI COMPARISON OF SPOT-BLOT AND MICROTITRE PLATE METHODS FOR THE DETECTION OF HIV-1 PCR PRODUCTS SO MOLECULAR AND CELLULAR PROBES LA English DT Article DE PCR; HIV-1; MICROTITRE PLATE; SPOT-BLOT ID HUMAN-IMMUNODEFICIENCY-VIRUS; POLYMERASE CHAIN-REACTION; MONONUCLEAR-CELLS; DNA; AMPLIFICATION; INFECTION C1 DUPONT CO,MED PROD,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. RP CONWAY, B (reprint author), UNIV OTTAWA,DEPT MICROBIOL & IMMUNOL,OTTAWA K1N 6N5,ONTARIO,CANADA. FU NCI NIH HHS [CA12464, CA35020] NR 15 TC 18 Z9 18 U1 0 U2 0 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0890-8508 J9 MOL CELL PROBE JI Mol. Cell. Probes PD JUN PY 1992 VL 6 IS 3 BP 245 EP 249 DI 10.1016/0890-8508(92)90023-Q PG 5 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology GA HZ167 UT WOS:A1992HZ16700010 PM 1406733 ER PT J AU KEUTMANN, HT HUA, QX WEISS, MA AF KEUTMANN, HT HUA, QX WEISS, MA TI STRUCTURE OF A RECEPTOR-BINDING FRAGMENT FROM HUMAN LUTEINIZING-HORMONE BETA-SUBUNIT DETERMINED BY [H-1]NUCLEAR AND [N-15]NUCLEAR MAGNETIC-RESONANCE SPECTROSCOPY SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; ALPHA-SUBUNIT; PEPTIDES; LUTROPIN; IDENTIFICATION; INHIBITION; SEQUENCE; PROTEINS; EPITOPE; REGION AB The structure of the glycoprotein hormones (LH, CG, FSH, and TSH) and their mechanism of receptor recognition are problems of long-standing interest and speculation. Here we describe the two-dimensional [H-1]nuclear magnetic resonance ([H-1]NMR) analysis of a linear peptide model for the intercysteine sequence (38-57) from the beta-subunit of human (h) LH. This sequence contains functional determinants for receptor binding and postreceptor activation and is predicted by computer-based modeling to fold as a compact minidomain containing a central amphipathic helix. To test this prediction, an Arg-extended disulfide-free (38-57) analog of enhanced solubility was prepared for complementary circular-dichroic and two-dimensional NMR studies. The linear peptide retains ovarian membrane receptor-binding activity. Although the peptide is not highly structured in aqueous solution, circular-dichroic analysis shows partial alpha-helix formation in a lipophilic medium (50% trifluoroethanol). Complete sequential assignment is obtained in 50% trifluoroethanol based on homonuclear and [N-15]edited heteronuclear NMR methods. Alpha-Helix-related (i,i+3) connectivities are observed by nuclear-Overhauser effect spectroscopy that define an amphipathic alpha-helical segment (residues 41-48). Additional long range nuclear-Overhauser effects are observed in the C-terminal region that are consistent with beta-turns involving one or more proline residues; these may serve to reverse the direction of the peptide chain. A nuclear-Overhausesr effect contact is identified between residues 38 and 55 at opposite ends of the linear sequence, suggesting that a loop configuration is significantly populated in this solvent system. These results, taken together, characterize elements of ordered structure in the 38-57 peptide, which appear to be distinguishing features of hLH (and the homologous region of hCG). We propose that the structure of this peptide provides a model for the structure of the corresponding region of native hLH in the hormone-receptor complex. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. RP KEUTMANN, HT (reprint author), MASSACHUSETTS GEN HOSP, DEPT MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. FU NICHD NIH HHS [HD-12851] NR 38 TC 9 Z9 10 U1 0 U2 0 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 JUN PY 1992 VL 6 IS 6 BP 904 EP 913 DI 10.1210/me.6.6.904 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ964 UT WOS:A1992HZ96400007 PM 1495492 ER PT J AU SWARTZ, KJ KOROSHETZ, WJ REES, AH HUETTNER, JE AF SWARTZ, KJ KOROSHETZ, WJ REES, AH HUETTNER, JE TI COMPETITIVE ANTAGONISM OF GLUTAMATE RECEPTOR CHANNELS BY SUBSTITUTED BENZAZEPINES IN CULTURED CORTICAL-NEURONS SO MOLECULAR PHARMACOLOGY LA English DT Article ID METHYL-D-ASPARTATE; AMINO-ACID RECEPTORS; INSENSITIVE GLYCINE RECEPTOR; CENTRAL-NERVOUS-SYSTEM; MOUSE CENTRAL NEURONS; HIPPOCAMPAL-NEURONS; XENOPUS-OOCYTES; STRUCTURAL REQUIREMENTS; DIVALENT-CATIONS; MODULATORY SITE AB Whole-cell recordings from rat cortical neurons in dissociated cell culture were used to study the antagonism of glutamate receptors by several lipophilic benzazepine analogues of 2,5-dihydro-2,5-dioxo-3-hydroxy-1H-benzazepine (DDHB). DDHB and three substituted derivatives, 4-bromo-, 7-methyl-, and 8-methyl-DDHB, inhibited the activation of N-methyl-D-aspartate (NMDA) receptors at both the NMDA recognition site and the glycine allosteric site. In addition, all four compounds blocked the activation of non-NMDA receptors by kainate and L-glutamate. Antagonism by the four benzazepines was equivalent at holding potentials from -80 mV to +50 mV. Both the onset of and recovery from block of the agonist-gated currents were complete within seconds. Antagonist affinity was calculated from the displacement of steady state concentration-response curves for kainate, L-glutamate, glycine, and NMDA, based on the Gaddum-Schild relationship (dose ratio = 1 + [antagonist]/K(B)). The most potent blocker, 8-Me-DDHB, had an apparent dissociation constant (K(B)) Of 470 nm at the glycine allosteric site and 27-mu-m at the NMDA recognition site. The apparent dissociation constant of 8-Me-DDHB for non-NMDA receptors was 6.4-mu-M when kainate was the agonist and 9.6-mu-M when L-glutamate was the agonist. Unsubstituted DDHB showed slightly higher affinity for the NMDA recognition site (K(B) = 16-mu-M) but was less potent than 8-Me-DDHB at the glycine allosteric site and at non-NMDA receptors (K(B) = 3 and 65-mu-M, respectively). At all three sites, the inhibitory actions of these benzazepine derivatives were consistent with a simple competitive mechanjsm of antagonism. In addition, the antagonist Potency of the parent compound, DDHB, against kainate, NMDA, and glycine was equal to or greater than that of other bicyclic antagonists, including kynurenic acid, indole-2-carboxylic acid, and quinoxaline-2,3-dione. Substituted benzazepines represent a new class of glutamate receptor antagonists that show competitive action, significant potency at multiple sites, and a high degree of lipophilicity. C1 WASHINGTON UNIV,SCH MED,DEPT CELL BIOL & PHYSIOL,660 S EUCLID AVE,BOX 8228,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. TRENT UNIV,DEPT CHEM,PETERBOROUGH K9J 7B8,ONTARIO,CANADA. RI Huettner, James/C-5219-2012 FU NINDS NIH HHS [NS 02253, NS 10828] NR 60 TC 28 Z9 28 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0026-895X J9 MOL PHARMACOL JI Mol. Pharmacol. PD JUN PY 1992 VL 41 IS 6 BP 1130 EP 1141 PG 12 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA JA586 UT WOS:A1992JA58600021 PM 1352036 ER PT J AU DONAHOE, PK AF DONAHOE, PK TI MULLERIAN INHIBITING SUBSTANCE IN REPRODUCTION AND CANCER SO MOLECULAR REPRODUCTION AND DEVELOPMENT LA English DT Article; Proceedings Paper CT SYMP ON TGF-BETA AND RELATED PROTEINS IN DEVELOPMENT CY SEP 20-23, 1991 CL IOWA STATE UNIV, AMES, IA SP NIH, IOWA STATE UNIV, BIOTECHNOL COUNCIL, IOWA STATE UNIV, GRAD COLL, CELTRIX LABS, GENENTECH, IOWA BEEF IND COUNCIL, JOHNSON & JOHNSON, LILLY RES LABS, NATL ANIM DIS CTR AMES, MIDLAND UNITED DAIRY IND ASSOC HO IOWA STATE UNIV DE MIS; OVARIAN CANCER; FETAL TESTES; OCULAR MELANOMA ID GROWTH FACTOR-BETA; OOCYTE MEIOSIS; NUDE-MICE; CELLS; INVITRO; BOVINE; EXPRESSION; RECEPTOR; ONTOGENY; FOLLICLE AB During embryogenesis normal male phenotypic development requires the action of Mullerian Inhibiting Substance (MIS) which is secreted by Sertoli cells of the fetal testis. As testes differentiate in genetic (XY) males, they produce MIS which causes regression of the Mullerian ducts, the anlagen of the female reproductive tract. Soon thereafter, testicular androgens stimulate the Wolffian ducts. In females, on the other hand, MIS is not produced by grandulosa cells until after birth, before which, estrogens induce Mullerian duct development, while the Wolffian ducts passively atrophy in the absence of androgenic stimulation. High serum MIS levels in males are maintained until puberty, whereupon they fall to baseline levels. In females MIS is undetectable in serum until the peripubertal period when values approach the baseline levels of males. This distinct pattern of sexual and ontogenic expression presupposes and requires tight regulation. MIS may play a role in gonadal function and development. Our laboratory has shown that an important role for ovarian MIS is to inhibit oocyte meiosis, perhaps providing maximal oocyte maturation prior to selection for ovulation and subsequent fertilization. Furthermore, Vigier et al. (Development 100:43-55) have recently obtained evidence that MIS may influence testicular differentiation, coincident with inhibition of aromatase activity. Current structure-function studies demonstrate that MIS, like other growth regulators in its protein family, requires proteolytic cleavage to exhibit full biological activity. MIS can be inhibited by epidermal growth factor. This antagonism, which is common to all MIS functions so far investigated, is associated with inhibition of EGF receptor autophosphorylation. We have provided evidence that bovine MIS can inhibit female reproductive tract tumors arising in adults. More recent work with highly purified recombinant human MIS (rhMIS) has extended these early observations, showing that this recombinantly made fetal inhibitor can also suppress tumors of Mullerian duct origin and thus may prove to be useful in the clinical management of gynecologic neoplasms. Recent investigations have identified ocular melanoma as another potential target for rhMIS therapy in humans. RP DONAHOE, PK (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT SURG RES UNIT,BOSTON,MA 02114, USA. NR 45 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 1040-452X J9 MOL REPROD DEV JI Mol. Reprod. Dev. PD JUN PY 1992 VL 32 IS 2 BP 168 EP 172 DI 10.1002/mrd.1080320213 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology SC Biochemistry & Molecular Biology; Cell Biology; Developmental Biology; Reproductive Biology GA HY940 UT WOS:A1992HY94000012 PM 1637555 ER PT J AU BATES, GP VALDES, J HUMMERICH, H BAXENDALE, S LEPASLIER, DL MONACO, AP TAGLE, D MACDONALD, ME ALTHERR, M ROSS, M BROWNSTEIN, BH BENTLEY, D WASMUTH, JJ GUSELLA, JF COHEN, D COLLINS, F LEHRACH, H AF BATES, GP VALDES, J HUMMERICH, H BAXENDALE, S LEPASLIER, DL MONACO, AP TAGLE, D MACDONALD, ME ALTHERR, M ROSS, M BROWNSTEIN, BH BENTLEY, D WASMUTH, JJ GUSELLA, JF COHEN, D COLLINS, F LEHRACH, H TI CHARACTERIZATION OF A YEAST ARTIFICIAL CHROMOSOME CONTIG SPANNING THE HUNTINGTONS-DISEASE GENE CANDIDATE REGION SO NATURE GENETICS LA English DT Article ID DNA MARKERS; LIBRARY; CONSTRUCTION; TELOMERE; CLONES; LOCUS; D4S95; G8 AB The Huntington's disease (HD) gene has been localized by recombination events to a region covering 2.2 megabases (Mb) DNA within chromosome 4p16.3. We have screened three yeast artificial chromosome (YAC) libraries in order to isolate and characterize 44 YAC clones mapping to this region. Approximately 50% of the YACs were chimaeric. Unstable YACs were identified across the whole region, but were particularly prevalent around the D4S183 and D4S43 loci. The YACs have been assembled into a contig extending from D4S126 to D4S98 covering roughly 2 Mb DNA except for a gap of about 250 kilobases (kb). The establishment of a YAC contig which spans the region most likely to contain the HD mutation is an essential step in the isolation of the HD gene. C1 CTR ETUD POLYMORPHISME HUMAIN,F-75010 PARIS,FRANCE. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED & HUMAN GENET,ANN ARBOR,MI 48109. JOHN RADCLIFFE HOSP,INST MOLEC MED,IMPERIAL CANC RES FUND,HUMAN GENET LAB,OXFORD OX3 9DU,ENGLAND. MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV CALIF IRVINE,COLL MED,DEPT BIOL CHEM,IRVINE,CA 92717. WASHINGTON UNIV,SCH MED,DEPT GENET,ST LOUIS,MO 63110. GUYS HOSP,DIV MED & MOLEC GENET,LONDON SE1 9RT,ENGLAND. RP BATES, GP (reprint author), IMPERIAL CANC RES FUND,GENOME ANAL LAB,44 LINCOLNS INN FIELDS,LONDON WC2A 3PX,ENGLAND. RI Monaco, Anthony/A-4495-2010; Bates, Gillian/E-1146-2012 OI Monaco, Anthony/0000-0001-7480-3197; Bates, Gillian/0000-0002-4041-6305 NR 48 TC 73 Z9 73 U1 0 U2 0 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 JUN PY 1992 VL 1 IS 3 BP 180 EP 187 DI 10.1038/ng0692-180 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA JC982 UT WOS:A1992JC98200009 PM 1303232 ER PT J AU CHEN, ZY HENDRIKS, RW JOBLING, MA POWELL, JF BREAKEFIELD, XO SIMS, KB CRAIG, IW AF CHEN, ZY HENDRIKS, RW JOBLING, MA POWELL, JF BREAKEFIELD, XO SIMS, KB CRAIG, IW TI ISOLATION AND CHARACTERIZATION OF A CANDIDATE GENE FOR NORRIE DISEASE SO NATURE GENETICS LA English DT Article ID PRENATAL-DIAGNOSIS; DNA; SEQUENCES; DELETION; FAMILY; LOCUS AB Previous analysis has refined the location of the gene for Norrie disease, a severe, X-linked, recessive neurodevelopmental disorder, to a yeast artificial chromosome subfragment of 160 kilobases (kb). This fragment was used to screen cDNA libraries from human fetal and adult retina. As a result, we have identified an evolutionarily conserved cDNA, which is expressed in fetal and adult brain and encodes a predicted protein of 133 amino acids. The cDNA detects genomic sequences which span a maximum of 50 kb, and which are partly deleted in several typical Norrie disease patients. An EcoRI polymorphism with a calculated heterozygosity value of 43% was observed. The locus identified is a strong candidate for the Norrie disease gene. C1 UNIV OXFORD,DEPT BIOCHEM,GENET LAB,S PARKS RD,OXFORD OX1 3QU,ENGLAND. INST PSYCHIAT,DEPT NEUROSCI,LONDON SE5 8AF,ENGLAND. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,MOLEC NEUROGENET LAB,BOSTON,MA 02114. RI Powell, John/G-4412-2011 OI Powell, John/0000-0001-6124-439X FU Wellcome Trust NR 34 TC 160 Z9 163 U1 0 U2 7 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 JUN PY 1992 VL 1 IS 3 BP 204 EP 208 DI 10.1038/ng0692-204 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JC982 UT WOS:A1992JC98200014 PM 1303236 ER PT J AU ROSENFELD, PJ COWLEY, GS MCGEE, TL SANDBERG, MA BERSON, EL DRYJA, TP AF ROSENFELD, PJ COWLEY, GS MCGEE, TL SANDBERG, MA BERSON, EL DRYJA, TP TI A NULL MUTATION IN THE RHODOPSIN GENE CAUSES ROD PHOTORECEPTOR DYSFUNCTION AND AUTOSOMAL RECESSIVE RETINITIS-PIGMENTOSA SO NATURE GENETICS LA English DT Article ID RETINAL DEGENERATION; SPLICING MUTATION; TRANSDUCIN; DROSOPHILA; DEFECTS; MUTANTS; DNA; IDENTIFICATION; TRANSCRIPTION; SEQUENCE AB Mutations within the rhodopsin gene are known to give rise to autosomal dominant retinitis pigmentosa (RP), a common hereditary form of retinal degeneration. We now describe a patient with autosomal recessive RP who is homozygous for a nonsense mutation at codon 249 within exon 4 of the rhodopsin gene. This null mutation, the first gene defect identified in autosomal recessive retinitis pigmentosa, should result in a functionally inactive rhodopsin protein that is missing the sixth and seventh transmembrane domains including the 11-cis-retinal attachment site. We also found a different null mutation carried heterozygously by an unrelated unaffected individual. Heterozygous carriers of either mutation had normal ophthalmologic examinations but their electroretinograms revealed an abnormality in rod photoreceptor function. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,HOWE LAB,243 CHARLES ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 50 TC 299 Z9 301 U1 1 U2 3 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 JUN PY 1992 VL 1 IS 3 BP 209 EP 213 DI 10.1038/ng0692-209 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JC982 UT WOS:A1992JC98200015 PM 1303237 ER PT J AU GOTTLIEB, D LEVINE, DN AF GOTTLIEB, D LEVINE, DN TI LIMB ATAXIA RELATED TO MONOCULAR OPHTHALMOPLEGIA SO NEURO-OPHTHALMOLOGY LA English DT Article DE OCULOMOTOR PALSY; PAST POINTING; ATAXIA ID SPATIAL LOCALIZATION; STRABISMUS AB Oculomotor palsies are known to cause past pointing in reaching for visual targets. Disturbances of gait may also occur, but have not been reported extensively. The authors present two patients with an oculomotor palsy, one of central and the other of peripheral origin, who complained of unsteady gait. When using their affected eye, they showed gait deviations characterized by veering in the direction of action of the paralyzed medial rectus. The ataxia was present only when they were looking monocularly with the affected eye and disappeared when the intact eye was used. The authors suggest that the gait ataxia was caused by a 'past-stepping' analogous to the past-pointing of the upper extremity. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP GOTTLIEB, D (reprint author), SPAULDING REHABIL HOSP,NEUROL SERV,125 NASHUA ST,BOSTON,MA 02114, USA. NR 23 TC 0 Z9 0 U1 0 U2 0 PU AEOLUS PRESS PI BUREN PA PO BOX 740, 4116 ZJ BUREN, NETHERLANDS SN 0165-8107 J9 NEURO-OPHTHALMOLOGY JI Neuro-Ophthalmol. PD JUN PY 1992 VL 12 IS 3 BP 147 EP 151 DI 10.3109/01658109209058132 PG 5 WC Clinical Neurology; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA HY505 UT WOS:A1992HY50500003 ER PT J AU FRANK, JI ROPPER, AH ZUNIGA, G AF FRANK, JI ROPPER, AH ZUNIGA, G TI VASODEPRESSOR CAROTID-SINUS SYNCOPE ASSOCIATED WITH A NECK MASS SO NEUROLOGY LA English DT Article ID OVERLOOKED CAUSE; HYPERSENSITIVITY AB We present the hemodynamic and autonomic features of recurrent purely vasodepressor syncope episodes in a patient with left-sided malignant cervical adenopathy involving the carotid sinus. Extreme hypotension lasting 10 to 30 minutes, without change in heart rate, occurred spontaneously and 20 seconds after head-turning. The baseline respiratory sinus arrhythmia, heart rate response to standing and Valsalva's maneuver, and cold-induced blood pressure elevation were normal, indicating normal baroreceptor function between episodes. The episodes abated after 1 week of bedrest but reappeared within 1 day of discharge from the hospital. Syncope no longer occurred after intracranial section of the left glossopharyngeal nerve and upper rootlets of the left vagus. Autonomic testing remained normal postoperatively. A review of the literature indicates that purely vasodepressor syncope has been more common with left carotid sinus lesions. C1 ST ELIZABETH HOSP, DIV NEUROL, BOSTON, MA USA. MASSACHUSETTS GEN HOSP, NEUROL NEUROSURG INTENS CARE UNIT, BOSTON, MA 02114 USA. NR 38 TC 11 Z9 12 U1 0 U2 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 EI 1526-632X J9 NEUROLOGY JI Neurology PD JUN PY 1992 VL 42 IS 6 BP 1194 EP 1197 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA HX959 UT WOS:A1992HX95900012 PM 1603347 ER PT J AU LEI, SZ PAN, ZH AGGARWAL, SK CHEN, HSV HARTMAN, J SUCHER, NJ LIPTON, SA AF LEI, SZ PAN, ZH AGGARWAL, SK CHEN, HSV HARTMAN, J SUCHER, NJ LIPTON, SA TI EFFECT OF NITRIC-OXIDE PRODUCTION ON THE REDOX MODULATORY SITE OF THE NMDA RECEPTOR CHANNEL COMPLEX SO NEURON LA English DT Article ID VASCULAR SMOOTH-MUSCLE; AMINO-ACID RECEPTORS; RELAXING FACTOR; ORGANIC NITRATES; ADP-RIBOSYLTRANSFERASE; GLYCERYL TRINITRATE; N-ACETYLCYSTEINE; CEREBRAL-CORTEX; GANGLION-CELLS; BLOOD-FLOW AB Nitric oxide (NO) is an important messenger both systemically and in the CNS. In digital Ca2+ imaging and patch-clamp experiments, clinically available nitroso compounds that generate NO are shown to inhibit responses mediated by the NMDA subtype of the glutamate receptor on rat cortical neurons in vitro. A mechanism of action for this effect was investigated by using the specific NO-generating agent S-nitrosocysteine. We propose that free sulfhydryl groups on the NMDA receptor-channel complex react to form one or more S-nitrosothiols in the presence of NO. If vicinal thiol groups react in this manner, they can form a disulfide bond(s), which is thought to constitute the redox modulatory site of the receptor, resulting in a relatively persistent blockade of NMDA responses. These reactions with NO can afford protection from NMDA receptor-mediated neurotoxicity. Our results demonstrate a new pathway for NO regulation of physiological function that is not via cGMP, but instead involves reactions with membrane-bound thiol groups on the NMDA receptor-channel complex. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,PROGRAM NEUROSCI,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,PROGRAM NEUROSCI,BOSTON,MA 02115. RP LEI, SZ (reprint author), CHILDRENS HOSP MED CTR,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115, USA. OI Sucher, Nikolaus/0000-0001-6233-1612 FU NEI NIH HHS [EY05477, EY09024]; NINDS NIH HHS [NS07264] NR 62 TC 670 Z9 684 U1 0 U2 5 PU CELL PRESS PI CAMBRIDGE PA 1050 MASSACHUSETTES AVE, CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD JUN PY 1992 VL 8 IS 6 BP 1087 EP 1099 DI 10.1016/0896-6273(92)90130-6 PG 13 WC Neurosciences SC Neurosciences & Neurology GA JA429 UT WOS:A1992JA42900009 PM 1376999 ER PT J AU FRIM, DM BARKER, FG POLETTI, CE HAMILTON, AJ AF FRIM, DM BARKER, FG POLETTI, CE HAMILTON, AJ TI POSTOPERATIVE LOW-DOSE HEPARIN DECREASES THROMBOEMBOLIC COMPLICATIONS IN NEUROSURGICAL PATIENTS SO NEUROSURGERY LA English DT Article DE DEEP VEIN THROMBOSIS; LOW-DOSE HEPARIN; PNEUMATIC COMPRESSION BOOTS; PULMONARY EMBOLUS ID DEEP-VEIN THROMBOSIS; VENOUS THROMBOEMBOLISM; PROPHYLAXIS; COMPRESSION; THERAPY; SURGERY AB Thromboembolic complications are a major cause of postoperative morbidity and mortality in the neurosurgical patient. Prophylaxis with lower extremity pneumatic compression boots (PCBs) reduces the incidence of lower extremity deep vein thrombosis (DVT) but has not been shown to affect the incidence of pulmonary embolism (PE). Prophylaxis with low-dose heparin has consistently reduced the incidence of both DVT and PE in studies on general surgical patients but has not been adopted for use in neurosurgery primarily for fear of causing catastrophic hemorrhage. We report on a series of 138 consecutive adult patients who underwent major neurosurgical procedures on a general neurosurgical service at our institution. Patients were treated with intraoperative PCBs and, starting on the morning of the first postoperative day, with a regimen of 5000 U of heparin administered subcutaneously twice daily. This treatment was continued until patients were fully ambulatory. PCBs were discontinued 24 hours after the first administration of heparin. None of the heparin-treated patients suffered postoperative hemorrhage. We compared this series with a control group of 473 adult patients who had previously undergone major neurosurgical procedures on the same neurosurgical service. These patients had been treated with intraoperative and postoperative PCBs alone. The control group had a 3.2% incidence of thromboembolic complications (15 of 473; eight DVT, seven PE). Prophylaxis with PCBs plus heparin significantly (P = 0.020) reduced the incidence of thromboembolic complications: no PCBs/heparin-treated patient exhibited clinical evidence of PE or DVT (0%, 0/138). We conclude that a combination of intraoperative PCBs and postoperative low-dose heparin is a safe and effective method by which to reduce thromboembolic complications in the neurosurgical patient. C1 UNIV ARIZONA,ARIZONA HLTH SCI CTR,NEUROSURG SECT,TUCSON,AZ 85724. RP FRIM, DM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,NEUROSURG SERV,WHITE 5,14 FRUIT ST,BOSTON,MA 02114, USA. NR 23 TC 82 Z9 85 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0148-396X J9 NEUROSURGERY JI Neurosurgery PD JUN PY 1992 VL 30 IS 6 BP 830 EP 833 PG 4 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HV274 UT WOS:A1992HV27400002 PM 1614582 ER PT J AU BORODIC, GE AF BORODIC, GE TI BOTULINUM-A TOXIN FOR (EXPRESSIONISTIC) PTOSIS OVERCORRECTION AFTER FRONTALIS SLING SO OPHTHALMIC PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article DE BOTULINUM-A TOXIN; FRONTALIS SLING; PTOSIS; FRONTALIS MUSCLE; CHEMODENERVATION AB Botulinum A toxin was injected into the frontalis muscle in two patients with complete third nerve palsies to limit intermittent upper lid retraction after a frontalis sling procedure. This form of lid retraction is noted during periods of active facial movement with occipitofrontalis muscle contraction. Although upper lid position may be symmetric when the facial muscles are adynamic, the upper lid may retract during periods of active facial expression. This type of lid retraction was corrected using Botulinum A toxin injections into the frontalis muscles, without affecting the lid position when the facial muscles are adynamic. Both improvement in appearance and intermittent exposure were noted in both cases. Additionally, a blunting of the transverse forehead creases occurred over a defined area after this injection, representing a clinical example of a denervation field produced by a point injection of botulinum toxin. RP BORODIC, GE (reprint author), BOSTON UNIV,MASSACHUSETTS EYE & EAR INFIRM,GUNDERSON EYE CLIN,100 CHARLES RIVER PLAZA,BOSTON,MA 02114, USA. NR 0 TC 11 Z9 11 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0740-9303 J9 OPHTHALMIC PLAST REC JI Ophthalmic Plast. Reconstr. Surg. PD JUN PY 1992 VL 8 IS 2 BP 137 EP 142 DI 10.1097/00002341-199206000-00010 PG 6 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA HX368 UT WOS:A1992HX36800010 PM 1520657 ER PT J AU STEINERT, RF POST, CT BRINT, SF FRITCH, CD HALL, DL WILDER, LW FINE, IH LICHTENSTEIN, SB MASKET, S CASEBEER, C OKSMAN, H HOLLADAY, JT AF STEINERT, RF POST, CT BRINT, SF FRITCH, CD HALL, DL WILDER, LW FINE, IH LICHTENSTEIN, SB MASKET, S CASEBEER, C OKSMAN, H HOLLADAY, JT TI A PROSPECTIVE, RANDOMIZED, DOUBLE-MASKED COMPARISON OF A ZONAL PROGRESSIVE MULTIFOCAL INTRAOCULAR-LENS AND A MONOFOCAL INTRAOCULAR-LENS SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT, 1991 CL ANAHEIM, CA SP AMER ACAD OPHTHALMOL ID MULTIZONE BIFOCAL IMPLANT; OPTICAL-PERFORMANCE; CONTRAST AB Introduction: Multifocal intraocular lenses (IOLs) have been designed to provide improved near visual acuity without spectacles compared with monofocal IOLs. Early studies have reported variable amounts of decreased visual acuity and contrast sensitivity with multifocal IOLs, and some patients have experienced halos and glare. Methods: The authors performed a prospective, double-masked, multicenter evaluation of 62 patients randomized between a new zonal-progressive optic multifocal IOL and a monofocal IOL. Results: Mean postoperative spherical equivalent, astigmatism, and uncorrected and best-corrected distance visual acuity were similar between the two groups. Patients with a multifocal IOL achieved significantly better uncorrected near visual acuity than patients with monofocal IOLs (J3+ versus J7; P < 0.0001). With distance correction only, mean near visual acuity was J2 versus J5- (P = 0.0001). Best-corrected near visual acuity was J1 for both groups, with 1.36 diopters (D) for the multifocal group versus 2.37 D for the monofocal group (P < 0.0001). Regan contrast sensitivity was lower for the multifocal patients at all contrast levels, and achieved statistical significance at very low contrast (11% contrast; P = 0.0024). Fifty-two percent of patients with a multifocal IOL reported that they did not need spectacles at all or used them only for their fellow eye, compared with 25% of the patients with monofocal IOLs. Conclusion: Both monofocal and multifocal implant patients were very satisfied with the results of their cataract extraction and IOL implant surgery. A small loss of contrast sensitivity with the multifocal IOL was demonstrated, consistent with theoretical predictions. The functional significance of the loss of contrast sensitivity appears to be small and counterbalanced by the advantage of improved uncorrected near visual acuity. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. TULANE UNIV,SCH MED,NEW ORLEANS,LA 70112. UNIV CALIF LOS ANGELES,LOS ANGELES,CA 90024. JULES STEIN EYE INST,LOS ANGELES,CA. UNIV SO CALIF,DOHENY EYE INST,LOS ANGELES,CA 90089. UNIV KANSAS,COLL HLTH SCI,WICHITA,KS. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. THOMAS JEFFERSON UNIV,JEFFERSON MED COLL,WILLS EYE HOSP,PHILADELPHIA,PA 19107. UNIV CALIF IRVINE,IRVINE,CA 92717. LOUISIANA STATE UNIV,SHREVEPORT,LA 71105. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. UNIV TEXAS,SCH MED,HERMANN EYE CTR,HOUSTON,TX 77025. RP STEINERT, RF (reprint author), CTR EYE RES,OPHTHALM CONSULTANTS BOSTON,50 STANIFORD ST,BOSTON,MA 02114, USA. NR 17 TC 100 Z9 103 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD JUN PY 1992 VL 99 IS 6 BP 853 EP 861 PG 9 WC Ophthalmology SC Ophthalmology GA HX373 UT WOS:A1992HX37300010 PM 1630773 ER PT J AU AIELLO, LP IWAMOTO, M GUYER, DR AF AIELLO, LP IWAMOTO, M GUYER, DR TI PENETRATING OCULAR FISH-HOOK INJURIES - SURGICAL-MANAGEMENT AND LONG-TERM VISUAL OUTCOME SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT, 1991 CL ANAHEIM, CA SP AMER ACAD OPHTHALMOL AB Background. Ocular penetrating fish-hook injuries represent a rare yet potentially devastating ocular trauma. To date, only five cases have been reported in the medical literature. The authors present five new cases with long-term follow-up. Methods. All individuals who presented to the Wilmer Ophthalmological Institute emergency room with ocular fish-hook injuries between 1974 and 1990 were identified, and ophthalmic follow-up evaluations were performed. Results: Individuals were male, between the ages of 10 and 27, with follow-up evaluation of 2.0 to 15.5 years (mean, 6.7 years). The left eye was involved in 80% and in no instance had a single hook penetrated the lid and globe simultaneously. Initial visual acuity was uniformly poor (20/200 or worse). Using specialized surgical techniques, ultimate visual outcome was excellent in 80% of cases (4 of 5 with visual acuity of 20/30 or better). One eye was enucleated because of panendophthalmitis after delayed wound closure. Similar overall results are achieved when previous reports are included in the analysis (90% with visual acuity of 20/40 or better). Conclusions: These results suggest that penetrating ocular fish-hook injuries may have an excellent long-term prognosis if prompt, appropriate surgical intervention is accomplished. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. RP AIELLO, LP (reprint author), JOHNS HOPKINS UNIV HOSP,WILMER OPHTHALMOL INST,600 N WOLFE ST,WILMER B-23,BALTIMORE,MD 21205, USA. NR 6 TC 25 Z9 27 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 JUN PY 1992 VL 99 IS 6 BP 862 EP 866 PG 5 WC Ophthalmology SC Ophthalmology GA HX373 UT WOS:A1992HX37300011 PM 1630774 ER PT J AU HURLEY, JD MEMINGER, SR AF HURLEY, JD MEMINGER, SR TI A RELAPSE-PREVENTION PROGRAM - EFFECTS OF ELECTROMYOGRAPHIC TRAINING ON HIGH AND LOW-LEVELS OF STATE AND TRAIT ANXIETY SO PERCEPTUAL AND MOTOR SKILLS LA English DT Article ID RELAXATION AB This study involved 40 college subjects and investigated the effects of EMG training on high and low state- and trait-anxiety scores. At pretreatment assessment subjects were administered the Spielberger State-Trait Anxiety Inventory (1970). Subjects were treated with EMG training with an established treatment criterion of 3 microvolts. All subjects achieved the treatment criterion within six 20-min. training sessions. Daily homework practice sessions were recorded on behavioral data cards. Two-way analysis of variance indicated significant mean differences on both state and trait anxiety at the conclusion of treatment. Interactions were significant, with EMG affecting subjects high in anxiety differently from subjects low in anxiety. Multiple t tests indicated high state-anxiety scores dropped significantly more than high trait-anxiety scores. A 6-mo. follow-up assessment, employing biweekly mailing of behavioral data cards along with a protective contingency instituted by informing subjects they would be contacted by phone if the data cards were not received, showed that state-anxiety scores remained significantly lower, while trait-anxiety scores returned to pretreatment levels. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP HURLEY, JD (reprint author), STONEHILL COLL,DEPT PSYCHOL,N EASTON,MA 02357, USA. NR 20 TC 0 Z9 1 U1 1 U2 1 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 JUN PY 1992 VL 74 IS 3 BP 699 EP 705 PN 1 PG 7 WC Psychology, Experimental SC Psychology GA HX385 UT WOS:A1992HX38500005 PM 1608706 ER PT J AU PRAHL, SA VITKIN, IA BRUGGEMANN, U WILSON, BC ANDERSON, RR AF PRAHL, SA VITKIN, IA BRUGGEMANN, U WILSON, BC ANDERSON, RR TI DETERMINATION OF OPTICAL-PROPERTIES OF TURBID MEDIA USING PULSED PHOTOTHERMAL RADIOMETRY SO PHYSICS IN MEDICINE AND BIOLOGY LA English DT Article ID LAYERED MATERIALS AB Pulsed photothermal radiometry (PPTR) measures blackbody radiation emitted by a sample after absorption of an optical pulse. Three techniques for obtaining the absorption coefficient of absorbing-only, semi-infinite samples are examined and shown to give comparable results. An analytic theory for the time dependence of the PPTR signal in semi-infinite scattering and absorbing media has been derived and tested in a series of controlled gel phantoms. This theory, based on the diffusion approximation of the radiative transport equation, is shown to model the time course of the detected signal accurately. Furthermore, when the incident fluence is known, the theory can be used in a non-linear, two-parameter fitting algorithm to determine the absorption and reduced scattering coefficients of a turbid sample with an accuracy of 10-15% for transport albedos ranging from 0.42-0.88. C1 HAMILTON REG CANC CTR,HAMILTON L8V 1C3,ONTARIO,CANADA. MCMASTER UNIV,DEPT PHYS,HAMILTON L8V 1C3,ONTARIO,CANADA. RP PRAHL, SA (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN RES LABS PHOTOMED,BOSTON,MA 02114, USA. RI Vitkin, Alex/I-8166-2012 FU NIAMS NIH HHS [5R01AR25395-11] NR 24 TC 96 Z9 96 U1 0 U2 5 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 JUN PY 1992 VL 37 IS 6 BP 1203 EP 1217 DI 10.1088/0031-9155/37/6/001 PG 15 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Radiology, Nuclear Medicine & Medical Imaging GA HY517 UT WOS:A1992HY51700001 PM 1626021 ER PT J AU BERN, S BURD, A MAY, JW AF BERN, S BURD, A MAY, JW TI THE BIOPHYSICAL AND HISTOLOGIC PROPERTIES OF CAPSULES FORMED BY SMOOTH AND TEXTURED SILICONE IMPLANTS IN THE RABBIT SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID BREAST IMPLANTS; CONTRACTURE AB Capsular contracture remains the major complication of reconstructive and aesthetic breast surgery. The purpose of this investigation was to determine if a silicone implant with a textured surface will form a capsule of significantly different biophysical and histologic properties than conventional smooth silicone. Thirty smooth and 30 textured silicone tissue expanders were implanted under the panniculus carnosus of rabbits. After 3 months, measurements related to contracture were performed on anesthetized animals in an investigator-blinded, controlled manner. Intraexpander pressures were measured as saline was injected over time. We found a significant correlation between intraexpander pressures, applanation tonometry, and Baker class. Histology revealed a thicker, more adherent, and inflammatory capsule around the textured silicone implants as compared with the smooth silicone implants. Dynamic pressures were plotted against volume of saline within the two types of implants. Statistical analysis revealed that the textured implants form a tighter and thicker capsule than the smooth implants after 3 months of observation (p < 0.005). C1 SHRINERS BURN INST,WOUND HEALING LAB,BOSTON,MA. MASSACHUSETTS GEN HOSP,HAND SURG SERV,BOSTON,MA 02114. RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,DIV PLAST SURG,ACC-4,SUITE 453,BOSTON,MA 02114, USA. NR 18 TC 50 Z9 52 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUN PY 1992 VL 89 IS 6 BP 1037 EP 1042 DI 10.1097/00006534-199206000-00005 PG 6 WC Surgery SC Surgery GA HX386 UT WOS:A1992HX38600005 PM 1584865 ER PT J AU MAY, JW AF MAY, JW TI THE VALUE OF BASIC EDUCATION IN PLASTIC-SURGERY - A LESSON LEARNED FROM ABROAD SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Editorial Material RP MAY, JW (reprint author), MASSACHUSETTS GEN HOSP,ACC,SUITE 353,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0032-1052 J9 PLAST RECONSTR SURG JI Plast. Reconstr. Surg. PD JUN PY 1992 VL 89 IS 6 BP 1132 EP 1132 DI 10.1097/00006534-199206000-00021 PG 1 WC Surgery SC Surgery GA HX386 UT WOS:A1992HX38600021 PM 1584876 ER PT J AU DEUTSCH, T WAYNANT, R AF DEUTSCH, T WAYNANT, R TI PROLOG TO THE SPECIAL SECTION ON LASERS IN MEDICINE SO PROCEEDINGS OF THE IEEE LA English DT Editorial Material C1 US FDA,CDRH,ROCKVILLE,MD 20857. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP DEUTSCH, T (reprint author), MASSACHUSETTS GEN HOSP,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9219 J9 P IEEE JI Proc. IEEE PD JUN PY 1992 VL 80 IS 6 BP 831 EP 832 PG 2 WC Engineering, Electrical & Electronic SC Engineering GA JG019 UT WOS:A1992JG01900005 ER PT J AU KOCHEVAR, IE AF KOCHEVAR, IE TI BIOLOGICAL EFFECTS OF EXCIMER LASER-RADIATION SO PROCEEDINGS OF THE IEEE LA English DT Article ID UNSCHEDULED DNA-SYNTHESIS; HUMAN-SKIN FIBROBLASTS; MAMMALIAN-CELLS; ACTION SPECTRA; 193 NM; CYTO-TOXICITY; ULTRAVIOLET WAVELENGTHS; CORNEAL SURGERY; STRAND BREAKS; 308 NM AB Excimer laser radiation at 193 nm (ArF) and 308 nm (XeCl) is being used for medical applications. Because ultraviolet radiation is absorbed by DNA and causes cell killing, mutagenesis, and carcinogenesis, the effects of 193- and 308-nm excimer laser radiation on biological material have been studied. Radiation at 193 nm causes less cell killing than conventional 254 nm germicidal light per incident photon. Radiation at 193 nm showed very low potential for causing mutation because proteins absorb strongly at 193 nm thereby reducing the photon flux reaching the nuclear DNA. In addition, the quantum yield of a cytotoxic and mutagenic photoproduct of DNA is lower for 193 nm than for 254 nm. Radiation at 308 nm is cytotoxic and mutagenic. Results of in vitro assays indicate that the relative ability of excimer laser radiation to cause DNA damage decreases in the order 248 nm > 308 nm > 193 nm. RP KOCHEVAR, IE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114, USA. NR 29 TC 11 Z9 11 U1 0 U2 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI NEW YORK PA 345 E 47TH ST, NEW YORK, NY 10017-2394 SN 0018-9219 J9 P IEEE JI Proc. IEEE PD JUN PY 1992 VL 80 IS 6 BP 833 EP 837 DI 10.1109/5.149447 PG 5 WC Engineering, Electrical & Electronic SC Engineering GA JG019 UT WOS:A1992JG01900006 ER PT J AU KODUKULA, K AMTHAUER, R CINES, D YEH, ETH BRINK, L THOMAS, LJ UDENFRIEND, S AF KODUKULA, K AMTHAUER, R CINES, D YEH, ETH BRINK, L THOMAS, LJ UDENFRIEND, S TI BIOSYNTHESIS OF PHOSPHATIDYLINOSITOL-GLYCAN (PI-G)-ANCHORED MEMBRANE-PROTEINS IN CELL-FREE SYSTEMS - PI-G IS AN OBLIGATORY COSUBSTRATE FOR COOH-TERMINAL PROCESSING OF NASCENT PROTEINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE TRANSAMIDASE ID PLACENTAL ALKALINE-PHOSPHATASE; CLEAVAGE ATTACHMENT SITE; ANCHOR; SELECTIVITY; DEFECT AB It is generally recognized that nascent proteins destined to be processed to a phosphatidylinositol-glycan (PI-G)-anchored membrane form contain a hydrophobic signal peptide at both their NH2 and COOH termini. In previous studies we showed that rough microsomal membranes (RM) prepared from CHO cells can carry out COOH-terminal processing. We have now investigated RM prepared from many additional cell types, including frog oocytes, B cells, and T cells, and found that all are competent with respect to COOH-terminal processing. Exceptions were certain mutant T cells that had been shown to be defective at various steps of PI-G anchor biosynthesis [Sugiyama, E., De Gasperi, R., Urakaze, M., Chang, H.-M., Thomas, L. J., Hyman, R., Warren, C. D. & Yeh, E. T. H. (1991) J. Biol. Chem. 266, 12119-12122]. In one such defective mutant, COOH-terminal processing activity of RM could be restored either by transfecting the intact cells with the gene for the deficient step in PI-G synthesis or by adding PI-G extracts to the RM in vitro. Cleavage of the COOH-terminal signal peptide in the RM is therefore dependent on the presence of intact PI-G incorporated into the mature protein. C1 ROCHE INST MOLEC BIOL,ROCHE RES CTR,DEPT NEUROSCI,NUTLEY,NJ 07110. UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PATHOL,PHILADELPHIA,PA 19104. MASSACHUSETTS GEN HOSP,DEPT MED,ARTHRITIS UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL 40387, HL 45851] NR 25 TC 30 Z9 30 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 JUN 1 PY 1992 VL 89 IS 11 BP 4982 EP 4985 DI 10.1073/pnas.89.11.4982 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX168 UT WOS:A1992HX16800042 PM 1594603 ER PT J AU ARDMAN, B SIKORSKI, MA STAUNTON, DE AF ARDMAN, B SIKORSKI, MA STAUNTON, DE TI CD43 INTERFERES WITH LYMPHOCYTE-T ADHESION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; WISKOTT-ALDRICH SYNDROME; LEUKOCYTE-COMMON ANTIGEN; SURFACE GLYCOPROTEIN; MOLECULE-1 ICAM-1; CELL-ADHESION; LFA-1; SIALOGLYCOPROTEIN; DEFICIENCY; DISTINCT AB CD43 is a cell-surface sialoglycoprotein of uncertain physiologic function expressed to various degrees by most leukocytes. We tested whether or not CD43 participates in intercellular adhesion by comparing the binding of human T lymphocytes to transfected HeLa cells stably expressing CD43 and sham-transfected HeLa cells (CD43-negative). Significantly fewer T lymphocytes adhered to the CD43-positive HeLa cells than to the CD43-negative HeLa cells. Diminished T-cell adherence to the CD43-positive HeLa cells was seen for all T lymphocytes tested, irrespective of their source or derivation. Antibody-blocking experiments revealed that CD43 interference with T-cell adhesion largely represented interference with T-cell leukocyte function-associated antigen 1 binding to HeLa cell intercellular adhesion molecule 1. The CD43 anti-adhesion effect was not overcome by treating cells with phorbol 12-myristate 13-acetate, a chemical that increases the binding avidity of leukocyte function-associated antigen 1 for intercellular adhesion molecule 1. However, neuraminidase treatment of the HeLa cell transfectants diminished the CD43 anti-adhesion effect. These data indicate that CD43 expression by opposing cells can interfere with cell-cell adhesion. The data also suggest that CD43 might regulate T-cell adhesion by interfering with leukocyte function-associated 1 binding to intercellular adhesion molecule 1, a major activation-induced adhesion pathway among lymphocytes. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ARDMAN, B (reprint author), NEW ENGLAND MED CTR HOSP,DEPT MED,BOSTON,MA 02111, USA. FU NIAID NIH HHS [AI-27729] NR 32 TC 150 Z9 150 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 JUN 1 PY 1992 VL 89 IS 11 BP 5001 EP 5005 DI 10.1073/pnas.89.11.5001 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HX168 UT WOS:A1992HX16800046 PM 1594606 ER PT J AU RAGIN, RC DONAHOE, PK KENNEALLY, MK AHMAD, MF MACLAUGHLIN, DT AF RAGIN, RC DONAHOE, PK KENNEALLY, MK AHMAD, MF MACLAUGHLIN, DT TI HUMAN MULLERIAN INHIBITING SUBSTANCE - ENHANCED PURIFICATION IMPARTS BIOCHEMICAL STABILITY AND RESTORES ANTIPROLIFERATIVE EFFECTS SO PROTEIN EXPRESSION AND PURIFICATION LA English DT Article ID GROWTH FACTOR-BETA; AMINO-ACID-SEQUENCE; DUCT REGRESSION; COLONY GROWTH; PROTEINS; BOVINE; FAMILY; CELLS; FETAL; GENE C1 MASSACHUSETTS GEN HOSP, DIABET UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT SURG & MED, BOSTON, MA 02115 USA. RP MASSACHUSETTS GEN HOSP, PEDIAT SURG RES LABS, BOSTON, MA 02114 USA. FU NCI NIH HHS [1RO1-CA17393] NR 48 TC 53 Z9 55 U1 0 U2 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1046-5928 EI 1096-0279 J9 PROTEIN EXPRES PURIF JI Protein Expr. Purif. PD JUN PY 1992 VL 3 IS 3 BP 236 EP 245 DI 10.1016/1046-5928(92)90020-W PG 10 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology GA HZ849 UT WOS:A1992HZ84900009 PM 1392620 ER PT J AU MAHLER, ME AF MAHLER, ME TI BEHAVIORAL MANIFESTATIONS ASSOCIATED WITH MULTIPLE-SCLEROSIS SO PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID MINI-MENTAL STATE; COGNITIVE FUNCTION; IMPAIRMENT; MEMORY; DISABILITY; DEPRESSION; PROFILES C1 W LOS ANGELES DEPT VET AFFAIRS MED CTR,NEUROBEHAV PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. NR 56 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 0193-953X J9 PSYCHIAT CLIN N AM JI Psychiatr. Clin. North Amer. PD JUN PY 1992 VL 15 IS 2 BP 427 EP 438 PG 12 WC Psychiatry SC Psychiatry GA KZ888 UT WOS:A1992KZ88800012 PM 1603734 ER PT J AU HOLTZ, JL AF HOLTZ, JL TI MAKING A CONSULTATION SERVICE WORK - AN ORGANIZATIONAL COMMENTARY SO PSYCHOSOMATICS LA English DT Article RP HOLTZ, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROSCI,WARREN 611,BOSTON,MA 02114, USA. NR 0 TC 4 Z9 4 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD SUM PY 1992 VL 33 IS 3 BP 324 EP 328 PG 5 WC Psychiatry; Psychology SC Psychiatry; Psychology GA JB243 UT WOS:A1992JB24300010 PM 1410205 ER PT J AU MIKULIS, DJ DIAZ, O EGGLIN, TK SANCHEZ, R AF MIKULIS, DJ DIAZ, O EGGLIN, TK SANCHEZ, R TI VARIANCE OF THE POSITION OF THE CEREBELLAR TONSILS WITH AGE - PRELIMINARY-REPORT SO RADIOLOGY LA English DT Article DE AGING; BRAIN, ANATOMY; BRAIN, GROWTH AND DEVELOPMENT; BRAIN, MR ID MR; MALFORMATION AB The position of the cerebellar tonsils relative to the foramen magnum was measured with sagittal magnetic resonance (MR) images in 221 patients aged 5 months to 89 years who were considered not to have disorders that would affect tonsillar position. All patients were grouped according to age. All measurements of the tonsils were obtained directly from the video console. Statistically significant (P < .05) differences in tonsillar position were found between the 1st and 9th decades (P < .001) and the 3rd and 9th decades (P < .003) of life. An obvious trend existed: tonsillar ascent with increasing age. Therefore, the authors believe that a single reference standard that indicates the normal distance of the cerebellar tonsils from the foramen magnum is inappropriate unless age is considered. They suggest that the following distances below the foramen magnum (more than 2 standard deviations out of the normal range) be used as criteria for ectopia of the cerebellar tonsils: 1st decade of life, 6 mm; 2nd and 3rd decades, 5 mm; 4th to 8th decades, 4 mm; and 9th decade, 3 mm. C1 SHIELDS HLTH CARE GRP,CAMBRIDGE MRI CTR,BROCKTON,MA. RP MIKULIS, DJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 12 TC 106 Z9 116 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 JUN PY 1992 VL 183 IS 3 BP 725 EP 728 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV578 UT WOS:A1992HV57800027 PM 1584927 ER PT J AU TASENDE, MSG GALE, GR SMITH, AB JONES, MM SINGH, PK AF TASENDE, MSG GALE, GR SMITH, AB JONES, MM SINGH, PK TI MONOISOAMYL MESO-2,3-DIMERCAPTOSUCCINATE - INTERACTION WITH METALLOTHIONEIN-BOUND CADMIUM INVITRO AND EVIDENCE OF ACTIVE-TRANSPORT INTO RENAL AND HEPATIC CELLS INVIVO SO RESEARCH COMMUNICATIONS IN CHEMICAL PATHOLOGY AND PHARMACOLOGY LA English DT Article ID TISSUE DISTRIBUTION; ANTAGONISTS; EXCRETION; DIETHYLDITHIOCARBAMATE; DERIVATIVES; AGENTS AB Monoisoamyl meso-2,3-dimercaptosuccinate (Mi-ADMS) and the unesterified 2,3-dimercaptosuccinic acid (DMSA) were evaluated for relative reactivities against metallothionein (MT)-bound cadmium (Cd) in vitro by elution of the reaction products through Sephadex G-75 gel. After 3 hr of incubation, Mi-ADMS removed about 70% of the Cd from Cd-MT, and a new peak emerged which corresponded to that obtained by elution of a 2:1 molar mixture of Mi-ADMS and Cd. Only about 15% of the Cd was removed from Cd-MT by DMSA. After 24 hr of incubation with Mi-ADMS, no evidence remained of the presence of Cd-MT; all of the Cd was recovered in a very high molecular weight fraction and in a fraction corresponding to Cd ion. In contrast, after 24 hr of incubation with DMSA, 25% of the Cd was still present as Cd-MT, while the remainder eluted in a fraction corresponding to a 2:1 molar complex of DMSA and Cd. When Mi-ADMS was administered to Cd-bearing mice which had received an inhibitor of organic anion transport, probenecid (PBC) or sulfinpyrazone (SPZ), prior to administration of thc monoester, there was a marked attenuation of the Cd mobilizing actions of Mi-ADMS as reflected in whole body Cd levels. Analysis of organ Cd concentrations revealed that PBC blocked primarily the mobilization of renal Cd by Mi-ADMS, while the principal action of SPZ in antagonizing the action of Mi-ADMS was on hepatic Cd mobilization. It was concluded that Mi-ADMS has a higher affinity for Cd in Cd-MT than does DMSA, and that the access of Mi-ADMS to intracellular Cd is, at least in part, mediated by the organic anion transport system. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29401. VANDERBILT UNIV,CTR MOLEC TOXICOL,NASHVILLE,TN 37235. VANDERBILT UNIV,DEPT CHEM,NASHVILLE,TN 37235. RP TASENDE, MSG (reprint author), RALPH H JOHNSON VET AFFAIRS MED CTR,RES SERV,109 BEE ST,CHARLESTON,SC 29401, USA. RI Garcia -Tasende, Soledad/H-6408-2015 OI Garcia -Tasende, Soledad/0000-0001-8738-6070 FU NIEHS NIH HHS [ES-02638] NR 23 TC 24 Z9 25 U1 0 U2 2 PU P J D PUBLICATIONS LTD PI WESTBURY PA PO BOX 966, WESTBURY, NY 11590 SN 0034-5164 J9 RES COMMUN CHEM PATH PD JUN PY 1992 VL 76 IS 3 BP 323 EP 339 PG 17 WC Pathology; Pharmacology & Pharmacy SC Pathology; Pharmacology & Pharmacy GA JB323 UT WOS:A1992JB32300006 PM 1636055 ER PT J AU NEUFELD, GR SCHWARDT, JD GOBRAN, SR BAUMGARDNER, JE SCHREINER, MS AUKBURG, SJ SCHERER, PW AF NEUFELD, GR SCHWARDT, JD GOBRAN, SR BAUMGARDNER, JE SCHREINER, MS AUKBURG, SJ SCHERER, PW TI MODELING STEADY-STATE PULMONARY ELIMINATION OF HE, SF6 AND CO2 - EFFECT OF MORPHOMETRY SO RESPIRATION PHYSIOLOGY LA English DT Article DE EXPIROGRAM; MORPHOMETRY, GAS EXCHANGE; ALVEOLAR, MODELING; MODELS, ALVEOLAR GAS EXCHANGE, MORPHOMETRY ID GAS-TRANSPORT; HUMAN-LUNG; WASHOUT; ACINUS; DIFFUSION; EXCHANGE AB We studied the influence of acinar morphometry on the shape of simulated expirograms computed from a single path convection-diffusion model that includes a source term for gas evolution from the blood (Scherer et al., J. Appl. Physiol. 64: 1022-1029, 1988). Acinar structure was obtained from published data of 3 different lung morphometries. The simulations were performed over a range of tidal volumes (VT) and breathing frequencies (f) comparable to those observed in a previously reported human study. Airways dead space (VDaw) increased with VT in all the morphometric models tested and in the experimental data. The increase in VDaw with VT was inversely related to the diffusivity of the evolving gas and to the rate of increase in airway cross-section of the most mouthward (proximal) alveolated generations of the models. Normalized phase III slope for all the gases decreased with increasing VT in all the models as was previously reported for healthy human subjects. In the model simulations, the greatest sensitivity of phase III slope to VT was seen with the least diffusible gas using the airway morphometry with the smallest cross-sectional areas in the proximal alveolated generations. We conclude that both VDaw and phase III slope of an evolving gas are sensitive to the geometry of the proximal acinar airways and that this is manifest by their dependence on tidal volume, breathing frequency, molecular diffusivity and alveolar/blood source emission rate. The model simulations indicate that heterogeneity of gas washout is not required to explain the magnitude of the phase III slope in healthy human subjects. C1 UNIV PENN,SCH MED,DEPT ANESTHESIA,PHILADELPHIA,PA 19104. UNIV PENN,SCH ENGN & APPL SCI,DEPT BIOENGN,PHILADELPHIA,PA 19104. PHILADELPHIA VET AFFAIRS MED CTR,PHILADELPHIA,PA. CHILDRENS HOSP PHILADELPHIA,PHILADELPHIA,PA 19104. FU NHLBI NIH HHS [HL-33891] NR 27 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0034-5687 J9 RESP PHYSIOL JI Respir. Physiol. PD JUN PY 1992 VL 88 IS 3 BP 257 EP 275 DI 10.1016/0034-5687(92)90001-D PG 19 WC Physiology; Respiratory System SC Physiology; Respiratory System GA HW902 UT WOS:A1992HW90200001 PM 1615224 ER PT J AU SLEDGE, GW ANTMAN, KH AF SLEDGE, GW ANTMAN, KH TI PROGRESS IN CHEMOTHERAPY FOR METASTATIC BREAST-CANCER SO SEMINARS IN ONCOLOGY LA English DT Review ID BONE-MARROW TRANSPLANTATION; INTENSIVE INDUCTION CHEMOTHERAPY; PREVIOUSLY UNTREATED PATIENTS; HIGH-DOSE CYCLOPHOSPHAMIDE; REFRACTORY SOLID TUMORS; HUMAN CELL-LINES; PHASE-II; COMBINATION CHEMOTHERAPY; RANDOMIZED TRIAL; ALKYLATING-AGENTS C1 INDIANA UNIV,SCH MED,DEPT MED,INDIANAPOLIS,IN 46202. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. FU NCI NIH HHS [P01CA-38493] NR 130 TC 82 Z9 82 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0093-7754 J9 SEMIN ONCOL JI Semin. Oncol. PD JUN PY 1992 VL 19 IS 3 BP 317 EP 332 PG 16 WC Oncology SC Oncology GA JA077 UT WOS:A1992JA07700013 PM 1609297 ER PT J AU SCHWESINGER, WH AF SCHWESINGER, WH TI LASER TREATMENT OF ESOPHAGEAL AND GASTRIC-LESIONS SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Article ID ND-YAG LASER; BLEEDING PEPTIC-ULCERS; UPPER GASTROINTESTINAL-TRACT; PALLIATIVE TREATMENT; MALIGNANT DYSPHAGIA; ENDOSCOPIC PALLIATION; ESOPHAGOGASTRIC CANCER; PHOTO-COAGULATION; RANDOMIZED TRIAL; THERAPY C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,GEN SURG SECT,SAN ANTONIO,TX 78284. NR 75 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD JUN PY 1992 VL 72 IS 3 BP 581 EP 595 PG 15 WC Surgery SC Surgery GA LA547 UT WOS:A1992LA54700007 PM 1589833 ER PT J AU SCHWESINGER, WH HUNTER, JG AF SCHWESINGER, WH HUNTER, JG TI DIXON,JOHN,A. SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Editorial Material C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV UTAH,MED CTR,DEPT SURG,SALT LAKE CITY,UT 84112. 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 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD JUN PY 1992 VL 72 IS 3 BP R3 EP R3 PG 1 WC Surgery SC Surgery GA LA547 UT WOS:A1992LA54700001 ER PT J AU SCHWESINGER, WH HUNTER, JG AF SCHWESINGER, WH HUNTER, JG TI LASERS IN GENERAL-SURGERY - PREFACE SO SURGICAL CLINICS OF NORTH AMERICA LA English DT Editorial Material C1 UNIV UTAH,MED CTR,DEPT SURG,SALT LAKE CITY,UT 84132. AUDIE L MURPHY MEM VET ADM MED CTR,GEN SURG SECT,SAN ANTONIO,TX 78284. 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 0039-6109 J9 SURG CLIN N AM JI Surg. Clin.-North Am. PD JUN PY 1992 VL 72 IS 3 BP R15 EP R16 PG 2 WC Surgery SC Surgery GA LA547 UT WOS:A1992LA54700003 ER PT J AU LU, HR GOLD, HK WU, ZM YASUDA, T PAUWELS, P RAPOLD, HJ NAPIER, M BUNTING, S COLLEN, D AF LU, HR GOLD, HK WU, ZM YASUDA, T PAUWELS, P RAPOLD, HJ NAPIER, M BUNTING, S COLLEN, D TI G4120, AN ARG-GLY-ASP CONTAINING PENTAPEPTIDE, ENHANCES ARTERIAL EVERSION GRAFT RECANALIZATION WITH RECOMBINANT TISSUE-TYPE PLASMINOGEN-ACTIVATOR IN DOGS SO THROMBOSIS AND HAEMOSTASIS LA English DT Article ID ANTIPLATELET GPIIB/IIIA ANTIBODY; GLYCOPROTEIN-IIB/IIIA RECEPTOR; PLATELET-AGGREGATION INHIBITOR; MONOCLONAL-ANTIBODY; THROMBOLYTIC THERAPY; MODEL; POTENTIATION; REPERFUSION; THROMBOSIS; VENOM AB The effects of G4120, a cyclic Arg-Gly-Asp (RGD) containing peptide which inhibits fibrinogen binding to the platelet receptor GPIIb/IIIa, on thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) were investigated in a combined arterial and venous thrombosis model in heparinized dogs. The arterial thrombus model consisted of a 3 cm everted (inside-out) carotid arterial segment inserted into a transsected femoral artery which occludes within 30 min with platelet-rich material and which is resistant to recanalization with 0.5 mg/kg rt-PA. The venous thrombus was a I-125-fibrin labeled whole blood clot produced in the contralateral femoral vein. In 5 dogs given an intravenous bolus of 0.05 mg/kg G4120 followed by a continuous infusion of 0.05 mg/kg per hour for 3 h (group I), arterial occlusion persisted throughout a 4 h observation period and was still present at 24 h in all dogs; the extent of venous clot lysis after 120 min was 27 +/- 7%. In 5 dogs given the same infusion of G4120 in combination with 0.5 mg/kg rt-PA over 60 min, recanalization of the arterial graft occurred in all dogs, within 13 +/- 2 min and persisted throughout the observation period of 4 h (p = 0.01 versus G4120 or rt-PA alone); at 24 h, however, all grafts were occluded. Venous clot lysis in this group was 75 +/- 8% (p = 0.002 versus G4120 alone and p = NS versus rt-PA alone). Pathologic analysis revealed platelet-rich or mixed thrombus with platelet-rich and erythrocyte-rich zones. The last 6 dogs were given a reduced dose of G4120 consisting either of a 0.05 mg/kg bolus followed by an infusion of 0.05 mg/kg over 1 h in 3 dogs (group III) or of a single 0.05 mg/kg bolus in 3 dogs (group IV), both given in combination with 0.5 mg/kg rt-PA infused over 60 min. These protocols produced recanalization within 15 +/- 2 and 34 +/- 8 min, respectively, which was maintained throughout the 4 h observation period. Venous lysis in these groups was 63 +/- 4 and 97 +/- 1% respectively. Bleeding times prolonged from 1 to 2 min to > 30 min with G4120, but returned towards baseline within 2 h after the end of the infusion. Platelet aggregation with ADP was completely inhibited with G4120 but partially recovered within 1 h after the end of the infusion. No fibrinogen breakdown was observed in association with the rt-PA infusion. Thus, G4120, a synthetic GPIIb/IIIa receptor antagonist, enhances and accelerates lysis of platelet-rich arterial thrombosis with rt-PA and prevents reocclusion during and within 3 h after the infusion. It may be useful for the conjunctive use with thrombolytic agents in patients with arterial thromboembolic disease. C1 CATHOLIC UNIV LEUVEN,CTR THROMBOSIS & VASC RES,CAMPUS GASTHUISBERG,O & N,HERESTR 49,B-3000 LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,EXPTL CARDIOL LAB,B-3000 LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,DEPT HISTOPATHOL,B-3000 LOUVAIN,BELGIUM. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH LOW TEMP ENGN PHYS,CARDIAC UNIT,BOSTON,MA 02114. GENENTECH INC,DEPT CARDIOVASC RES,SAN FRANCISCO,CA 94080. NR 30 TC 24 Z9 24 U1 0 U2 0 PU F K SCHATTAUER VERLAG GMBH PI STUTTGART PA P O BOX 10 45 45, LENZHALDE 3, D-70040 STUTTGART, GERMANY SN 0340-6245 J9 THROMB HAEMOSTASIS JI Thromb. Haemost. PD JUN 1 PY 1992 VL 67 IS 6 BP 686 EP 691 PG 6 WC Hematology; Peripheral Vascular Disease SC Hematology; Cardiovascular System & Cardiology GA HZ356 UT WOS:A1992HZ35600018 PM 1509410 ER PT J AU MALDONADO, LS MURATA, GH HERSHMAN, JM BRAUNSTEIN, GD AF MALDONADO, LS MURATA, GH HERSHMAN, JM BRAUNSTEIN, GD TI DO THYROID-FUNCTION TESTS INDEPENDENTLY PREDICT SURVIVAL IN THE CRITICALLY ILL SO THYROID LA English DT Article ID NONTHYROIDAL ILLNESSES; SERUM TRIIODOTHYRONINE; ACUTE PHYSIOLOGY; HORMONE BINDING; ICU PATIENTS; THYROXINE; THYROTROPIN; MORTALITY; PROTEINS; DISEASE AB We studied the ability of thyroid function tests to predict hospital survival in 116 critically ill patients and compared the results with independent predictions of survival made by critical care physicians. Eleven patients (9.5%) had clinically unsuspected hypothyroidism and were less likely to survive (p = 0.03). In patients critically ill with nonthyroidal disease, low T3, low FT3I, low T4, low FT4I, high TSH, and high T3U levels each showed significant correlation with nonsurvival (all p < 0.02). Of these, however, only low T3 (P < 0.001) and high TSH (p = 0.016) showed significant independent prediction of nonsurvival, and only low T3 (p = 0.011) added any significant independent prediction of nonsurvival beyond that made clinically by the group of critical care physicians. C1 UNIV CALIF LOS ANGELES,CEDARS SINAI MED CTR,SCH MED,DEPT MED,DIV ENDOCRINOL,LOS ANGELES,CA 90048. UNIV CALIF LOS ANGELES,SCH MED,W LOS ANGELES VET ADM MED CTR,DEPT MED,ENDOCRINOL SECT,LOS ANGELES,CA 90024. RP MALDONADO, LS (reprint author), UNIV CALIF LOS ANGELES,CEDARS SINAI MED CTR,SCH MED,DEPT MED,DIV GEN INTERNAL MED,ROOM B114,LOS ANGELES,CA 90048, USA. NR 39 TC 63 Z9 66 U1 1 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 1050-7256 J9 THYROID JI Thyroid PD SUM PY 1992 VL 2 IS 2 BP 119 EP 123 DI 10.1089/thy.1992.2.119 PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HZ352 UT WOS:A1992HZ35200004 PM 1525579 ER PT J AU SURGENOR, DM WALLACE, EL CHURCHILL, WH HAO, SHS CHAPMAN, RH COLLINS, JJ AF SURGENOR, DM WALLACE, EL CHURCHILL, WH HAO, SHS CHAPMAN, RH COLLINS, JJ TI RED-CELL TRANSFUSIONS IN CORONARY-ARTERY BYPASS-SURGERY (DRGS-106 AND DRGS-107) SO TRANSFUSION LA English DT Article ID BLOOD AB To study red cell transfusion practice in 3216 coronary artery bypass graft (CABG) cases in 11 hospitals in 1988 abstracted patient records were stratified by diagnosis related group (DRG) (that is, DRG 106, coronary artery bypass without catheterization, or DRG 107, coronary artery bypass with catheterization) and International Classification of Diseases, 9th revision, Clinical Modification (ICD-9-CM) surgical procedure code. Means of units per transfused patient, age and length of stay, and in-hospital mortality rates were significantly greater for patients in DRG 106 than DRG 107. Gender was a significant factor for transfusion outcomes; female patients were more likely to undergo transfusion, and, when transfused, they received more units of red cells than male patients. For a given DRG/ICD-9-CM surgical procedure class, significant differences were found between hospitals in the percentage of patients transfused, but not in mean units of red cells per transfused patient. However, within individual hospitals, the proportion of patients transfused and the number of units per transfused patient did not vary significantly across DRG/ICD-9-CM procedure classes. These results suggest that circumstances operating within a hospital, still to be identified, had more influence on transfusion decisions than the nature of the surgical intervention. C1 CTR MANAGEMENT SYST,WILLIAMSVILLE,NY. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT CLIN LABS,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DIV THORAC & CARDIAC SURG,BOSTON,MA 02115. SUNY BUFFALO,CTR MANAGEMENT SYST,BUFFALO,NY 14260. RP SURGENOR, DM (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NHLBI NIH HHS [HL-33774] NR 13 TC 69 Z9 69 U1 0 U2 0 PU AMER ASSOC BLOOD BANKS PI BETHESDA PA 8101 GLENBROOK RD, BETHESDA, MD 20814-2749 SN 0041-1132 J9 TRANSFUSION JI Transfusion PD JUN PY 1992 VL 32 IS 5 BP 458 EP 464 DI 10.1046/j.1537-2995.1992.32592327721.x PG 7 WC Hematology SC Hematology GA JB606 UT WOS:A1992JB60600014 PM 1626350 ER PT J AU OKUMURA, M MESTER, M AF OKUMURA, M MESTER, M TI THE COMING OF AGE OF SMALL-BOWEL TRANSPLANTATION - A HISTORICAL-PERSPECTIVE SO TRANSPLANTATION PROCEEDINGS LA English DT Article ID INTESTINAL TRANSPLANTATION C1 UNIV SAO PAULO,FAC MED,HOSP CLIN,SCH MED,SAO PAULO,BRAZIL. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 15 TC 9 Z9 15 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 JUN PY 1992 VL 24 IS 3 BP 1241 EP 1242 PG 2 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA HY795 UT WOS:A1992HY79500243 PM 1604601 ER PT J AU MOORE, JP SIMPSON, G MCKEATING, JA BURAKOFF, SJ SCHREIBER, SL WEISS, RA AF MOORE, JP SIMPSON, G MCKEATING, JA BURAKOFF, SJ SCHREIBER, SL WEISS, RA TI CPF-DD IS AN INHIBITOR OF INFECTION BY HUMAN-IMMUNODEFICIENCY-VIRUS AND OTHER ENVELOPED VIRUSES INVITRO SO VIROLOGY LA English DT Article ID HUMAN RETROVIRUS; HTLV-III/LAV; T4 MOLECULE; NEUTRALIZING ANTIBODIES; SOLUBLE CD4; AIDS; RECEPTOR; BINDING; CELLS; HIV-1 C1 INST CANC RES,CHESTER BEATTY LABS,LONDON SW3 6JB,ENGLAND. HARVARD UNIV,DEPT CHEM,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OI McKeating, Jane/0000-0002-7229-5886 NR 44 TC 13 Z9 13 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 JUN PY 1992 VL 188 IS 2 BP 537 EP 544 DI 10.1016/0042-6822(92)90508-M PG 8 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100014 PM 1316672 ER PT J AU CAPUTO, A HASELTINE, WA AF CAPUTO, A HASELTINE, WA TI REEXAMINATION OF THE CODING POTENTIAL OF THE HTLV-1 PX REGION SO VIROLOGY LA English DT Article ID T-CELL LEUKEMIA; VIRUS TYPE-I; TROPICAL SPASTIC PARAPARESIS; COMPLETE NUCLEOTIDE-SEQUENCE; ENV PROTEIN EXPRESSION; P27REX REGULATES GAG; LYMPHOTROPIC VIRUS; MOLECULAR-CLONING; RETROVIRUS; LYMPHOCYTES C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT HUMAN RETROVIROL,44 BINNEY ST,BOSTON,MA 02115. FU NCI NIH HHS [R01CA36974] NR 39 TC 11 Z9 11 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 JUN PY 1992 VL 188 IS 2 BP 618 EP 627 DI 10.1016/0042-6822(92)90516-R PG 10 WC Virology SC Virology GA HU511 UT WOS:A1992HU51100022 PM 1585637 ER PT J AU PARK, SS WALKER, W AOYAMA, T LAPENSON, DP WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV AF PARK, SS WALKER, W AOYAMA, T LAPENSON, DP WAXMAN, DJ GONZALEZ, FJ GELBOIN, HV TI MONOCLONAL-ANTIBODIES TO RAT-LIVER MICROSOMAL CYTOCHROME-B5 SO BIOCHEMICAL PHARMACOLOGY LA English DT Article ID FISH STENOTOMUS-CHRYSOPS; CATALYTIC ACTIVITY; PURIFICATION; METABOLISM; FORMS; CARCINOGENESIS; SEQUENCE; ENZYMES; TISSUES; CDNA AB Hybridomas obtained by the fusion of spleen cells from rat cytochrome b5-immunized mice with mouse myeloma cells produced five groups of monoclonal antibodies (MAbs) with three mouse immunoglobulin subtypes: IgG1, IgG2b and IgM. All of the MAbs bound strongly to rat cytochrome b5 as measured by radioimmunoassay (RIA). Four clones of MAbs were also strongly immunoreactive with cytochrome b5 when tested by Western blotting, but only one of the MAbs (1-39-2) weakly immunoprecipitated cytochrome b5 in an Ouchterlony double-immunodiffusion test. Two of the MAbs partially inhibited cytochrome b5-mediated NADH cytochrome c reduction catalyzed by liver microsomes (24-36%). Expression of immunodetectable cytochrome b5 was highest in the liver, next highest in the kidney, and quite low in the other tissues examined with MAb 1-17-1 by Western blotting. This MAb recognized homologous cytochrome b5 of human liver microsomes and in homogenates of TK- cells infected with recombinant vaccinia virus encoding human cytochrome b5. These MAbs to cytochrome b5 will be useful for the identification, quantification, and purification of cytochrome b5 from animal and human tissues, and for understanding its role in cytochrome P450 catalyzed drug metabolism and carcinogen activation with respect to tissue, organ and individual differences. C1 NCI,MOLEC CARCINOGENESIS LAB,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. NR 32 TC 3 Z9 3 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0006-2952 J9 BIOCHEM PHARMACOL JI Biochem. Pharmacol. PD MAY 28 PY 1992 VL 43 IS 10 BP 2201 EP 2208 DI 10.1016/0006-2952(92)90179-M PG 8 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HZ254 UT WOS:A1992HZ25400020 PM 1599506 ER PT J AU EZEKOWITZ, RAB MULLIKEN, JB FOLKMAN, J AF EZEKOWITZ, RAB MULLIKEN, JB FOLKMAN, J TI INTERFERON ALFA-2A THERAPY FOR LIFE-THREATENING HEMANGIOMAS OF INFANCY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID ACQUIRED IMMUNODEFICIENCY SYNDROME; VASCULAR MALFORMATIONS; KAPOSIS SARCOMA; CHILDREN; MANAGEMENT; CYCLOPHOSPHAMIDE; CLASSIFICATION; EMBOLIZATION; INHIBITION; DISEASE AB Background and Methods. Most hemangiomas are small, harmless birthmarks that appear soon after birth, proliferate for 8 to 18 months, and then slowly regress over the next 5 to 8 years, leaving normal or slightly blemished skin. In rare cases, hemangiomas can endanger vital structures, with a mortality of up to 60 percent. About a third of these life-threatening hemangiomas respond to treatment with corticosteroids, but for the others there is no safe and effective treatment. We evaluated the effects of daily subcutaneous injections of interferon alfa-2a (up to 3 million units per square meter of body-surface area) in 20 neonates and infants with life-threatening or vision-threatening hemangiomas that failed to respond to corticosteroid therapy. Results. In 18 of the 20 patients the hemangiomas regressed by 50 percent or more after an average of 7.8 months of treatment (range, 2 to 13). One infant died of refractory proliferation of a lesion and consumptive coagulopathy. The condition of three other patients who had large hemangiomas associated with consumptive coagulopathies that were unresponsive to conventional therapies stabilized after seven days of treatment with interferon alfa-2a alone. Transient side effects of treatment with interferon alfa-2a included fever, neutropenia (one patient), and skin necrosis (one patient). No long-term toxicity has been observed after a mean follow-up of 16 months. Conclusions. Interferon alfa-2a appears to induce the early regression of life-threatening corticosteroid-resistant hemangiomas of infancy. C1 CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT ANAT & CELLULAR BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DIV PLAST SURG,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DIV HEMATOL & ONCOL,BOSTON,MA 02115. RP EZEKOWITZ, RAB (reprint author), CHILDRENS HOSP MED CTR,DANA FARBER CANC INST,DEPT PEDIAT,ENDERS BLDG,7TH FL,BOSTON,MA 02115, USA. FU NCRR NIH HHS [M01 RR02172] NR 39 TC 720 Z9 739 U1 0 U2 6 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 28 PY 1992 VL 326 IS 22 BP 1456 EP 1463 DI 10.1056/NEJM199205283262203 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HV469 UT WOS:A1992HV46900003 PM 1489383 ER PT J AU MANKIN, HJ AF MANKIN, HJ TI CURRENT CONCEPTS - NONTRAUMATIC NECROSIS OF BONE (OSTEONECROSIS) SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID SYSTEMIC LUPUS-ERYTHEMATOSUS; TOTAL HIP-REPLACEMENT; FEMORAL-HEAD; AVASCULAR NECROSIS; RENAL-TRANSPLANTATION; STEROID-THERAPY; FOLLOW-UP; DISEASE; SCINTIGRAPHY; DIAGNOSIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MANKIN, HJ (reprint author), MASSACHUSETTS GEN HOSP,ORTHOPAED SERV,FRUIT ST,BOSTON,MA 02114, USA. NR 73 TC 445 Z9 468 U1 2 U2 16 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 28 PY 1992 VL 326 IS 22 BP 1473 EP 1479 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HV469 UT WOS:A1992HV46900006 PM 1574093 ER PT J AU PAPOULAS, O WILLIAMS, NG KINGSTON, RE AF PAPOULAS, O WILLIAMS, NG KINGSTON, RE TI DNA-BINDING ACTIVITIES OF C-MYC PURIFIED FROM EUKARYOTIC CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID AVIAN MYELOCYTOMATOSIS VIRUS; LOOP-HELIX PROTEINS; LEUCINE ZIPPER; NUCLEAR-LOCALIZATION; TRANSCRIPTION FACTOR; SEX DETERMINATION; GENE FAMILY; EXPRESSION; ONCOGENE; SEQUENCE AB c-Myc is a nuclear phosphoprotein which contains both a leucine zipper and a helix-loop-helix dimerization motif. These are adjacent to a basic region believed to make specific contacts with DNA upon dimerization. We report the purification of full-length c-Myc to near homogeneity from two independent eukaryotic systems: the baculovirus overexpression system using an insect cell host, and Chinese hamster ovary cells containing heat-inducible c-myc genes. The DNA binding capabilities of these preparations were characterized. Both preparations contain two distinct activities that bind specifically to sequences with a core of CACGTG. The Myc protein is solely responsible for one of these binding activities. Specific sequences that bound to c-Myc were selected from a large pool of random DNA sequence. Sequencing of individual binding sites selected by this procedure yielded a 12-base consensus, PuACCACGTGCTC, for c-Myc binding. Both protein preparations additionally demonstrated a distinct complex, containing both c-Myc and a copurifying 26-29-kDa protein, that bound to DNA with higher affinity than Myc alone. Selection of specific DNA sequences by this complex revealed a consensus binding site similar to the 12-base consensus described above. These data demonstrate that c-Myc isolated from eukaryotic cells is capable of sequence-specific DNA binding and further refine the optimal sequence for c-Myc binding. These protein preparations should prove useful in further characterizing the biochemical properties of c-Myc. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,WELLMAN 10,FRUIT ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,PROGRAM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 60 TC 49 Z9 50 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 MAY 25 PY 1992 VL 267 IS 15 BP 10470 EP 10480 PG 11 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000042 PM 1587829 ER PT J AU ABBOTT, AM BUENO, R PEDRINI, MT MURRAY, JM SMITH, RJ AF ABBOTT, AM BUENO, R PEDRINI, MT MURRAY, JM SMITH, RJ TI INSULIN-LIKE GROWTH FACTOR-I RECEPTOR GENE STRUCTURE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID MESSENGER-RNA; SEQUENCE; PROMOTER; FAMILY AB The insulin-like growth factor I (IGF I) receptor is a tyrosine kinase-containing transmembrane protein that plays an important role in cell growth control. We have isolated and characterized human genomic DNA clones containing the entire coding sequence of the IGF I receptor. Results of restriction analysis and sequencing of multiple overlapping clones were consistent with the existence of a single IGF I receptor gene. The complete receptor coding sequence is contained in 21 exons. There is striking homology with the insulin receptor gene in overall size (approximately 100 kilobases) and in the number and size of individual exons. An exon analogous to the alternatively spliced exon 11 of the insulin receptor gene could not be detected. An alternative internal splice site corresponding to a known alternatively spliced mRNA transcript was shown to be located at the 5' end of exon 14. Knowledge of the structure of the IGF I receptor gene should facilitate further studies on the structural determinants of receptor function, the relationships between insulin and IGF I receptors, and the molecular basis for multiple IGF I receptor species. C1 JOSLIN DIABET CTR,DIV RES,ELLIOT P JOSLIN RES LAB,1 JOSLIN PL,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK36836, DK07260]; NIGMS NIH HHS [GM36428] NR 26 TC 109 Z9 118 U1 0 U2 2 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 25 PY 1992 VL 267 IS 15 BP 10759 EP 10763 PG 5 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV090 UT WOS:A1992HV09000083 PM 1316909 ER PT J AU ZHANG, DX LIPTON, SA AF ZHANG, DX LIPTON, SA TI L-HOMOCYSTEIC ACID SELECTIVELY ACTIVATES N-METHYL-D-ASPARTATE RECEPTORS OF RAT RETINAL GANGLION-CELLS SO NEUROSCIENCE LETTERS LA English DT Article DE EXCITATORY AMINO ACID; RODENT RETINAL GANGLION CELL; PATCH-CLAMP ID RABBIT RETINA; RESPONSES; GLUTAMATE; INVITRO; NEURONS; TRANSMITTER; AGONIST AB To explore the possible role Of L-homocysteic acid (HCA) as a retinal transmitter, whole-cell recordings with patch electrodes were performed on isolated rat retinal ganglion cells (RGCs) in culture. HCA elicited an inward current at -60 mV. Similar to currents evoked at this potential in RGCs by N-methyl-D-aspartate (NMDA), HCA-activated currents were of relatively small amplitude (10-150 pA), and the noise level increased dramatically during the response. When HCA was co-applied with concentrations of NMDA that elicited a maximal response, the current was not increased over that of NMDA alone. HCA-evoked currents were almost completely blocked by the NMDA antagonists D-2-amino-5-phosphonovalerate (D-AP5), Mg2+, or 7-chlorokynurenate (7-Cl KYN). Unlike its effects on other preparations, even millimolar concentrations of HCA did not activate kainate- like currents. These observations suggest that HCA specifically activates the NMDA receptor-channel complex of rat RGCs. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT NEUROL,CELLULAR & MOLEC NEUROSCI LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY05477-08] NR 23 TC 16 Z9 16 U1 0 U2 0 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD MAY 25 PY 1992 VL 139 IS 2 BP 173 EP 177 DI 10.1016/0304-3940(92)90545-I PG 5 WC Neurosciences SC Neurosciences & Neurology GA HW694 UT WOS:A1992HW69400008 PM 1351663 ER PT J AU WALL, C HARRIS, LR LATHAN, CE AF WALL, C HARRIS, LR LATHAN, CE TI INTERACTIONS BETWEEN OTOLITHS AND VISION REVEALED BY THE RESPONSE TO Z-AXIS LINEAR MOVEMENTS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID MOTION C1 YORK UNIV, DEPT PSYCHOL, N YORK M3J 1P3, ONTARIO, CANADA. MIT, DEPT PSYCHOL, CAMBRIDGE, MA 02139 USA. RP WALL, C (reprint author), MASSACHUSETTS EYE & EAR INFIRM, VESTIBULAR TESTING LAB, BOSTON, MA 02114 USA. NR 6 TC 1 Z9 1 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 22 PY 1992 VL 656 BP 898 EP 900 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM221 UT WOS:A1992JM22100093 PM 1599214 ER PT J AU NORRIS, CM GOODMAN, ML WEBER, AL SCULLY, RE JOSEPH, MP DEMIRJIAN, ZN SEIDEN, MV AF NORRIS, CM GOODMAN, ML WEBER, AL SCULLY, RE JOSEPH, MP DEMIRJIAN, ZN SEIDEN, MV TI A 65-YEAR-OLD MAN WITH A MASS THAT INVOLVED THE BASE OF THE SKULL - MULTIPLE-MYELOMA, PRESENTING AS PLASMACYTOMA OF BONE EXTENDING INTO SPHENOID SINUS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID PARA-NASAL SINUSES; EXTRA-MEDULLARY PLASMACYTOMA; CAVERNOUS SINUS; PITUITARY-ADENOMA; MR FINDINGS; FEATURES; TUMORS; CT; ESTHESIONEUROBLASTOMA; CHONDROSARCOMAS C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,HEAD & NECK ONCOL CLIN,BOSTON,MA 02115. HARVARD UNIV,SCH MED,OTOLARYNGOL,BOSTON,MA 02115. RP NORRIS, CM (reprint author), NEW ENGLAND DEACONESS HOSP,DIV OTOLARYNGOL HEAD & NECK SURG,BOSTON,MA 02215, USA. NR 62 TC 10 Z9 10 U1 0 U2 2 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 21 PY 1992 VL 326 IS 21 BP 1417 EP 1424 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HU890 UT WOS:A1992HU89000008 ER PT J AU FERRUCCI, JT AF FERRUCCI, JT TI CLINICAL PROBLEM-SOLVING - TRAPPED BY AN INCIDENTAL FINDING SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP FERRUCCI, JT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 1 Z9 1 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 MAY 21 PY 1992 VL 326 IS 21 BP 1432 EP 1432 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HU890 UT WOS:A1992HU89000024 PM 1569988 ER PT J AU TIERNEY, MR GRUBER, ML AF TIERNEY, MR GRUBER, ML TI CASE-32-1991 - TESTS FOR NEUROSYPHILIS - REPLY SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter RP TIERNEY, MR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 21 PY 1992 VL 326 IS 21 BP 1434 EP 1434 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA HU890 UT WOS:A1992HU89000031 ER PT J AU KOPANS, DB AF KOPANS, DB TI DETECTING BREAST-CANCER NOT VISIBLE BY MAMMOGRAPHY SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID GD-DTPA; SEQUENCES; DENSITY RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,15 FRUIT ST,BOSTON,MA 02114, USA. NR 21 TC 13 Z9 13 U1 0 U2 0 PU NATL CANCER INSTITUTE PI BETHESDA PA 9030 OLD GEORGETOWN RD, BETHESDA, MD 20814 SN 0027-8874 J9 J NATL CANCER I JI J. Natl. Cancer Inst. PD MAY 20 PY 1992 VL 84 IS 10 BP 745 EP 747 DI 10.1093/jnci/84.10.745 PG 3 WC Oncology SC Oncology GA HU582 UT WOS:A1992HU58200003 PM 1573658 ER PT J AU COLEY, CM FIELD, TS ABRAHAM, SA BOUCHER, CA EAGLE, KA AF COLEY, CM FIELD, TS ABRAHAM, SA BOUCHER, CA EAGLE, KA TI USEFULNESS OF DIPYRIDAMOLE-THALLIUM SCANNING FOR PREOPERATIVE EVALUATION OF CARDIAC RISK FOR NONVASCULAR SURGERY SO AMERICAN JOURNAL OF CARDIOLOGY LA English DT Article ID PERIPHERAL VASCULAR-SURGERY; NONCARDIAC SURGERY; SURGICAL-PROCEDURES; REDISTRIBUTION; MORBIDITY; DISEASE; INDEX AB The ability to stratify cardiac risk before nonvascular surgery using clinical markers and dipyridamole-thallium scanning (DTS) was assessed for patients with known or suspected coronary artery disease unable to exercise. Of 100 consecutively studied patients who proceeded to nonvascular surgery, 9 (9%) experienced greater-than-or-equal-to 1 perioperative cardiac ischemic event, including death in 2 patients (2%) and nonfatal myocardial infarction in 2 (2%). Logistic regression identified 2 clinical predictors (age > 70 years and history of heart failure), and 1 DTS (thallium redistribution) predictor of events. Of 45 patients with neither clinical variable, none (0%; 95% confidence intervals [CI] 0 to 8%) had events. Of 55 patients with greater-than-or-equal-to 1 clinical marker, 9 (16.4%; 95% CI 7 to 26%) had events. Within this subgroup, 1 of 31 patients (3.2%; 95% CI 0 to 16%) without thallium redistribution had events compared with 8 of 24 (33.3%; 95% CI 14 to 52%) with redistribution. An algorithm combining 5 independent clinical and 2 DTS predictors, derived previously in vascular surgery patients, was validated in the 100 nonvascular surgery patients. It is concluded that preoperative planar DTS is most useful to stratify selected nonvascular surgery patients at intermediate or high risk by clinical assessment. However, for almost half of those patients with known or suspected coronary artery disease, DTS may be unnecessary because of sufficiently low predictive value based on simple clinical descriptors. C1 MASSACHUSETTS GEN HOSP,DEPT MED,GEN INTERNAL MED UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,BOSTON,MA 02114. NR 28 TC 53 Z9 53 U1 0 U2 0 PU EXCERPTA MEDICA INC PI NEW YORK PA 245 WEST 17TH STREET, NEW YORK, NY 10011 SN 0002-9149 J9 AM J CARDIOL JI Am. J. Cardiol. PD MAY 15 PY 1992 VL 69 IS 16 BP 1280 EP 1285 DI 10.1016/0002-9149(92)91221-O PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HU939 UT WOS:A1992HU93900007 PM 1585860 ER PT J AU EVANS, AA LEFKOPOULOU, M MUELLER, NE AF EVANS, AA LEFKOPOULOU, M MUELLER, NE TI METHODS FOR INFERENCE ON TRANSMISSION IN SEROPREVALENCE DATA FOR MULTIPLE INFECTIONS SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Article DE CROSS-SECTIONAL STUDIES; EPIDEMIOLOGIC METHODS; HEPATITIS-B VIRUS; HEPATITIS-C VIRUS; MODELS, STATISTICAL; PREVALENCE; SEROLOGY ID NON-B-HEPATITIS; CATEGORICAL OUTCOMES; RISK-FACTORS; NON-A; VIRUS; ASSOCIATION; ANTIBODIES; MODELS AB When risk factors for an infectious disease are unknown, a method commonly employed is to investigate parallels with known infections (covariate infections). Data sets of value here are those for specified populations in which the seroprevalence of antibodies for multiple infections has been ascertained, The use of markers of covariate infections in multivariable analyses is problematic when the covariate infection is not itself an independent risk factor for the outcome of interest. In the performance of these analyses, the authors recommend the following strategy: 1) For estimates of the effects of measured risk factors on the outcome, adjustment for the covariate infection should not be done; this will avoid problems of overadjustment. 2) After control for the measured risk factors, an estimate of the "effect" of the covariate infection may be used as an indicator of the presence of unmeasured shared risk factors. 3) When shared, measured risk factors exist, the authors propose the use of methods developed for analysis of repeated measures of categorical variables to assist in inference about shared mechanisms of action of these risk factors. This analytic strategy takes advantage of the method of analogy for building understanding of transmission of new agents through their parallels with better known ones and is useful in the development of hypotheses. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT & EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. FU NIEHS NIH HHS [5T32 ES07069] NR 16 TC 6 Z9 6 U1 0 U2 0 PU JOHNS HOPKINS UNIV SCHOOL HYGIENE PUB HEALTH PI BALTIMORE PA 111 MARKET PLACE, STE 840, BALTIMORE, MD 21202-6709 SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. PD MAY 15 PY 1992 VL 135 IS 10 BP 1156 EP 1165 PG 10 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA JF484 UT WOS:A1992JF48400010 PM 1632425 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 INTRACAMERALLY INJECTED ETHACRYNIC-ACID ON INTRAOCULAR-PRESSURE IN PATIENTS WITH GLAUCOMA SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Article AB We studied the effect of ethacrynic acid on intraocular pressure in eyes with advanced open-angle glaucoma. Five to 15-mu-l of ethacrynic acid (3.3 to 9.8-mu-g) was injected intracamerally after retrobulbar anesthesia was achieved in five eyes of five patients with advanced glaucoma. Intraocular pressure before treatment ranged from 26 to 46 mm Hg with maximal medical treatment. A reduction in intraocular pressure from 9 to 31 mm Hg was observed in all patients three to 24 hours after treatment, and this effect lasted for three days, with a gradual return of intraocular pressure to pretreatment values one week after treatment. No acute corneal or anterior chamber side effects were observed and results of corneal endothelial cell counts were essentially unchanged two months after treatment. We suggest that ethacrynic acid may represent a new class of antiglaucoma medication. Intracameral administration of ethacrynic acid or a derivative might be contemplated in the future at the time of other ocular surgical procedures to treat short-term intraocular pressure increase. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,GLAUCOMA SERV,BOSTON,MA 02114. RP MELAMED, S (reprint author), TEL AVIV UNIV,SHEBA MED CTR,SACKLER FAC MED,GOLDSCHLEGER EYE INST,GLAUCOMA SERV,IL-52621 TEL HASHOMER,ISRAEL. NR 16 TC 30 Z9 32 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAY 15 PY 1992 VL 113 IS 5 BP 508 EP 512 PG 5 WC Ophthalmology SC Ophthalmology GA HR541 UT WOS:A1992HR54100004 PM 1575224 ER PT J AU MORLEY, MG FREDERICK, AR AF MORLEY, MG FREDERICK, AR TI MELTED HAPTIC AS A COMPLICATION OF THE INDIRECT OPHTHALMIC LASER DELIVERY SYSTEM SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter ID CORNEAL C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,BOSTON,MA 02114. TUFTS UNIV,NEW ENGLAND MED CTR,SCH MED,BOSTON,MA 02111. RP MORLEY, MG (reprint author), OPHTHALM CONSULTANTS BOSTON,50 STANIFORD ST,BOSTON,MA 02114, USA. NR 3 TC 7 Z9 7 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAY 15 PY 1992 VL 113 IS 5 BP 584 EP 586 PG 3 WC Ophthalmology SC Ophthalmology GA HR541 UT WOS:A1992HR54100017 PM 1575235 ER PT J AU RUBIN, PAD AF RUBIN, PAD TI ECTROPION CAUSED BY EYEGLASSES SO AMERICAN JOURNAL OF OPHTHALMOLOGY LA English DT Letter C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 1 TC 1 Z9 1 U1 0 U2 0 PU OPHTHALMIC PUBL CO PI CHICAGO PA 77 WEST WACKER DR, STE 660, CHICAGO, IL 60601 SN 0002-9394 J9 AM J OPHTHALMOL JI Am. J. Ophthalmol. PD MAY 15 PY 1992 VL 113 IS 5 BP 590 EP 591 PG 2 WC Ophthalmology SC Ophthalmology GA HR541 UT WOS:A1992HR54100021 PM 1575239 ER PT J AU KRUMHOLZ, HM DOUGLAS, PS LAUER, MS PASTERNAK, RC AF KRUMHOLZ, HM DOUGLAS, PS LAUER, MS PASTERNAK, RC TI SELECTION OF PATIENTS FOR CORONARY ANGIOGRAPHY AND CORONARY REVASCULARIZATION EARLY AFTER MYOCARDIAL-INFARCTION - IS THERE EVIDENCE FOR A GENDER BIAS SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE MYOCARDIAL INFARCTION; CORONARY ANGIOGRAPHY; CORONARY ARTERY BYPASS; SEX FACTORS; ANGIOPLASTY, TRANSLUMINAL, PERCUTANEOUS CORONARY; WOMENS HEALTH; SELECTION BIAS ID ARTERY BYPASS-SURGERY; WOMEN; MORTALITY; SEX; DISEASE; MEN AB Objective: To determine whether a gender bias exists in the selection of patients for diagnostic and therapeutic cardiovascular procedures early after myocardial infarction. Design: A retrospective cohort study. Setting: A community-based tertiary care teaching hospital. Patients: A total of 2473 consecutive patients with a principal discharge diagnosis of acute myocardial infarction and a peak creatine kinase MB fraction of at least 4%. Measurements: Comparison of men and women regarding the frequency with which they underwent various cardiac procedures. Results: Women had coronary angiography during hospitalization for myocardial infarction much less frequently than men (odds ratio, 0.55; 95% Cl, 0.46 to 0.65), but the age-adjusted rates were similar in women and men (odds ratio, 0.91; Cl, 0.75 to 1.12). An abnormal ejection fraction (< 50%) was equally frequent in women and men who underwent left ventriculography (odds ratio, 0.85; Cl, 0.56 to 1.30). Among patients who had coronary angiography, women had a significantly lower rate of severe coronary artery disease, defined as either a left main stenosis of more than 50%, three-vessel disease, or two-vessel disease with a proximal left anterior descending stenosis of more than 70% (odds ratio, 0.67; Cl, 0.48 to 0.93). When adjustments were made for age, women had percutaneous transluminal coronary angioplasty as often as men (odds ratio, 1.16; Cl, 0.83 to 1.62) but had coronary artery bypass graft surgery significantly less frequently (odds ratio, 0.58; Cl, 0.37 to 0.91). When adjustments were made for age and the severity of coronary artery disease, the difference in rates was of borderline significance (odds ratio, 0.65; Cl, 0.41 to 1.01). Conclusions: No evidence of a difference in the rate of coronary angiography early after myocardial infarction between women and men was found after age adjustment. Among patients who have cardiac catheterization early after myocardial infarction, women and men are equally likely to have angioplasty, but women are less likely than men to have coronary artery bypass surgery. C1 MASSACHUSETTS GEN HOSP,CELL BIOL UNIT,32 FRUIT ST,BOSTON,MA 02114. BETH ISRAEL HOSP,DIV CARDIOVASC,BOSTON,MA 02215. LAHEY CLIN FDN,MED CTR,CARDIOL SECT,BURLINGTON,MA 01805. RI Lauer, Michael/L-9656-2013 OI Lauer, Michael/0000-0002-9217-8177 FU NHLBI NIH HHS [HL-07374] NR 22 TC 236 Z9 240 U1 0 U2 0 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAY 15 PY 1992 VL 116 IS 10 BP 785 EP 790 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HT802 UT WOS:A1992HT80200001 PM 1567092 ER PT J AU ZIEGLER, TR YOUNG, LS BENFELL, K SCHELTINGA, M HORTOS, K BYE, R MORROW, FD JACOBS, DO SMITH, RJ ANTIN, JH WILMORE, DW AF ZIEGLER, TR YOUNG, LS BENFELL, K SCHELTINGA, M HORTOS, K BYE, R MORROW, FD JACOBS, DO SMITH, RJ ANTIN, JH WILMORE, DW TI CLINICAL AND METABOLIC EFFICACY OF GLUTAMINE-SUPPLEMENTED PARENTERAL-NUTRITION AFTER BONE-MARROW TRANSPLANTATION - A RANDOMIZED, DOUBLE-BLIND, CONTROLLED-STUDY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE BONE MARROW TRANSPLANTATION; GLUTAMINE; PARENTERAL NUTRITION; COST CONTROL ID RAT SKELETAL-MUSCLE; NITROGEN-BALANCE; LIQUID-CHROMATOGRAPHY; INTESTINAL-MUCOSA; PROTEIN-SYNTHESIS; IMMUNE-SYSTEM; RECIPIENTS; COMPLICATIONS; SURGERY; HYPERALIMENTATION AB Objective: To determine whether glutamine-supplemented parenteral nutrition improves nitrogen retention and reduces hospital morbidity compared with standard parenteral nutrition after bone marrow transplantation. Design: Double-blind, randomized, controlled clinical trial. Setting: University teaching hospital. Patients: Forty-five adults receiving allogeneic bone marrow transplants for hematologic malignancies. Intervention: Parenteral nutrition was initiated the day after bone marrow transplantation (day 1). The experimental solution was supplemented with L-glutamine (0.57 g/kg body weight per day) and provided estimated requirements for energy and protein. The control solution was a standard, glutamine-free, isonitrogenous, isocaloric formula. Measurements: Nitrogen balance was determined between days 4 and 11 in the initial 23 patients. The incidence of clinical infection and microbial colonization, time until bone marrow engraftment, indices of clinical care, and other data related to hospital morbidity were recorded for all patients. Results: The glutamine-supplemented patients (n = 24) were clinically similar to the controls (n = 21) at entrY. Nutrient intake was similar in both groups; however, nitrogen balance was improved in the glutamine-supplemented patients relative to the controls (- 1.4 +/- 0.5 g/d compared with - 4.2 +/- 1.2; P = 0.002). Fewer experimental patients developed clinical infection (three compared with nine in the control group; P = 0.041), and the incidence of microbial colonization was also significantly reduced. Hospital stay was shortened in patients receiving glutamine supplementation (29 +/-1 d compared with 36 +/- 2 d; P = 0.017). Conclusion: Patients receiving glutamine-supplemented parenteral nutrition after bone marrow transplantation had improved nitrogen balance, a diminished incidence of clinical infection, lower rates of microbial colonization, and shortened hospital stay compared with patients receiving standard parenteral nutrition. These effects occurred despite no differences between groups in the incidence of fever, antibiotic requirements, or time to neutrophil engraftment. C1 BRIGHAM & WOMENS HOSP,DEPT SURG,75 FRANCIS ST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV DIABET & METAB,BOSTON,MA 02115. JOSLIN DIABET CTR,BOSTON,MA 02215. BRIGHAM & WOMENS HOSP,SURG METAB & NUTR LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,DIV HEMATOL & ONCOL,BOSTON,MA 02115. FREE UNIV AMSTERDAM,DEPT SURG,1081 HV AMSTERDAM,NETHERLANDS. MT CLEMENS GEN HOSP,DEPT MED,MT CLEMENS,MI 48062. TUFTS UNIV,USDA,HUMAN NUTR RES CTR AGING,BOSTON,MA 02111. FU NCI NIH HHS [CA 39542]; NIGMS NIH HHS [5P50 GM36428] NR 52 TC 526 Z9 538 U1 0 U2 4 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD MAY 15 PY 1992 VL 116 IS 10 BP 821 EP 828 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HT802 UT WOS:A1992HT80200006 PM 1567096 ER PT J AU GRAZIANI, A LING, LE ENDEMANN, G CARPENTER, CL CANTLEY, LC AF GRAZIANI, A LING, LE ENDEMANN, G CARPENTER, CL CANTLEY, LC TI PURIFICATION AND CHARACTERIZATION OF HUMAN ERYTHROCYTE PHOSPHATIDYLINOSITOL 4-KINASE - PHOSPHATIDYLINOSITOL 4-KINASE AND PHOSPHATIDYLINOSITOL 3-MONOPHOSPHATE 4-KINASE ARE DISTINCT ENZYMES SO BIOCHEMICAL JOURNAL LA English DT Article ID KINASE-ACTIVITY; GROWTH-FACTOR; CELLS; POLYPHOSPHOINOSITIDES; TRANSFORMATION; PROTEINS; HEAD AB PtdIns 4-kinase has been purified 83 000-fold from human erythrocyte membranes. The major protein detected by SDS/PAGE is of molecular mass 56 kDa, and enzymic activity can be renatured from this band of the gel. The characteristics of this enzyme are similar to other type II PtdIns kinases previously described: PtdIns presented in Triton X-100 micelles is preferred as a substrate over PtdIns vesicles, the enzyme possesses a relatively low K(m) for ATP (20-mu-M), and adenosine is an effective inhibitor. A monoclonal antibody raised against bovine brain type II PtdIns 4-kinase is an effective inhibitor of the purified enzyme. PtdIns(4,5)P2 inhibits by approx. 50% when added in equimolar amounts with PtdIns; PtdIns4P has little effect on activity. A PtdIns3P 4-kinase activity has also been detected in erythrocyte lysates. Approximately two-thirds of this activity is in the cytosolic fraction and one-third in the membrane fraction. No PtdIns3P 4-kinase activity could be detected in the purified type II PtdIns 4-kinase preparation, nor could this activity be detected in a bovine brain type III PtdIns 4-kinase preparation. The monoclonal antibody that inhibits the type II PtdIns 4-kinase does not affect the PtdIns3P 4-kinase activity in the membrane fraction. The cytosolic PtdIns3P 4-kinase can be efficiently recovered from a 60%-satd.-(NH4)2SO4 precipitate that is virtually free of PtdIns 4-kinase activity. We conclude that PtdIns3P 4-kinase is a new enzyme distinct from previously characterized PtdIns 4-kinases, and that this enzyme prefers PtdIns3P over PtdIns as a substrate. C1 TUFTS UNIV,SCH MED,DEPT PHYSIOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. STANFORD UNIV,MED CTR,SCH MED,DEPT CELL BIOL,STANFORD,CA 94305. MASSACHUSETTS GEN HOSP,HEMATOL ONCOL UNIT,BOSTON,MA 02114. RI Graziani, Andrea/B-2554-2009; Cantley, Lewis/D-1800-2014 OI Graziani, Andrea/0000-0002-6302-2317; Cantley, Lewis/0000-0002-1298-7653 FU NIGMS NIH HHS [GM 36624, GM 41890, R01 GM041890] NR 26 TC 40 Z9 41 U1 0 U2 2 PU PORTLAND PRESS PI LONDON PA 59 PORTLAND PLACE, LONDON, ENGLAND W1N 3AJ SN 0264-6021 J9 BIOCHEM J JI Biochem. J. PD MAY 15 PY 1992 VL 284 BP 39 EP 45 PN 1 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HV223 UT WOS:A1992HV22300006 PM 1318025 ER PT J AU KALIN, NH SHELTON, SE TURNER, JG AF KALIN, NH SHELTON, SE TURNER, JG TI EFFECTS OF BETA-CARBOLINE ON FEAR-RELATED BEHAVIORAL AND NEUROHORMONAL RESPONSES IN INFANT RHESUS-MONKEYS SO BIOLOGICAL PSYCHIATRY LA English DT Article ID BENZODIAZEPINE RECEPTORS; DEFENSIVE BEHAVIORS; PREFRONTAL CORTEX; RAT-BRAIN; ANTAGONISM; ANXIETY; METABOLISM; ALPRAZOLAM; PRIMATES; STRESS AB We examined the effects of the inverse benzodiazepine agonist ethyl-beta-carboline-3-carboxylate (beta-CCE) oh behavioral, hormonal, and neurochemical responses in infant rhesus monkeys exposed to fearful situations. Our paradigm elicits three distinct adaptive patterns of defensive behavior. From previous work, we hypothesized that behaviors induced by attachment bond disruption are predominantly mediated by opiate systems, whereas behaviors induced by the threat of attack are mediated by benzodiazepine systems. When beta-CCE (0, 125, 250, and 500-mu-g/kg) was administered immediately after maternal separation, the 500-mu-g/kg dose increased freezing and the 250 and 500-mu-g/kg doses reduced environmental exploration. Test conditions produced increased plasma ACTH and cortisol concentrations and increased cerebrospinal fluid (CSF) concentrations of MHPG and DOPAC; beta-CCE did not further affect these metabolites. A dose of 1000-mu-g/kg of beta-CCE increased CSF concentrations of DOPAC and MHPG in infants left with their mothers. During test conditions, it further increased CSF MHPG (but not DOPAC) concentrations, and reduced cooing while increasing freezing and barking and other hostile behaviors. Our results thus confirm that benzodiazepine systems mediate threat-related behaviors and suggest that coos, which were thought to predominantly reflect the degree of distress during separation, can be modulated by the infant's level of fear. Beta-CCE also activated stress-related pituitary-adrenal hormonal systems and brain norepinephrine (NE) and dopamine (DA) systems. These effects occurred when animals remained undisturbed in their home cages with their mothers, suggesting that benzodiazepine receptors directly modulate brain NE and DA systems. C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI 53705. RP KALIN, NH (reprint author), UNIV WISCONSIN,SCH MED,DEPT PSYCHIAT,CTR CLIN SCI,600 HIGHLAND AVE,MADISON,WI 53792, USA. FU NIMH NIH HHS [R01 MH046729, MH-46729] NR 27 TC 22 Z9 22 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD MAY 15 PY 1992 VL 31 IS 10 BP 1008 EP 1019 DI 10.1016/0006-3223(92)90094-G PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA JH869 UT WOS:A1992JH86900005 PM 1324744 ER PT J AU BAKSHI, R NI, RX FADEN, AI AF BAKSHI, R NI, RX FADEN, AI TI N-METHYL-D-ASPARTATE (NMDA) AND OPIOID RECEPTORS MEDIATE DYNORPHIN-INDUCED SPINAL-CORD INJURY - BEHAVIORAL AND HISTOLOGICAL STUDIES SO BRAIN RESEARCH LA English DT Article DE DYNORPHIN; OPIOID RECEPTOR; NMDA RECEPTOR; EXCITOTOXIN; PARALYSIS; SPINAL CORD INJURY ID RAT HINDLIMB PARALYSIS; CENTRAL NERVOUS-SYSTEM; TAIL-FLICK REFLEX; BINDING-SITES; AMINO-ACIDS; NOR-BINALTORPHIMINE; BLOOD-FLOW; AUTORADIOGRAPHIC LOCALIZATION; INTRATHECAL INJECTION; NONOPIOID MECHANISMS AB Both N-methyl-D-aspartate (NMDA) and opioid receptors have been implicated in the pathophysiology of traumatic spinal cord injury and dynorphin-induced paralysis. The present studies compared the effects of the non-competitive NMDA antagonist dextrorphan (Dex) and the kappa-selective opioid antagonist nor-binaltorphimine (nor-BNI) on the acute motor deficits and chronic neuropathological alterations caused by intrathecally administered dynorphin A-(1-17) (Dyn A). Infusion of Dyn A into the rat lower thoracic spinal subarachnoid space produced acute, reversible hindlimb paresis. Histological evaluations of spinal cord sections from these animals at 2 weeks post-infusion revealed ventral grey matter necrosis, neuronal loss and gliosis as well as axonal loss in adjacent white matter; however, there was minimal alteration in serotonin immunocytochemistry caudal to the injury zone. Dex or nor-BNI pretreatment each significantly (P < 0.05) reduced, and to a similar degree, the acute motor deficits and certain histological changes associated with Dyn A administration. These findings further support the hypothesis that dynorphin-induced spinal cord injury involves both NMDA receptors and opioid receptors. C1 GEORGETOWN UNIV,MED CTR,SCH MED,OFF DEAN RES,DEPT NEUROL,MED DENT BLDG,NW 101,WASHINGTON,DC 20007. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. GEORGETOWN UNIV,SCH MED,DEPT PHARMACOL,WASHINGTON,DC 20057. VET AFFAIRS MED CTR,NEUROL SERV,SAN FRANCISCO,CA 94143. FU NINDS NIH HHS [R01 NS23422]; PHS HHS [CCR 903623] NR 68 TC 47 Z9 48 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 MAY 15 PY 1992 VL 580 IS 1-2 BP 255 EP 264 DI 10.1016/0006-8993(92)90952-6 PG 10 WC Neurosciences SC Neurosciences & Neurology GA HZ747 UT WOS:A1992HZ74700034 PM 1380394 ER PT J AU VONDEIMLING, A EIBL, RH OHGAKI, H LOUIS, DN VONAMMON, K PETERSEN, I KLEIHUES, P CHUNG, RY WIESTLER, OD SEIZINGER, BR AF VONDEIMLING, A EIBL, RH OHGAKI, H LOUIS, DN VONAMMON, K PETERSEN, I KLEIHUES, P CHUNG, RY WIESTLER, OD SEIZINGER, BR TI P53 MUTATIONS ARE ASSOCIATED WITH 17P ALLELIC LOSS IN GRADE-II AND GRADE-III ASTROCYTOMA SO CANCER RESEARCH LA English DT Note ID HUMAN-MALIGNANT ASTROCYTOMA; HUMAN GLIOBLASTOMA; HETEROZYGOSITY; CANCER; GENE; CHROMOSOME-17P; TUMORIGENESIS; ALLELOTYPE; DELETIONS; OCCUR AB Loss of genetic material on the short arm of chromosome 17 is observed in approximately 40% of human astrocytomas (WHO grades II and III) and in approximately 30% of cases of glioblastoma multiforme (WHO grade IV). Previous studies of glioblastoma multiforme have shown that the p53 gene, located on the short arm of chromosome 17, is frequently mutated in these glioblastomas. To explore whether lower-grade astrocytomas are also associated with corresponding mutations of the p53 gene, we have investigated a series of 22 human astrocytomas of WHO grades II and III both for loss of heterozygosity on chromosome 17p and for p53 mutations. Mutations in the conserved regions of the p53 gene were identified by single strand conformation polymorphism analysis of exons 5, 6, 7, and 8 and were verified by direct DNA sequencing of the polymerase chain reaction products. p53 mutations were observed in 3 of 8 grade II astrocytomas and 4 of 14 grade II astrocytomas. In all 22 tumors, allelic loss of the short arm of chromosome 17 was investigated :bv restriction fragment length polymorphism analysis. One-half of the grade II astrocytomas (4 of 8) and grade III astrocytomas (7 of 14) exhibited allelic loss on chromosome 17p. Mutations in the p53 gene were exclusively observed in tumors with allelic loss on 17p. Our results show that p53 mutations are not restricted to glioblastoma multiforme and may be important in the tumorigenesis of lower-grade astrocytomas and that p53 mutations in lower-grade astrocytomas are associated with loss of chromosome 17p. These findings are consistent with a recessive mechanism of action of p53 in WHO grade II and III astrocytoma tumorigenesis. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV ZURICH,DEPT PATHOL,NEUROPATHOL LAB,CH-8091 ZURICH,SWITZERLAND. UNIV ZURICH,DEPT NEUROSURG,CH-8091 ZURICH,SWITZERLAND. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP VONDEIMLING, A (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02129, USA. RI Eibl, Robert/C-1249-2008; von Deimling, Andreas/F-7774-2013 OI Eibl, Robert/0000-0002-6687-5286; von Deimling, Andreas/0000-0002-5863-540X FU NCI NIH HHS [1 F32 CA 09144]; NIGMS NIH HHS [2 T32 GMO 7753-12, T32 GM007753] NR 30 TC 273 Z9 274 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 15 PY 1992 VL 52 IS 10 BP 2987 EP 2990 PG 4 WC Oncology SC Oncology GA HU222 UT WOS:A1992HU22200036 PM 1349850 ER PT J AU YOSHIZUMI, M KOUREMBANAS, S TEMIZER, DH CAMBRIA, RP QUERTERMOUS, T LEE, ME AF YOSHIZUMI, M KOUREMBANAS, S TEMIZER, DH CAMBRIA, RP QUERTERMOUS, T LEE, ME TI TUMOR-NECROSIS-FACTOR INCREASES TRANSCRIPTION OF THE HEPARIN-BINDING EPIDERMAL GROWTH FACTOR-LIKE GROWTH-FACTOR GENE IN VASCULAR ENDOTHELIAL-CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID EXPRESSION; ATHEROSCLEROSIS; PATHOGENESIS; CHAIN; ACID AB Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a recently identified, potent vascular smooth muscle cell (SMC) mitogen of macrophage origin. To determine whether this gene is transcribed and regulated in vascular endothelial cells, we measured HB-EGF mRNA levels in human umbilical vein endothelial cells (HUVEC) by RNA blot analysis with an HB-EGF cDNA probe. The base-line level of HB-EFG mRNA in HUVEC in culture was low. However, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta markedly increased HB-EGF mRNA levels in HUVEC by 12- and 7-fold, respectively, and induction of the gene by TNF-alpha was both dose- and time-dependent. In response to TNF-alpha, HB-EGF mRNA levels quickly increased and peaked at 1 h, indicating that HB-EGF belongs to the family of immediate early genes. In nuclear run-off experiments, TNF-alpha increased the rate of HB-EGF gene transcription by 3.2-fold. To our knowledge this is the first demonstration that the HB-EGF gene is transcribed in vascular endothelial cells. The inducible transcription of this potent SMC mitogen gene in endothelial cells suggests that HB-EGF may have an important role in the pathogenesis of atherosclerosis. C1 MASSACHUSETTS GEN HOSP,GEN MED SERV,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. UNIV TOKYO,FAC MED,DEPT INTERNAL MED 3,TOKYO 113,JAPAN. CHILDRENS HOSP MED CTR,JOINT PROGRAM NEONATOL,BOSTON,MA 02115. NR 26 TC 132 Z9 132 U1 0 U2 4 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9467 EP 9469 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500005 PM 1577791 ER PT J AU KLEYMAN, TR COUPAYEGERARD, B ERNST, SA AF KLEYMAN, TR COUPAYEGERARD, B ERNST, SA TI ALDOSTERONE DOES NOT ALTER APICAL CELL-SURFACE EXPRESSION OF EPITHELIAL NA+ CHANNELS IN THE AMPHIBIAN CELL LINE-A6 SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CULTURED KIDNEY-CELLS; PROTEIN KINASE-C; TOAD BLADDER; SODIUM-TRANSPORT; HORMONAL-REGULATION; TIGHT EPITHELIA; AMILORIDE; SUBUNIT; MECHANISMS; A6 AB The steroid hormone aldosterone regulates reabsorptive Na+ transport across specific high resistance epithelia. The increase in Na+ transport induced by aldosterone is dependent on protein synthesis and is due, in part, to an increase in Na+ conductance of the apical membrane mediated by amiloride-sensitive Na+ channels. To examine whether an increment in the biochemical pool of Na+ channels expressed at the apical cell surface is a mechanism by which aldosterone increases apical membrane Na+ conductance, apical cell-surface proteins from the epithelial cell line A6 were specifically labeled by an enzyme-catalyzed radioiodination procedure following exposure of cells to aldosterone. Labeled Na+ channels were immunoprecipitated to quantify the biochemical pool of Na+ channels at the apical cell surface. The activation of Na+ transport across A6 cells by aldosterone was not accompanied by alterations in the biochemical pool of Na+ channels at the apical plasma membrane, despite a 3.7-4.2-fold increase in transepithelial Na+ transport. Similarly, no change in the distribution of immunoreactive protein was resolved by immunofluorescence microscopy. The oligomeric subunit composition of the channel remained unaltered, with one exception. A 75,000-Da polypeptide and a broad 70,000-Da polypeptide were observed in controls. Following addition of aldosterone, the 75,000-Da polypeptide was not resolved, and the 70,000-Da polypeptide was the major polypeptide found in this molecular mass region. Aldosterone did not alter rates of Na+ channel biosynthesis. These data suggest that neither changes in rates of Na+ channel biosynthesis nor changes in its apical cell-surface expression are required for activation of transepithelial Na+ transport by aldosterone. Post-translational modification of the Na+ channel, possibly the 75,000 or 70,000-Da polypeptide, may be one of the cellular events required for Na+ channel activation by aldosterone. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. UNIV MICHIGAN,DEPT ANAT & CELL BIOL,ANN ARBOR,MI 48109. RP KLEYMAN, TR (reprint author), UNIV PENN,DEPT MED,PHILADELPHIA,PA 19104, USA. FU NIDDK NIH HHS [DK 34933] NR 41 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 MAY 15 PY 1992 VL 267 IS 14 BP 9622 EP 9628 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500029 PM 1315763 ER PT J AU DEGASPERI, R DANIEL, PF WARREN, CD AF DEGASPERI, R DANIEL, PF WARREN, CD TI A HUMAN LYSOSOMAL ALPHA-MANNOSIDASE SPECIFIC FOR THE CORE OF COMPLEX GLYCANS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID URINARY OLIGOSACCHARIDES; GLYCOPROTEIN CATABOLISM; SWAINSONINE; ENZYME; SHEEP; 1,4-DIDEOXY-1,4-IMINO-D-MANNITOL; BIOSYNTHESIS; SEPARATION; CATTLE; KIDNEY AB A novel lysosomal alpha-mannosidase, with unique substrate specificity, has been partially purified from human spleen by chromatography through concanavalin A-Sepharose, DEAE-Sephadex, and Sephacryl S-300. This enzyme can catalyze the hydrolysis of only 1 mannose residue, that which is alpha(1 --> 6)-linked to the beta-linked mannose in the core of N-linked glycans, as found in the oligosaccharides Man-alpha(1 --> 6)[Man-alpha(1 --> 3] Man-beta(1 --> 4)GlcNAc and Man-alpha(1 --> 6)Man-beta(1 --> 4) GlcNAc. The newly described alpha-mannosidase does not catalyze the hydrolysis of mannose residues outside of the core, even if they are alpha(1 --> 6)-linked, and is not active on the other alpha-linked mannose in the core, which is (1 --> 3)-linked. The narrow specificity of the novel mannosidase contrasts sharply with that of the major lysosomal alpha-mannosidase, which is able to catalyze the degradation of oligosaccharides containing diverse linkage and branching patterns of the mannose residues. Importantly, although the major mannosidase readily catalyzes the hydrolysis of the core alpha(1 --> 3)-linked mannose, it is poorly active towards the alpha(1 --> 6)-linked mannose, i.e. the very same mannose residue for which the newly characterized mannosidase is specific. The novel enzyme is further differentiated from the major lysosomal alpha-mannosidase by its inability to catalyze the efficient hydrolysis of the synthetic substrate p-nitrophenyl alpha-mannoside, and by the strong stimulation of its activity by Co2+ and Zn2+. Similarly to the major mannosidase, it is strongly inhibited by swainsonine and 1,4-dideoxy-1,4-imino-D-mannitol, but not by deoxymannojirimycin. The presence of this novel alpha-mannosidase activity in human tissues provides the best explanation, to date, for the structures of the oligosaccharides stored in human alpha-mannosidosis. In this condition the major lysosomal alpha-mannosidase activity is severely deficient, but apparently the alpha(1 --> 6)-mannosidase is unaffected, so that the oligosaccharide structures reflect the unique specificity of this enzyme. C1 HARVARD UNIV,SCH MED,LOVETT LABS,CARBOHYDRATE UNIT,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,WALTHAM,MA 02254. FU NCRR NIH HHS [SO7 RR 05486-28]; NICHD NIH HHS [HD 16942]; NIDDK NIH HHS [DK 40930] NR 35 TC 31 Z9 31 U1 1 U2 3 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9706 EP 9712 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500041 PM 1577805 ER PT J AU DUZIC, E COUPRY, I DOWNING, S LANIER, SM AF DUZIC, E COUPRY, I DOWNING, S LANIER, SM TI FACTORS DETERMINING THE SPECIFICITY OF SIGNAL TRANSDUCTION BY GUANINE NUCLEOTIDE-BINDING PROTEIN-COUPLED RECEPTORS .1. COUPLING OF ALPHA-2-ADRENERGIC RECEPTOR SUBTYPES TO DISTINCT G-PROTEINS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID ADRENERGIC-RECEPTOR; ADENYLATE-CYCLASE; HIGH-AFFINITY; ALPHA-2B-ADRENERGIC RECEPTOR; CELL LINE; EXPRESSION; CLONING; IDENTIFICATION; SYSTEMS; BRAIN AB Alpha-2-adrenergic receptor (alpha-2-AR) subtypes couple to pertussis toxin (PT)-sensitive G-proteins to elicit both stimulatory and inhibitory cell responses. Signal specificity may be generated by the ability of the receptor subtypes to "recognize" distinct G-proteins with different affinity. To address this issue we stably expressed three alpha-2-AR subtypes, RNG-alpha-2 (alpha-2B-AR), RG10 (alpha-2C-AR), and RG20 (alpha-2D-AR), in NIH-3T3 fibroblasts, which express two PT-sensitive G-proteins (G(i-alpha-2), G(i-alpha-3), and analyzed receptor/G-protein interactions by determining: 1) functional coupling to adenylylcyclase and 2) the ability of the receptors to exist in a high affinity state for agonist. In alpha-2D-AR transfectants expressing 200 or 2,200 fmol of receptor/mg of protein, epinephrine (10-mu-M) inhibited forskolin-induced elevation of cellular cAMP by 26 +/- 4.8% and 72 +/- 6.2%, respectively. Similar results were obtained in alpha-2B-AR transfectants. However, in alpha-2C-AR transfectants (200 fmol/mg) the forskolin-induced elevation of cellular cAMP was not altered by agonist treatment. In alpha-2C-AR transfectants expressing higher receptor densities (650-1,200 fmol/mg), epinephrine inhibited the effect of forskolin by 30 +/- 3.2%. This difference in functional coupling among the alpha-2-AR subtypes is reflected at the receptor/G-protein interface. In membrane preparations of alpha-2B and alpha-2D-AR but not alpha-2c-AR transfectants, agonist competition curves were biphasic, indicating high and low affinity states of the receptor for agonist. The high affinity state was guanyl-5'-yl imidodiphosphate- and PT-sensitive, indicative of receptor/G-protein coupling. These data suggest that the alpha-2c-AR differs from the alpha-2B and alpha-2D-AR subtypes in its ability to recognize PT-sensitive G-proteins expressed in NIH-3T3 fibroblasts. The alpha-2c-AR may couple preferentially to PT-sensitive G-proteins (G(i1), G(o1,2) not expressed in NIH-3T3 fibroblasts and thereby elicit different cellular responses. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,171 ASHLEY AVE,CHARLESTON,SC 29425. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CELLULAR & MOLEC RES LAB,BOSTON,MA 02114. RI COUPRY, Isabelle/L-4900-2014 FU FIC NIH HHS [3 FO5 TW4313-02]; NINDS NIH HHS [NS-24821] NR 51 TC 73 Z9 73 U1 0 U2 1 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9844 EP 9851 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500064 PM 1349606 ER PT J AU COUPRY, I DUZIC, E LANIER, SM AF COUPRY, I DUZIC, E LANIER, SM TI FACTORS DETERMINING THE SPECIFICITY OF SIGNAL TRANSDUCTION BY GUANINE NUCLEOTIDE-BINDING PROTEIN-COUPLED RECEPTORS .2. PREFERENTIAL COUPLING OF THE ALPHA-2C-ADRENERGIC RECEPTOR TO THE GUANINE NUCLEOTIDE-BINDING PROTEIN, GO SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID PURIFIED MUSCARINIC RECEPTORS; ALPHA-2-ADRENERGIC RECEPTOR; HIGH-AFFINITY; REGULATORY PROTEINS; FUNCTIONAL RECONSTITUTION; PHOSPHOLIPID-VESICLES; MOLECULAR-CLONING; CALCIUM CHANNELS; ALPHA-SUBUNIT; HYBRID-CELLS AB Cell to cell communication by many hormones and neurotransmitters involves three major entities: receptor (R), G-protein (G), and effector molecule (E). Plasticity in this system is conferred by the existence of each entity as isoforms or closely related subtypes that are expressed in a tissue-specific and developmentally regulated manner. Factors that determine signal specificity in this system are poorly understood. Such factors include the relative affinity and stoichiometry of R-G or G-E and the possible colocalization of R-G-E in cellular microdomains. Utilizing the alpha-2-adrenergic receptor (alpha-2-AR) system as a representative subfamily of this class of signal transducers, we determined the relative importance of these factors. By analysis of R-G coupling in mammalian cells cotransfected With alpha-2-AR genes and G(alpha) cDNA, we demonstrate preferential coupling between an alpha-2-AR subtype and G(o). Our data implicate R-G affinity as an important determinant of signal transduction specificity and indicate that a critical level of G(o-alpha) is required for coupling. This report indicates the utility of R-G cotransfection in mammalian cells as a "natural environment model" to characterize events occurring at the R-G and G-E interface. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CELLULAR & MOLEC RES LAB,BOSTON,MA 02114. RI COUPRY, Isabelle/L-4900-2014 FU FIC NIH HHS [3 FO5 TW4313]; NINDS NIH HHS [NS-24821] NR 46 TC 37 Z9 37 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 15 PY 1992 VL 267 IS 14 BP 9852 EP 9857 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT965 UT WOS:A1992HT96500065 PM 1349607 ER PT J AU ROCK, KL ROTHSTEIN, L FLEISCHACKER, C GAMBLE, S AF ROCK, KL ROTHSTEIN, L FLEISCHACKER, C GAMBLE, S TI INHIBITION OF CLASS-I AND CLASS-II MHC-RESTRICTED ANTIGEN PRESENTATION BY CYTOTOXIC LYMPHOCYTES-T SPECIFIC FOR AN EXOGENOUS ANTIGEN SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MONOCLONAL-ANTIBODY; SOLUBLE-PROTEIN; CELL HYBRIDOMAS; RECOGNITION; INDUCTION; RESPONSIVENESS; GENERATION; MECHANISM; RECEPTORS AB Ag in the extracellular fluids can be internalized, processed, and presented in association with class I MHC molecules on specialized APC in normal spleen. We examine the fate of these APC after they present Ag to a CTL. When splenocytes present exogenous OVA to CTL, their ability to subsequently present native Ag in association with both class I and class II molecules is inhibited. CTL do not inhibit the ability of splenocytes to present processing independent peptides with class I or class II molecules. Inhibition of Ag presentation is only observed in the presence of the specific Ag recognized by the CTL. This inhibition is MHC-restricted. In the presence of specific Ag, CTL inhibit the ability of APC to present unrelated Ag. However, bystander APC are not affected by activated CTL. Taken together these results indicate that when APC present exogenous Ag to CTL, they are inhibited or killed. The CTL that mediates this activity has a conventional CD4-CD8+ phenotype and utilizes a TCR-alpha-beta. The potential significance of these findings and their possible relationship to phenomena associated with Ts cells are discussed. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ROCK, KL (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115, USA. FU NIAID NIH HHS [AI-20248] NR 36 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 MAY 15 PY 1992 VL 148 IS 10 BP 3028 EP 3033 PG 6 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600008 PM 1578128 ER PT J AU WANG, Y SMITH, JA GEFTER, ML PERKINS, DL AF WANG, Y SMITH, JA GEFTER, ML PERKINS, DL TI IMMUNODOMINANCE - INTERMOLECULAR COMPETITION BETWEEN MHC CLASS-II MOLECULES BY COVALENTLY LINKED T-CELL EPITOPES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; ANTIGEN-BINDING SITE; RECOGNITION; HYBRIDOMAS; IA; PEPTIDES; IDENTIFICATION; PROLIFERATION; DETERMINANT; CAPACITY AB The T cell response to complex protein Ag typically focuses on a few, and frequently a single, immunodominant epitope. Several groups have proposed that the mechanism of immunodominance is determined by the steps of Ag processing and presentation including protein unfolding, the sites of proteolytic cleavage, and the affinity of binding to MHC molecules. Also, the failure of the TCR repertoire to recognize MHC-bound peptides, termed a hole in the repertoire, can prevent recognition of a potentially dominant processed peptide. In the present study, we demonstrate that immunodominance can be determined by intermolecular competition for binding to MHC class II molecules between covalently linked T cell epitopes. In addition, we have analyzed the factors controlling T cell recognition of the covalently linked epitopes. In our system, T cell recognition of the dominant epitope is not altered by Ag processing, and is not simply a function of MHC-binding affinity. We propose that adjacent sequences can subtly alter the conformation of an epitope, creating significant changes in T cell recognition. These observations are discussed in terms of the mechanisms of immunodominance and in terms of the development of synthetic peptide vaccines. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP PERKINS, DL (reprint author), BRIGHAM & WOMENS HOSP,IMMUNOGENET & TRANSPLANTAT LAB,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK01693] NR 32 TC 33 Z9 33 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3034 EP 3041 PG 8 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600009 PM 1578129 ER PT J AU PIKE, MC COSTELLO, KM LAMB, KA AF PIKE, MC COSTELLO, KM LAMB, KA TI IL-8 STIMULATES PHOSPHATIDYLINOSITOL-4-PHOSPHATE KINASE IN HUMAN POLYMORPHONUCLEAR LEUKOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NEUTROPHIL CHEMOTACTIC FACTOR; ACTIVATING FACTOR; RABBIT NEUTROPHILS; GENE-EXPRESSION; HUMAN-MONOCYTES; FACTOR MDNCF; RECEPTOR; PEPTIDE; CELLS; DIACYLGLYCEROL AB IL-8 is a neutrophil-specific chemoattractant and cellular activator which exists in at least three forms, 69, 72, and 77 amino acids. The predominant monocyte product has 72 amino acids, whereas endothelial cells secrete the 77-amino acid form. The 72-amino acid form has been shown to increase intracellular calcium in neutrophils, but the exact biochemical pathways involved in stimulation of these cells is unknown. N-formyl peptide chemoattractants in neutrophils stimulate the formation of phosphatidylinositol-4,5-bisphosphate (PIP2), a reservoir for second messenger molecules and regulator of actin assembly through its association with the actin-binding proteins, profilin, and gelsolin. The present study examined. whether IL-8 altered the enzyme which synthesizes PIP2, phosphatidylinositol-4-phosphate (PIP) kinase. Incubation of intact neutrophils with 10 nM IL-8 caused approximately a twofold increase in the activity of the enzyme. All forms of IL-8 stimulated PIP kinase activity in concentrations ranging from 1 to 50 nM, and the dose-response curves exactly correlated with the order of potency of these cytokines for interacting with the IL-8R on the surface of neutrophils. Lineweaver-Burk analysis of the kinetics of PIP kinase assayed in the presence of 0.03 to 0.7 MM ATP showed that 10 nM IL-8 increased the V(max) of the enzyme 38 to 70.5%, with no significant change in the apparent K(m) for ATP or for PIP. The stimulation of PIP kinase activity could not be explained by decreased degradation of PIP2 by phospholipase C or phosphomonoesterase activity in the membranes isolated from cells treated with IL-8 or by a decrease in the degradation of ATP. The microfilament disruptor, cytochalasin b, inhibited IL-8 induced stimulation of PIP kinase. These findings demonstrate that all forms of IL-8 stimulate PIP kinase in human neutrophils. This event may provide molecular signals to these cells that are necessary to maintain or change the state of microfilament assembly during cellular activation. RP PIKE, MC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ARTHRITIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. FU NIAID NIH HHS [P01 AI28465, R01 AI28386] NR 41 TC 13 Z9 13 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3158 EP 3164 PG 7 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600027 PM 1315831 ER PT J AU SUNDT, TM LEGUERN, C GERMANA, S SMITH, CV NAKAJIMA, K LUNNEY, JK SACHS, DH AF SUNDT, TM LEGUERN, C GERMANA, S SMITH, CV NAKAJIMA, K LUNNEY, JK SACHS, DH TI CHARACTERIZATION OF A POLYMORPHISM OF CD4 IN MINIATURE SWINE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CLASS-II MHC; MONOCLONAL-ANTIBODIES; T-CELLS; SIGNAL TRANSDUCTION; EPITOPE; HETEROGENEITY; LYMPHOCYTES; ANTIGENS; BINDING; OKT4 AB A polymorphism of CD4 in miniature swine has been identified by failure of cells from some animals to react with mAb 74-12-4. The phenotypic, molecular genetic, and functional characteristics of these animals have been defined. Cells from heterozygous animals bear approximately 50% the number of 74-12-4-reactive molecules on their surface as do cells from animals homozygous for the wild type. Animals of both phenotypes demonstrate similar flow cytometric profiles for CD8+ T cells. Northern blot analysis confirms the presence of mRNA for CD4 among PBL of animals failing to stain with 74-12-4. CD4 allelism is confirmed by Southern blot analysis, revealing RFLP. Function of the CD4 subset in vivo, as demonstrated by antibody production against a T cell-dependent Ag, is similar between animals of both phenotypes. Proliferative responses to PHA and alloantigen stimulation by a full haplotype mismatch or a class II mismatch alone are equivalent for animals of both phenotypes. These data suggest that the allelic form of CD4, designated CD4.2 in contrast to the wild-type CD4.1, is capable of performing normally as an accessory molecule in the generation of immune responses. Furthermore, antixenogeneic responses to C57B10.BR were equivalent, suggesting that both CD4 molecular types may be capable of interacting with xenogeneic class II molecules. Although the polymorphism includes differences in exons 3 and 4, regions thought to encode portions of the molecule interacting with MHC class II, these results imply that this naturally occurring CD4 polymorphism does not affect the interaction with class II molecules. C1 MASSACHUSETTS GEN HOSP,TRANSPLANTAT BIOL RES CTR,MGH E,BLDG 149,13TH ST,BOSTON,MA 02129. NCI,IMMUNOL BRANCH,TRANSPLANTAT BIOL SECT,BETHESDA,MD 20892. NR 29 TC 15 Z9 17 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3195 EP 3201 PG 7 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600032 PM 1578144 ER PT J AU HOLLSBERG, P WUCHERPFENNIG, KW AUSUBEL, LJ CALVO, V BIERER, BE HAFLER, DA AF HOLLSBERG, P WUCHERPFENNIG, KW AUSUBEL, LJ CALVO, V BIERER, BE HAFLER, DA TI CHARACTERIZATION OF HTLV-I INVIVO INFECTED T-CELL CLONES - IL-2-INDEPENDENT GROWTH OF NONTRANSFORMED T-CELLS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID TROPICAL SPASTIC PARAPARESIS; PEPTIDYL-PROLYL ISOMERASE; RECEPTOR GENE-EXPRESSION; VIRUS TYPE-I; LEUKEMIA-VIRUS; IMMUNOSUPPRESSANT FK506; IL-2 RECEPTOR; LYMPHOCYTES-T; MULTIPLE-SCLEROSIS; MACROLIDES FK-506 AB Mononuclear cells from subjects infected with human T lymphotropic virus type I (HTLV-1) display a unique ability to proliferate in vitro in the absence of mitogens or exogenous growth factors. Subjects who have developed an HTLV-I-associated myelopathy (HAM) show an even higher degree of spontaneous proliferation concomitant with transcription of the HTLV-I provirus. The mechanism underlying HTLV-I-induced T cell activation was investigated by characterizing a series of HTLV-I-infected T cell clones generated from the blood of subjects with HAM. Approximately 15% of the T cell clones generated were HTLV-I infected as determined by polymerase chain reaction and Southern blotting. Infected T cell clones displayed altered growth kinetics as they continued to incorporate tritiated thymidine 7 to 14 days after stimulation, a time when noninfected T cell clones had returned to a resting state. This was not due to transformation as all the T cell clones required periodic restimulation with mitogens and feeder cells for continued growth. Although HTLV-I-infected T cell clones showed increased expression of the IL-2 receptor p55 chain, the spontaneous clonal proliferation was not inhibited by anti-IL-2 receptor mAb. Moreover, the spontaneous clonal proliferation was insensitive to cyclosporin A and FK 506 while being highly sensitive to rapamycin, which is known to inhibit IL-2-mediated signaling. Together these results demonstrate that IL-2 is not required for the HTLV-I-induced spontaneous clonal proliferation and further suggest that HTLV-I may induce signaling pathways replacing an IL-2 receptor signal proximal to the site of action of rapamycin. C1 HARVARD UNIV,DANA FARBER CANC INST,DIV PEDIAT ONCOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,DEPT MED,DIV HEMATOL,BOSTON,MA 02115. RP HOLLSBERG, P (reprint author), BRIGHAM & WOMENS HOSP,CTR NEUROL DIS,DEPT MED,DIV NEUROL,221 LONGWOOD AVE,BOSTON,MA 02115, USA. RI Calvo, Victor/L-5024-2014 OI Calvo, Victor/0000-0002-5913-7058 NR 44 TC 72 Z9 72 U1 0 U2 1 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3256 EP 3263 PG 8 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600041 PM 1374452 ER PT J AU STAUNTON, DE GAUR, A CHAN, PY SPRINGER, TA AF STAUNTON, DE GAUR, A CHAN, PY SPRINGER, TA TI INTERNALIZATION OF A MAJOR GROUP HUMAN RHINOVIRUS DOES NOT REQUIRE CYTOPLASMIC OR TRANSMEMBRANE DOMAINS OF ICAM-1 SO JOURNAL OF IMMUNOLOGY LA English DT Article ID INTERCELLULAR-ADHESION MOLECULE-1; INDUCED CONFORMATIONAL CHANGE; HUMAN-IMMUNODEFICIENCY-VIRUS; SEMLIKI-FOREST VIRUS; HEP-2 CELLS; RECEPTOR; LIGAND; MEMBRANE; LFA-1; IMMUNOGLOBULIN AB Intercellular adhesion molecule-1 (CD54), a cell adhesion molecule and the receptor for the major group of rhinoviruses, is a class 1 membrane protein with five Ig-like domains in its extracellular region, a transmembrane domain, and a short cytoplasmic domain. The amino-terminal domains (D1 and D2) are sufficient for virus binding and the first is most important (1). We have investigated whether other extracellular domains, transmembrane or cytoplasmic domains are required for virus entry as determined by postinfection virion protein biosynthesis. We demonstrate that cytoplasmic, transmembrane, and Ig-like domains 3, 4, and 5 are not essential for rhinovirus entry into transfected COS cells. The efficiency of rhinovirus infection directly correlates with the efficiency of rhinovirus binding and a form of intercellular adhesion molecule-1 that is glycophosphatidylinositol anchored, and thus does not extend into the inner leaflet of the membrane bilayer or the cytoplasm efficiently supports virus entry. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STAUNTON, DE (reprint author), CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115, USA. FU NIAID NIH HHS [1 UO1 AI31921] NR 30 TC 48 Z9 48 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 15 PY 1992 VL 148 IS 10 BP 3271 EP 3274 PG 4 WC Immunology SC Immunology GA HU686 UT WOS:A1992HU68600043 PM 1349619 ER PT J AU NGUYEN, TV KOSOFSKY, BE BIRNBAUM, R COHEN, BM HYMAN, SE AF NGUYEN, TV KOSOFSKY, BE BIRNBAUM, R COHEN, BM HYMAN, SE TI DIFFERENTIAL EXPRESSION OF C-FOS AND ZIF268 IN RAT STRIATUM AFTER HALOPERIDOL, CLOZAPINE, AND AMPHETAMINE SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MESSENGER-RNA; GROWTH-FACTORS; GENE; NEURONS; ACTIVATION; ENCODES; BINDING; D1 AB Antipsychotic drugs are monoamine receptor antagonists. However, the mechanisms by which these direct actions are translated into therapeutic effects are unknown. Candidate mechanisms include receptor-mediated regulation of gene expression in target neurons. Inducible transcription factors, including certain immediate early genes (IEGs), may mediate between receptor-activated second messenger systems and expression of genes involved in the differentiated functions of neurons. We examined the specificity of induction of the IEGs c-fos and zif268 after acute administration of several antipsychotic drugs and, for comparison, the stimulant amphetamine, which has pharmacologic effects relatively opposite to those of antipsychotics. Antipsychotic drugs with potent dopamine D2 receptor antagonist properties, such as haloperidol, induced both c-fos and zif268 mRNA in the caudate-putamen; however, the atypical antipsychotic drug clozapine induced zif268 but not c-fos mRNA in that region. Similarly, haloperidol, but not clozapine, induced c-Fos-like immunoreactivity in the caudate-putamen. In contrast, both drugs induced c-Fos-like immunoreactivity in the nucleus accumbens. Like haloperidol, amphetamine induced both c-fos and zif268 mRNA in the caudate-putamen, but the anatomic patterns of induction of c-Fos-like immunoreactivity by the two drugs were dramatically different. Haloperidol and amphetamine induced AP-1 binding activity in cell extracts from the caudate-putamen, indicating that drug-induced IEG expression results in protein products that may function in the regulation of target gene expression. Thus these data demonstrate that inductions of IEG expression by haloperidol, clozapine, and amphetamine are specific, may be biologically relevant, and suggest avenues for further investigation. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. MCLEAN HOSP,MAILMAN RES CTR,BELMONT,MA 02178. RP NGUYEN, TV (reprint author), MASSACHUSETTS GEN HOSP,MOLEC NEUROBIOL LAB,BOSTON,MA 02114, USA. FU NIDA NIH HHS [DA07134]; NIMH NIH HHS [MH00892, MH42543] NR 19 TC 327 Z9 328 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 MAY 15 PY 1992 VL 89 IS 10 BP 4270 EP 4274 DI 10.1073/pnas.89.10.4270 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700011 PM 1374894 ER PT J AU HOCHSTENBACH, F DAVID, V WATKINS, S BRENNER, MB AF HOCHSTENBACH, F DAVID, V WATKINS, S BRENNER, MB TI ENDOPLASMIC-RETICULUM RESIDENT PROTEIN OF 90 KILODALTONS ASSOCIATES WITH THE T-CELL AND B-CELL ANTIGEN RECEPTORS AND MAJOR HISTOCOMPATIBILITY COMPLEX ANTIGENS DURING THEIR ASSEMBLY SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MOLECULAR CHAPERONE ID GLUCOSE-REGULATED PROTEIN; CHAIN BINDING-PROTEIN; HEAT-SHOCK; MONOCLONAL-ANTIBODY; ALPHA-CHAIN; EXPRESSION; GLYCOPROTEIN; POLYPEPTIDE; HYBRIDOMAS; SUBUNIT AB In the endoplasmic reticulum (ER), newly synthesized subunits of the T-cell antigen receptor (TCR), membrane-bound immunoglobulin (mIg), and major histocompatibility complex (MHC) class I antigens must fold correctly and assemble completely into multimeric protein complexes prior to transport to the cell surface. Although folding and assembly may occur spontaneously, the concept that molecular chaperones facilitate these events is emerging. Here, an intracellular protein of 90-kDa apparent molecular mass, denoted IP90, was shown to be an ER resident protein that associated with partial complexes of the TCR, mIg, and MHC class I proteins but was absent from fully assembled complexes. We speculate that IP90 might participate in folding and assembly processes of these and other multisubunit protein complexes during their transit through the ER. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOCHEM LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RHEUMATOL & IMMUNOL,LYMPHOCYTE BIOL SECT,BOSTON,MA 02115. UNIV PITTSBURGH,DEPT NEUROBIOL ANAT & CELL SCI,PITTSBURGH,PA 15206. RI Hochstenbach, Frans/B-5232-2008 NR 29 TC 258 Z9 258 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 MAY 15 PY 1992 VL 89 IS 10 BP 4734 EP 4738 DI 10.1073/pnas.89.10.4734 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU977 UT WOS:A1992HU97700106 PM 1584811 ER PT J AU KRISHNA, S BENAROCH, P PILLAI, S AF KRISHNA, S BENAROCH, P PILLAI, S TI TETRAMERIC CELL-SURFACE MHC CLASS-I MOLECULES SO NATURE LA English DT Article ID MONOCLONAL-ANTIBODIES; ANTIGEN; COMPLEX; MOUSE AB PURIFIED major histocompatibility complex (MHC) class I molecules have been studied at high resolution by X-ray crystallography 1; the structure is a complex of a single heavy chain, a beta-2-microglobulin light chain and a tightly bound peptide moiety. We show here that complete MHC class I molecules are post-translationally assembled into tetramers (made up of four heavy chains and four beta-2-microglobulin units) and that this tetrameric species is expressed on the cell surface. The multivalent tetrameric structure of class I molecules can be reconciled with models of T-cell activation that invoke antigen-receptor crosslinking, as opposed to models that depend on an allosteric change. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP KRISHNA, S (reprint author), MASSACHUSETTS GEN HOSP,CTR CANC,MOLEC GENET GRP,MOLEC IMMUNOL LAB,BLDG 149,13TH ST,BOSTON,MA 02129, USA. NR 15 TC 33 Z9 33 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 MAY 14 PY 1992 VL 357 IS 6374 BP 164 EP 167 DI 10.1038/357164a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HU122 UT WOS:A1992HU12200060 PM 1579167 ER PT J AU MALKIN, D JOLLY, KW BARBIER, N LOOK, AT FRIEND, SH GEBHARDT, MC ANDERSEN, TI BORRESEN, AL LI, FP GARBER, J STRONG, LC AF MALKIN, D JOLLY, KW BARBIER, N LOOK, AT FRIEND, SH GEBHARDT, MC ANDERSEN, TI BORRESEN, AL LI, FP GARBER, J STRONG, LC TI GERMLINE MUTATIONS OF THE P53 TUMOR-SUPPRESSOR GENE IN CHILDREN AND YOUNG-ADULTS WITH 2ND MALIGNANT NEOPLASMS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID CANCER FAMILY SYNDROME; RETINOBLASTOMA GENE; ANTIGEN; EXPRESSION; CHILDHOOD; PROTEIN; SARCOMA; 17P13; RISK AB Background. Acquired mutations in the p53 tumor-suppressor gene have been detected in several human cancers, including colon, breast, and lung cancer. Inherited mutations (transmitted through the germline) of this gene can underlie the Li-Fraumeni syndrome, a rare familial association of breast cancer in young women, childhood sarcomas, and other malignant neoplasms. We investigated the possibility that p53 mutations in the germline are associated with second primary cancers that arise in children and young adults who would not be considered as belonging to Li-Fraumeni families. Methods. Genomic DNA was extracted from the blood leukocytes of 59 children and young adults with a second primary cancer. The polymerase chain reaction, in combination with denaturant-gel electrophoresis and sequencing, was used to identify p53 gene mutations. Results. Mutations of p53 that changed the predicted amino acid sequence were identified in leukocyte DNA from 4 of the 59 patients (6.8 percent). In three cases, the mutations were identical to ones previously found in the p53 gene. The fourth mutation was the first germline mutation to be identified in exon 9, at codon 325. Analysis of leukocyte DNA from close relatives of three of the patients indicated that the mutations were inherited, but cancer had developed in only one parent at the start of the study. Conclusions. These findings identify an important subgroup of young patients with cancer who carry germline mutations in the p53 tumor-suppressor gene but whose family histories are not indicative of the Li-Fraumeni syndrome. The early detection of such mutations would be useful not only in treating these patients, but also in identifying family members who may be at high risk for the development of tumors. C1 MASSACHUSETTS GEN HOSP, CTR CANC, DIV MOLEC GENET, BLDG 149, 13TH ST, BOSTON, MA 02129 USA. UNIV TEXAS, MD ANDERSON CANC CTR, DEPT EXPTL PEDIAT & GENET, HOUSTON, TX 77025 USA. HARVARD UNIV, SCH MED,DANA FARBER CANC INST,INST CANC RES, DEPT GENET, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DEPT EPIDEMIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT PEDIAT, MEMPHIS, TN 38163 USA. MASSACHUSETTS GEN HOSP, DEPT ORTHOPED SURG, BOSTON, MA 02114 USA. CHILDRENS HOSP MED CTR, DEPT ORTHOPED SURG, BOSTON, MA 02115 USA. CHILDRENS HOSP MED CTR, DIV HEMATOL & ONCOL, BOSTON, MA 02115 USA. ST JUDE CHILDRENS RES HOSP, DEPT HEMATOL & ONCOL, MEMPHIS, TN 38101 USA. FU NCI NIH HHS [CA-20180, CA-21765, CA-23099] NR 39 TC 326 Z9 330 U1 0 U2 4 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 14 PY 1992 VL 326 IS 20 BP 1309 EP 1315 DI 10.1056/NEJM199205143262002 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA HT803 UT WOS:A1992HT80300002 PM 1565144 ER PT J AU BLUMENTHAL, D EPSTEIN, AM AF BLUMENTHAL, D EPSTEIN, AM TI PHYSICIAN-PAYMENT REFORM - UNFINISHED BUSINESS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article C1 HARVARD UNIV,SCH MED,DEPT HLTH CARE POLICY,25 SHATTUCK ST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,GEN MED UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED,HLTH POLICY RES & DEV UNIT,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT MED,DIV GEN MED,HLTH SERV & POLICY RES SECT,BOSTON,MA 02115. NR 13 TC 15 Z9 15 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 14 PY 1992 VL 326 IS 20 BP 1330 EP 1334 DI 10.1056/NEJM199205143262005 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HT803 UT WOS:A1992HT80300005 PM 1304717 ER PT J AU HAMILTON, JD HARTIGAN, PM SIMBERKOFF, MS AF HAMILTON, JD HARTIGAN, PM SIMBERKOFF, MS TI THE EFFECT OF ZIDOVUDINE ON PATIENT SUBGROUPS SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Letter RP HAMILTON, JD (reprint author), US DEPT VET AFFAIRS,AIDS COOPERAT STUDIES GRP,DURHAM,NC, 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 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD MAY 13 PY 1992 VL 267 IS 18 BP 2472 EP 2473 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HT068 UT WOS:A1992HT06800021 PM 1573722 ER PT J AU CALNE, DB HOCHBERG, FH SNOW, BJ NYGAARD, T AF CALNE, DB HOCHBERG, FH SNOW, BJ NYGAARD, T TI THEORIES OF NEURODEGENERATION SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; CHAIN C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. COLUMBIA UNIV COLL PHYS & SURG,NEW YORK,NY 10032. RP CALNE, DB (reprint author), UNIV HOSP BRITISH COLUMBIA,CTR NEURODEGENERAT,UBC SITE,2211 WESBROOK MALL,VANCOUVER V6T 1W5,BC,CANADA. NR 15 TC 9 Z9 10 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 MAY 11 PY 1992 VL 648 BP 1 EP 5 DI 10.1111/j.1749-6632.1992.tb24518.x PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM216 UT WOS:A1992JM21600003 PM 1637039 ER PT J AU MARTIN, JB BEAL, MF AF MARTIN, JB BEAL, MF TI HUNTINGTONS-DISEASE AND NEUROTOXINS SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID QUINOLINIC ACID; STRIATAL NEURONS; NEUROPEPTIDE-Y; INTRASTRIATAL INJECTIONS; EXCITOTOXIN LESIONS; SOMATOSTATIN; BRAIN; RECEPTOR; CHOREA; RATS C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. RP MARTIN, JB (reprint author), UNIV CALIF SAN FRANCISCO,SCH MED,SAN FRANCISCO,CA 94143, USA. NR 28 TC 10 Z9 10 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 MAY 11 PY 1992 VL 648 BP 169 EP 175 DI 10.1111/j.1749-6632.1992.tb24535.x PG 7 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM216 UT WOS:A1992JM21600020 PM 1386201 ER PT J AU CARSON, JL KELLEY, MA DUFF, A WEG, JG FULKERSON, WJ PALEVSKY, HI SCHWARTZ, JS THOMPSON, BT POPOVICH, J HOBBINS, TE SPERA, MA ALAVI, A TERRIN, ML AF CARSON, JL KELLEY, MA DUFF, A WEG, JG FULKERSON, WJ PALEVSKY, HI SCHWARTZ, JS THOMPSON, BT POPOVICH, J HOBBINS, TE SPERA, MA ALAVI, A TERRIN, ML TI THE CLINICAL COURSE OF PULMONARY-EMBOLISM SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Article ID VENOUS THROMBOSIS; LATE PROGNOSIS; FILTER AB Background. Pulmonary embolism is a potentially fatal disorder. Information about the outcome of clinically recognized pulmonary embolism is sparse, particularly given that new treatments for more seriously ill patients are now available. Methods. We prospectively followed 399 patients with pulmonary embolism diagnosed by lung scanning and pulmonary angiography, who were enrolled in a multicenter diagnostic trial. We reviewed all hospitalizations, all new investigations of pulmonary embolism, and all deaths among the patients within one year of diagnosis. Results. Of the 399 patients, 375 (94 percent) received treatment for pulmonary embolism, usually conventional anticoagulation. Only 10 patients (2.5 percent) died of pulmonary embolism; 9 of them had clinically suspected recurrent pulmonary embolism. Clinically apparent pulmonary embolism recurred in 33 patients (8.3 percent), of whom 45 percent died during follow-up. Ninety-five patients with pulmonary embolism (23.8 percent) died within one year. The conditions associated with these deaths were cancer (relative risk, 3.8; 95 percent confidence interval, 2.3 to 6.4), left-sided congestive heart failure (relative risk, 2.7; 95 percent confidence interval, 1.5 to 4.6), and chronic lung disease (relative risk, 2.2; 95 percent confidence interval, 1.2 to 4.0). The most frequent causes of death in patients with pulmonary embolism were cancer (in 34.7 percent), infection (22.1 percent), and cardiac disease (16.8 percent). Conclusions. When properly diagnosed and treated, clinically apparent pulmonary embolism was an uncommon cause of death, and it recurred in only a small minority of patients. Most deaths were due to underlying diseases. Patients with pulmonary embolism who had cancer, congestive heart failure, or chronic lung disease had a higher risk of dying within one year than did other patients with pulmonary embolism. C1 UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT RADIOL,PHILADELPHIA,PA 19104. LEONARD DAVIS INST HLTH ECON,PHILADELPHIA,PA. UNIV MICHIGAN,SCH MED,DEPT MED,ANN ARBOR,MI 48104. DUKE UNIV,SCH MED,DEPT MED,DURHAM,NC 27706. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HENRY FORD HOSP,DEPT MED,DETROIT,MI 48202. MARYLAND MED RES INST,BALTIMORE,MD. RP CARSON, JL (reprint author), UNIV MED & DENT NEW JERSEY,ROBERT WOOD JOHNSON MED SCH,DEPT MED,DIV GEN INTERNAL MED,NEW BRUNSWICK,NJ 08903, USA. NR 35 TC 708 Z9 742 U1 0 U2 6 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD MAY 7 PY 1992 VL 326 IS 19 BP 1240 EP 1245 DI 10.1056/NEJM199205073261902 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA HR447 UT WOS:A1992HR44700002 PM 1560799 ER PT J AU GRANSTEIN, RD BARNHILL, RL MARK, EJ KANG, SW PARRISH, JA AF GRANSTEIN, RD BARNHILL, RL MARK, EJ KANG, SW PARRISH, JA TI A 56-YEAR-OLD MAN WITH WALDENSTROMS MACROGLOBULINEMIA AND CUTANEOUS AND ORAL VESICLES - PARANEOPLASTIC PEMPHIGUS, WITH INVOLVEMENT OF SKIN, MUCOSA (BUCCAL CAVITY), LARYNX, AND TRACHEA - MALIGNANT-LYMPHOMA, SMALL-CELL LYMPHOCYTIC TYPE, WITH PLASMACYTOID FEATURES CONSISTENT WITH WALDENSTROMS MACROGLOBULINEMIA SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID LINEAR IGA DISEASE; GLUTEN-FREE DIET; ERYTHEMA MULTIFORME; DERMATITIS-HERPETIFORMIS; LUPUS-ERYTHEMATOSUS; COMPLEMENT-FIXATION; IMMUNE-COMPLEXES; EPIDERMAL-CELLS; FOLLOW-UP; VULGARIS C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP GRANSTEIN, RD (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 92 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 MAY 7 PY 1992 VL 326 IS 19 BP 1276 EP 1284 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA HR447 UT WOS:A1992HR44700008 ER PT J AU FAMULOK, M SZOSTAK, JW AF FAMULOK, M SZOSTAK, JW TI STEREOSPECIFIC RECOGNITION OF TRYPTOPHAN AGAROSE BY INVITRO SELECTED RNA SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Note ID ANALYTICAL AFFINITY-CHROMATOGRAPHY; BINDING-SITE; TETRAHYMENA; RIBOZYME C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 13 TC 128 Z9 130 U1 2 U2 10 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD MAY 6 PY 1992 VL 114 IS 10 BP 3990 EP 3991 DI 10.1021/ja00036a065 PG 2 WC Chemistry, Multidisciplinary SC Chemistry GA HT801 UT WOS:A1992HT80100065 ER PT J AU WHITE, RT DAMM, D HANCOCK, N ROSEN, BS LOWELL, BB USHER, P FLIER, JS SPIEGELMAN, BM AF WHITE, RT DAMM, D HANCOCK, N ROSEN, BS LOWELL, BB USHER, P FLIER, JS SPIEGELMAN, BM TI HUMAN ADIPSIN IS IDENTICAL TO COMPLEMENT FACTOR-D AND IS EXPRESSED AT HIGH-LEVELS IN ADIPOSE-TISSUE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SERINE PROTEASE HOMOLOG; AMINO-ACID-SEQUENCE; INSULIN-RECEPTOR; MESSENGER-RNA; FACTOR-B; BIOSYNTHESIS; PROTEINS; MONOCYTES; PATHWAY; CELLS AB A cDNA for human adipsin was isolated and shown to encode a protein sharing 98% amino acid sequence similarity with the protein sequence previously determined for purified natural human complement factor D. Like mouse adipsin, recombinant human adipsin displays the enzymatic activity of human complement factor D, cleaving complement factor B only when B is complexed with activated complement component C3. We conclude that human adipsin is equivalent to complement factor D and that adipsin is the homologue of factor D in rodents. Adipose tissue is a major site of synthesis of human adipsin/complement factor D mRNA, but unlike the case in rodents, human adipsin mRNA is also expressed in monocytes/macrophages. The data presented here, demonstrating the equivalence of human adipsin to complement factor D and its high level of expression in fat, suggest a previously unsuspected role for adipose tissue in immune system biology. C1 UNIV EDINBURGH,AGR & FOOD RES COUNCIL,CTR GENOME RES,EDINBURGH EH9 3JQ,SCOTLAND. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. RP WHITE, RT (reprint author), CALIF BIOTECHNOL INC,2450 BAYSHORE PKWY,MT VIEW,CA 94043, USA. FU NIDDK NIH HHS [DK31405, DK42539] NR 26 TC 221 Z9 229 U1 1 U2 8 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD MAY 5 PY 1992 VL 267 IS 13 BP 9210 EP 9213 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HR854 UT WOS:A1992HR85400077 PM 1374388 ER PT J AU TALAL, N DAUPHINEE, M AHMED, SA AF TALAL, N DAUPHINEE, M AHMED, SA TI CD5 B-CELLS IN AUTOIMMUNITY SO ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article ID PRIMARY SJOGRENS-SYNDROME; RETROVIRAL PROTEINS; SERUM ANTIBODIES; MICE; IMMUNODEFICIENCY; AUTOANTIBODIES; EXOCRINOPATHY; SUPERANTIGEN; LYMPHOCYTES; ASSOCIATION C1 AUDIE L MURPHY MEM VET ADM MED CTR, SAN ANTONIO, TX 78284 USA. RP TALAL, N (reprint author), UNIV TEXAS, HLTH SCI CTR, DEPT MED, DIV CLIN IMMUNOL, 7703 FLOYD CURL DR, SAN ANTONIO, TX 78284 USA. NR 28 TC 0 Z9 0 U1 0 U2 0 PU NEW YORK ACAD SCIENCES PI NEW YORK PA 2 E 63RD ST, NEW YORK, NY 10021 USA SN 0077-8923 J9 ANN NY ACAD SCI JI Ann.NY Acad.Sci. PD MAY 4 PY 1992 VL 651 BP 551 EP 556 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA JM219 UT WOS:A1992JM21900074 ER PT J AU FISHER, CM AF FISHER, CM TI STROKE SO LANCET LA English DT Letter RP FISHER, CM (reprint author), MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114, USA. NR 2 TC 1 Z9 1 U1 2 U2 2 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0140-6736 J9 LANCET JI Lancet PD MAY 2 PY 1992 VL 339 IS 8801 BP 1112 EP 1113 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA HR446 UT WOS:A1992HR44600032 PM 1349124 ER PT J AU RUPRECHT, RM SOSA, MAG DEGASPERI, R PATARCA, R AF RUPRECHT, RM SOSA, MAG DEGASPERI, R PATARCA, R TI UNUSUAL DNA STRUCTURES WITHIN AN HIV-1 PROVIRAL CLONE - STRUCTURAL AND FUNCTIONAL-ANALYSIS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,VIRAL PATHOGENESIS LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 870 EP 870 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300083 ER PT J AU TERWILLIGER, E GABUZDA, D LANGHOFF, E HASELTINE, W AF TERWILLIGER, E GABUZDA, D LANGHOFF, E HASELTINE, W TI FUNCTIONS OF THE VPR AND VPX GENES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 870 EP 870 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300085 ER PT J AU REINHERZ, EL AF REINHERZ, EL TI THE T-CELL RECEPTOR - A 1991 PERSPECTIVE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,IMMUNOBIOL LAB,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 2 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 908 EP 908 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300217 ER PT J AU HOLLSBERG, P WUCHERPFENNIG, KW BIERER, BE HAFLER, DA AF HOLLSBERG, P WUCHERPFENNIG, KW BIERER, BE HAFLER, DA TI HTLV-I INDUCED SPONTANEOUS T-CELL CLONAL PROLIFERATION IS RAPAMYCIN SENSITIVE SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 910 EP 910 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300223 ER PT J AU HASELTINE, WA AF HASELTINE, WA TI NEW PERSPECTIVES ON REPLICATION AND PATHOGENESIS OF HIV-1 SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 913 EP 913 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300236 ER PT J AU MARGALITH, M MEDINA, D HSIUNG, GD SKOLNIK, P HIRSCH, MS AF MARGALITH, M MEDINA, D HSIUNG, GD SKOLNIK, P HIRSCH, MS TI HIV-CMV INTERACTIONS IN CHRONICALLY INFECTED HUMAN OSTEOSARCOMA CELLS SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 TUFTS UNIV,SCH MED,BOSTON,MA 02111. YALE UNIV,SCH MED,NEW HAVEN,CT 06510. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. VET ADM MED CTR,W HAVEN,CT 06516. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 920 EP 920 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300259 ER PT J AU JASSOY, C JOHNSON, RP NAVIA, B MAZARRA, G WALKER, BD AF JASSOY, C JOHNSON, RP NAVIA, B MAZARRA, G WALKER, BD TI FREQUENT DETECTION OF HIV-1-SPECIFIC CYTOTOXIC LYMPHOCYTES-T (CTL) IN CEREBROSPINAL-FLUID (CSF) OF PERSONS WITH AIDS DEMENTIA COMPLEX SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. APPL BIOTECHNOL,CAMBRIDGE,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 928 EP 928 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300288 ER PT J AU PAUL, JR TROCHA, A EARL, P MOSS, B BUCHANAN, TM WALKER, BD AF PAUL, JR TROCHA, A EARL, P MOSS, B BUCHANAN, TM WALKER, BD TI EFFECTS OF GAG AND ENVELOPE SEQUENCE VARIATION ON EPITOPE RECOGNITION BY HIV-1-SPECIFIC CYTOTOXIC LYMPHOCYTE-T CLONES SO AIDS RESEARCH AND HUMAN RETROVIRUSES LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NIAID,BETHESDA,MD 20892. UNIV WASHINGTON,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 SN 0889-2229 J9 AIDS RES HUM RETROV JI Aids Res. Hum. Retrovir. PD MAY PY 1992 VL 8 IS 5 BP 945 EP 945 PG 1 WC Immunology; Infectious Diseases; Virology SC Immunology; Infectious Diseases; Virology GA JA513 UT WOS:A1992JA51300349 ER PT J AU GRAHAM, DY AF GRAHAM, DY TI GASTROENTEROLOGY TODAY AND TOMORROW SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material C1 BAYLOR COLL MED,HOUSTON,TX 77030. RP GRAHAM, DY (reprint author), VET ADM MED CTR 111D,DEPT MED,DIGEST DIS SECT,2002 HOLCOME BLVD,HOUSTON,TX 77030, USA. NR 2 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD MAY PY 1992 VL 87 IS 5 BP 559 EP 561 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HT843 UT WOS:A1992HT84300004 PM 1595640 ER PT J AU KENNELLY, W AF KENNELLY, W TI PHARMACISTS SHOULD NOT ACCEPT GIFTS FROM INDUSTRY SO AMERICAN JOURNAL OF HOSPITAL PHARMACY LA English DT Letter RP KENNELLY, W (reprint author), WILLIAM S MIDDLETON MEM VET ADM MED CTR,PHARM SERV,2500 OVERLOOK TERRACE,MADISON,WI 53705, USA. NR 1 TC 1 Z9 1 U1 1 U2 1 PU AMER SOC HEALTH-SYSTEM PHARMACISTS PI BETHESDA PA 7272 WISCONSIN AVE, BETHESDA, MD 20814 SN 0002-9289 J9 AM J HOSP PHARM JI Am. J. Hosp. Pharm. PD MAY PY 1992 VL 49 IS 5 BP 1108 EP 1108 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA HR493 UT WOS:A1992HR49300004 PM 1595730 ER PT J AU MCCLATCHEY, AI TROFATTER, J MCKENNAYASEK, D RASKIND, W BIRD, T PERICAKVANCE, M GILCHRIST, J ARAHATA, K RADOSAVLJEVIC, D WORTHEN, HG VANDENBERGH, P HAINES, JL GUSELLA, JF BROWN, RH AF MCCLATCHEY, AI TROFATTER, J MCKENNAYASEK, D RASKIND, W BIRD, T PERICAKVANCE, M GILCHRIST, J ARAHATA, K RADOSAVLJEVIC, D WORTHEN, HG VANDENBERGH, P HAINES, JL GUSELLA, JF BROWN, RH TI DINUCLEOTIDE REPEAT POLYMORPHISMS AT THE SCN4A LOCUS SUGGEST ALLELIC HETEROGENEITY OF HYPERKALEMIC PERIODIC PARALYSIS AND PARAMYOTONIA-CONGENITA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MULTILOCUS LINKAGE ANALYSIS; CHANNEL ALPHA-SUBUNIT; MUSCLE SODIUM-CHANNEL; RAT-BRAIN; SKELETAL-MUSCLE; EXPRESSION; MYOTONIA; HUMANS; GENE; CDNA AB Two polymorphic dinucleotide repeats - one (dGdA)n and one (dGdT)n - have been identified at the SCN4A locus, encoding the alpha-subunit of the adult skeletal muscle sodium channel. When typed using PCR, the dinucleotide repeats display 4 and 10 alleles, respectively, with a predicted heterozygosity of .81 for the combined haplotype. We have applied these polymorphisms to the investigation of hyperkalemic periodic paralysis and paramyotonia congenita, distinct neuromuscular disorders both of which are thought to involve mutation at SCN4A. Our data confirm the genetic linkage of both disorders with SCN4A. Haplotype analysis also indicates the strong likelihood of allelic heterogeneity in both disorders. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,13TH ST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DAY NEUROMUSCULAR RES,BOSTON,MA 02114. HARVARD MED SCH,BOSTON,MA. UNIV WASHINGTON,DEPT MED,SEATTLE,WA 98195. VET AFFAIRS HOSP,DIV NEUROL,SEATTLE,WA. DUKE UNIV,DEPT MED,DIV NEUROL,DURHAM,NC 27706. BROWN UNIV,RHODE ISL HOSP,DEPT NEUROL,PROVIDENCE,RI 02903. NATL CTR NEUROL & PSYCHIAT,NATL INST NEUROSCI,KODAIRA,TOKYO,JAPAN. INST MOLEC GENET & GENET ENGN,BELGRADE,YUGOSLAVIA. CAMBRIDGE FAMILY HLTH,CAMBRIDGE,MA. CATHOLIC UNIV LOUVAIN CLIN,DEPT NEUROL,B-1200 BRUSSELS,BELGIUM. RI Haines, Jonathan/C-3374-2012 FU NINDS NIH HHS [NS22224, NS24279, NS26630] NR 30 TC 45 Z9 45 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD MAY PY 1992 VL 50 IS 5 BP 896 EP 901 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA HR473 UT WOS:A1992HR47300003 PM 1315122 ER PT J AU WAZNA, J SHENKER, Y AF WAZNA, J SHENKER, Y TI ATRIAL-NATRIURETIC-PEPTIDE - ALIVE AND WELL SO AMERICAN JOURNAL OF HYPERTENSION LA English DT Editorial Material C1 WILLIAM S MIDDLETON MEM VET ADM MED CTR,ENDOCRINOL SECT,2500 OVERLOOK TERRACE,MADISON,WI 53705. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0895-7061 J9 AM J HYPERTENS JI Am. J. Hypertens. PD MAY PY 1992 VL 5 IS 5 BP 336 EP 337 PN 1 PG 2 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HR679 UT WOS:A1992HR67900015 PM 1533772 ER PT J AU SAMET, JH LIBMAN, H STEGER, KA DHAWAN, RK CHEN, J SHEVITZ, AH DEWEESDUNK, R LEVENSON, S KUFE, D CRAVEN, DE AF SAMET, JH LIBMAN, H STEGER, KA DHAWAN, RK CHEN, J SHEVITZ, AH DEWEESDUNK, R LEVENSON, S KUFE, D CRAVEN, DE TI COMPLIANCE WITH ZIDOVUDINE THERAPY IN PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS, TYPE-1 - A CROSS-SECTIONAL STUDY IN A MUNICIPAL HOSPITAL CLINIC SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID INTRAVENOUS-DRUG-USERS; MEDICATION COMPLIANCE; HIV INFECTION; CONTROLLED TRIAL; AIDS; HYPERTENSION; DIGOXIN; PHARMACOKINETICS; PREVENTION; ADHERENCE AB PURPOSE: To determine the extent of and clinical variables associated with zidovudine compliance. PATIENTS AND METHODS: A survey of 83 patients infected with human immunodeficiency virus (HIV) followed in a municipal hospital clinic was performed. Compliance histories were validated by serum and urine zidovudine levels. Patient characteristics included 46% white, 63% with a history of intravenous drug use, and 59% reporting a diagnosis of acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC). The main outcome measure was greater than 80% compliance with prescribed doses of zidovudine over the previous week. RESULTS: Sixty-seven percent of the study patients reported greater than 80% compliance with prescribed doses of zidovudine over the previous week. The most common explanations given for missing a dose were "forgot to take zidovudine" and "did not have the medication with me." Five variables were independently associated with greater than 80% compliance as determined by stepwise multiple logistic regression: patient belief that zidovudine prolongs life (odds ratio [OR] 9.3, [95 % confidence interval (CI) 2.4, 36.7]), a diagnosis of AIDS or ARC (OR 5.5, [CI 1.5, 20.4]), use of a medication timer (OR 4.4, [CI 1.0, 19.11), no history of intravenous drug use (OR 3.7, [CI 1.0, 14.2]), and taking one to three other medications with zidovudine. CONCLUSIONS: High compliance with zidovudine was achieved by HIV-infected patients in a municipal hospital clinic, many of whom had a history of intravenous drug use. Compliance with zidovudine may be enhanced by a patient's belief that it prolongs life and the use of a medication timer for proper dosing. C1 BOSTON UNIV,SCH MED,DEPT MED,BOSTON,MA 02118. BOSTON CITY HOSP,THORNDIKE MEM LAB,CLIN AIDS PROGRAM,INFECT DIS SECT,BOSTON,MA 02118. BOSTON UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL & BIOSTAT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP SAMET, JH (reprint author), BOSTON CITY HOSP,GEN INTERNAL MED SECT,ACC-3,818 HARRISON AVE,BOSTON,MA 02118, USA. NR 47 TC 173 Z9 175 U1 2 U2 4 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 MAY PY 1992 VL 92 IS 5 BP 495 EP 502 DI 10.1016/0002-9343(92)90746-X PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA HU612 UT WOS:A1992HU61200008 PM 1580296 ER PT J AU ACKERMAN, RH CANDIA, MR AF ACKERMAN, RH CANDIA, MR TI ASSESSMENT OF CAROTID-ARTERY STENOSIS BY MR ANGIOGRAPHY SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Note DE ARTERIES, CAROTID; ARTERIES, STENOSIS AND OCCLUSION; MAGNETIC RESONANCE ANGIOGRAPHY (MRA); ULTRASOUND, DOPPLER C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP ACKERMAN, RH (reprint author), ARMED FORCES INST PATHOL,DEPT RADIOL PATHOL,WASHINGTON,DC 20306, USA. NR 6 TC 24 Z9 24 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD MAY-JUN PY 1992 VL 13 IS 3 BP 1005 EP 1008 PG 4 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA HU246 UT WOS:A1992HU24600029 ER PT J AU LITT, AW RUGGIERI, PM ROSEN, BR AF LITT, AW RUGGIERI, PM ROSEN, BR TI 3RD INTERNATIONAL WORKSHOP ON MAGNETIC-RESONANCE ANGIOGRAPHY, LAQUILA, ITALY, OCTOBER 13-15, 1991 SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Editorial Material C1 CLEVELAND CLIN EDUC FDN,DEPT RADIOL,CLEVELAND,OH 44106. MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. RP LITT, AW (reprint author), NYU MED CTR,DEPT RADIOL,560 1ST AVE,NEW YORK,NY 10016, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD MAY-JUN PY 1992 VL 13 IS 3 BP 1040 EP 1042 PG 3 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA HU246 UT WOS:A1992HU24600039 ER PT J AU YOUNG, LHY JOAG, SV LIN, PY LUO, SF ZHENG, LM LIU, CC YOUNG, JDE AF YOUNG, LHY JOAG, SV LIN, PY LUO, SF ZHENG, LM LIU, CC YOUNG, JDE TI EXPRESSION OF CYTOLYTIC MEDIATORS BY SYNOVIAL-FLUID LYMPHOCYTES IN RHEUMATOID-ARTHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID CYTO-TOXIC LYMPHOCYTES; SERINE ESTERASE GENE; PORE-FORMING PROTEIN; T-CELL SUBSETS; PERIPHERAL-BLOOD; MONOCLONAL-ANTIBODIES; MESSENGER-RNA; INVIVO EXPRESSION; CD8+ LYMPHOCYTES; GAMMA-DELTA AB To understand the role of cytolytic lymphocytes in the pathogenesis of rheumatoid arthritis, we investigated the expression of lymphocyte cytotoxicity mediators, perforin, and serine esterases, in lymphocytes derived from the synovial fluid of 15 patients with rheumatoid arthritis. Previous work has shown that CD8+ lymphocytes that possess markers of activation appear to be present in rheumatoid arthritis (RA). By means of in situ hybridization techniques and immunohistochemical analysis, the authors show that perforin and two serine esterases (serine esterase 1/Hanukah factor/granzyme A, and serine esterase 2/granzyme B) are expressed by subpopulations of CD8+ and CD56+ lymphocytes obtained from synovial fluid. The presence of these cytotoxic mediators suggests a possible mechanism for tissue damage, and provides evidence implicating cytolytic lymphocytes in the pathogenesis of RA. C1 ROCKEFELLER UNIV,MOLEC IMMUNOL & CELL BIOL LAB,1230 YORK AVE,NEW YORK,NY 10021. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BOSTON,MA 02114. CHANG GUNG MEM HOSP,DEPT PATHOL,TAIPEI,TAIWAN. CHANG GUNG MEM HOSP,DEPT INTERNAL MED,TAIPEI,TAIWAN. CHANG GUNG MED COLL,TAIPEI,TAIWAN. FU NCI NIH HHS [CA47307] NR 45 TC 34 Z9 34 U1 0 U2 5 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD MAY PY 1992 VL 140 IS 5 BP 1261 EP 1268 PG 8 WC Pathology SC Pathology GA HU007 UT WOS:A1992HU00700029 PM 1580335 ER PT J AU YU, YM BURKE, JF VOGT, JA CHAMBERS, L YOUNG, VR AF YU, YM BURKE, JF VOGT, JA CHAMBERS, L YOUNG, VR TI SPLANCHNIC AND WHOLE-BODY L-[1-C-13,N-15]LEUCINE KINETICS IN RELATION TO ENTERAL AND PARENTERAL AMINO-ACID SUPPLY SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE METABOLISM; KETOISOCAPROATE; AMINO ACID FEEDING; ARTERIOVENOUS DIFFERENCE; SPLANCHNIC REGION; LIVER; GUT ID FED RATS; GLUCOSE-METABOLISM; LEUCINE METABOLISM; PROTEIN-SYNTHESIS; STABLE ISOTOPE; GUT MASS; NUTRITION; ROUTE; DOG; TRANSLOCATION AB The effect of the route of administration of a complete amino acid solution (0.24 g.kg-1.h-1) on leucine (Leu) and alpha-ketoisocaproate (KIC) metabolism in the splanchnic region (Sp) was assessed in nine chronically catheterized mongrel dogs receiving, for 6 h, amino acids by jugular vein (PN feeding). Results were compared with those obtained previously [Y. M. Yu, D. A. Wagner, E. E. Tredget, J. A. Waleszewski, J. F. Burke, and V. R. Young. Am. J. Physiol. 259 (Endocrinol. Metab. 22): E36-E51, 1990] in eight dogs similarly studied but given amino acids by constant enteral feeding (EN). We used primed continuous intravenous infusions of L-[1-C-13, N-15]Leu and measurements of arteriovenous isotope and Leu balance across the gut, liver, and Sp to estimate parameters of whole body and organ Leu metabolism [Leu-N and Leu-C flux, Leu --> KIC; KIC --> Leu, Leu oxidation and rates of Leu appearance (B) from and disappearance (S) into proteins]. Whole body Leu kinetics were the same for both routes of amino acid administration. With PN, KIC --> Leu, Leu --> KIC, and total metabolic processing were lower than for EN in Sp, and overall Leu balance (S - B) was higher in Sp for EN. Leu appearance from protein breakdown in gut was higher with PN. The rate of KIC --> Leu was higher in liver for EN. These findings reveal that route of amino acid (Leu) administration, under these acute feeding conditions, alters the processing and metabolic fate of Leu in Sp but that whole body parameters of Leu metabolism are stable. The implications of these metabolic findings in relation to the maintenance of intestinal function and integrity are discussed. C1 MIT,HUMAN NUTR LAB,RM E18-613,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SHRINERS BURN INST,BOSTON,MA 02114. FU NIDDK NIH HHS [DK-36616, DK-15856]; NIGMS NIH HHS [GM-02700] NR 52 TC 47 Z9 47 U1 0 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 MAY PY 1992 VL 262 IS 5 BP E687 EP E694 PN 1 PG 8 WC Physiology SC Physiology GA HV370 UT WOS:A1992HV37000050 PM 1590378 ER PT J AU ERCOLANI, L BROWN, D STUARTTILLEY, A ALPER, SL AF ERCOLANI, L BROWN, D STUARTTILLEY, A ALPER, SL TI COLOCALIZATION OF GAPDH AND BAND-3 (AE1) PROTEINS IN RAT ERYTHROCYTES AND KIDNEY INTERCALATED CELL-MEMBRANES SO AMERICAN JOURNAL OF PHYSIOLOGY LA English DT Article DE GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; ANION EXCHANGER; IMMUNOCYTOCHEMISTRY; KIDNEY COLLECTING DUCT ID ANION-EXCHANGE PROTEIN; GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE; ASSOCIATION; MICROSCOPY; BINDING; ATPASE; GENE AB Glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.2.12) (GAPDH) is a multifunctional protein that associates with the cytoplasmic face of intact human erythrocyte membranes. This association has been postulated to be critically dependent on the interaction of GAPDH with the highly acidic NH2-terminal domain of the principal integral membrane protein of the erythrocyte plasma membrane, the band 3 anion exchanger (AE1). This domain is not conserved in murine erythrocyte AE1 and is fully deleted in the alternatively spliced AE1 isoform that is expressed in the kidney. The lack of conservation of this domain has been proposed to explain the reported absence of GAPDH association with rodent erythrocyte membranes. To determine whether GAPDH could be associated with AE1 proteins in rodent cell membranes, specific rabbit antibodies to peptide sequences of rat GAPDH and mouse AE1 were used to immunolocalize these proteins in sequential semithin sections of rat erythrocytes and kidney medulla. In rat erythrocytes, GAPDH immunoreactivity was predominantly membrane associated and colocalized with AE1. In the kidney medulla, GAPDH was concentrated in the basolateral membrane of type A intercalated cells, where it colocalized with the alternatively spliced kidney form of AE1. GAPDH immunoreactivity was not detected in the plasma membrane of any other cell type in the kidney, indicating its predominant association with AE1-rich membranes. If this membrane interaction occurs via AE1 binding, then GAPDH must have binding sites in addition to those previously described for such binding in human AE1. C1 MASSACHUSETTS GEN HOSP,RENAL UNIT,BOSTON,MA 02114. BETH ISRAEL HOSP,MOLEC MED UNIT,BOSTON,MA 02215. BETH ISRAEL HOSP,RENAL UNIT,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. FU NIDDK NIH HHS [DK-01506, DK-43495, DK-38452] NR 28 TC 22 Z9 23 U1 0 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 MAY PY 1992 VL 262 IS 5 BP F892 EP F896 PN 2 PG 5 WC Physiology SC Physiology GA HV372 UT WOS:A1992HV37200100 PM 1590432 ER PT J AU DAWSON, SL MUELLER, PR LEE, MJ SAINI, S KELSEY, P NISHIOKA, NS AF DAWSON, SL MUELLER, PR LEE, MJ SAINI, S KELSEY, P NISHIOKA, NS TI TREATMENT OF BILE-DUCT STONES BY LASER LITHOTRIPSY - RESULTS IN 12 PATIENTS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID BILIARY CALCULI; FRAGMENTATION AB We used a pulsed tunable dye laser (operating at 60 mJ per pulse, 504-nm wavelength) to fragment large (0.8-4.5 cm) stones retained in the hepatic ducts or common bile duct in 12 patients after cholecystectomy. Attempts to extract stones via a T-tube or endoscope had been unsuccessful in all patients. In nine of 12 patients, all stone fragments were successfully eliminated during the initial treatment. In one patient, fragmentation occurred but debris remained, requiring endoscopic stenting. Pseudomonas sepsis developed in this patient 30 days after the procedure and was treated by extraction of the stone fragments. Fragments remaining after lithotripsy were cleared at the same sitting by using saline flushing or endoscopic or percutaneous basket extraction. In two of 12 patients, the treatment was unsuccessful because of laser malfunction. The treatment was performed without complications, except for clinically insignificant hyperamylasemia, which occurred in two patients. Our experience suggests that laser lithotripsy offers a safe alternative for nonsurgical treatment of large retained biliary stones for patients in whom traditional treatments have failed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT GASTROENTEROL,BOSTON,MA 02114. RP DAWSON, SL (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 17 Z9 17 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAY PY 1992 VL 158 IS 5 BP 1007 EP 1009 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HQ193 UT WOS:A1992HQ19300013 PM 1348901 ER PT J AU GAZELLE, GS HAAGA, JR AF GAZELLE, GS HAAGA, JR TI HEPATIC NEOPLASMS - SURGICALLY RELEVANT SEGMENTAL ANATOMY AND IMAGING TECHNIQUES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article AB With advances in imaging and surgical techniques, the diagnosis and treatment of primary and secondary liver neoplasms have improved. Advances in imaging have contributed to the early detection of the tumors and have allowed more precise preoperative characterization and localization of the lesions. Refinements in surgical technique have permitted more extensive resections, while at the same time placing even greater importance on accurate preoperative imaging of the tumor. Presurgical planning requires precise definition of the extent of the tumor vis-a-vis hepatic segmental anatomy. The goal of this essay is to discuss the segmental anatomy of the liver, the types of segmental resections possible, and the strengths and weaknesses of the various imaging techniques used in the preoperative assessment of potential candidates for hepatic resection. Staging of hepatic malignant tumors and technical details of the imaging techniques are not discussed. C1 UNIV HOSP CLEVELAND,DEPT RADIOL,CLEVELAND,OH 44106. RP GAZELLE, GS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 4 TC 30 Z9 30 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAY PY 1992 VL 158 IS 5 BP 1015 EP 1018 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HQ193 UT WOS:A1992HQ19300015 PM 1566658 ER PT J AU DISLER, DG CHEW, FS AF DISLER, DG CHEW, FS TI ADRENAL PHEOCHROMOCYTOMA SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Editorial Material ID LOCALIZATION; MANAGEMENT; DIAGNOSIS; CT C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 4 TC 5 Z9 5 U1 0 U2 0 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR, SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD MAY PY 1992 VL 158 IS 5 BP 1056 EP 1056 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HQ193 UT WOS:A1992HQ19300023 PM 1566666 ER PT J AU LOPEZ, RR BENNER, KG IVANCEV, K KEEFFE, EB DEVENEY, CW PINSON, CW AF LOPEZ, RR BENNER, KG IVANCEV, K KEEFFE, EB DEVENEY, CW PINSON, CW TI MANAGEMENT OF BILIARY COMPLICATIONS AFTER LIVER-TRANSPLANTATION SO AMERICAN JOURNAL OF SURGERY LA English DT Article; Proceedings Paper CT 78TH ANNUAL MEETING OF THE NORTH PACIFIC SURGICAL ASSOC CY NOV 08-09, 1991 CL PORTLAND, OR SP N PACIFIC SURG ASSOC ID TRACT COMPLICATIONS; SURGICAL COMPLICATIONS; DIAGNOSIS; STENTS AB Biliary tract complications after liver transplantation are common, and the evaluation of newer treatment options compared with standard surgical treatment is important. In 62 fiver transplants performed in 55 adult patients, the biliary tract was reconstructed with choledochocholedochostomy (CC) in 52 (84%) and Roux-en-Y choledochojejunostomy (RYCJ) in 10 (16%). Seventeen biliary tract complications occurred in 16 patients (29%). The incidence of complications, was the same after CC and RYCJ. Eight complications (47%) occurred within the first month and nine (53%) thereafter. Only 6 of 17 (35%) biliary tract complications required operation. One patient died of a biliary tract complication. No other allografts were lost due to biliary tract complications. Four patients transplanted at other centers were also treated, for a total of 21 biliary tract complications. Overall, there were nine bile leaks, eight bile duct strictures, two Roux loop hemorrhages, one choledocholithiasis, and one ampullary dyskinesia. Temporary or permanent stents were used successfully in seven of eight strictures. Five bile leaks were managed without operation. Nonsurgical management is appropriate for a selected majority of patients with late bile leaks, biliary tract strictures, or choledocholithiasis after liver transplantation. C1 OREGON HLTH SCI UNIV,DEPT MED,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT RADIOL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT SURG,PORTLAND,OR 97201. PORTLAND VET AFFAIRS MED CTR,PORTLAND,OR. RP LOPEZ, RR (reprint author), VANDERBILT UNIV,MED CTR,SCH MED,CTR TRANSPLANT,DEPT SURG,NASHVILLE,TN 37232, USA. NR 27 TC 97 Z9 97 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD MAY PY 1992 VL 163 IS 5 BP 519 EP 524 DI 10.1016/0002-9610(92)90401-C PG 6 WC Surgery SC Surgery GA HT109 UT WOS:A1992HT10900015 PM 1575311 ER PT J AU FLETCHER, EC LUCKETT, RA GOODNIGHTWHITE, S MILLER, CC QIAN, W COSTARANGOSGALARZA, C AF FLETCHER, EC LUCKETT, RA GOODNIGHTWHITE, S MILLER, CC QIAN, W COSTARANGOSGALARZA, C TI A DOUBLE-BLIND TRIAL OF NOCTURNAL SUPPLEMENTAL OXYGEN FOR SLEEP DESATURATION IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE AND A DAYTIME PAO2 ABOVE 60 MM HG SO AMERICAN REVIEW OF RESPIRATORY DISEASE LA English DT Article ID LONG-TERM OXYGEN; OXYHEMOGLOBIN DESATURATION; HEMODYNAMIC-RESPONSE; THERAPY AB The efficacy of nasal oxygen during sleep was evaluated in patients with COPD, episodic rapid eye movement sleep desaturation, and a daytime PaO2 > 60 mm Hg. The double-blind, randomized 3-yr trial used nasal oxygen versus room air in two groups of nocturnal sleep desaturating subjects. The setting was the outpatient chest clinic of a Veterans Affairs Medical Center. There were 51 patients with moderate to severe COPD, daytime PaO2 greater-than-or-equal-to 60 mm Hg: 38 with proven REM sleep desaturation and 13 without desaturation. Nocturnal oxygen at 3 L/min was delivered by concentrator to 19 desaturating subjects, and room air at 3 L/min was delivered by defective concentrator to the remaining 19 desaturating subjects. There was no gas therapy for the 13 nondesaturating subjects. The nocturnal desaturator group who received supplemental oxygen during sleep over 36 months showed a significant downward trend in pulmonary artery pressure (-3.7 mm Hg) compared with desaturating patients treated with room air (+3.9 mm Hg). Nonvascular parameters of hypoxia, such as hemoglobin and red blood cell mass, did not differ between the sham- and oxygen-treated groups. Mortality was decidedly higher In the desaturating patients compared with nondesaturating subjects, but there was no significant difference between oxygen- and sham-treated desaturating subjects. We conclude that nasal supplemental oxygen used during sleep to reverse episodic desaturation in COPD patients whose daytime PaO2 is above 60 mm Hg has a beneficial effect in reducing pulmonary artery pressure. Further study Is needed to examine the usefulness of supplemental oxygen in reducing mortality in COPD patients with nocturnal desaturation who do not qualify for home oxygen by current criteria. C1 HOUSTON VET AFFAIRS MED CTR,DEPT MED,PULM DIS SECT,HOUSTON,TX. BAYLOR COLL MED,HOUSTON,TX 77030. NR 24 TC 99 Z9 104 U1 1 U2 6 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 MAY PY 1992 VL 145 IS 5 BP 1070 EP 1076 PG 7 WC Respiratory System SC Respiratory System GA HU614 UT WOS:A1992HU61400016 PM 1586049 ER PT J AU MARTYN, JAJ WHITE, DA GRONERT, GA JAFFE, RS WARD, JM AF MARTYN, JAJ WHITE, DA GRONERT, GA JAFFE, RS WARD, JM TI UP-AND-DOWN REGULATION OF SKELETAL-MUSCLE ACETYLCHOLINE-RECEPTORS - EFFECTS ON NEUROMUSCULAR BLOCKERS SO ANESTHESIOLOGY LA English DT Review DE ACETYLCHOLINE RECEPTOR, AGONISTS; ANTAGONISTS; BUNGAROTOXIN BINDING; DOWN-REGULATION; UP-REGULATION; CHOLINESTERASE INHIBITORS, IRREVERSIBLE; REVERSIBLE; COMPLICATIONS, DENERVATION; IMMOBILIZATION; INFECTION; MYASTHENIA GRAVIS; NEURONAL INJURY; ORGANOPHOSPHORUS POISONING; INJURY, BURNS; MUSCLE; NEURONAL; NEUROMUSCULAR RELAXANTS, DRUG INTERACTION; HYPERKALEMIA; NONDEPOLARIZING; PHARMACOKINETICS; PHARMACODYNAMICS; RESISTANCE; SENSITIVITY; SUCCINYLCHOLINE ID SUCCINYLCHOLINE-INDUCED HYPERKALEMIA; CRITICALLY ILL PATIENTS; SUXAMETHONIUM-INDUCED HYPERKALEMIA; CHRONIC NEOSTIGMINE TREATMENT; BUNGAROTOXIN BINDING-SITES; EATON-LAMBERT SYNDROME; MOTOR-NEURON LESIONS; MESSENGER-RNA LEVELS; SMALL-CELL-CARCINOMA; MYASTHENIA-GRAVIS C1 UNIV CALIF DAVIS,SCH MED,DEPT ANESTHESIA,DAVIS,CA 95616. SHRINERS BURN INST,BOSTON,MA. RP MARTYN, JAJ (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [GM31569] NR 261 TC 208 Z9 218 U1 3 U2 8 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAY PY 1992 VL 76 IS 5 BP 822 EP 843 PG 22 WC Anesthesiology SC Anesthesiology GA HR032 UT WOS:A1992HR03200022 PM 1575351 ER PT J AU SIMON, BA HURFORD, WE ALFILLE, PH HASPEL, K BEHRINGER, EC AF SIMON, BA HURFORD, WE ALFILLE, PH HASPEL, K BEHRINGER, EC TI AN AID IN THE DIAGNOSIS OF MALPOSITIONED DOUBLE-LUMEN TUBES SO ANESTHESIOLOGY LA English DT Letter RP SIMON, BA (reprint author), MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114, USA. RI Hurford, William/G-6386-2013 OI Hurford, William/0000-0003-1201-0313 NR 1 TC 18 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD MAY PY 1992 VL 76 IS 5 BP 862 EP 863 DI 10.1097/00000542-199205000-00033 PG 2 WC Anesthesiology SC Anesthesiology GA HR032 UT WOS:A1992HR03200033 PM 1575357 ER PT J AU RAUCH, SD AF RAUCH, SD TI MALFORMATION AND DEGENERATION IN THE INNER-EAR OF MOS TRANSGENIC MICE SO ANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY LA English DT Article DE INNER EAR; MOUSE DEAFNESS; TRANSGENIC MUTANT ID PROTO-ONCOGENE; GUINEA-PIG; PRODUCT; PROTOONCOGENE; LOCALIZATION; MATURATION; PATHOLOGY; FEATURES; OTOCONIA; DEFECTS AB Transgenic mice carrying the mos proto-oncogene linked to a retroviral transcriptional control sequence display behavioral abnormalities including circling, hyperactivity. head tilt, and bobbing. Axonal degeneration, neuronal chromatolysis, spongiform encephalopathy, gliosis, and inflammatory infiltrates are reportedly found in the central nervous systems of all mutants with the behavioral traits. Hearing was tested by means of broadband free-field rarefaction clicks with auditory brain stem response recorded between vertex and mouth electrodes. No detectable auditory response was elicited in transgenic animals, in contrast to five distinct positive peaks observed in littermate control animals. Light microscopic survey of temporal bone histopathology in mutants revealed extensive degeneration of the organ of Corti with loss of hair cells in all cochlear turns and loss of supporting cells and atrophy of spiral ganglion cells. The spiral limbus was deformed, with replacement of the usual convexity of the superior surface by a flattened trough configuration. Hair cells of the vestibular end organs appeared normal. Pathologic alteration in levels of mos transgene RNA appears to have a direct effect on the structural integrity of the inner ear. RP RAUCH, SD (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NIDCD NIH HHS [K08-DC00012] NR 30 TC 4 Z9 4 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 MAY PY 1992 VL 101 IS 5 BP 430 EP 436 PG 7 WC Otorhinolaryngology SC Otorhinolaryngology GA HT267 UT WOS:A1992HT26700010 PM 1570938 ER PT J AU HERMAN, TS TEICHER, BA VARSHNEY, A KHANDEKAR, V BRANN, T AF HERMAN, TS TEICHER, BA VARSHNEY, A KHANDEKAR, V BRANN, T TI EFFECT OF HYPOXIA AND ACIDOSIS ON THE CYTOTOXICITY OF MITOXANTRONE, BISANTRENE AND AMSACRINE AND THEIR PLATINUM COMPLEXES AT NORMAL AND HYPERTHERMIC TEMPERATURES SO ANTICANCER RESEARCH LA English DT Article DE MITOXANTRONE; HYPOXIA; ACIDOSIS; BISANTRENE; AMSACRINE; PLATINUM COMPLEXES; HYPERTHERMIC TEMPERATURE ID CHINESE-HAMSTER CELLS; MOUSE MAMMARY-TUMOR; II-MEDIATED LESIONS; CYTO-TOXICITY; LEUKEMIA-CELLS; INVITRO; DNA; INVIVO; ANTITUMOR; DRUGS AB In an effort to synthesize drugs which would become much more cytotoxic at clinically achievable hyperthermic temperatures, complexes of the tetrachloro-platinum(II) dianion were made with two anthracene dye derivatives, MITOX and BISANT, and the acridine dye derivative m-AMSA. As compared with the parent drug, PtCl4(MITOX)2 was less cytotoxic at 37-degrees-C and more cytotoxic at 42-degrees-C and 43-degrees-C especially at pH 6.45. In contrast, the PtCl4(BISANT)2 was more cytotoxic than BISANT under all condition's. M-AMSA was again shown to be less cytotoxic at elevated temperatures but PtCl4(m-AMSA)2 was more cytotoxic especially at 43-degrees-C and pH 6.45. Platinum levels in cells treated for 1 hr with 25-mu-M at 37-degrees-C, 42-degrees-C and at pH 7.40 versus pH 6.45 demonstrated no significant differences depending on temperature or pH except for PtCl4(MITOX)2 where approximately 4 times higher intracellular platinum levels were present at pH 6.45 versus pH 7.40, although this finding did not correlate with cytotoxicitY. These results suggest that PtCl4(MITOX)2 and PtCl4(m-AMSA)2 may be highly interactive drugs with local hyperthermia. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. NR 39 TC 4 Z9 4 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD MAY-JUN PY 1992 VL 12 IS 3 BP 827 EP 836 PG 10 WC Oncology SC Oncology GA JB316 UT WOS:A1992JB31600038 PM 1622142 ER PT J AU TANAKA, J HOLDEN, SA HERMAN, TS TEICHER, BA AF TANAKA, J HOLDEN, SA HERMAN, TS TEICHER, BA TI RESPONSE OF SUBPOPULATIONS OF THE FSALLC FIBROSARCOMA TO LOW-DOSE X-RAYS AND VARIOUS POTENTIAL ENHANCING AGENTS SO ANTICANCER RESEARCH LA English DT Article DE FIBROSARCOMA; LOW DOSE X-RAYS; HYPOXIA; TUMOR SUBPOPULATIONS ID CELL-SURVIVAL; FIBRO-SARCOMA; MURINE TUMOR; RADIATION; HYPERTHERMIA; CIS-DIAMMINEDICHLOROPLATINUM(II); PERFLUOROCHEMICALS; RADIOSENSITIZATION; SELECTION; THERAPY AB The effectiveness of various oxygen carrying treatments in sensitizing subpopulations of the FSallC fibrosarcoma to low doses of radiation was assessed, and compared with survivals obtained with the same cells after in vivo irradiation under normally oxygenated or hypoxic conditions. FSallC tumors were treated with 2-10 Gray then the Hoechst 33342 dye diffusion method was used to separate the tumor into bright (enriched in normally oxygenated cells) and dim (enriched in hypoxic cells) subpopulations. There was good agreement between the survival of normally oxygenated cells in culture and bright cells from tumors and between hypoxic cells in culture and dim cells from tumors over a radiation dosage range of 2-5 Gray. At 10 Gray bright cells from tumors were minimally less sensitive to the radiation doese than normally oxygenated cells in vivo. When maximally effective doses of perfluorochemical emulsions (F44E at 4 g PFC/kg or Fluosol-DA at 2.4 g PFC/kg) or a purified bovine hemoglobin solution (PBHS at 1.32 g protein/kg) were administered 1 hr. prior to radiation therapy with carbogen (95% O2, 5% CO2) breathing prior to and during radiation delivery, low single doses of x-ray (2-5 Gray) were measurably more cytotoxic toward both FSallC tumor cell subpopulations. These results indicate that perfluorochemical emulsions or purified bovine hemoglobin preparations along with carbogen breathing may be able to increase tumor radiosensitivity to the relatively low radiation doses per fraction used in the clinic. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. FU NCI NIH HHS [P01-CA19589] NR 23 TC 8 Z9 8 U1 0 U2 1 PU INT INST ANTICANCER RESEARCH PI ATHENS PA EDITORIAL OFFICE 1ST KM KAPANDNTIOU-KALAMOU RD KAPANDRITI, POB 22, ATHENS 19014, GREECE SN 0250-7005 J9 ANTICANCER RES JI Anticancer Res. PD MAY-JUN PY 1992 VL 12 IS 3 BP 1029 EP 1033 PG 5 WC Oncology SC Oncology GA JB316 UT WOS:A1992JB31600069 PM 1622113 ER PT J AU HOOPER, DC WOLFSON, JS BOZZA, MA NG, EY AF HOOPER, DC WOLFSON, JS BOZZA, MA NG, EY TI GENETICS AND REGULATION OF OUTER-MEMBRANE PROTEIN EXPRESSION BY QUINOLONE RESISTANCE LOCI NFXB, NFXC, AND CFXB SO ANTIMICROBIAL AGENTS AND CHEMOTHERAPY LA English DT Note ID ESCHERICHIA-COLI K-12; DNA GYRASE; MICF RNA; OMPF; NORFLOXACIN; ACCUMULATION; TETRACYCLINE; MUTANTS; PORIN; CHLORAMPHENICOL AB Quinolone resistance mutations (cfxB1, marA1, and soxQ1) that reduce porin outer membrane protein OmpF map near 34 min on the Escherichia coli chromosome. Another such mutation, nfxC1, was found in strain KF131 (nfxB, 19 min). nfxC1 and cfxB1 mutants (selected with quinolones) differed slightly but reproducibly from marA1 (selected with tetracycline) and soxQ1 (selected with menadione) mutants in quinolone resistance and linkage to zdd2208::Tn10kan (33.7 min). For nfxB nfxC1 and cfxB1 mutants, as previously shown for marA mutants, resistance and reduced OmpF required the micF locus encoding an antisense RNA complementary to ompF mRNA and were associated with increased micF expression. RP HOOPER, DC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114, USA. FU NIAID NIH HHS [AI23988] NR 30 TC 34 Z9 36 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 MAY PY 1992 VL 36 IS 5 BP 1151 EP 1154 PG 4 WC Microbiology; Pharmacology & Pharmacy SC Microbiology; Pharmacology & Pharmacy GA HT589 UT WOS:A1992HT58900048 PM 1510409 ER PT J AU CORREIA, MA YAO, KQ WRIGHTON, SA WAXMAN, DJ RETTIE, AE AF CORREIA, MA YAO, KQ WRIGHTON, SA WAXMAN, DJ RETTIE, AE TI DIFFERENTIAL APOPROTEIN LOSS OF RAT-LIVER CYTOCHROMES-P450 AFTER THEIR INACTIVATION BY 3,5-DICARBETHOXY-2,6-DIMETHYL-4-ETHYL-1,4-DIHYDROPYRIDINE - A CASE FOR DISTINCT PROTEOLYTIC MECHANISMS SO ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS LA English DT Article ID GLUCOCORTICOID-RESPONSIVE CYTOCHROME-P-450P; UBIQUITIN-DEPENDENT PROTEOLYSIS; PRIMARY MONOLAYER-CULTURE; N-ALKYLPROTOPORPHYRIN-IX; HEPATIC CYTOCHROME-P-450; 4-ALKYL ANALOGS; SUBSTITUTED DIHYDROPYRIDINES; MACROLIDE ANTIBIOTICS; ALKYL GROUP; DEGRADATION C1 UNIV CALIF SAN FRANCISCO,CTR LIVER,SAN FRANCISCO,CA 94143. ELI LILLY & CO,LILLY CORP CTR,LILLY RES LABS,INDIANAPOLIS,IN 46285. HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV WASHINGTON,DEPT MED CHEM,SEATTLE,WA 98195. RP CORREIA, MA (reprint author), UNIV CALIF SAN FRANCISCO,DEPT PHARMACOL,BOX 0450,SAN FRANCISCO,CA 94143, USA. FU NIDDK NIH HHS [DK 26506, DK 33765]; NIGMS NIH HHS [GM 44037] NR 42 TC 40 Z9 40 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0003-9861 J9 ARCH BIOCHEM BIOPHYS JI Arch. Biochem. Biophys. PD MAY 1 PY 1992 VL 294 IS 2 BP 493 EP 503 DI 10.1016/0003-9861(92)90716-A PG 11 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA HN472 UT WOS:A1992HN47200025 PM 1567205 ER PT J AU GREEN, HA BURD, E NISHIOKA, NS BRUGGEMANN, U COMPTON, CC AF GREEN, HA BURD, E NISHIOKA, NS BRUGGEMANN, U COMPTON, CC TI MIDDERMAL WOUND-HEALING - A COMPARISON BETWEEN DERMATOMAL EXCISION AND PULSED CARBON-DIOXIDE LASER ABLATION SO ARCHIVES OF DERMATOLOGY LA English DT Article ID CO2-LASER TISSUE ABLATION; THERMAL-DAMAGE; CONTINUOUS-WAVE; SKIN INCISIONS; SCALPEL; REGENERATION; VAPORIZATION; DURATION AB Background. - Continuous-wave carbon dioxide lasers are not widely used for the surgical removal of most skin lesions because it is difficult to control laser ablation and the extensive laser-induced thermal damage slows healing. Pulsed lasers provide means to reduce thermal damage produced during laser ablation and permit precise control of tissue removed during ablation. Using a swine model, we compared on a gross and microscopic level the healing of middermal wounds of similar depth and area created by a dermatome and a focused pulsed CO2 laser. Results. - Pulsed CO2 laser ablation removed skin precisely and bloodlessly with 85 +/- 15-mu-m (mean +/- SD)of residual thermal damage covering the surface of the wound. Compared with the dermatome, tissue reepithelialization was delayed in the laser wounds at day 3. By day 7, epithelial coverage of the laser-created wounds was not significantly different from the dermatome-created wounds. No significant difference in the appearance of the two wounds was noted at 42 days. Conclusions. - We conclude that the focused pulsed CO2 laser is capable of precisely and bloodlessly ablating skin with conservation of residual subjacent adnexal elements, minimal early interference with epibolic epithelial outgrowth, and no pathologic effects on the wound healing process. Pulsed CO2 lasers may be a valuable instrument for the conservative ablation of skin and skin lesions. C1 DEPT HISTOPATHOL,BRISTOL,ENGLAND. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,SHRINERS BURN INST,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT DERMATOL,BOSTON,MA 02115. RP GREEN, HA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN 2,BOSTON,MA 02114, USA. NR 61 TC 69 Z9 69 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-987X J9 ARCH DERMATOL JI Arch. Dermatol. PD MAY PY 1992 VL 128 IS 5 BP 639 EP 645 DI 10.1001/archderm.128.5.639 PG 7 WC Dermatology SC Dermatology GA HU003 UT WOS:A1992HU00300008 PM 1575527 ER PT J AU KELLER, MB LAVORI, PW KANE, JM GELENBERG, AJ ROSENBAUM, JF WALZER, EA BAKER, LA AF KELLER, MB LAVORI, PW KANE, JM GELENBERG, AJ ROSENBAUM, JF WALZER, EA BAKER, LA TI SUBSYNDROMAL SYMPTOMS IN BIPOLAR DISORDER - A COMPARISON OF STANDARD AND LOW SERUM LEVELS OF LITHIUM SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID MANIC-DEPRESSIVE ILLNESS; NATIONAL INSTITUTE; CARBONATE; PROPHYLAXIS; PREVENTION; IMIPRAMINE; UNIPOLAR; RELAPSE AB Ninety-four patients with bipolar disorder participating in a random-assignment, double-blind, prospective maintenance trial of standard- (0.8 to 1.0 mmol/L) vs low-range (0.4 to 0.6 mmol/L) serum lithium levels were assessed to determine the presence and significance of subsyndromal symptoms during periods of remission and recovery. A significant relationship was found between prescribed serum lithium level and the probability of major affective relapse and the occurrence of subsyndromal symptoms. Patients given lithium carbonate to achieve low-range levels had 2.6 times the risk of major affective relapse as those given lithium for standard-range levels and nearly twice the risk of developing subsyndromal symptoms. Patients given the low-range therapy showed a greater variance in weekly Psychiatric Status Rating measures, and their symptoms were more likely to worsen at any time than were symptoms in their standard-level group counterparts. The first occurrence of subsyndromal symptoms increased the risk of major affective relapse fourfold. Following the onset of subsyndromal symptoms, the patients originally randomized to receive standard-range lithium therapy were still better protected from relapse than were patients randomized to receive low-range lithium treatment. Patients were two times more likely to develop depressive than hypomanic symptoms between acute episodes of illness. However, onset of hypomanic symptoms predicted subsequent major affective relapse twice as strongly as did depressive symptoms. Seventy-six percent of patients who became hypomanic had a major affective relapse, compared with 39% of patients who were subclinically depressed. C1 LONG ISL JEWISH MED CTR,HILLSIDE HOSP,NEW YORK,NY. ALBERT EINSTEIN COLL MED,NEW YORK,NY. UNIV ARIZONA,DEPT PSYCHIAT,TUCSON,AZ 85721. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,CAMBRIDGE,MA 02138. RP KELLER, MB (reprint author), BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912, USA. FU NIMH NIH HHS [MH35787, MH37576, R01 MH025478] NR 28 TC 162 Z9 162 U1 1 U2 5 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD MAY PY 1992 VL 49 IS 5 BP 371 EP 376 PG 6 WC Psychiatry SC Psychiatry GA HV122 UT WOS:A1992HV12200005 PM 1586272 ER PT J AU KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR AF KROENKE, K LAWRENCE, VA THEROUX, JF TULEY, MR TI OPERATIVE RISK IN PATIENTS WITH SEVERE OBSTRUCTIVE PULMONARY-DISEASE SO ARCHIVES OF INTERNAL MEDICINE LA English DT Article ID UPPER ABDOMINAL-SURGERY; PREOPERATIVE SPIROMETRY; SURGICAL PROCEDURES; CARDIAC-SURGERY; CLINICAL COURSE; COMPLICATIONS; ANESTHESIA; PREVENTION; INDEX AB Background. - We wanted to determine the risk of postoperative pulmonary complications and mortality in patients with severe chronic obstructive pulmonary disease. Methods. - We reviewed 107 consecutive operations performed in 89 patients with severe chronic obstructive pulmonary disease (forced expiratory volume in 1 second, < 50% of predicted). Results. - Postoperative pulmonary complications occurred in 31 operations (29%) and were significantly related to the type and duration of surgery. Also, American Society of Anesthesiologists class approached significance as a predictor. Postoperative pulmonary complications occurred at higher rates in coronary artery bypass grafting and major abdominal procedures (60% and 56%) than in other operations involving general or spinal anesthesia (27%) or in procedures performed with the patient under regional or local anesthesia (16%). When the durations of the operations were classified as less than 1 hour, 1 to 2 hours, 2 to 4 hours, and more than 4 hours, the rates of postoperative pulmonary complications were 4%, 23%, 38%, and 73%, respectively. Regarding American Society of Anesthesiologists class, postoperative pulmonary complications occurred in 10% of patients in class II, 28% of those in class III, and 46% of those in class IV. In terms of life-threatening complications, there were six deaths and only two cases of nonfatal ventilatory failure. Notably, mortality clustered primarily in coronary artery bypass graft procedures. Five of 10 patients receiving coronary artery bypass grafts died, compared with one death after 97 non-coronary artery bypass graft operations (50% vs 1%). Conclusions. - Although the risk of coronary artery bypass grafting deserves further study, noncardiac surgery carries an acceptable operative risk in patients with severe chronic obstructive pulmonary disease. C1 WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV GEN INTERNAL MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. BROOKE ARMY MED CTR,FT SAM HOUSTON,TX 78234. RP KROENKE, K (reprint author), UNIFORMED SERV UNIV HLTH SCI,DEPT MED,BETHESDA,MD 20814, USA. NR 30 TC 84 Z9 93 U1 0 U2 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9926 J9 ARCH INTERN MED JI Arch. Intern. Med. PD MAY PY 1992 VL 152 IS 5 BP 967 EP 971 DI 10.1001/archinte.152.5.967 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA HU616 UT WOS:A1992HU61600011 PM 1580723 ER PT J AU JUNEAU, P SCHOENE, WC BLACK, P AF JUNEAU, P SCHOENE, WC BLACK, P TI MALIGNANT-TUMORS IN THE PITUITARY-GLAND SO ARCHIVES OF NEUROLOGY LA English DT Article ID CARCINOMA; FEATURES AB Malignant tumors of the pituitary gland may mimic pituitary adenomas both in clinical presentation and in imaging, and often present with neurologic findings including visual field loss and extraocular movement palsies. We describe a 58-year-old woman without known malignancy who presented with extraocular movement weakness, loss of facial sensation, and a sellar plasmacytoma; a 49-year-old woman with oculomotor palsy, no known malignancy, and rapidly failing vision who had metastatic lung carcinoma; and a 70-year-old woman with metastatic breast carcinoma who presented with rapidly failing vision and a metastasis to the anterior lobe of the pituitary. These cases illustrate several important features of malignancy in the pituitary fossa: that it can mimic a "nonfunctioning" pituitary adenoma in clinical presentation and imaging; that rapidly progressive visual loss, extraocular movement palsies, or facial sensory loss may help to distinguish it from a benign adenoma; and that when the pathologist evaluates an alleged "nonsecretory" or "nonfunctional" adenoma, metastases should be included in the differential diagnosis. C1 BRIGHAM & WOMENS HOSP,NEUROSURG SERV,75 FRANCIS ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,NEUROPATHOL SERV,BOSTON,MA 02115. NR 19 TC 26 Z9 26 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 MAY PY 1992 VL 49 IS 5 BP 555 EP 558 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA HT678 UT WOS:A1992HT67800022 PM 1580820 ER PT J AU TINGEY, DP SCHROEDER, A EPSTEIN, MPM EPSTEIN, DL AF TINGEY, DP SCHROEDER, A EPSTEIN, MPM EPSTEIN, DL TI EFFECTS OF TOPICAL ETHACRYNIC-ACID ADDUCTS ON INTRAOCULAR-PRESSURE IN RABBITS AND MONKEYS SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article AB We evaluated the effect of topical ethacrynic acid on rabbit and monkey intraocular pressure. In a preliminary experiment, 100-mmol/L ethacrynic acid applied topically to Dutch-Belted rabbit eyes was associated with an 8-mm Hg lowering of intraocular pressure. However, corneal edema was severe, and the corneal epithelium sloughed off. To try to maintain the pressure-lowering effect but reduce the corneal side effects, we attempted to create an adduct of ethacrynic acid by utilizing ethacrynic acid's sulfhydryl reactivity. Ethacrynic acid was mixed with equimolar cysteine to bind the sulfhydryl-reactive sites on ethacrynic acid. The goal was to expose the cornea to adducted ethacrynic acid, which might then dissociate in the anterior chamber via a retro-Michael reaction. Intraocular pressure decreased 8.9 mm Hg (n = 40) with this treatment, and corneal edema was lessened (32 of 40 eyes had mild to no edema). However, we observed that when the eye was treated before ethacrynic acid-cysteine administration with topical acetylcysteine, the corneal side effects were reduced further and the intraocular pressure effect remained. In living cynomolgus monkeys receiving a single pretreatment drop of 75-mmol/L acetylcysteine followed by two drops of 130-mmol/L ethacrynic acid and 130-mmol/L cysteine, an intraocular pressure lowering of 9.9 mm Hg was observed (n = 7). However, in three of seven eyes corneal edema developed. Pretreatment with two drops of acetylcysteine eliminated the pressure-lowering effect but did not confer any added corneal protection. Our results indicate that topical ethacrynic acid-cysteine is effective in lowering the intraocular pressure of rabbits and cynomolgus monkeys and, when combined with acetylcysteine pretreatment, may offer the potential for a new topical therapeutic regimen for use in glaucoma. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,HOWE LAB OPHTHALMOL,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY0 1894, R01 EY01894] NR 11 TC 25 Z9 26 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0003-9950 J9 ARCH OPHTHALMOL-CHIC JI Arch. Ophthalmol. PD MAY PY 1992 VL 110 IS 5 BP 699 EP 702 PG 4 WC Ophthalmology SC Ophthalmology GA HT822 UT WOS:A1992HT82200033 PM 1580849 ER PT J AU SINGER, S ANTMAN, K CORSON, JM EBERLEIN, TJ FOSTER, RS PATTERSON, WB AF SINGER, S ANTMAN, K CORSON, JM EBERLEIN, TJ FOSTER, RS PATTERSON, WB TI LONG-TERM SALVAGEABILITY FOR PATIENTS WITH LOCALLY RECURRENT SOFT-TISSUE SARCOMAS SO ARCHIVES OF SURGERY LA English DT Article; Proceedings Paper CT 72ND ANNUAL MEETING OF THE NEW ENGLAND SURGICAL SOC CY SEP 28, 1991 CL QUEBEC, CANADA SP NEW ENGLAND SURG SOC ID RADIATION-THERAPY; RANDOMIZED TRIAL; POSTOPERATIVE RADIOTHERAPY; ADJUVANT CHEMOTHERAPY; LIMB SALVAGE; SURGERY; EXTREMITIES; DOXORUBICIN; EXPERIENCE; AMPUTATION AB Between 1971 and 1988, 39 patients were referred because of local recurrence of soft-tissue sarcomas and data from their patient records were analyzed to determine the parameters governing local recurrence. Mean follow-up was 11.1 years, with a mean time to local recurrence of 22 months. Twenty-one patients had local recurrence only, without metastatic disease. Salvage was provided for 14 (67%) of these patients after reexcision of local recurrence, and all 14 patients remained free of disease (mean follow-up, 112 months). We conclude that (1) excisional biopsy of tumors larger than 3 cm leads to potential contamination of clean tissue planes, limits ability to achieve an adequate margin of resection, and may compromise the definitive excision, and (2) in patients with local recurrence only, there is a high rate of long-term salvage (67% for follow-up of 9.3 years) after radical compartmental excision with or without postoperative radiation thera . C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. RP SINGER, S (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT SURG,DIV SURG ONCOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 31 TC 36 Z9 38 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0004-0010 J9 ARCH SURG-CHICAGO JI Arch. Surg. PD MAY PY 1992 VL 127 IS 5 BP 548 EP 554 PG 7 WC Surgery SC Surgery GA HT555 UT WOS:A1992HT55500008 PM 1575625 ER PT J AU RAHMAN, MU CHEEMA, MA SCHUMACHER, HR HUDSON, AP AF RAHMAN, MU CHEEMA, MA SCHUMACHER, HR HUDSON, AP TI MOLECULAR EVIDENCE FOR THE PRESENCE OF CHLAMYDIA IN THE SYNOVIUM OF PATIENTS WITH REITERS-SYNDROME SO ARTHRITIS AND RHEUMATISM LA English DT Article ID REACTIVE ARTHRITIS; BORRELIA-BURGDORFERI; DISEASE; TRACHOMATIS; HYBRIDIZATION; FLUID; DNA; PATHOGENESIS; INFECTION; RESPONSES AB Objective. There is much evidence indicating that chlamydial antigens in the synovium may be critical in the pathogenesis of Reiter's syndrome (RS), but it is not known whether intact organisms are present in that tissue in any stage of the disease. The present study was undertaken to begin to address this question. Methods. We used a highly specific and sensitive molecular hybridization screening system which detects chlamydial RNA, to examine synovial biopsy samples from 22 patients with various arthropathies, including 9 with RS. Results. Seven of the 9 RS patients were positive for chlamydial RNA, while 3 of the 13 non-RS patients were also positive; positive results in the non-RS patients probably indicate the actual presence of the organism, since these patients had arthritis that was otherwise incompletely explained. Conclusion. The detection of chlamydial RNA, in combination with previous findings of chlamydia-like particles and/or chlamydial antigens in the synovium of RS patients, suggests that whole bacterial cells are present in that tissue. C1 DEPT VET AFFAIRS MED CTR,CTR ARTHRIT IMMUNOL,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19104. DEPT VET AFFAIRS MED CTR,RES SERV,PHILADELPHIA,PA 19104. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,DIV RHEUMATOL,PHILADELPHIA,PA 19129. UNIV PENN,SCH MED,PHILADELPHIA,PA 19104. FU NCRR NIH HHS [RR-00040] NR 51 TC 133 Z9 134 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0004-3591 J9 ARTHRITIS RHEUM JI Arthritis Rheum. PD MAY PY 1992 VL 35 IS 5 BP 521 EP 529 DI 10.1002/art.1780350506 PG 9 WC Rheumatology SC Rheumatology GA HV713 UT WOS:A1992HV71300006 PM 1374250 ER PT J AU LEE, FJS AF LEE, FJS TI MODIFIED PROTOCOL FOR YEAST DNA MINI-PREPARATION SO BIOTECHNIQUES LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NR 1 TC 23 Z9 23 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD MAY PY 1992 VL 12 IS 5 BP 677 EP 677 PG 1 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT696 UT WOS:A1992HT69600010 PM 1325162 ER PT J AU BUBLEY, GJ ASHBURNER, BP BALK, SP ARA, G VARSHANEY, A TEICHER, BA AF BUBLEY, GJ ASHBURNER, BP BALK, SP ARA, G VARSHANEY, A TEICHER, BA TI IDENTIFICATION OF CIS-DIAMMINEDICHLORO-PLATINUM(II) ADDUCTS IN DNA FROM DRUG-TREATED HUMAN CELL-NUCLEI SO BIOTECHNIQUES LA English DT Note ID CIS-DIAMMINEDICHLOROPLATINUM(II); INVITRO; TERMINATION; POLYMERASE; SEQUENCES C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP BUBLEY, GJ (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,CHARLES A DANA RES INST,THORNDIKE LAB,330 BROOKLINE AVE,BOSTON,MA 02215, USA. FU NCI NIH HHS [CA51438] NR 9 TC 6 Z9 6 U1 0 U2 0 PU EATON PUBLISHING CO PI NATICK PA 154 E. CENTRAL ST, NATICK, MA 01760 SN 0736-6205 J9 BIOTECHNIQUES JI Biotechniques PD MAY PY 1992 VL 12 IS 5 BP 694 EP & PG 0 WC Biochemical Research Methods; Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA HT696 UT WOS:A1992HT69600017 PM 1515136 ER PT J AU BADER, A RINKES, IHB CLOSS, EI RYAN, CM TONER, M CUNNINGHAM, JM TOMPKINS, RG YARMUSH, ML AF BADER, A RINKES, IHB CLOSS, EI RYAN, CM TONER, M CUNNINGHAM, JM TOMPKINS, RG YARMUSH, ML TI A STABLE LONG-TERM HEPATOCYTE CULTURE SYSTEM FOR STUDIES OF PHYSIOLOGICAL PROCESSES - CYTOKINE STIMULATION OF THE ACUTE PHASE RESPONSE IN RAT AND HUMAN HEPATOCYTES SO BIOTECHNOLOGY PROGRESS LA English DT Article ID TUMOR-NECROSIS-FACTOR; HEPATIC PROTEIN-SYNTHESIS; SERUM AMYLOID-A; MURINE RECOMBINANT INTERLEUKIN-1; C-REACTIVE PROTEIN; MESSENGER-RNA; PLASMA-PROTEINS; FACTOR-ALPHA; MOLECULAR-CLONING; LIVER AB Prior studies on the in vitro hepatic acute phase response have involved either hepatoma cell lines or conventional short-term cultures of primary hepatocytes. No data are available on the response of primary hepatocytes in stable long-term culture systems. In this study, the acute phase response of rat and human hepatocytes in a new long-term culture system was examined in response to interleukin-6 (IL-6), interleukin-1-beta (IL-1-beta), and tumor necrosis factor-alpha (TNF-alpha). The cultured cells were sandwiched between two layers of collagen in a (double-gel) configuration which has been shown to preserve both hepatocyte function and morphology over prolonged periods of time. The stability of this culture configuration enabled us to investigate, for the first time, the temporal aspects of the response in addition to the effects of the mediators on protein secretion. Exposure of rat hepatocytes to IL-6 after culture for 16 days resulted in a 2-fold reduction of albumin secretion and a 15-fold increase in the secretion rates of fibrinogen and alpha(2)-macroglobulin. In all instances, the peak response occurred at 48 h after IL-6 exposure, and all protein secretion rates returned to pretreatment values within 5 days post-treatment. Changes in the mRNA levels of these proteins in response to IL-6 corresponded with those changes seen with the secreted products, indicating pretranslational regulation. Administration of IL-1-beta to rat hepatocytes produced a similar decline of albumin secretion and a 5-fold increase of fibrinogen secretion, whereas alpha(2)-macroglobulin secretion remained undisturbed. In contrast, TNF-alpha did not affect the secretion of any protein examined. Human hepatocytes in a double-gel culture configuration reacted to IL-6 and IL-1-beta with an approximate 40-fold increase in serum amyloid A secretion, peaking at day 3 posttreatment. Both the secretion pattern and temporal response of these cultured hepatocytes to cytokines appear to closely mimic the in vivo hepatocellular response. The double-gel culture system is a stable, attractive tool for further investigation of the acute phase and other hepatocellular responses to physiologic stimuli. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BIGELOW 1302,BOSTON,MA 02114. HARVARD UNIV,SCH MED,SHRINERS BURNS INST,DEPT SURG,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HOWARD HUGHES MED INST,BOSTON,MA 02115. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. FU NIDDK NIH HHS [DK41709, DK01746]; NIGMS NIH HHS [GM 21700] NR 55 TC 71 Z9 71 U1 0 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 SN 8756-7938 J9 BIOTECHNOL PROGR JI Biotechnol. Prog. PD MAY-JUN PY 1992 VL 8 IS 3 BP 219 EP 225 DI 10.1021/bp00015a007 PG 7 WC Biotechnology & Applied Microbiology; Food Science & Technology SC Biotechnology & Applied Microbiology; Food Science & Technology GA HZ243 UT WOS:A1992HZ24300008 PM 1368259 ER PT J AU DRUKER, B OKUDA, K MATULONIS, U SALGIA, R ROBERTS, T GRIFFIN, JD AF DRUKER, B OKUDA, K MATULONIS, U SALGIA, R ROBERTS, T GRIFFIN, JD TI TYROSINE PHOSPHORYLATION OF RASGAP AND ASSOCIATED PROTEINS IN CHRONIC MYELOGENOUS LEUKEMIA-CELL LINES SO BLOOD LA English DT Note ID P210 BCR-ABL; PHILADELPHIA-CHROMOSOME; HEMATOPOIETIC-CELLS; GENE; ESTABLISHMENT; TRANSFORMATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CELLULAR & MOLEC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA36167, CA34183] NR 30 TC 96 Z9 96 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 MAY 1 PY 1992 VL 79 IS 9 BP 2215 EP 2220 PG 6 WC Hematology SC Hematology GA HW884 UT WOS:A1992HW88400004 PM 1571536 ER PT J AU ROBERTSON, MJ SOIFFER, RJ FREEDMAN, AS RABINOWE, SL ANDERSON, KC ERVIN, TJ MURRAY, C DEAR, K GRIFFIN, JD NADLER, LM RITZ, J AF ROBERTSON, MJ SOIFFER, RJ FREEDMAN, AS RABINOWE, SL ANDERSON, KC ERVIN, TJ MURRAY, C DEAR, K GRIFFIN, JD NADLER, LM RITZ, J TI HUMAN BONE-MARROW DEPLETED OF CD33-POSITIVE CELLS MEDIATES DELAYED BUT DURABLE RECONSTITUTION OF HEMATOPOIESIS - CLINICAL-TRIAL OF MY9 MONOCLONAL ANTIBODY-PURGED AUTOGRAFTS FOR THE TREATMENT OF ACUTE MYELOID-LEUKEMIA SO BLOOD LA English DT Article ID ACUTE MYELOGENOUS LEUKEMIA; ACUTE NONLYMPHOCYTIC LEUKEMIA; COLONY-FORMING CELLS; ACUTE MYELOBLASTIC-LEUKEMIA; LONG-TERM CULTURE; CLONOGENIC CELLS; DIFFERENTIATION ANTIGENS; PROGENITOR CELLS; STEM-CELLS; TRANSPLANTATION C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOPHYS & THEORET BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ROBERTSON, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,44 BINNEY ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA 34183] NR 49 TC 86 Z9 86 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 MAY 1 PY 1992 VL 79 IS 9 BP 2229 EP 2236 PG 8 WC Hematology SC Hematology GA HW884 UT WOS:A1992HW88400007 PM 1571539 ER PT J AU CAVINESS, VS FILIPEK, PA KENNEDY, DN AF CAVINESS, VS FILIPEK, PA KENNEDY, DN TI QUANTITATIVE MAGNETIC-RESONANCE-IMAGING AND STUDIES OF DEGENERATIVE DISEASES OF THE DEVELOPING HUMAN BRAIN SO BRAIN & DEVELOPMENT LA English DT Article DE RETT SYNDROME; MRI; DEGENERATIVE DISEASE ID MORPHOMETRY; INVIVO AB The Rett syndrome is a progressive disorder which is associated with regression of psychomotor development and precipitous deceleration of brain growth during the first year of life. General histopathological surveys in postmortem specimens have identified degeneration of subpopulations of neurons of the nigrostriatal system but no other evidence of degenerative process. Magnetic resonance imaging-based morphometry may usefully guide application of rigorous but demanding quantitative histologic search for evidence of neuronal degeneration. The volumes of the principal set of cortical and nuclear structures of principal interest in the disorder may be measured by currently available MRI-based methods. Optimized levels of precision now allow detection of volumetric changes over time in the same brain of approximately 10% at the 95% confidence level. C1 MASSACHUSETTS GEN HOSP, CTR NEUROSCI, CTR MORPHOMETR ANAL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, DIV CHILD NEUROL, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT RADIOL, DIV CHILD NEUROL, BOSTON, MA 02114 USA. RI Kennedy, David/H-3627-2012 FU PHS HHS [P01 20489, P01 24279] NR 17 TC 8 Z9 8 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD MAY PY 1992 VL 14 SU S BP S80 EP S85 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA HW947 UT WOS:A1992HW94700013 PM 1626638 ER PT J AU BALDESSARINI, RJ HUSTONLYONS, D CAMPBELL, A MARSH, E COHEN, BM AF BALDESSARINI, RJ HUSTONLYONS, D CAMPBELL, A MARSH, E COHEN, BM TI DO CENTRAL ANTIADRENERGIC ACTIONS CONTRIBUTE TO THE ATYPICAL PROPERTIES OF CLOZAPINE SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID CEREBROSPINAL-FLUID NORADRENALINE; TERM NEUROLEPTIC TREATMENT; SCHIZOPHRENIC-PATIENTS; RAT-BRAIN; PLASMA NOREPINEPHRINE; DOPAMINE HYPOTHESIS; ANTIPSYCHOTIC-DRUGS; AUTONOMIC AROUSAL; CLONIDINE; NEURONS AB Full neuropharmacological understanding of the atypical antipsychotic agent clozapine remains elusive. Antidopaminergic actions of most neuroleptics probably contribute to their antipsychotic benefits, but also to neurological side-effects. Clinical evidence of abnormalities of dopamine (DA) and serotonin (5-HT) in psychotic disorders is inconsistent, but there is substantial metabolic and post-mortem evidence for hyperactivity of noradrenalin (NA). Clozapine is only weakly antidopaminergic but is a potent antagonist at brain alpha-1-adrenergic, 5-HT2-serotonergic, and muscarinic receptors. Its apparent limbic-over-extrapyramidal neurophysiological selectivity can be mimicked by combining a typical neuroleptic with a central alpha-1 antagonist. Clozapine strongly upregulates alpha-1 but not DA, receptor abundance, and may supersensitise alpha-1 but not DA receptors in rat brain. Clozapine also selectively increases activity of NA neurons and metabolic turnover in NA more than DA areas of rat brain, and also increases NA, but not DA or 5-HT, metabolites in human CSF. Potential psychotropic effects of selective central antiadrenergic agents may deserve reconsideration. C1 HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHIAT RES LABS,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHOT DISORDERS PROGRAM,BELMONT,MA 02178. RP BALDESSARINI, RJ (reprint author), HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115, USA. NR 57 TC 102 Z9 102 U1 0 U2 0 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD MAY PY 1992 VL 160 SU 17 BP 12 EP 16 PG 5 WC Psychiatry SC Psychiatry GA HU104 UT WOS:A1992HU10400002 ER PT J AU KRUPP, F HIPPIUS, H MELTZER, HP KANE, JM GERLACH, J NABER, D COWARD, DM BALDESSARINI, RJ BUNNEY, BS FARDE, L AF KRUPP, F HIPPIUS, H MELTZER, HP KANE, JM GERLACH, J NABER, D COWARD, DM BALDESSARINI, RJ BUNNEY, BS FARDE, L TI CLOZAPINE - THE ATYPICAL ANTIPSYCHOTIC - DISCUSSION SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Discussion ID INDUCED AGRANULOCYTOSIS; DRUGS C1 UNIV MUNICH,HOSP PSYCHIAT,W-8000 MUNICH 2,GERMANY. UNIV HOSP CLEVELAND,CLEVELAND,OH 44106. LONG ISL JEWISH MED CTR,HILLSIDE HOSP,DEPT PSYCHIAT,GLEN OAKS,NY 11004. YESHIVA UNIV ALBERT EINSTEIN COLL MED,BRONX,NY 10461. ST HANS HOSP,DEPT P,DK-4000 ROSKILDE,DENMARK. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,NEUROSCI PROGRAM,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHIAT RES LABS,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,MCLEAN DIV,MAILMAN RES CTR,PSYCHOT DISORDERS PROGRAM,BELMONT,MA 02178. YALE UNIV,SCH MED,DEPT PSYCHIAT,NEW HAVEN,CT 06519. YALE UNIV,SCH MED,DEPT PHARMACOL,NEW HAVEN,CT 06519. KAROLINSKA INST,DEPT PSYCHIAT & PSYCHOL,ULF LUNDAHL RES UNIT,S-10401 STOCKHOLM 60,SWEDEN. KAROLINSKA HOSP,S-10401 STOCKHOLM 60,SWEDEN. RP KRUPP, F (reprint author), SANDOZ PHARMA LTD,CTR DRUG MONITORING,CLIN RES & DEV,CH-4002 BASEL,SWITZERLAND. NR 8 TC 1 Z9 1 U1 0 U2 2 PU ROYAL COLLEGE OF PSYCHIATRISTS PI LONDON PA BRITISH JOURNAL OF PSYCHIATRY 17 BELGRAVE SQUARE, LONDON, ENGLAND SW1X 8PG SN 0007-1250 J9 BRIT J PSYCHIAT JI Br. J. Psychiatry PD MAY PY 1992 VL 160 SU 17 BP 60 EP 64 PG 5 WC Psychiatry SC Psychiatry GA HU104 UT WOS:A1992HU10400011 ER PT J AU COTE, CJ DANIELS, AL CONNOLLY, M SZYFELBEIN, SK WICKENS, CD AF COTE, CJ DANIELS, AL CONNOLLY, M SZYFELBEIN, SK WICKENS, CD TI TONGUE OXIMETRY IN CHILDREN WITH EXTENSIVE THERMAL-INJURY - COMPARISON WITH PERIPHERAL OXIMETRY SO CANADIAN JOURNAL OF ANAESTHESIA-JOURNAL CANADIEN D ANESTHESIE LA English DT Article DE ANESTHESIA, PEDIATRIC; COMPLICATIONS, BURNS; MEASUREMENT TECHNIQUES, OXIMETERS; MONITORING, OXYGEN ID PULSE OXIMETRY AB We undertook a prospective study of standard peripheral pulse oximetry versus a modified pulse oximeter probe applied to the tongue in order to determine the efficacy of this alternative monitoring site in children with thermal injuries. Ten patients with a mean age (+/- SD) of 7.5 +/- 4.5 yr were studied on 15 occasions. The mean weight (+/- SD) was 31.4 +/- 13.7 kg and percent surface area burn (+/- SD) was 56 +/- 21%. A total of 1,992 min of anaesthesia time was monitored. Both sites functioned simultaneously 47% of the time; the lingual but not the peripheral site functioned 28% of the time and only the peripheral site and not the lingual functioned 22% of the time. Neither site functioned 3% of the time. The tongue oximeter provided 563 min more monitoring time than the peripheral sites. The tongue oximeter also functioned in children with peripheral vasoconstriction when the peripheral sensor failed and was less susceptible to electrocautery interference. The tongue oximeter is a reasonable adjunct but not a substitute for peripheral oximetry since its application is limited to paralyzed, intubated patients. C1 SHRINERS BURN INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP COTE, CJ (reprint author), HARVARD UNIV,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02115, USA. NR 10 TC 8 Z9 8 U1 0 U2 1 PU CANADIAN ANAESTHETISTS SOC INC PI TORONTO PA 1 EGLINTON AVE EAST, SUITE 208, TORONTO ON M4P 3A1, CANADA SN 0832-610X J9 CAN J ANAESTH JI Can. J. Anaesth.-J. Can. Anesth. PD MAY PY 1992 VL 39 IS 5 BP 454 EP 457 PN 1 PG 4 WC Anesthesiology SC Anesthesiology GA HU958 UT WOS:A1992HU95800006 PM 1596969 ER PT J AU WEN, PY BLANCHARD, KL BLOCK, CC LOEFFLER, JS DAVIS, DG LACROIX, LA ANTIN, JH AF WEN, PY BLANCHARD, KL BLOCK, CC LOEFFLER, JS DAVIS, DG LACROIX, LA ANTIN, JH TI DEVELOPMENT OF LHERMITTE SIGN AFTER BONE-MARROW TRANSPLANTATION SO CANCER LA English DT Article ID SUBACUTE COMBINED DEGENERATION; THORACIC CORD COMPRESSION; HEMATOLOGIC MALIGNANCIES; SPINAL-CORD; COMPLICATIONS; CHEMOTHERAPY; DISCHARGES AB The authors observed Lhermitte's sign in four patients after bone marrow transplantation (BMT) for hematologic malignancies. Three patients had acute myelogenous leukemia (AML), and one had chronic myelogenous leukemia. Before BMT, the patients with AML received daunorubicin, cytosine arabinoside and etoposide, whereas the patient with chronic myelogenous leukemia received hydroxyurea. One patient with AML received MY-9 antibody-depleted autologous BMT. The other patients received human lymphocyte antigen-identical, allogeneic BMT. Preparative therapy for BMT was cytosine arabinoside, cyclophosphamide, and total body exposure to radiation for two patients, and busulfan, cyclophosphamide, and no exposure to radiation in two other patients. Lhermitte's sign appeared 4 to 8 months after BMT and resolved spontaneously after 2 to 5 months. Neurologic sequelae had developed in none of the patients 16 to 34 months after BMT. No unifying etiologic factor could be identified in these patients. The development of Lhermitte's sign after BMT appears to be a benign, self-limited phenomenon that requires no specific treatment. C1 BRIGHAM & WOMENS HOSP,DIV HEMATOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. UNIV KENTUCKY,DEPT PATHOL,LEXINGTON,KY 40506. RP WEN, PY (reprint author), BRIGHAM & WOMENS HOSP,DIV NEUROL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [K11 CAO1492] NR 40 TC 11 Z9 11 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAY 1 PY 1992 VL 69 IS 9 BP 2262 EP 2266 DI 10.1002/1097-0142(19920501)69:9<2262::AID-CNCR2820690909>3.0.CO;2-J PG 5 WC Oncology SC Oncology GA HP194 UT WOS:A1992HP19400008 PM 1562971 ER PT J AU LEBLANC, GA KANTOFF, PW NG, SF FREI, E WAXMAN, DJ AF LEBLANC, GA KANTOFF, PW NG, SF FREI, E WAXMAN, DJ TI HORMONAL PERTURBATIONS IN PATIENTS WITH TESTICULAR CANCER TREATED WITH CISPLATIN SO CANCER LA English DT Article ID HUMAN CHORIONIC-GONADOTROPIN; CIS-PLATINUM; COMBINATION CHEMOTHERAPY; STEROID-BIOSYNTHESIS; GYNECOMASTIA; ENZYMES; SURGERY; TESTIS AB Patients with testicular cancer treated with cisplatin can undergo feminization that is understood poorly. Rat model studies recently showed that cisplatin can feminize in part the profile of hepatic steroid-metabolizing enzymes and circulating hormone levels. This study was undertaken to determine whether cisplatin similarly might contribute to the perturbations in gonadotropin or steroid hormone levels that can occur in patients undergoing cisplatin-based treatment for testicular cancer. Analysis of serum free testosterone, total testosterone, and androstenedione levels revealed that these hormones were not altered significantly in patients during a 38-week period of cisplatin-based treatment and follow-up. Estradiol levels were elevated before chemotherapy and were reduced to normal levels during treatment. This reduction was attributed to the cytotoxic effect of chemotherapy on the tumors and the resultant reduction in serum chorionic gonadotropin levels. Serum dihydrotestosterone (DHT) levels were normal before chemotherapy but progressively became elevated during treatment with cisplatin in five of ten patients examined. The rise in DHT may relate to the previously described increase in hepatic androgen 5-alpha-reductase activity in cisplatin-treated rats. Levels of the gonadotropins, luteinizing hormone, and follicle-stimulating hormone (FSH) were normal before cisplatin-based treatment was administered; however, FSH was elevated selectively during chemotherapy. This selective induction of FSH may reflect an effect of cisplatin on the hypothalamic secretion of gonadotropin-releasing hormone. Taken together, these findings suggest that cisplatin contributes to the perturbation of steroid and peptide hormone levels in patients with testicular cancer and perhaps in others undergoing cisplatin-based chemotherapy. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT BIOL CHEM & MOLEC PHARMACOL,ROOM JF-525,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CLIN ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED,BOSTON,MA 02115. N CAROLINA STATE UNIV,DEPT TOXICOL,RALEIGH,NC 27695. NR 22 TC 13 Z9 13 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0008-543X J9 CANCER JI Cancer PD MAY 1 PY 1992 VL 69 IS 9 BP 2306 EP 2310 DI 10.1002/1097-0142(19920501)69:9<2306::AID-CNCR2820690917>3.0.CO;2-F PG 5 WC Oncology SC Oncology GA HP194 UT WOS:A1992HP19400016 PM 1562977 ER PT J AU BENNETT, WT PANDOLFI, F GROVE, BH HAWES, GE BOYLE, LA KRADIN, RL KURNICK, JT AF BENNETT, WT PANDOLFI, F GROVE, BH HAWES, GE BOYLE, LA KRADIN, RL KURNICK, JT TI DOMINANT REARRANGEMENTS AMONG HUMAN TUMOR-INFILTRATING LYMPHOCYTES - ANALYSIS OF T-CELLS DERIVED FROM 32 PATIENTS WITH MELANOMA, LUNG, AND RENAL-CELL CARCINOMA SO CANCER LA English DT Article ID RECEPTOR GENE REARRANGEMENTS; BETA-CHAIN GENES; CLONAL DOMINANCE; EXPRESSION; ARTHRITIS; CANCER; INTERLEUKIN-2; IMMUNOTHERAPY AB Dominant rearrangements of T-cell receptor (TCR) beta-chain genes are reported among tumor-infiltrating lymphocytes (TIL). After interleukin-2 expansion of TIL from renal and lung carcinoma and melanoma biopsy tissues, rearrangements of TCR beta-chain genes were analyzed by Southern blotting. Nongermline restriction fragments, indicating dominant rearrangements, were detected among the TIL from all 6 patients with renal cell carcinoma, 17 of 20 patients with melanoma, and 3 of 6 patients with lung tumors. The restriction-fragment sizes of these dominant rearrangements were heterogeneous among the various patients. Rearrangements into C-beta-1 were more common than C-beta-2 rearrangements. Phenotypic analyses indicated that dominant rearrangements occurred in both CD4 and CD8 predominant TIL populations. The TIL populations that were extracted were expanded to derive large cell numbers suitable for in vivo transfer in an interleukin-2 and TIL immunotherapy program. The data indicated that the cells delivered to these patients usually were characterized by dominant populations of T-cells with selective TCR gene rearrangements. The significance of selective TCR use requires evaluation of the function and specificity of the TIL comprising these dominant populations both in their native in vivo setting and in the context of therapeutic transfer. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. FU NCI NIH HHS [CA43244, CA 44324]; NIAMS NIH HHS [AR39993] NR 29 TC 35 Z9 35 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 MAY 1 PY 1992 VL 69 IS 9 BP 2379 EP 2384 DI 10.1002/1097-0142(19920501)69:9<2379::AID-CNCR2820690928>3.0.CO;2-W PG 6 WC Oncology SC Oncology GA HP194 UT WOS:A1992HP19400027 PM 1314129 ER PT J AU PEREY, L HAYES, DF MAIMONIS, P ABE, M OHARA, C KUFE, DW AF PEREY, L HAYES, DF MAIMONIS, P ABE, M OHARA, C KUFE, DW TI TUMOR SELECTIVE REACTIVITY OF A MONOCLONAL-ANTIBODY PREPARED AGAINST A RECOMBINANT PEPTIDE DERIVED FROM THE DF3 HUMAN BREAST CARCINOMA-ASSOCIATED ANTIGEN SO CANCER RESEARCH LA English DT Article ID HUMAN-MILK; DIFFERENTIATION ANTIGENS; CARCINOEMBRYONIC ANTIGEN; EPITHELIAL SIALOMUCIN; CANCER; MUCIN; CELLS; GLYCOPROTEINS; POLYMORPHISM; PROTEIN AB The DF3 antigen is a member of a family of high molecular weight glycoproteins aberrantly expressed in malignant mammary epithelium. We have generated a monoclonal antibody (MAb), designated DF3-P, against a recombinant DF3/beta-galactosidase fusion protein. Characterization of this MAb has demonstrated reactivity with immature precursors of DF3 antigen and not with the secreted form. These findings are in contrast to those obtained with MAb DF3, a previously described antibody with predominant reactivity against the mature glycoprotein. The finding that deglycosylation of secreted DF3 antigen with neuraminidase and endo-alpha-N-acetylgalactosaminidase is associated with increased MAb DF3-P reactivity provided additional support for the selectivity of this antibody against the protein core. Epitope mapping studies demonstrate that both the DF3-P and DF3 epitopes are located at a TRPAPGS domain in the 20-amino acid tandem repeat. The results of competition studies with synthetic peptides indicate that the proline in this domain is involved in both epitopes, while the potential glycosylation sites at threonine and serine may contribute to the differential reactivity of MAbs DF3 and DF3-P. Taken together, these findings suggest that both antibodies react with a similar epitope that is modified by the presence of carbohydrate moieties. The results of immunoperoxidase staining studies further demonstrate that while MAb DF3-P reacts with formalin-fixed sections of breast carcinomas, this antibody exhibits little if any reactivity with normal mammary epithelium. Selective expression of the DF3-P epitope in malignant breast cells may be useful in identifying this transformed phenotype. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,44 BINNEY ST,BOSTON,MA 02115. BOSTON UNIV,MED CTR,MALLORY INST PATHOL,BOSTON,MA 02118. NR 29 TC 81 Z9 82 U1 1 U2 3 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 1 PY 1992 VL 52 IS 9 BP 2563 EP 2568 PG 6 WC Oncology SC Oncology GA HR290 UT WOS:A1992HR29000030 PM 1373671 ER PT J AU SUNDAY, ME WILLETT, CG AF SUNDAY, ME WILLETT, CG TI INDUCTION AND SPONTANEOUS REGRESSION OF INTENSE PULMONARY NEUROENDOCRINE CELL-DIFFERENTIATION IN A MODEL OF PRENEOPLASTIC LUNG INJURY SO CANCER RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON INVESTIGATIONAL STRATEGIES FOR DETECTION AND INTERVENTION IN EARLY LUNG CANCER CY APR 21-24, 1991 CL ANNAPOLIS, MD SP NCI ID GASTRIN-RELEASING PEPTIDE; ONCOGENE INDUCES DIFFERENTIATION; SUPPRESSOR GENES; ENDOCRINE-CELLS; GROWTH-FACTOR; FETAL LUNG; APUD CELLS; DIETHYLNITROSAMINE; BOMBESIN; HAMSTERS AB Pulmonary neuroendocrine cell (PNEC) hyperplasia is associated with chronic lung diseases in humans, where it is thought to play a role in reparative responses to lung injury. To investigate the kinetics of strongly induced PNEC hyperplasia in an animal model, we exposed hamsters to a combination of hyperoxia (60% O2) and diethylnitrosamine (DEN) for up to 20 weeks. We thus demonstrate not only the induction but also spontaneous regression of intense PNEC differentiation and growth, which are much more intense than those observed with DEN alone. Lung tissues were immunostained for serotonin, calcitonin gene-related peptide (CGRP), calcitonin (CT), and gastrin-releasing peptide (GRP) (mammalian bombesin). Between 9 and 12 weeks of treatment, the number of CGRP- and serotonin-positive neuroepithelial bodies per cm airway epithelium increased over 10-fold, and CT became detectable. The number of neuroepithelial bodies immunostained for CGRP, serotonin, and CT peaked at 12-14 weeks of treatment, thereafter regressing to near-control levels by 20 weeks, in spite of continued DEN/O2 treatment. Simultaneously, by 6-7 weeks of treatment, there was a significant increase in the mean number of CGRP-positive cells per neuroepithelial body, which continued to rise up to double control levels, with a plateau at 13-20 weeks. GRP and pro-GRP immunostaining were not detectable at any time point. Polymerase chain reaction analyses of neuroendocrine-specific mRNAs demonstrated that CGRP, CT, and GRP mRNAs (normalized for beta-actin) peaked in lung tissues from most animals at 9-14 weeks after the beginning of DEN/O2 treatment, with decreased expression at 16-20 weeks. These data suggest that regulation of levels of these neuropeptides may be primarily transcriptional. This model may be a valuable system for analyzing mechanisms of induction and regression of normal PNEC differentiation and growth. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP SUNDAY, ME (reprint author), BRIGHAM & WOMENS HOSP,DEPT PATHOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 80 TC 38 Z9 38 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD MAY 1 PY 1992 VL 52 IS 9 SU S BP S2677 EP S2686 PG 10 WC Oncology SC Oncology GA HT047 UT WOS:A1992HT04700007 ER PT J AU MARGOSSIAN, SS WHITE, HD CAULFIELD, JB NORTON, P TAYLOR, S SLAYTER, HS AF MARGOSSIAN, SS WHITE, HD CAULFIELD, JB NORTON, P TAYLOR, S SLAYTER, HS TI LIGHT CHAIN-2 PROFILE AND ACTIVITY OF HUMAN VENTRICULAR MYOSIN DURING DILATED CARDIOMYOPATHY - IDENTIFICATION OF A CAUSAL AGENT FOR IMPAIRED MYOCARDIAL-FUNCTION SO CIRCULATION LA English DT Article DE LIGHT CHAINS; CARDIOMYOPATHY; MYOSIN ID RABBIT SKELETAL-MUSCLE; HEAVY-CHAIN; ALPHA-MYOSIN; ACTIN; THROMBOSPONDIN; EXPRESSION; ISOENZYMES; SUBFRAGMENT-1; PURIFICATION; FILAMENTS AB Background. A number of parameters reflecting the effects of idiopathic dilated cardiomyopathy (IDC) on the structure and function of myosin from the human myocardium were analyzed. Methods and Results. The content of the regulatory light chain, LC2, was reduced in myopathic heart myosin in contrast to the controls in which it was present in stoichiometric amounts relative to the essential light chain, LC1. In IDC hearts, the absence or significant reduction in amount of LC2 was related to the presence of an active protease, which was isolated and purified about 130-fold. The protease exhibited a significant degree of specificity: It cleaved LC2 almost totally (but not the heavy chains) in human control heart myosin but only partially cleaved LC2 in canine heart or in rabbit skeletal muscle myosins. The protease was present at a very low level or was inactive in control heart tissue. When the LC1/LC2 molar ratio was calculated, it was found to be 1:1.0 in control heart myosin and remained constant in various samples analyzed, whereas in myopathic myosin from different individuals, this ratio varied from 1:0.1 to 1:0.69. The rates of ATP binding to control and myopathic myosins were similar, whereas the V(m) of actin-activated ATPase of myopathic myosin was about 25% less than that of the control. However, ATP binding and its hydrolysis by control S1, i.e., the myosin head, were faster by a factor of 2 than that of the myopathic S1. In addition, control myosin synthetic thick filament length as well as turbidity in solution, measured by light scattering, were twice as large as those of the myopathic heart myosin. These effects induced by myopathy in both filament assembly and turbidity were reversed upon reassociation of IDC myosin with LC2. Conclusions. The changes in myosin structure and function were linked to a protease-mediated cleavage of LC2 in myosin; a possible role for the protease in the degenerative effects of idiopathic dilated cardiomyopathy is thus defined. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELLULAR & MOLEC PHYSIOL,BOSTON,MA 02115. MONTEFIORE MED CTR,DEPT BIOCHEM,BRONX,NY 10467. EASTERN VIRGINIA MED SCH,DEPT BIOCHEM,NORFOLK,VA 23501. UNIV ALABAMA,DEPT PATHOL,BIRMINGHAM,AL 35294. RP MARGOSSIAN, SS (reprint author), MONTEFIORE MED CTR,DEPT ORTHOPAED RES,ORTHOPED RES LABS,111 E 210TH ST,BRONX,NY 10467, USA. FU NHLBI NIH HHS [HL-26569, HL-35358, HL-41776] NR 55 TC 88 Z9 89 U1 0 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD MAY PY 1992 VL 85 IS 5 BP 1720 EP 1733 PG 14 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA HR947 UT WOS:A1992HR94700009 PM 1572030 ER PT J AU RODRIGUEZ, L ANCONINA, J FLACHSKAMPF, FA WEYMAN, AE LEVINE, RA THOMAS, JD AF RODRIGUEZ, L ANCONINA, J FLACHSKAMPF, FA WEYMAN, AE LEVINE, RA THOMAS, JD TI IMPACT OF FINITE ORIFICE SIZE ON PROXIMAL FLOW CONVERGENCE - IMPLICATIONS FOR DOPPLER QUANTIFICATION OF VALVULAR REGURGITATION SO CIRCULATION RESEARCH LA English DT Article DE FLOW RATE CALCULATION; PROXIMAL FLOW CONVERGENCE; FLUID DYNAMICS; FINITE-DIFFERENCE MODELING; INVITRO MODELING; DOPPLER ECHOCARDIOGRAPHY ID MITRAL REGURGITATION; INVITRO; ECHOCARDIOGRAPHY; MOMENTUM; JETS AB Analysis of velocity acceleration proximal to a regurgitant valve has been proposed as a method to quantify the regurgitant flow rate (Q(o)). Previous work has assumed inviscid flow through an infinitesimal orifice, predicting hemispheric isovelocity shells, with calculated flow rate given by Q(c) = 2-tau-r(N)2v(N), where v(N) is user-selected velocity of interest and r(N) is the distance from that velocity to the orifice. To validate this approach more rigorously and investigate the impact of finite orifice size on the assumption of hemispheric symmetry, numerical and in vitro modeling was used. Finite-difference modeling demonstrated hemispheric shape for contours more than two orifice diameters from the orifice. More proximal than this (where the measured velocity v(N) exceeded 3% of the orifice velocity v(o)), flow was progressively underestimated, with a proportional error DELTA-Q/Q(o) nearly identical to the ratio of contour velocity to orifice velocity, v(N)/v(o). For the in vitro investigations, flow rates from 4.3 to 150 cm3/sec through 0.3 and 1.0 cm2 circular orifices were imaged with color Doppler with aliasing velocities from 19 to 36 cm/sec. Overall, the calculated flow (assuming hemispheric symmetry) correlated well with the true How, Q(c) = 0.88Q(o) - 7.82 (r = 0.945, SD = 12.2 cm3/sec, p < 0.0001, n = 48), but progressively underestimated flow when the v(N) approached the orifice velocity v(o). Applying a correction factor predicted by the numerical modeling, DELTA-Q was improved from - 13.81 +/- 13.01 cm3/sec (mean +/- SD) to + 1.54 +/- 5.67 cm3/sec. These data indicate that flow can be accurately calculated using the hemispheric assumption as Q(c) = 2-tau-r(N)2v(N) when v(N) << V(o). For larger v(N), flow is systematically underestimated, but a more accurate estimate may be obtained by multiplying Q(c) by v(o)/(v(o) - v(N)). These observations lend additional support for the clinical use of the proximal acceleration concept and suggest a simple correction factor to make a more accurate estimation of valvular regurgitation. C1 MASSACHUSETTS GEN HOSP,DEPT MED,CARDIAC UNIT,NONINVAS CARDIAC LAB,ZERO EMERSON PL,SUITE 2F,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 24 TC 111 Z9 111 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7330 J9 CIRC RES JI Circ.Res. PD MAY PY 1992 VL 70 IS 5 BP 923 EP 930 PG 8 WC Cardiac & Cardiovascular Systems; Hematology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Hematology GA HQ041 UT WOS:A1992HQ04100006 PM 1568302 ER PT J AU SCHUMACHER, HR AF SCHUMACHER, HR TI HYPERTROPHIC OSTEOARTHROPATHY - RHEUMATOLOGIC MANIFESTATIONS SO CLINICAL AND EXPERIMENTAL RHEUMATOLOGY LA English DT Article; Proceedings Paper CT 1ST INTERNATIONAL WORKSHOP ON HYPERTROPHIC OSTEOARTHROPATHY CY JUN 21-24, 1992 CL FLORENCE, ITALY SP UNIV FLORENCE, INST INTERNAL MED 4, UNIV ZAGREB, MED FAC, DEPT PHYS MED & RHEUMATOL, INST NACL CARDIOL IGNACIO CHAVEZ, DEPT RHEUMATOL DE HYPERTROPHIC OSTEOARTHROPATHY; DIGITAL CLUBBING; PACHYDERMOPERIOSTOSIS ID ARTICULAR MANIFESTATIONS; AORTIC PROSTHESIS; PACHYDERMOPERIOSTOSIS; CARCINOMA; INFECTION; TISSUE AB Arthropathy can occasionally be an early clue to the diagnosis of hypertrophic osteoarthropathy (HOA). Joint effusions are typically relatively non-inflammatory, while synovial membrane biopsies show a variety of vascular changes that suggest the consideration of several factors possibly involved in the pathogenesis of HOA. C1 VET AFFAIRS MED CTR,PHILADELPHIA,PA. RP SCHUMACHER, HR (reprint author), UNIV PENN,3RD RAVDIN BLDG HOSP,34TH & SPRUCE ST,PHILADELPHIA,PA 19104, USA. NR 29 TC 20 Z9 20 U1 0 U2 0 PU CLINICAL & EXPER RHEUMATOLOGY PI PISA PA VIA SANTA MARIA 31, 56126 PISA, ITALY SN 0392-856X J9 CLIN EXP RHEUMATOL JI Clin. Exp. Rheumatol. PD MAY-JUN PY 1992 VL 10 SU 7 BP 35 EP 40 PG 6 WC Rheumatology SC Rheumatology GA JC382 UT WOS:A1992JC38200009 PM 1623671 ER PT J AU WONG, TK PEKARY, AE HOO, GS BRADLEY, ME HERSHMAN, JM AF WONG, TK PEKARY, AE HOO, GS BRADLEY, ME HERSHMAN, JM TI COMPARISON OF METHODS FOR MEASURING FREE-THYROXINE IN NONTHYROIDAL ILLNESS SO CLINICAL CHEMISTRY LA English DT Article DE FLUORESCENCE POLARIZATION IMMUNOASSAY; RADIOIMMUNOASSAY; IMMUNORADIOMETRIC ASSAY ID TUMOR-NECROSIS-FACTOR; CRITICALLY ILL PATIENTS; NON-THYROIDAL ILLNESSES; FACTOR-ALPHA; EQUILIBRIUM DIALYSIS; SERUM; RADIOIMMUNOASSAY; ULTRAFILTRATION; INTERLEUKIN-1; MECHANISM AB Patients with severe nonthyroidal illness (NTI) often have decreased serum thyroxin (T4) concentrations and sometimes have decreased free T4 (FT4) and increased tumor necrosis factor-alpha (TNF-alpha) concentrations. We evaluated four commercial methods for measuring FT4 [Abbott IMx, Amersham Amerlex MAB, Nicholas, and Diagnostic Products Corporation (DPC) RIA] and one method for TNF-alpha in 41 NTI patients, 24 euthyroid control subjects, and 10 hypothyroid patients. Free T4 index (FTI) was also measured by the Abbott IMx method. Euthyroid subjects' results were in the stated normal ranges. NTI FT4 was subnormal in 2.4%, 61%, and 29% by the Nichols, DPC, and Amerlex methods, respectively. The DPC, Amersham Amerlex, and Abbott IMx methods gave significantly lower FT4 values for the NTI group than for the controls. There were good correlations between the various FT4 methods in the NTI group. FTI concentrations correlated well with FT4 for the euthyroid and hypothyroid groups but poorly for the NTI group. The Abbott IMx and Nichols RIA methods yield values in the hypothyroid range for only a small proportion of NTI patients. C1 W LOS ANGELES VET AFFAIRS MED CTR,ENDOCRINOL & METAB SECT,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. NR 29 TC 29 Z9 29 U1 0 U2 0 PU AMER ASSOC CLINICAL CHEMISTRY PI WASHINGTON PA 2101 L STREET NW, SUITE 202, WASHINGTON, DC 20037-1526 SN 0009-9147 J9 CLIN CHEM JI Clin. Chem. PD MAY PY 1992 VL 38 IS 5 BP 720 EP 724 PG 5 WC Medical Laboratory Technology SC Medical Laboratory Technology GA HU749 UT WOS:A1992HU74900020 PM 1582025 ER PT J AU OYEN, WJG CLAESSENS, RAMJ VANDERMEER, JWM RUBIN, RH STRAUSS, HW CORSTENS, FHM AF OYEN, WJG CLAESSENS, RAMJ VANDERMEER, JWM RUBIN, RH STRAUSS, HW CORSTENS, FHM TI INDIUM-111-LABELED HUMAN NONSPECIFIC IMMUNOGLOBULIN-G - A NEW RADIOPHARMACEUTICAL FOR IMAGING INFECTIOUS AND INFLAMMATORY FOCI SO CLINICAL INFECTIOUS DISEASES LA English DT Review ID POLYCLONAL HUMAN-IMMUNOGLOBULIN; CHRONIC OSTEOMYELITIS; MONOCLONAL-ANTIBODY; CLINICAL-EVALUATION; GA-67; SCINTIGRAPHY; CANCER; BONE; LEUKOCYTES; IN-111 AB Indium-111-labeled human nonspecific immunoglobulin G (In-111-IgG) is a newly developed radiopharmaceutical for imaging infectious and inflammatory foci. This article presents an over-view of the literature concerning In-111-IgG scintigraphy. The current theory about the mechanism of accumulation suggests that In-111-IgG accumulates in lesions as a result of enhanced vascular permeability and subsequent entrapment of the radiolabeled protein. Human studies show excellent results in imaging bone and joint, abdominal, and intravascular infection. Of special interest is the ability to depict infectious foci in granulocytopenic patients. The value of In-111-IgG scintigraphy for detection of infection is compared with that of gallium-67, labeled-leukocyte, and technetium-99m (Tc-99m) nanocolloid scintigraphy. The significance of differences between In-111-IgG scintigraphy and two other new scintigraphic techniques, Tc-99m-labeled IgG and Tc-99m-labeled murine monoclonal anti-granulocyte antibody BW 250/183, are discussed. C1 UNIV HOSP NIJMEGEN,DEPT INTERNAL MED,6500 HB NIJMEGEN,NETHERLANDS. MASSACHUSETTS GEN HOSP,MED SERV,INFECT DIS UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT NUCL MED,BOSTON,MA 02114. RP OYEN, WJG (reprint author), UNIV HOSP NIJMEGEN,DEPT NUCL MED,POB 9101,6500 HB NIJMEGEN,NETHERLANDS. RI Oyen, Wim/D-4178-2009; van der Meer, Jos/C-8521-2013 OI Oyen, Wim/0000-0001-8235-7078; van der Meer, Jos/0000-0001-5120-3690 NR 66 TC 41 Z9 41 U1 0 U2 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 1058-4838 J9 CLIN INFECT DIS JI Clin. Infect. Dis. PD MAY PY 1992 VL 14 IS 5 BP 1110 EP 1118 PG 9 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HQ569 UT WOS:A1992HQ56900019 PM 1600013 ER PT J AU LAWNER, P AF LAWNER, P TI NEW PERSPECTIVES ON NARCISSISM - PLAKUN,EM SO CONTEMPORARY PSYCHOLOGY LA English DT Book Review C1 MASSACHUSETTS GEN HOSP,POSTDOCTORAL FELLOWSHIP PROGRAM PSYCHOANALYT PSYCHOTHERAPY,BOSTON,MA 02114. RP LAWNER, P (reprint author), HARVARD UNIV,SCH MED,BOSTON,MA 02115, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD MAY PY 1992 VL 37 IS 5 BP 452 EP 453 PG 2 WC Psychology, Multidisciplinary SC Psychology GA HT086 UT WOS:A1992HT08600039 ER PT J AU FOSTER, CS AF FOSTER, CS TI TRICHIASIS PRECEDING CONJUNCTIVAL CHANGES IN CICATRICIAL PEMPHIGOID - REPLY SO CORNEA LA English DT Letter RP FOSTER, CS (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0277-3740 J9 CORNEA JI Cornea PD MAY PY 1992 VL 11 IS 3 BP 272 EP 273 PG 2 WC Ophthalmology SC Ophthalmology GA HQ033 UT WOS:A1992HQ03300017 ER PT J AU JANG, IK GOLD, HK LEINBACH, RC RIVERA, AG FALLON, JT BUNTING, S COLLEN, D AF JANG, IK GOLD, HK LEINBACH, RC RIVERA, AG FALLON, JT BUNTING, S COLLEN, D TI PERSISTENT INHIBITION OF ARTERIAL THROMBOSIS BY A 1-HOUR INTRAVENOUS-INFUSION OF ARGATROBAN, A SELECTIVE THROMBIN INHIBITOR SO CORONARY ARTERY DISEASE LA English DT Article DE ARTERIAL THROMBOSIS; ARGATROBAN; ASPIRIN; HEPARIN; THROMBIN INHIBITION ID PLASMINOGEN-ACTIVATOR; CORONARY THROMBOLYSIS; UNSTABLE ANGINA; PLATELET; ANGIOPLASTY; MECHANISMS; ASPIRIN; HEPARIN; PLAQUE; RICH AB Background: Thrombin plays a pivotal role in early platelet-mediated arterial thrombosis. Methods: The efficacy of a 1-hour infusion of the competitive synthetic thrombin inhibitor, argatroban, (2R,4R)-4-methyl-1-[N2-(3-methyl-1,2,3,4-tetrahydro-8-quinoline-sulfonyl)-L-arginyl]-2-piperidine-carboxylic acid monohydrate, relative to that of heparin, for the prevention of delayed (24 hours postinfusion) arterial thrombosis was studied. Results: Intravenous infusion of 50 U/kg heparin over 60 minutes was associated with arterial graft patency in only one of 11 animals after 24 hours. Heparin in combination with intravenous aspirin (17 mg/kg) maintained everted arterial graft patency at 24 hours in two of six rabbits, (P=0.51 vs heparin alone). Infusion of 100-mu-g/kg/min argatroban for 60 minutes prevented arterial graft occlusion in seven of 10 animals after 24 hours (P=0.008 vs heparin). The combination of argatroban and aspirin prevented occlusion within 24 hours in six of eight rabbits (P=0.28 vs heparin and aspirin). Pathologic examination of the grafts at 24 hours revealed that graft segment thrombosis was significantly less extensive in the group receiving argatroban alone than in the group receiving heparin alone (P=0.013). Conclusions: These findings indicate that a 1-hour intravenous infusion of the selective thrombin inhibitor, argatroban, reduces delayed (24 hours) arterial eversion graft thrombosis much more efficiently than heparin. C1 MASSACHUSETTS GEN HOSP,CARDIAC UNIT,ACC 480,15 PARKMAN ST,BOSTON,MA 02114. GENENTECH INC,SAN FRANCISCO,CA 94080. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 18 TC 13 Z9 13 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0954-6928 J9 CORONARY ARTERY DIS JI Coronary Artery Dis. PD MAY PY 1992 VL 3 IS 5 BP 407 EP 414 DI 10.1097/00019501-199205000-00009 PG 8 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HX878 UT WOS:A1992HX87800009 ER PT J AU ARCECI, RJ PAMPFER, S POLLARD, JW AF ARCECI, RJ PAMPFER, S POLLARD, JW TI EXPRESSION OF CSF-1/C-FMS AND SF/C-KIT MESSENGER-RNA DURING PREIMPLANTATION MOUSE DEVELOPMENT SO DEVELOPMENTAL BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; TYROSINE KINASE RECEPTOR; FMS PROTO-ONCOGENE; STEM-CELL FACTOR; C-KIT; GROWTH-FACTOR; W-LOCUS; SI-LOCUS; PLACENTAL DEVELOPMENT; FACTOR-I C1 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT DEV BIOL & CANC,BRONX,NY 10461. RP ARCECI, RJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115, USA. FU NCI NIH HHS [P30-CA1330]; NICHD NIH HHS [HD25076]; NIGMS NIH HHS [GM38156] NR 39 TC 79 Z9 79 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 0012-1606 J9 DEV BIOL JI Dev. Biol. PD MAY PY 1992 VL 151 IS 1 BP 1 EP 8 DI 10.1016/0012-1606(92)90207-W PG 8 WC Developmental Biology SC Developmental Biology GA HT364 UT WOS:A1992HT36400001 PM 1374350 ER PT J AU ZIESKE, JD BUKUSOGLU, G YANKAUCKAS, MA WASSON, ME KEUTMANN, HT AF ZIESKE, JD BUKUSOGLU, G YANKAUCKAS, MA WASSON, ME KEUTMANN, HT TI ALPHA-ENOLASE IS RESTRICTED TO BASAL CELLS OF STRATIFIED SQUAMOUS EPITHELIUM SO DEVELOPMENTAL BIOLOGY LA English DT Article ID EPIDERMAL GROWTH-FACTOR; NON-NEURONAL ENOLASE; RAT-BRAIN ENOLASE; MESSENGER-RNA; FACTOR RECEPTORS; STEM-CELLS; DIFFERENTIATION; CULTURE; FIBROBLASTS; EXPRESSION C1 MASSACHUSETTS GEN HOSP,CORNEA UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP ZIESKE, JD (reprint author), MASSACHUSETTS GEN HOSP,EYE RES INST,BOSTON,MA 02114, USA. FU NEI NIH HHS [R01-EY05665] NR 52 TC 65 Z9 65 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 SN 0012-1606 J9 DEV BIOL JI Dev. Biol. PD MAY PY 1992 VL 151 IS 1 BP 18 EP 26 DI 10.1016/0012-1606(92)90209-Y PG 9 WC Developmental Biology SC Developmental Biology GA HT364 UT WOS:A1992HT36400003 PM 1577187 ER PT J AU COHEN, RM NATHAN, DM CLEMENTS, RS AF COHEN, RM NATHAN, DM CLEMENTS, RS TI HYPERPROINSULINEMIA IN TYPE-II DIABETES SO DIABETES CARE LA English DT Letter ID INSULIN; PROINSULIN; MELLITUS; SPLIT C1 UNIV CINCINNATI,COLL MED,DEPT INTERNAL MED,CINCINNATI,OH 45221. HARVARD UNIV,SCH MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. UNIV PENN,SCH MED,DEPT MED,PHILADELPHIA,PA 19104. NR 16 TC 15 Z9 15 U1 0 U2 0 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1660 DUKE ST, ALEXANDRIA, VA 22314 SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD MAY PY 1992 VL 15 IS 5 BP 723 EP 724 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HR039 UT WOS:A1992HR03900020 PM 1516496 ER PT J AU XAVIER, RJ STEIN, CM KIIRE, CF ARROW, J KITAI, I AF XAVIER, RJ STEIN, CM KIIRE, CF ARROW, J KITAI, I TI VALUE OF THE HISTORY AND STOOL OCCULT BLOOD-TEST IN SELECTION OF PATIENTS FOR UPPER ENDOSCOPY IN ZIMBABWE SO EAST AFRICAN MEDICAL JOURNAL LA English DT Article ID OPEN-ACCESS ENDOSCOPY; ULCER-LIKE DYSPEPSIA AB Patients with abdominal pain and no definite diagnosis referred for endoscopy were studied to define discriminating features in the history, and the value of a stool occult blood test, in predicting the presence of upper gastrointestinal disease. Endoscopy was performed in 116 patients; pathology was seen in 32 (duodenal ulcer 17, gastric carcinoma 4, gastric ulcer 3, miscellaneous 8) and no pathology was seen in 84 patients. Features that predicted upper gastrointestinal pathology were, in descending order of rank: a positive pointing sign, a positive stool Fecult test, a history of vomiting, loss or weight, and alcohol intake. Using these discriminating features together it was possible to correctly predict 95% of patients with abnormal endoscopy and 82% of patients with a normal endoscopy. The history and the stool occult blood test are useful predictors of the presence of upper gastrointestinal pathology and may aid rational selection of patients for endoscopy. C1 UNIV ZIMBABWE,SCH MED,HARARE,ZIMBABWE. RP XAVIER, RJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114, USA. NR 17 TC 0 Z9 0 U1 0 U2 0 PU EAST AFRICAN MEDICAL JOURNAL PI NAIROBI PA CHYULU ROAD PO BOX 41632, NAIROBI, KENYA SN 0012-835X J9 E AFR MED J JI East Afr. Med. J. PD MAY PY 1992 VL 69 IS 5 BP 268 EP 271 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA JR821 UT WOS:A1992JR82100010 PM 1644046 ER PT J AU FEHMANN, HC HABENER, JF AF FEHMANN, HC HABENER, JF TI GALANIN INHIBITS PROINSULIN GENE-EXPRESSION STIMULATED BY THE INSULINOTROPIC HORMONE GLUCAGON-LIKE PEPTIDE-I(7-37) IN MOUSE INSULINOMA BETA-TC-1 CELLS SO ENDOCRINOLOGY LA English DT Article ID PEPTIDE-I; RAT PANCREAS; K+ CHANNELS; ENDOCRINE PANCREAS; ADENYLATE-CYCLASE; SECRETING CELLS; RINM5F CELLS; G-PROTEIN; RELEASE; RECEPTORS AB The neuropeptide hormone galanin, released by sympathetic stimulation of nerve terminals in the endocrine pancreas, inhibits insulin secretion via a receptor-linked pertussis toxin-sensitive (G(i)) transmembrane signaling pathway. Glucagon-like peptide-I(7-37) [GLP-I(7-37)] is an intestinal hormone shown to have potent insulin-releasing activities in pancreatic B-cells and is believed to serve a physiological role in the augmentation of nutrient-induced insulin release. GLP-1(7-37) binds to specific G8- and adenylate cyclase-coupled receptors on pancreatic B-cells and directly stimulates proinsulin gene transcription, thereby increasing cellular levels of proinsulin messenger RNA (mRNA) and proinsulin biosynthesis. This study examines the effects of galanin on GLP-I(7-37)-stimulated proinsulin gene expression in mouse beta-TC1 cells. The degree of proinsulin gene transcription was assessed by measuring the activity of chloramphenicol acetyl transferase (CAT) expressed from a CAT reporter plasmid linked to the rat insulin-I gene promoter transferred to beta-TC1 cells and by measuring proinsulin mRNA levels by Northern blot analysis. Galanin inhibited both CAT activity and the rise in proinsulin mRNA levels stimulated by either GLP-1(7-37) or forskolin (0.1-mu-m). Notably, galanin was without effect on CAT activity induced by the cAMP analog, 8-bromo-cAMP, the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, or higher concentrations of forskolin. The inhibitory effects of galanin on GLP-1(7-37) and forskolin-induced CAT activity were reversed by the addition of pertussis toxin, a toxin that inactivates inhibitory G-proteins (G(i)). We conclude that galanin inhibits GLP-1(7-37)-stimulated proinsulin gene expression by inhibiting the activation of adenylate cyclase by GLP-I(7-37) and subsequently the production of cAMP in B-cells. Further, our data suggest that these actions of galanin are mediated by a pertussis toxin sensitive pathway involving one or more G(i)s that inhibit adenylate cyclase. Thus, in addition to its well known inhibitory effects on insulin secretion galanin can inhibit proinsulin gene expression stimulated by GLP-1(7-37) activation of the cAMP signaling pathway. These findings may be a unique demonstration of the inhibition of proinsulin gene expression by a substance (galanin) released endogenously within the pancreas. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,MOLEC ENDOCRINOL LAB,BOSTON,MA 02114. FU NIDDK NIH HHS [DK-30834] NR 55 TC 28 Z9 28 U1 0 U2 3 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAY PY 1992 VL 130 IS 5 BP 2890 EP 2896 DI 10.1210/en.130.5.2890 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HR339 UT WOS:A1992HR33900060 PM 1374016 ER PT J AU WILSON, JM GROSSMAN, M THOMPSON, AR LUPASSIKIS, C ROSENBERG, A POTTS, JT KRONENBERG, HM MULLIGAN, RC NUSSBAUM, SR AF WILSON, JM GROSSMAN, M THOMPSON, AR LUPASSIKIS, C ROSENBERG, A POTTS, JT KRONENBERG, HM MULLIGAN, RC NUSSBAUM, SR TI SOMATIC GENE-TRANSFER IN THE DEVELOPMENT OF AN ANIMAL-MODEL FOR PRIMARY HYPERPARATHYROIDISM SO ENDOCRINOLOGY LA English DT Article ID MICROCARRIER-ATTACHED HEPATOCYTES; PARATHYROID-HORMONE; SKIN FIBROBLASTS; HYPERCALCEMIA; THERAPY; IDENTIFICATION; EXPRESSION; VECTORS; CANCER; CELLS AB The overproduction of hormones is associated with a variety of endocrinological disorders. We have used somatic cell gene transfer of human PTH (hPTH) to develop an animal model of hypercalcemia and osteoclastic skeletal resorption. Recombinant retroviruses were used to transduce a functional hPTH gene into cultured rat fibroblasts. The recombinant-derived preproparathyroid hormone peptide was appropriately processed in this ectopic cell, and intact hPTH (1-84) was secreted at a high level (2-5 ng/10(6) cells/24 h). Transplantation of the PTH-secreting cells into syngeneic rat recipients was associated with the development of hypercalcemia mediated by increasing serum concentrations of hPTH. Thyroparathyroidectomy in these hypercalcemic rats producing hPTH did not result in hypocalcemia and tetany, which was observed in control animals undergoing thyroparathyroidectomy. Chronic overproduction of hPTH (60 days) was associated with severe hypercalcemia, metastatic calcification, and histological changes of osteoclastic resorption of bone. This animal model will be useful in studying the pathophysiology of severe hyperparathyroidism in humans and should help in the evaluation of new medical therapies for hypercalcemia. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MED SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. MIT,WHITEHEAD INST,DEPT BIOL,CAMBRIDGE,MA 02139. RP WILSON, JM (reprint author), UNIV MICHIGAN,SCH MED,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109, USA. RI Wilson, James/F-9220-2011 OI Wilson, James/0000-0002-9630-3131 NR 28 TC 5 Z9 5 U1 0 U2 2 PU ENDOCRINE SOC PI BETHESDA PA 4350 EAST WEST HIGHWAY SUITE 500, BETHESDA, MD 20814-4110 SN 0013-7227 J9 ENDOCRINOLOGY JI Endocrinology PD MAY PY 1992 VL 130 IS 5 BP 2947 EP 2954 DI 10.1210/en.130.5.2947 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HR339 UT WOS:A1992HR33900067 PM 1315263 ER PT J AU LIANG, JJN LI, XY AF LIANG, JJN LI, XY TI SPECTROSCOPIC STUDIES ON THE INTERACTION OF CALF LENS MEMBRANES WITH CRYSTALLINS SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE CRYSTALLIN; MEMBRANE; LIPOSOME; FLUORESCENCE; CIRCULAR DICHROISM ID ALPHA-CRYSTALLIN; PLASMA-MEMBRANES; BOVINE; FLUORESCENCE; AFFINITY; BINDING C1 HARVARD UNIV,SCH MED,MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB OPHTHALMOL,DEPT OPHTHALMOL,BOSTON,MA 02115. FU NEI NIH HHS [EY05803] NR 18 TC 22 Z9 22 U1 0 U2 4 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD MAY PY 1992 VL 54 IS 5 BP 719 EP 724 DI 10.1016/0014-4835(92)90026-O PG 6 WC Ophthalmology SC Ophthalmology GA HY289 UT WOS:A1992HY28900008 PM 1623956 ER PT J AU LARUSSA, VF GRIFFIN, JD KESSLER, SW CUTTING, MA KNIGHT, RD BLATTLER, WA LAMBERT, JM WRIGHT, DG AF LARUSSA, VF GRIFFIN, JD KESSLER, SW CUTTING, MA KNIGHT, RD BLATTLER, WA LAMBERT, JM WRIGHT, DG TI EFFECTS OF ANTI-CD33 BLOCKED RICIN IMMUNOTOXIN ON THE CAPACITY OF CD34+ HUMAN MARROW-CELLS TO ESTABLISH INVITRO HEMATOPOIESIS IN LONG-TERM MARROW CULTURES SO EXPERIMENTAL HEMATOLOGY LA English DT Article DE ANTI-CD33 IMMUNOTOXIN; HEMATOPOIESIS; CD34; MARROW TRANSPLANTATION; LONG-TERM MARROW CULTURES ID COLONY-FORMING CELLS; HUMAN-BONE-MARROW; PROGENITOR CELLS; LIMITING DILUTION; PRECURSORS; EXPRESSION; UNIPOTENT; ANTIGEN; MOUSE AB Human marrow cells that express the CD34 antigen but lack CD33 are able to initiate sustained, multilineage in vitro hematopoiesis in long-term Dexter cultures and are believed to include the primitive stem cells responsible for effecting long-term hematopoietic reconstitution in vivo following marrow transplantation. In studies described in this report we investigated the effects of a novel anti-CD33 immunotoxin on the clonogenic potential of normal human CD34+ marrow cells and on the ability of these cells to initiate hematopoiesis in two-stage Dexter cultures (long-term marrow cultures, LTMC). This immunotoxin (anti-CD33-bR), shown previously to kill both clonogenic myelogenous leukemia cells and normal mature myeloid progenitor cells (granulocyte-macrophage colony-forming units, CFU-GM), consists of an anti-CD33 monoclonal antibody conjugated to purified ricin that has been modified by blocking the carbohydrate binding domains of the ricin B-chain to eliminate nonspecific binding. For our studies, normal CD34+ human marrow cells were isolated from the light-density (< 1.070 g/ml) cells of aspirated marrow by positive selection with immunomagnetic beads linked to the monoclonal antibody K6.1. These cell isolates were highly enriched with both multipotential and lineage-restricted clonogenic, hematopoietic progenitors (mixed lineage colony-forming units, CFU-Mix; CFU-GM; and erythroid burst-forming units, BFU-E) which constituted greater-than-or-equal-to 20% of the cells. Recovery of clonogenic progenitors from these CD34+ cell preparations, following treatment with anti-CD33-bR (10 nM), was reduced by greater-than-or-equal-to 85% for CFU-GM and 20%-40% for CFU-Mix and BFU-E. However, the capacity of these cells to initiate hematopoietic LTMC was preserved. Indeed, the production of high proliferative potential (HPP) CFU-GM, BFU-E, and CFU-Mix in cultures seeded with 10(5) anti-CD33-bR-treated CD34+ marrow cells was substantially greater than that observed in LTMC seeded with equivalent numbers of untreated CD34+ cells. Moreover, concentrations of long-term culture initiating cells in CD34+ cell isolates, quantified by a limiting dilution technique, were found to be increased following anti-CD33-bR treatment. These findings support the potential usefulness of anti-CD33-bR for in vitro marrow purging or in vivo treatment to eliminate CD33+ leukemic clones, while sparing normal CD34+/CD33- stem cells that support normal hematopoiesis and hematopoietic reconstitution in vivo. C1 USN,RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20814. IMMUNOGEN INC,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. RP LARUSSA, VF (reprint author), WALTER REED ARMY MED CTR,DIV MED,DEPT HEMATOL,WASHINGTON,DC 20307, USA. NR 30 TC 29 Z9 29 U1 0 U2 0 PU CARDEN JENNINGS PUBL CO LTD PI CHARLOTTESVILLE PA BLAKE CTR, STE 200, 1224 W MAIN ST, CHARLOTTESVILLE, VA 22903 SN 0301-472X J9 EXP HEMATOL JI Exp. Hematol. PD MAY PY 1992 VL 20 IS 4 BP 442 EP 448 PG 7 WC Hematology; Medicine, Research & Experimental SC Hematology; Research & Experimental Medicine GA HT028 UT WOS:A1992HT02800013 PM 1373688 ER PT J AU POLK, WH DEMPSEY, PJ RUSSELL, WE BROWN, PI BEAUCHAMP, RD BARNARD, JA COFFEY, RJ AF POLK, WH DEMPSEY, PJ RUSSELL, WE BROWN, PI BEAUCHAMP, RD BARNARD, JA COFFEY, RJ TI INCREASED PRODUCTION OF TRANSFORMING GROWTH-FACTOR ALPHA FOLLOWING ACUTE GASTRIC INJURY SO GASTROENTEROLOGY LA English DT Article ID MESSENGER-RNA; MUCOSAL GROWTH; RAT; UROGASTRONE; CELLS; EXPRESSION; PRECURSOR; DAMAGE; SURFACE; MUCUS C1 VANDERBILT UNIV,DEPT MED,NASHVILLE,TN 37232. VANDERBILT UNIV,DEPT SURG,NASHVILLE,TN 37240. VANDERBILT UNIV,DEPT PEDIAT,NASHVILLE,TN 37240. VANDERBILT UNIV,DEPT CELL BIOL,NASHVILLE,TN 37240. UNIV TEXAS,MED BRANCH,DEPT SURG,GALVESTON,TX 77550. MASSACHUSETTS GEN HOSP,CHILDRENS SERV,BOSTON,MA 02114. RI Russell, William/A-7307-2009 FU NCI NIH HHS [CA 01309, CA 08815-02, CA 46413] NR 48 TC 149 Z9 150 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 MAY PY 1992 VL 102 IS 5 BP 1467 EP 1474 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HR049 UT WOS:A1992HR04900003 PM 1568557 ER PT J AU TARGAN, SR LANDERS, CJ KING, NW PODOLSKY, DJ SHANAHAN, F AF TARGAN, SR LANDERS, CJ KING, NW PODOLSKY, DJ SHANAHAN, F TI ULCERATIVE-COLITIS LINKED ANTINEUTROPHIL CYTOPLASMIC ANTIBODY IN THE COTTON-TOP TAMARIN MODEL OF COLITIS SO GASTROENTEROLOGY LA English DT Article ID EPSTEIN-BARR VIRUS; TUMOR INCIDENCE; VIRAL-DNA; MARMOSETS; DISEASE; AUTOANTIBODIES; INOCULATION; RESPONSES; LYMPHOMA; INVITRO C1 HARVARD UNIV,SCH MED,NEW ENGLAND PRIMATE CTR,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP TARGAN, SR (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DIV GASTROENTEROL,900 VET AVE,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [AI 15332]; NIDDK NIH HHS [DK 40057, DK 34422] NR 30 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 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD MAY PY 1992 VL 102 IS 5 BP 1493 EP 1498 PG 6 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HR049 UT WOS:A1992HR04900006 PM 1568559 ER PT J AU WALSH, RM ACKROYD, FW SHELLITO, PC AF WALSH, RM ACKROYD, FW SHELLITO, PC TI ENDOSCOPIC RESECTION OF LARGE SESSILE COLORECTAL POLYPS SO GASTROINTESTINAL ENDOSCOPY LA English DT Article ID EXCISION AB Colonoscopic removal of large, sessile polyps is difficult, but can be successfully carried out by experienced endoscopists. "Piecemeal" resection with an electrocautery snare was performed at our institution in 108 patients with 132 such lesions. The mean size of the unresected polyps was 3.0 cm. Complications occurred in 3.0% of polypectomies (3.8% of patients), with bleeding necessitating transfusion in 2.3% of polypectomies (2.8% of patients), and microperforation (probable) in the remainder. No patient required emergency surgery due to a complication. In 65 patients (60%), colonoscopic resection and follow-up alone was carried out. Of these, adenomas recurred/persisted in 28%, most of which were successfully re-resected. Nearly half of all recurrent polyps occurred after at least one negative intervening examination. Carcinoma later appeared in 17% of the recurrences despite apparent initial complete resection of a previously benign polyp. Cure was ultimately achieved in 88% of endoscopically managed patients. Surgical resection was required in 27% of patients, mostly following the initial polypectomy when invasive carcinoma was found in the specimen. No residual tumor was later found in 41% of the colon specimens from these patients. Ninety-one percent of cancers were favorable stage, whether discovered early or late. Follow-up colonoscopy was achieved in 77% of patients over an average of 3.7 years. Metachronous polyps were excised in 52 patients (63%) and metachronous carcinoma was diagnosed in 3 patients (3.6%). An aggressive regimen of surveillance colonoscopy is warranted in these patients to detect and manage local recurrences and to remove subsequent adenomas. Endoscopic resection of large sessile adenomas can be safe and effective. C1 MASSACHUSETTS GEN HOSP,CTR AMBULATORY CARE,SURG SERV,336,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. NR 10 TC 135 Z9 141 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0016-5107 J9 GASTROINTEST ENDOSC JI Gastrointest. Endosc. PD MAY-JUN PY 1992 VL 38 IS 3 BP 303 EP 309 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HX668 UT WOS:A1992HX66800001 PM 1607080 ER PT J AU GUSELLA, JF ALTHERR, MR MCCLATCHEY, AI DOUCETTESTAMM, LA TAGLE, D PLUMMER, S GROOT, N BARNES, G HUMMERICH, H COLLINS, FS HOUSMAN, DE LEHRACH, H MACDONALD, ME BATES, G WASMUTH, JJ AF GUSELLA, JF ALTHERR, MR MCCLATCHEY, AI DOUCETTESTAMM, LA TAGLE, D PLUMMER, S GROOT, N BARNES, G HUMMERICH, H COLLINS, FS HOUSMAN, DE LEHRACH, H MACDONALD, ME BATES, G WASMUTH, JJ TI SEQUENCE-TAGGED SITES (STSS) SPANNING-4P16.3 AND THE HUNTINGTON DISEASE CANDIDATE REGION SO GENOMICS LA English DT Article ID HUMAN GENOME; CELL HYBRID; DNA MARKERS; GENE; CHROMOSOME-4; TELOMERE; SEGMENT; LOCUS C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02129. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. RP GUSELLA, JF (reprint author), MASSACHUSETTS GEN HOSP,NEUROGENET LAB,BOSTON,MA 02129, USA. RI Bates, Gillian/E-1146-2012 OI Bates, Gillian/0000-0002-4041-6305 FU NHGRI NIH HHS [HG00320, HG00169]; NINDS NIH HHS [NS16367] NR 37 TC 13 Z9 13 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 MAY PY 1992 VL 13 IS 1 BP 75 EP 80 DI 10.1016/0888-7543(92)90204-6 PG 6 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA HM699 UT WOS:A1992HM69900012 PM 1533609 ER PT J AU WANDALL, JH AF WANDALL, JH TI EFFECTS OF OMEPRAZOLE ON NEUTROPHIL CHEMOTAXIS, SUPER OXIDE PRODUCTION, DEGRANULATION, AND TRANSLOCATION OF CYTOCHROME-B-245 SO GUT LA English DT Article ID FACTOR-INDUCED ACTIVATION; GASTRIC-ACID SECRETION; SUBCELLULAR-LOCALIZATION; RESPIRATORY BURST; PLASMA-MEMBRANES; NA+/H+ EXCHANGE; PROTON PUMP; PH; INHIBITOR; MONOCYTES AB The effects of omeprazole on polymorphonuclear neutrophil (PMN) chemotaxis, superoxide generation, degranulation and translocation of cytochrome b-245 were investigated. Omeprazole (10(-6) - 5 X 10(-3) mol/l) reduced chemotaxis under agarose in a dose dependent manner, and the effect was irreversible. Superoxide anion generation was inhibited 50% at a concentration of 2.5 X 10(-5) mol/l and completely abolished at 5 X 10(-3) mol/l Acid degraded omeprazole also inhibited O2- generation. Omeprazole did not scavenge O2- generated in a cell free xanthin-xanthine oxidase system. Degranulation by PMNs was inhibited only by omeprazole in concentrations above 10(-4) mol/l. Translocation of cytochrome b-245, essential for generation Of O2-, was not affected by omeprazole. In conclusion, the anti-ulcer agent omeprazole in concentrations obtained during intravenous administration may inhibit the function of PMNs in vitro. C1 MASSACHUSETTS GEN HOSP,BLOOD TRANSFUS SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 28 TC 120 Z9 124 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0017-5749 J9 GUT JI Gut PD MAY PY 1992 VL 33 IS 5 BP 617 EP 621 DI 10.1136/gut.33.5.617 PG 5 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HU152 UT WOS:A1992HU15200011 PM 1319381 ER PT J AU LEFFERT, RD AF LEFFERT, RD TI THORACIC OUTLET SYNDROMES SO HAND CLINICS LA English DT Article RP LEFFERT, RD (reprint author), MASSACHUSETTS GEN HOSP,SURG UPPER EXTREM REHABIL UNIT,WHITE 10,BOSTON,MA 02114, USA. NR 0 TC 27 Z9 30 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0749-0712 J9 HAND CLIN JI Hand Clin. PD MAY PY 1992 VL 8 IS 2 BP 285 EP 297 PG 13 WC Orthopedics SC Orthopedics GA HV113 UT WOS:A1992HV11300009 PM 1613036 ER PT J AU LEO, MA KIM, CI LOWE, N LIEBER, CS AF LEO, MA KIM, CI LOWE, N LIEBER, CS TI INTERACTION OF ETHANOL WITH BETA-CAROTENE - DELAYED BLOOD CLEARANCE AND ENHANCED HEPATOTOXICITY SO HEPATOLOGY LA English DT Article ID VITAMIN-A; DEHYDROGENASE-ACTIVITY; ALCOHOL; CANCER; RAT; CONSUMPTION; RISK; LUNG; ANTIOXIDANT; CONVERSION AB Because we had found that ethanol interacts with retinol, we investigated whether it also affects its precursor, beta-carotene. In 14 baboons fed ethanol (50% of total energy) for 2 to 5 yr with a standard amount of beta-carotene (one 200-gm carrot/day), levels of beta-carotene were much higher than in controls fed isocaloric carbohydrate, both in plasma (122.5 +/- 30.9 nmol/dl vs. 6.3 +/- 1.4 nmol/dl; p < 0.005) and in liver (7.9 +/- 1.1 nmol/gm vs. 1.8 +/- 0.5 nmol/gm; p < 0.001). Even 20 days after withdrawal of the carrots, plasma beta-carotene levels remained higher in alcohol-fed baboons than in controls (10.1 +/- 3.8 nmol/dl vs. < 0.1 nmol/dl). Next, the diet was supplemented with beta-carotene beadlets: in four pairs of baboons given a low dose of beta-carotene (3 mg/1,000 kcal), plasma levels were significantly higher in alcohol-fed animals than in controls, even when expressed per cholesterol (although the latter increased with alcohol intake). Seven pairs of animals were given a higher dose (30 mg/1,000 kcal) of beta-carotene for 1 mo, followed, in four pairs, by 45 mg for another month. On cessation of beta-carotene treatment, plasma levels decreased more slowly in the alcohol-fed baboons than in the controls. Percutaneous liver biopsy specimens revealed that liver concentrations of beta-carotene correlated with plasma levels but were higher in the alcohol-fed baboons than in the control baboons, whereas the beta-carotene-induced increase in liver retinoids was lower (p < 0.02). Furthermore, the ethanol-induced liver depletion of total retinoids (432 +/- 103 nmol/gm vs. 1,711 +/- 103 in controls; p < 0.001) was not corrected (637 +/- 149 vs. 2,404 +/- 74; p < 0.001), despite the massive supplementation with beta-carotene. Moreover, in the animals fed alcohol with beta-carotene, multiple ultrastructural lesions appeared, with autophagic vacuoles, abundant myelin figures, degenerated mitochondria and increased blood levels of the mitochondrial enzyme glutamic dehydrogenase. The histological changes were either absent or much less prominent in the baboons given beta-carotene with the control diet or in animals fed the ethanol or control diets without beta-carotene. Thus the combination of an increase in plasma and liver beta-carotene after ethanol and a relative lack of a corresponding rise in retinol suggests interference with the conversion of beta-carotene to vitamin A. Because of an associated exacerbation of the liver toxicity, we conclude that beta-carotene must be administered cautiously in the presence of heavy alcohol consumption because the optimal human therapeutic dose remains to be defined. C1 BRONX VET AFFAIRS MED CTR,CTR ALCOHOL RES & TREATMENT,151-G,130 W KINGSBRIDGE RD,BRONX,NY 10468. CUNY MT SINAI SCH MED,NEW YORK,NY 10029. BRONX VET AFFAIRS MED CTR,LIVER DIS SECT,BRONX,NY. FU NIAAA NIH HHS [AA03508]; NIDDK NIH HHS [DK32810] NR 52 TC 78 Z9 79 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD MAY PY 1992 VL 15 IS 5 BP 883 EP 891 DI 10.1002/hep.1840150522 PG 9 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HR635 UT WOS:A1992HR63500021 PM 1568731 ER PT J AU JAMESON, JL HOLLENBERG, AN AF JAMESON, JL HOLLENBERG, AN TI RECENT ADVANCES IN STUDIES OF THE MOLECULAR-BASIS OF ENDOCRINE DISEASE SO HORMONE AND METABOLIC RESEARCH LA English DT Article DE INHERITED ENDOCRINE DISEASE; GENES; MUTATIONS; RECOMBINANT DNA; HORMONE RESISTANCE ID THYROXINE-BINDING GLOBULIN; THYROID-STIMULATING HORMONE; GROWTH-HORMONE; HYPOGONADOTROPIC HYPOGONADISM; HEREDITARY OSTEODYSTROPHY; RESISTANT RICKETS; DETERMINING GENE; G-PROTEIN; DEFICIENCY; MUTATION AB The molecular basis for a number of endocrine disorders has been determined in the last several years. Mutations have been described at multiple different steps in the pathways of hormone action. There are now examples of mutations in hormones themselves, hormone receptors, second messenger signalling pathways, and the transcription factors that transduce hormone signals. Several common themes emerge even from the relatively small number of mutations that have been described to date. First, the phenotypic variability that characterizes many endocrine diseases is also reflected in genetic heterogeneity. Some clinical phenotypes that were thought previously to represent distinct diseases can now be interpreted as manifestations of different types of mutations within a single gene. Second, the propensity of certain genes to be targets for frequent mutations may be explained in part by gene structure and organization. Third, although many of the mutations reported initially have been associated with severely affected patients, it is likely that mutations with less severe consequences will also be identified. Genetic polymorphisms within the normal population could also cause subtle differences in hormone or receptor activity, thereby constituting part of the basis for variability in hormone levels and activity. Finally, one can predict continued rapid advances in this field with transfer of genetic testing into clinical practice in the near future. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JAMESON, JL (reprint author), MASSACHUSETTS GEN HOSP,THYROID UNIT,JACKSON 1021,BOSTON,MA 02114, USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD23519]; NIDDK NIH HHS [DK42144] NR 49 TC 6 Z9 6 U1 0 U2 0 PU GEORG THIEME VERLAG PI STUTTGART PA P O BOX 30 11 20, D-70451 STUTTGART, GERMANY SN 0018-5043 J9 HORM METAB RES JI Horm. Metab. Res. PD MAY PY 1992 VL 24 IS 5 BP 201 EP 209 DI 10.1055/s-2007-1003294 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HV580 UT WOS:A1992HV58000001 PM 1398458 ER PT J AU YOUNG, RH GERSELL, DJ CLEMENT, PB SCULLY, RE AF YOUNG, RH GERSELL, DJ CLEMENT, PB SCULLY, RE TI HEPATOCELLULAR-CARCINOMA METASTATIC TO THE OVARY - A REPORT OF 3 CASES DISCOVERED DURING LIFE WITH DISCUSSION OF THE DIFFERENTIAL-DIAGNOSIS OF HEPATOID TUMORS OF THE OVARY SO HUMAN PATHOLOGY LA English DT Article DE OVARY; METASTATIC HEPATOMA; LIVER ID LUNG C1 WASHINGTON UNIV,BARNES HOSP,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. VANCOUVER GEN HOSP,DEPT PATHOL,VANCOUVER V5Z 1M9,BC,CANADA. UNIV BRITISH COLUMBIA,DEPT PATHOL,VANCOUVER V6T 1W5,BC,CANADA. RP YOUNG, RH (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114, USA. NR 21 TC 46 Z9 47 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD MAY PY 1992 VL 23 IS 5 BP 574 EP 580 DI 10.1016/0046-8177(92)90136-Q PG 7 WC Pathology SC Pathology GA HU056 UT WOS:A1992HU05600016 PM 1314779 ER PT J AU WALD, TG TOBACMAN, JK AF WALD, TG TOBACMAN, JK TI PREVENTION OF INFECTIOUS-DISEASES IN AMBULATORY CARE - IMMUNOPROPHYLAXIS AND CHEMOPROPHYLAXIS SO INFECTION CONTROL AND HOSPITAL EPIDEMIOLOGY LA English DT Article ID AMERICAN-HEART-ASSOCIATION; ACUTE RHEUMATIC-FEVER; IMMUNIZATION POLICIES; INFLUENZA VACCINATION; MISSED OPPORTUNITIES; UNITED-STATES; ENDOCARDITIS; RESURGENCE; REDUCTION; AREA AB OBJECTIVE: To review the current recommendations for immunoprophylaxis and chemoprophylaxis of infection in adults, including those who are at increased risk from occupation, lifestyle, travel, or pre-existing medical conditions. DESIGN: Review of the pertinent literature. SETTING: Adult ambulatory care. CONCLUSIONS: Guidelines for the prevention of several diseases including measles, tuberculosis, and bacterial endocarditis recently have been changed. Current recommendations for immunization, immune globulin therapy, and chemotherapy for these and other common infections are reviewed. C1 UNIV IOWA,COLL MED,DEPT INTERNAL MED,IOWA CITY,IA 52242. WILLIAM S MIDDLETON MEM VET ADM MED CTR,GERIAT SECT,MADISON,WI. NR 38 TC 0 Z9 0 U1 2 U2 2 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0899-823X J9 INFECT CONT HOSP EP JI Infect. Control Hosp. Epidemiol. PD MAY PY 1992 VL 13 IS 5 BP 272 EP 281 PG 10 WC Public, Environmental & Occupational Health; Infectious Diseases SC Public, Environmental & Occupational Health; Infectious Diseases GA HU432 UT WOS:A1992HU43200006 PM 1593110 ER PT J AU PAUL, SR SCHENDEL, P AF PAUL, SR SCHENDEL, P TI THE CLONING AND BIOLOGICAL CHARACTERIZATION OF RECOMBINANT HUMAN INTERLEUKIN-11 SO INTERNATIONAL JOURNAL OF CELL CLONING LA English DT Review DE INTERLEUKIN-11; HEMATOPOIETIC GROWTH FACTOR; BONE MARROW MICROENVIRONMENT ID MEGAKARYOCYTE COLONY FORMATION; LARGE T-ANTIGEN; CELL-GROWTH; STIMULATING FACTORS; BONE-MARROW; MOLECULAR-CLONING; LYMPHOCYTES-B; INVITRO; DIFFERENTIATION; PROLIFERATION AB Interleukin 11 (IL-11) is a pleiotropic hematopoietic growth factor with stimulatory effects on multiple hematopoietic progenitor cells. An immortalized primate bone marrow stromal cell line was established to facilitate the analysis of interactions between hematopoietic progenitors and the microenvironment. This line was found to produce a novel growth factor that directed the proliferation of a murine plasmacytoma cell line. A cDNA encoding this activity was isolated through functional expression cloning in mammalian cells. Preliminary characterization of the cytokine revealed that IL-11 stimulated T cell-dependent B cell immunoglobulin secretion and synergized with IL-3 in murine megakaryocyte formation. Subsequent analysis of the clone has demonstrated that it also synergizes with IL-3 and steel factor in the stimulation of early progenitors and affects early megakaryocyte formation and maturation. In addition, IL-11 induces secretion of acute phase proteins in the liver and may function in the hematopoietic microenvironment as an adipogenic antagonist in a paracrine manner. Further in vitro and in vivo analysis of IL-11 will be necessary to determine the biologic function and potential therapeutic use of the cytokine. C1 GENET INST,CAMBRIDGE,MA. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. NR 76 TC 37 Z9 39 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 0737-1454 J9 INT J CELL CLONING PD MAY PY 1992 VL 10 IS 3 BP 135 EP 143 PG 9 WC Biotechnology & Applied Microbiology SC Biotechnology & Applied Microbiology GA HT886 UT WOS:A1992HT88600002 PM 1535352 ER PT J AU FRISCH, RE WYSHAK, G ALBERT, LS SOBER, AJ AF FRISCH, RE WYSHAK, G ALBERT, LS SOBER, AJ TI DYSPLASTIC NEVI, CUTANEOUS MELANOMA, AND GYNECOLOGIC DISORDERS SO INTERNATIONAL JOURNAL OF DERMATOLOGY LA English DT Article ID REPRODUCTIVE-SYSTEM; MALIGNANT-MELANOMA; LOWER PREVALENCE; PRONE FAMILIES; RISK; CANCERS; BREAST AB We compared the frequency of reproductive system diseases and disorders among 206 female patients with dysplastic nevi (DN), and/or melanoma, in comparison with random samples of women of comparable age without melanoma. The highest odds ratio (OR) for these age-related diseases and reproductive disorders occurs among the youngest age group of the patients with DN alone (mean age 35.1 +/- 1.2 yr): 44.2% of the DN subjects had one or more reproductive disorders compared with 19.8% of the random sample (OR 3.2, 95% CL (1.6, 6.5), P < 0.001). The patients with melanoma and DN (mean age 41.5 +/- 1.4 yr) also had a significantly greater percentage of subjects with one or more reproductive disorders, though less so than the DN subjects: 49.4% compared to 33.7% (OR 1.9, 95% CL (1.1, 3.3), P = 0.02). C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP FRISCH, RE (reprint author), HARVARD UNIV,CTR POPULAT STUDIES,9 BOW ST,CAMBRIDGE,MA 02138, USA. NR 21 TC 15 Z9 15 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0011-9059 J9 INT J DERMATOL JI Int. J. Dermatol. PD MAY PY 1992 VL 31 IS 5 BP 331 EP 335 DI 10.1111/j.1365-4362.1992.tb03948.x PG 5 WC Dermatology SC Dermatology GA HR746 UT WOS:A1992HR74600007 PM 1587661 ER PT J AU HERZOG, DB NEWMAN, KL YEH, CJ WARSHAW, M AF HERZOG, DB NEWMAN, KL YEH, CJ WARSHAW, M TI BODY-IMAGE SATISFACTION IN HOMOSEXUAL AND HETEROSEXUAL WOMEN SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Note ID ANOREXIA-NERVOSA; PERCEPTION AB This study examined the relationship between sexual orientation and eating disorders in women using a non-clinical sample of 45 homosexual and 64 heterosexual women. Subjects completed two self-report inventories composed of questions regarding weight, body image satisfaction, eating attitudes, and eating behaviors. Homosexual women were significantly heavier than heterosexual women, desired a significantly heavier ideal weight, were less often concerned with weight and appearance, and had less drive for thinness. Homosexual women of normal weight were more satisfied with their bodies than heterosexual women. Homosexual women's greater body satisfaction and lower concern with weight and appearance may contribute to their lower rates of eating disorders. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HERZOG, DB (reprint author), MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 20 TC 48 Z9 48 U1 3 U2 6 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0276-3478 J9 INT J EAT DISORDER JI Int. J. Eating Disord. PD MAY PY 1992 VL 11 IS 4 BP 391 EP 396 DI 10.1002/1098-108X(199205)11:4<391::AID-EAT2260110413>3.0.CO;2-F PG 6 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA HP284 UT WOS:A1992HP28400012 ER PT J AU FISKEN, J ROULSTON, JE BEATTIE, G HAYES, DF LEONARD, RCF AF FISKEN, J ROULSTON, JE BEATTIE, G HAYES, DF LEONARD, RCF TI INVESTIGATION OF THE C-NEU PROTOONCOGENE RELATED PROTEIN, P185, IN THE SERUM OF PRIMARY EPITHELIAL OVARIAN-CANCER PATIENTS SO INTERNATIONAL JOURNAL OF GYNECOLOGICAL CANCER LA English DT Article DE ELISA; MONITORING; NEU; ONCOPROTEIN; OVARIAN CANCER; PROGNOSIS ID GROWTH-FACTOR RECEPTOR; EGF RECEPTOR; HUMAN-BREAST; PROTOONCOGENE; HER-2/NEU; CARCINOMA; SURVIVAL; PRODUCT; NEUROBLASTOMAS; OVEREXPRESSION AB The relatively high incidence of amplification and overexpression of the neu (c-erb B2/HER-2) oncogene in breast cancer, and its association with poor prognosis, particularly in node negative patients, may allow identification of patients who require aggressive therapy to prevent an early relapse. It's association with ovarian cancer, however, is less well defined than in breast cancer. An ELISA for the c-neu proto-oncogene related protein, p185, has been developed recently using the monoclonal antibodies NB3 and TA1. In the first study of it's kind, we assayed serum samples from patients with primary epithelial ovarian cancer for circulating c-neu p185. Elevated levels were found in 21/178 (11.8%) patients. No correlation was found between serum levels and either the presence or volume of tumor, when assessed either after primary or at second-look surgery. A change in c-neu p185 levels did not correlate with response to chemotherapy. When subjected to univariate and multivariate analyses together with other known prognostic factors, serum c-neu p185 was not a significant predictor of progression-free survival or overall survival. Although c-neu p185 may be involved in the pathogenesis of ovarian cancer, it's assay in serum has no value in prognosis or monitoring. C1 IMPERIAL COLL RES FUND,MED ONCOL UNIT,EDINBURGH,SCOTLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CLIN PHARMACOL LAB,BOSTON,MA 02115. RP FISKEN, J (reprint author), UNIV EDINBURGH,ROYAL INFIRM,DEPT CLIN CHEM,1 LAURISTON PL,EDINBURGH EH3 9YW,MIDLOTHIAN,SCOTLAND. NR 37 TC 1 Z9 1 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 1048-891X J9 INT J GYNECOL CANCER JI Int. J. Gynecol. Cancer PD MAY-JUN PY 1992 VL 2 IS 3 BP 134 EP 140 DI 10.1046/j.1525-1438.1992.02030134.x PG 7 WC Oncology; Obstetrics & Gynecology SC Oncology; Obstetrics & Gynecology GA HR647 UT WOS:A1992HR64700004 ER PT J AU SEDDON, JM EGAN, KM ZHANG, YQ GELLES, EJ GLYNN, RJ TUCKER, CA GRAGOUDAS, ES AF SEDDON, JM EGAN, KM ZHANG, YQ GELLES, EJ GLYNN, RJ TUCKER, CA GRAGOUDAS, ES TI EVALUATION OF SKIN MICROTOPOGRAPHY AS A MEASURE OF ULTRAVIOLET EXPOSURE SO INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE LA English DT Article DE EPIDEMIOLOGY; MICROTOPOGRAPHY; SKIN BIOPSY; SKIN IMPRESSIONS; ULTRAVIOLET EXPOSURE; UV MEASUREMENT ID RADIATION; RISK; SUNLIGHT; MELANOMA; DAMAGE AB A pilot study was conducted to investigate the use of skin microtopography as a semiquantitative noninvasive method for estimating cumulative sun exposure in epidemiologic studies of eye disease. The subjects received a kit through the mail containing material needed to make a replica of the skin texture of a sun-exposed area of the hand. Each subject previously had undergone a skin biopsy around the same site to evaluate elastotic degeneration, and all were interviewed about past sun exposures. A gradable skin impression was obtained from 96 of 115 (83%) participants after two mailings. The impressions were graded according to the degree of skin texture alteration using standard photographs; interobserver reliability was 0.73 using a weighted kappa statistic. The impression score was correlated most strongly with age (r = 0.53). Independent predictors of higher impression scores (more skin texture changes) were older age, cigar or pipe smoking, less education, lighter iris color, lighter skin color, male gender, and tendency to sunburn. After adjustment for age and the other predictor variables, the biopsy score was not correlated with the impression grade (r = 0.18, P = 0.13). Behaviors indexing sun exposure were not correlated with microtopography. These results suggest that skin microtopography as done in this study reflects aging from intrinsic parameters more than from actinic damage. C1 MASSACHUSETTS EYE & EAR INFIRM,RETINA SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02115. RP SEDDON, JM (reprint author), MASSACHUSETTS EYE & EAR INFIRM,EPIDEMIOL UNIT,243 CHARLES ST,BOSTON,MA 02114, USA. NR 17 TC 18 Z9 19 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 MAY PY 1992 VL 33 IS 6 BP 1903 EP 1908 PG 6 WC Ophthalmology SC Ophthalmology GA HV587 UT WOS:A1992HV58700012 PM 1582796 ER PT J AU REIMER, P WEISSLEDER, R NICKELEIT, V BRADY, TJ AF REIMER, P WEISSLEDER, R NICKELEIT, V BRADY, TJ TI ANIMAL-MODELS FOR MAGNETIC-RESONANCE-IMAGING RESEARCH OF THE LIVER SO INVESTIGATIVE RADIOLOGY LA English DT Article ID HEPATOCELLULAR-CARCINOMA; GALACTOSAMINE; RATS; HEPATITIS; CANCER C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NCI NIH HHS [CA 48279] NR 26 TC 10 Z9 11 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0020-9996 J9 INVEST RADIOL JI Invest. Radiol. PD MAY PY 1992 VL 27 IS 5 BP 390 EP 393 DI 10.1097/00004424-199205000-00014 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HR451 UT WOS:A1992HR45100011 PM 1582824 ER PT J AU YUCEL, EK DUMOULIN, CL WALTMAN, AC AF YUCEL, EK DUMOULIN, CL WALTMAN, AC TI MR ANGIOGRAPHY OF LOWER-EXTREMITY ARTERIAL-DISEASE - PRELIMINARY EXPERIENCE SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE ANEURYSM, FEMORAL; ANEURYSM, MR; ANEURYSM, POPLITEAL; ARTERIES, EXTREMITIES; ARTERIES, MR; ARTERIES, STENOSIS OR OBSTRUCTION; COMPARATIVE STUDIES; VASCULAR STUDIES AB Nineteen patients underwent magnetic resonance (MR) angiography for evaluation of lower-extremity arterial disease. The underlying conditions included atherosclerotic occlusive disease in 12 patients, femoral or popliteal aneurysms in four, and bypass graft stenoses or occlusion in four. In the patients with occlusive disease, the iliac and femoropopliteal vessels were classified as patent, moderately stenotic, severely stenotic, or occluded. Fifteen of 16 occlusions (accuracy = 94%) were correctly classified. In the one missed case, there was a long delay between MR angiography and x-ray angiography and it is likely that the occlusion occurred during the interval. Three of five severe stenoses were correctly classified with MR angiography. In two cases of iliac artery stenosis, there was a signal void at the point of maximal stenosis, which on the basis of anatomic features could be recognized as severe stenosis rather than an occlusion. Three of four moderate stenoses were correctly classified. Correlation with x-ray angiography or surgery demonstrated the ability of MR angiography to accurately depict the status of runoff vessels. RP YUCEL, EK (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 0 TC 39 Z9 39 U1 0 U2 0 PU SOC MAGNETIC RESONANCE IMAGING PI EASTON PA 1991 NORTHAMPTON ST, EASTON, PA 18042-3189 SN 1053-1807 J9 JMRI-J MAGN RESON IM JI JMRI-J. Magn. Reson. Imaging PD MAY-JUN PY 1992 VL 2 IS 3 BP 303 EP 309 DI 10.1002/jmri.1880020309 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HV081 UT WOS:A1992HV08100007 PM 1627865 ER PT J AU FLETCHER, EC LESSKE, J BEHM, R MILLER, CC STAUSS, H UNGER, T AF FLETCHER, EC LESSKE, J BEHM, R MILLER, CC STAUSS, H UNGER, T TI CAROTID CHEMORECEPTORS, SYSTEMIC BLOOD-PRESSURE, AND CHRONIC EPISODIC HYPOXIA MIMICKING SLEEP-APNEA SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE SLEEP APNEA SYNDROMES; ANOXIA; HYPOXEMIA; HYPERTENSION; HIGH BLOOD PRESSURE; CAROTID BODY; GLOMUS-CAROTICUM; PRESSORECEPTORS; BARORECEPTORS ID AWAKE RAT; TRACHEOSTOMY; HYPERTENSION; HYPERSOMNIA; RESPONSES; CATECHOLAMINES; BARORECEPTOR; HYPOXEMIA; PLASMA AB We have described a rat model that responds to repetitive episodic hypoxia (12-s infusions of nitrogen into daytime sleeping chambers every 30 s, 7 h/day for 35 days) with an increase in diurnal systemic blood pressure. We hypothesized that afferent information from the peripheral chemoreceptors may be necessary to produce diurnal blood pressure elevation in this hypoxia model. Carotid body denervation (CBD) was accomplished by severing both carotid sinus nerves in two groups of male Wistar rats (250-375 g). Group 4 CBD rats were subjected to intermittent hypoxia for 35 days (3-5% nadir ambient O2) as described above, whereas group 5 CBD rats remained unhandled in their usual cages. Additional sham-operated controls included group 2 sham-"hypoxia" rats, which were housed in chambers identical to the hypoxia rats but supplied with compressed air instead of nitrogen, group 1 (not denervated) rats, which remained unhandled in their usual cages, and group 3 sham-operated rats, which were subjected to 35 days of intermittent hypoxia identical to group 4 CBD rats. Femoral arterial basline and end-of-study blood pressures were measured in conscious rats. The group 3 rats exposed to episodic hypoxia displayed a 13-mmHg increase in mean blood pressure, whereas the other groups showed no significant change from baseline. Left ventricular hypertrophy was evident in all rats exposed to episodic hypoxia, but right ventricular hypertrophy was evident only in the group 4 rats. All CBD rats developed increased hematocrit and hemoglobin, while the group 3 rats (non-CBD, episodic hypoxia) did not. The baroreceptor reflex at baseline was not depressed in the CBD rats. We conclude that intact peripheral chemoreceptors are necessary for the blood pressure in rats to increase in response to episodic hypoxia patterned after that of sleep apnea in humans. C1 UNIV HEIDELBERG,DEPT PHARMACOL,W-6900 HEIDELBERG,GERMANY. UNIV HEIDELBERG,INST HIGH BLOOD PRESSURE RES,W-6900 HEIDELBERG,GERMANY. BAYLOR COLL MED,HOUSTON VET AFFAIRS MED CTR,DEPT MED,PULM DIS SECT,HOUSTON,TX 77030. OI Stauss, Harald/0000-0001-6647-1903 NR 37 TC 265 Z9 278 U1 2 U2 12 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 MAY PY 1992 VL 72 IS 5 BP 1978 EP 1984 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA HU331 UT WOS:A1992HU33100048 PM 1601808 ER PT J AU STOEBNER, JA BUTTERTON, JR CALDERWOOD, SB PAYNE, SM AF STOEBNER, JA BUTTERTON, JR CALDERWOOD, SB PAYNE, SM TI IDENTIFICATION OF THE VIBRIOBACTIN RECEPTOR OF VIBRIO-CHOLERAE SO JOURNAL OF BACTERIOLOGY LA English DT Article ID OUTER-MEMBRANE PROTEINS; ESCHERICHIA-COLI; IRON; SIDEROPHORE; VIRULENCE; TNPHOA AB Vibrio cholerae produces the novel phenolate siderophore vibriobactin and several outer membrane proteins in response to iron starvation. To determine whether any of these iron-regulated outer membrane proteins serves as the receptor for vibriobactin, the classical V. cholerae strain 0395 was mutagenized by using TnphoA, and iron-regulated fusions were analyzed for vibriobactin transport. One mutant, MBG14, was unable to bind or utilize exogenous vibriobactin and did not grow in low-iron medium. However, synthesis of the siderophore and transport of other iron complexes, including ferrichrome, hemin, and ferric citrate, were unaffected in MBG14. Analysis of membrane proteins by sodium dodecyl sulfate-polyacrylamide gel electrophoresis demonstrated the loss from the mutant of a 74-kDa iron-regulated outer membrane protein present in the parental strain when grown in iron-limiting conditions. This protein partitioned into the detergent phase during Triton X-114 extraction, suggesting that it is a hydrophobic membrane protein. DNA sequences encoding the gene into which TnphoA had inserted, designed viuA (vibriobactin uptake), restored the wild-type phenotype to the mutant; the complemented mutant expressed the 74-kDa outer membrane protein under iron-limiting conditions and possessed normal vibriobactin binding and uptake. These data indicate that the 74-kDa outer membrane protein of V. cholerae serves as the vibriobactin receptor. C1 UNIV TEXAS,DEPT MICROBIOL,AUSTIN,TX 78712. MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NIAID NIH HHS [AI27329] NR 24 TC 33 Z9 33 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0021-9193 J9 J BACTERIOL JI J. Bacteriol. PD MAY PY 1992 VL 174 IS 10 BP 3270 EP 3274 PG 5 WC Microbiology SC Microbiology GA HU938 UT WOS:A1992HU93800023 PM 1315733 ER PT J AU JAMES, SP JASTY, M DAVIES, J PIEHLER, H HARRIS, WH AF JAMES, SP JASTY, M DAVIES, J PIEHLER, H HARRIS, WH TI A FRACTOGRAPHIC INVESTIGATION OF PMMA BONE-CEMENT FOCUSING ON THE RELATIONSHIP BETWEEN POROSITY REDUCTION AND INCREASED FATIGUE LIFE SO JOURNAL OF BIOMEDICAL MATERIALS RESEARCH LA English DT Article ID SIMPLEX-P AB Fracture surfaces of both monotonic and fatigue loaded bone cement samples were examined to investigate the fractographic characteristics of PMMA. Classic cleavage step river patterns were observed on all monotonically loaded samples, running downstream in the direction of crack propagation. All fatigue cracks initiated at internal pores and the direction of crack propagation of many cracks was discernible. Porosity, pore size, and pore size distribution were found to affect the crack initiation and fatigue behavior of bone cement. Statistical analysis revealed a strong negative correlation between two-dimensional porosity present on the fracture surfaces and the cycles to failure. The fractographic observations of these fatigue samples elucidate one reason why porosity reduction by centrifugation or vacuum mixing increases the fatigue life of PMMA bone cement. C1 MIT,DEPT MAT SCI & ENGN,CAMBRIDGE,MA 02139. CARNEGIE MELLON UNIV,DEPT MET ENGN & MAT SCI,PITTSBURGH,PA 15213. MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,BOSTON,MA 02114. NR 13 TC 97 Z9 98 U1 0 U2 7 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9304 J9 J BIOMED MATER RES JI J. Biomed. Mater. Res. PD MAY PY 1992 VL 26 IS 5 BP 651 EP 662 DI 10.1002/jbm.820260507 PG 12 WC Engineering, Biomedical; Materials Science, Biomaterials SC Engineering; Materials Science GA HN541 UT WOS:A1992HN54100006 PM 1512284 ER PT J AU BARRACK, RL MULROY, RD HARRIS, WH AF BARRACK, RL MULROY, RD HARRIS, WH TI IMPROVED CEMENTING TECHNIQUES AND FEMORAL COMPONENT LOOSENING IN YOUNG-PATIENTS WITH HIP-ARTHROPLASTY - A 12-YEAR RADIOGRAPHIC REVIEW SO JOURNAL OF BONE AND JOINT SURGERY-BRITISH VOLUME LA English DT Article ID 10-YEAR FOLLOW-UP; REPLACEMENT; FIXATION AB To assess the effect of improved methods of femoral cementing on the loosening rates in young patients, we reviewed 50 'second-generation' cemented hip arthroplasties in 44 patients aged 50 years or less. The femoral stems were all collared and rectangular in cross-section with rounded corners. The cement was delivered by a gun into a medullary canal occluded distally with a cement plug. A clinical and radiographic review was undertaken at an average of 12 years (10 to 14.8) and no patient was lost to follow-up. No femoral component was revised for aseptic loosening, and only one stem was definitely loose by radiographic criteria. By contrast, 11 patients had undergone revision for symptomatic aseptic loosening of the acetabular component and 11 more had radiographic signs of acetabular loosening. C1 MASSACHUSETTS GEN HOSP,ORTHOPAED BIOMECH LAB,HIP & IMPLANT SURG UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 22 TC 491 Z9 511 U1 2 U2 9 PU BRITISH EDITORIAL SOC BONE JOINT SURGERY PI LONDON PA 22 BUCKINGHAM STREET, LONDON, ENGLAND WC2N 6ET SN 0301-620X J9 J BONE JOINT SURG BR JI J. Bone Joint Surg.-Br. Vol. PD MAY PY 1992 VL 74 IS 3 BP 385 EP 389 PG 5 WC Orthopedics; Surgery SC Orthopedics; Surgery GA HV659 UT WOS:A1992HV65900015 PM 1587883 ER PT J AU ROODMAN, GD AF ROODMAN, GD TI PERSPECTIVES - INTERLEUKIN-6 - AN OSTEOTROPIC FACTOR SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID HYBRIDOMA GROWTH-FACTOR; STIMULATORY FACTOR-II; HUMAN 26-KD PROTEIN; HEMATOPOIETIC PROGENITORS; PRODUCE IMMUNOGLOBULIN; PARATHYROID-HORMONE; COMPLEMENTARY-DNA; HUMAN-FIBROBLASTS; HUMAN-MONOCYTES; LYMPHOCYTES-B C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. RP ROODMAN, GD (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV 151,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [CA-40035]; NIADDK NIH HHS [AM35188]; NIAMS NIH HHS [AR39539] NR 37 TC 265 Z9 271 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD MAY PY 1992 VL 7 IS 5 BP 475 EP 478 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HV082 UT WOS:A1992HV08200001 PM 1615755 ER PT J AU MITLAK, BH WILLIAMS, DC BRYANT, HU PAUL, DC NEER, RM AF MITLAK, BH WILLIAMS, DC BRYANT, HU PAUL, DC NEER, RM TI INTERMITTENT ADMINISTRATION OF BOVINE PTH-(1-34) INCREASES SERUM 1,25-DIHYDROXYVITAMIN-D CONCENTRATIONS AND SPINAL BONE-DENSITY IN SENILE (23 MONTH) RATS SO JOURNAL OF BONE AND MINERAL RESEARCH LA English DT Article ID PARATHYROID-HORMONE; TRABECULAR BONE; MASS; OSTEOPOROSIS; CALCIUM; AGE AB We examined the effect of intermittent administration of bovine parathyroid hormone (1-34) (bPTH) on spinal bone mineral content (BMC) and bone mineral density (BMD), serum 1,25-dihydroxyvitamin D concentrations, and serum markers of osteoblast function in senile male and female rats (23 and 24 months of age, respectively). Sexually mature young (3 month) male rats were similarly treated for comparison. bPTH administration increased serum osteocalcin concentrations without changing serum inorganic phosphate or calcium concentrations in either group of old animals. In young animals, PTH administration increased the serum calcium and inorganic phosphate concentrations significantly (p < 0.05), although values remained within the normal range. In the vehicle-treated male rats, serum 1,25-dihydroxyvitamin D concentrations were lower in the senile than in the young animals (18 +/- 5 versus 47 +/- 6 pg/ml, p < 0.05). PTH administration resulted in significantly increased serum 1,25-dihydroxyvitamin D concentrations in the senile and young male animals (both, p < 0.05) and the final mean serum 1,25-dihydroxyvitamin D concentrations were not statistically different (68 +/- 9 versus 85 +/- 6 pg/ml respectively; p = NS). Serum 1,25-dihydroxy-vitamin D concentrations were significantly (p < 0.05) higher in the PTH-treated senile female rats than the sex-matched, vehicle-treated controls. The pretreatment spinal BMC and BMD as assessed by dual-energy x-ray absorptiometry (DEXA) were significantly higher in the senile male animals than in the young animals. Spinal BMC and BMD decreased in the vehicle-treated senile male rats (p < 0.05) over the 3 weeks of the study despite a gain in weight. bPTH administration prevented this fall in spinal BMC and increased spinal BMD (p < 0.05). Spinal BMC and BMD increased significantly (p < 0.05) in the young vehicle-treated rats, and PTH administration caused a further significant increase in both parameters of bone mass. Spinal BMD was significantly (p < 0.05) higher in the PTH-treated senile female rats than in vehicle-treated controls. These findings demonstrate that intermittent PTH administration increases serum 1,25-dihydroxyvitamin D concentrations of senile animals to the levels of PTH-treated, young, sexually mature animals. In addition, PTH administration arrests bone loss and increases spinal BMD of senile rats. C1 ELI LILLY & CO,LILLY RES LAB,INDIANAPOLIS,IN 46285. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MITLAK, BH (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BULFINCH 327,BOSTON,MA 02114, USA. NR 25 TC 36 Z9 36 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0884-0431 J9 J BONE MINER RES JI J. Bone Miner. Res. PD MAY PY 1992 VL 7 IS 5 BP 479 EP 484 PG 6 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HV082 UT WOS:A1992HV08200002 PM 1615756 ER PT J AU PARKOS, CA COLGAN, SP DELP, C ARNAOUT, MA MADARA, JL AF PARKOS, CA COLGAN, SP DELP, C ARNAOUT, MA MADARA, JL TI NEUTROPHIL MIGRATION ACROSS A CULTURED EPITHELIAL MONOLAYER ELICITS A BIPHASIC RESISTANCE RESPONSE REPRESENTING SEQUENTIAL EFFECTS ON TRANSCELLULAR AND PARACELLULAR PATHWAYS SO JOURNAL OF CELL BIOLOGY LA English DT Article ID BARRIER FUNCTION; ADHERENCE; LFA-1 AB Migration of polymorphonuclear leukocytes across epithelia is a hallmark of many inflammatory disease states. Neutrophils traverse epithelia by migrating through the paracellular space and crossing intercellular tight junctions. We have previously shown (Nash, S., J. Stafford, and J. L. Madara. 1987. J. Clin. Invest. 80:1104-1113), that leukocyte migration across T84 monolayers, a model human intestinal epithelium, results in enhanced tight junction permeability-an effect quantitated by the use of a simple, standard electrical assay of transepithelial resistance. Here we show that detailed time course studies of the transmigration-elicited decline in resistance has two components, one of which is unrelated to junctional permeability. The initial decrease in resistance, maximal 5-13 min after initiation of transmigration, occurs despite inhibition of transmigration by an antibody to the common beta subunit of neutrophil beta-2 integrins, and is paralleled by an increase in transepithelial short-circuit current. Chloride ion substitution and inhibitor studies indicate that the early-phase resistance decline is not attributable to an increase in tight junction permeability but is due to decreased resistance across epithelial cells resulting from chloride secretion. Since T84 cells are accepted models for studies of the regulation of Cl- and water secretion, our results suggest that neutrophil transmigration across mucosal surfaces (for example, respiratory and intestinal tracts) may initially activate flushing of the surface by salt and water. Equally important, these studies, by providing a concrete example of sequential transcellular and paracellular effects on transepithelial resistance, highlight the fact that this widely used assay cannot simply be viewed as a direct functional probe of tight junction permeability. C1 HARVARD UNIV,CTR DIGEST DIS,DEPT PATHOL,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP PARKOS, CA (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115, USA. RI Parkos, Charles/B-3896-2009; Colgan, Sean/B-4573-2009 FU NIAID NIH HHS [AI21964]; NIDDK NIH HHS [DK33506, DK35932] NR 26 TC 115 Z9 115 U1 0 U2 0 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 MAY PY 1992 VL 117 IS 4 BP 757 EP 764 DI 10.1083/jcb.117.4.757 PG 8 WC Cell Biology SC Cell Biology GA HT962 UT WOS:A1992HT96200005 PM 1577855 ER PT J AU NOZAKI, K BEAL, MF AF NOZAKI, K BEAL, MF TI NEUROPROTECTIVE EFFECTS OF L-KYNURENINE ON HYPOXIA ISCHEMIA AND NMDA LESIONS IN NEONATAL RATS SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE HYPOXIA ISCHEMIA; KYNURENINE; KYNURENIC ACID; NMDA; C-FOS; PROBENECID ID METHYL-D-ASPARTATE; CENTRAL NERVOUS-SYSTEM; AMINO-ACID RECEPTORS; INDUCED BRAIN INJURY; QUINOLINIC ACID; GLUTAMATE NEUROTOXICITY; CEREBROSPINAL-FLUID; GLYCINE RECEPTOR; MAMMALIAN BRAIN; CHOROID-PLEXUS AB Kynurenic acid is the only known endogenous excitatory amino acid receptor antagonist in the central nervous system. In the present study, we examined whether increasing brain concentrations of kynurenic acid by loading with its precursor L-kynurenine, or blocking its excretion with probenecid, could exert neuroprotective effects. Neuroprotective effects were examined in a neonatal model of hypoxia-ischemia, and following intrastriatal injection of N-methyl-D-aspartate (NMDA). Seven-day-old rats underwent unilateral ligation of the carotid artery, followed by exposure to 8% oxygen for 1.5 h. L-kynurenine administered 1 h before the hypoxia-ischemia showed a dose-dependent significant neuroprotective effect, with complete protection at a dose of 300 mg kg-1. The induction of c-fos immunoreactivity in cerebral cortex was also blocked by this dose Of L-kynurenine. Probenecid alone had moderate neuroprotective effects, while a combination of a low dose of probenecid with doses of 50-200 mg kg-1 of L-kynurenine showed significant dose-dependent neuroprotection. Kynurenine dose-dependently protected against NMDA neurotoxicity in 7-day-old rats. Neurochemical analysis confirmed that L-kynurenine with or without probenecid markedly increased concentrations of kynurenic acid in cerebral cortex of 7-day-old rats. These results show for the first time that pharmacologic manipulation of endogenous concentrations of kynurenic acid can exert neuroprotective effects. C1 MASSACHUSETTS GEN HOSP,NEUROCHEM LABS,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,STROKE RES LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NINDS NIH HHS [NS10828, NS16367] NR 62 TC 114 Z9 114 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD MAY PY 1992 VL 12 IS 3 BP 400 EP 407 PG 8 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA HP391 UT WOS:A1992HP39100006 PM 1569135 ER PT J AU WABER, DP TARBELL, NJ KAHN, CM GELBER, RD SALLAN, SE AF WABER, DP TARBELL, NJ KAHN, CM GELBER, RD SALLAN, SE TI THE RELATIONSHIP OF SEX AND TREATMENT MODALITY TO NEUROPSYCHOLOGICAL OUTCOME IN CHILDHOOD ACUTE LYMPHOBLASTIC-LEUKEMIA SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Article ID ACUTE LYMPHOCYTIC-LEUKEMIA; LONG-TERM SURVIVORS; CRANIAL IRRADIATION; INTRATHECAL METHOTREXATE; CNS PROPHYLAXIS; ANIMAL-MODEL; IQ SCORES; THERAPY; CHILDREN; MEMORY C1 CHILDRENS HOSP MED CTR,DIV HEMATOL ONCOL,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT RADIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT BIOSTAT,BOSTON,MA 02115. RP WABER, DP (reprint author), CHILDRENS HOSP MED CTR,DIV PSYCHIAT,300 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA19789]; NICHD NIH HHS [P30-HD18655]; NINDS NIH HHS [NS22108] NR 38 TC 106 Z9 107 U1 1 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAY PY 1992 VL 10 IS 5 BP 810 EP 817 PG 8 WC Oncology SC Oncology GA HR228 UT WOS:A1992HR22800018 PM 1569453 ER PT J AU STRAUSS, GM LANGER, MP ELIAS, AD SKARIN, AT SUGARBAKER, DJ AF STRAUSS, GM LANGER, MP ELIAS, AD SKARIN, AT SUGARBAKER, DJ TI MULTIMODALITY TREATMENT OF STAGE-IIIA NON-SMALL-CELL LUNG-CARCINOMA - A CRITICAL-REVIEW OF THE LITERATURE AND STRATEGIES FOR FUTURE-RESEARCH SO JOURNAL OF CLINICAL ONCOLOGY LA English DT Review ID THERAPY ONCOLOGY GROUP; RADIATION-THERAPY; BRONCHIAL-CARCINOMA; TUMOR-CONTROL; CANCER; SURVIVAL; CHEMOTHERAPY; IRRADIATION; CISPLATIN; TRIAL C1 HARVARD UNIV,COMMUNITY HLTH PLAN,DEPT ONCOL,CAMBRIDGE,MA 02138. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV MED ONCOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DIV THORAC SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP STRAUSS, GM (reprint author), BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,75 FRANCIS ST,BOSTON,MA 02115, USA. NR 38 TC 61 Z9 61 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0732-183X J9 J CLIN ONCOL JI J. Clin. Oncol. PD MAY PY 1992 VL 10 IS 5 BP 829 EP 838 PG 10 WC Oncology SC Oncology GA HR228 UT WOS:A1992HR22800021 PM 1314892 ER PT J AU HERZOG, DB KELLER, MB LAVORI, PW KENNY, GM SACKS, NR AF HERZOG, DB KELLER, MB LAVORI, PW KENNY, GM SACKS, NR TI THE PREVALENCE OF PERSONALITY-DISORDERS IN 210 WOMEN WITH EATING DISORDERS SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID BULIMIA AB Background. The purpose of this study was to assess the prevalence, reliability, and predictive value of comorbid personality disorders in a large sample of 210 women seeking treatment for anorexia nervosa (N = 31), bulimia nervosa (N = 91), or mixed disorder (N = 88). Method. All subjects were interviewed using the Structured Interview for DSM-III Personality Disorders as part of a longitudinal outcome study of eating disorders currently underway at Massachusetts General Hospital. Results: Of the 210 subjects, 27% had at least one personality disorder; the most commonly observed was borderline personality disorder in 18 subjects (9%). The highest prevalence of personality disorders was found in the anorexia nervosa/bulimia nervosa group at 39%, followed by 22% in the anorexics and 21% in the bulimic sample. We found statistically significant differences regarding the distribution of personality disorders across eating disorder groups. The dramatic personality disorder cluster was differentially distributed across groups; this finding was accounted for by higher rates of borderline personality disorder in the bulimia nervosa and anorexia nervosa/bulimia nervosa groups than in the anorexia nervosa group. The anxious personality disorder cluster was differentially distributed across groups with higher rates in the anorexia nervosa and anorexia nervosa/bulimia nervosa samples. Those subjects with a comorbid personality disorder had a significantly slower recovery rate than those without a comorbid personality disorder. Conclusion: The prevalence of personality disorders is not high in treatment-seeking women with eating disorders compared with previously studied samples. The greatest frequency of comorbid personality disorders is in the anorexia nervosa/bulimia nervosa group; this subset also had longer duration of eating disorder illness and much greater comorbid Axis I psychopathology compared with the rest of the sample. Future studies should address whether personality disorders have predictive value in the long-term course and outcome of eating disorders. C1 BROWN UNIV,DEPT PSYCHIAT & HUMAN BEHAV,PROVIDENCE,RI 02912. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP HERZOG, DB (reprint author), MASSACHUSETTS GEN HOSP,EATING DISORDERS UNIT,ACC 725,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R01 MH 38333-01A3] NR 27 TC 124 Z9 126 U1 0 U2 6 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD MAY PY 1992 VL 53 IS 5 BP 147 EP 152 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA HV957 UT WOS:A1992HV95700001 PM 1592839 ER PT J AU DENBESTEN, PK ITHARIANI, H AF DENBESTEN, PK ITHARIANI, H TI BIOLOGICAL MECHANISMS OF FLUOROSIS AND LEVEL AND TIMING OF SYSTEMIC EXPOSURE TO FLUORIDE WITH RESPECT TO FLUOROSIS SO JOURNAL OF DENTAL RESEARCH LA English DT Article; Proceedings Paper CT WORKSHOP ON CHANGING PATTERNS OF FLUORIDE INTAKE CY APR 23-25, 1991 CL UNIV N CAROLINA, CHAPEL HILL, NC HO UNIV N CAROLINA ID DEVELOPING BOVINE ENAMEL; ORGAN-CULTURE INVITRO; HAMSTER TOOTH-GERMS; DENTAL FLUOROSIS; ALKALINE-PHOSPHATASE; EXTRACELLULAR-MATRIX; SKELETAL FLUOROSIS; SECRETORY ENAMEL; RAT; CHILDREN AB Enamel fluorosis can occur following either an acute or chronic exposure to fluoride during tooth formation, Fluorosed enamel is characterized by a retention of amelogenins in the early-maturation stage, and by the formation of a more porous enamel with a subsurface hypomineralization. The mechanisms by which fluoride affects enamel development include specific effects on both the ameloblasts and on the developing enamel matrix. Maturation-stage ameloblast modulation is more rapid in fluorosed enamel as compared with control enamel, and proteolytic activity in fluorosed early-maturation enamel is reduced as compared with controls. Secretory enamel appears to be more susceptible to the effects of fluoride following acute fluoride exposure, such as may occur with the use of fluoride supplements. However, both human and animal studies show that the transition/early-maturation stage of enamel formation is most susceptible to the effects of chronic fluoride ingestion at above-optimal levels of fluoride in drinking water. RP DENBESTEN, PK (reprint author), FORSYTH DENT CTR,DEPT BIOCHEM,140 THE FENWAY,BOSTON,MA 02115, USA. NR 88 TC 84 Z9 94 U1 0 U2 4 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 MAY PY 1992 VL 71 IS 5 BP 1238 EP 1243 DI 10.1177/00220345920710051701 PG 6 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA HY704 UT WOS:A1992HY70400019 PM 1607440 ER PT J AU SILVA, JA SHARMA, KK LEONG, GB WEINSTOCK, R AF SILVA, JA SHARMA, KK LEONG, GB WEINSTOCK, R TI DANGEROUSNESS OF THE DELUSIONAL MISIDENTIFICATION OF CHILDREN SO JOURNAL OF FORENSIC SCIENCES LA English DT Article DE PSYCHIATRY; MENTAL ILLNESS; MISIDENTIFICATION; DANGEROUSNESS; VIOLENCE ID CAPGRAS SYNDROME AB Misidentification syndromes have been studied from a variety of perspectives, including phenomenological, biological, and nosological approaches. More recently, misidentification syndromes have been studied from a psychiatric-legal perspective, especially with regards to the problem of dangerousness. Capgras syndrome and other syndromes of misidentification can lead to hostile mood and subsequent physical violence. Little attention has so far been devoted to children as the objects of the psychotic person's misidentification delusion(s). We provide a review of cases from the anglophonic literature that have children as the misidentified objects, add three new cases, and then discuss the relationship between misidentification and potential harm to these children. C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV SO CALIF,INST PSYCHIAT & LAW,LOS ANGELES,CA 90089. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. NR 34 TC 11 Z9 11 U1 1 U2 1 PU AMER SOC TESTING MATERIALS PI W CONSHOHOCKEN PA 100 BARR HARBOR DR, W CONSHOHOCKEN, PA 19428-2959 SN 0022-1198 J9 J FORENSIC SCI JI J. Forensic Sci. PD MAY PY 1992 VL 37 IS 3 BP 830 EP 838 PG 9 WC Medicine, Legal SC Legal Medicine GA JY404 UT WOS:A1992JY40400022 PM 1629675 ER PT J AU GELBERMAN, RH AMIEL, D HARWOOD, F AF GELBERMAN, RH AMIEL, D HARWOOD, F TI GENETIC EXPRESSION FOR TYPE-I PROCOLLAGEN IN THE EARLY STAGES OF FLEXOR TENDON HEALING SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB To determine the precise mechanism by which contact tendon healing occurs at the cellular level, the production of pro alpha(I) collagen messenger RNA (mRNA) produced by fibroblasts of healing intrasynovial flexor tendons was determined by an in situ hybridization technique. The repair site and the proximal and distal tendon stumps of repaired tendons treated with early controlled passive mobilization were fixed and buffered in formalin, 3, 7, 10, and 17 days after repair. A complimentary DNA (cDNA) probe corresponding to alpha(I) procollagen mRNA was labeled with [P-32]d-CTP. After hybridization, autoradiography, and staining of the sections, the level of procollagen mRNA was assessed by microscopic examination. Rising levels of procollagen mRNA, indicating progressively increasing levels of synthetic collagen activity, were detected in the healing tendons through 10 days. A moderate decrease in procollagen mRNA was seen at 17 days. Genetic expression for procollagen mRNA was localized specifically to the epitenon cells on the tendon surface overlying the repair site and to cells in the gap between the tendon stumps. No detectable expression was noted in endotenon fibroblasts. The finding of high levels of expression for procollagen type I mRNA in the surface layer of healing tendons demonstrates that cells intrinsic to tendon epitenon contribute the greatest quantity of native tendon collagen to the repair site during these important early intervals after tendon suture. RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,WACC 527,BOSTON,MA 02114, USA. FU NIAMS NIH HHS [5R01-AR33097] NR 0 TC 64 Z9 70 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD MAY PY 1992 VL 17A IS 3 BP 551 EP 558 DI 10.1016/0363-5023(92)90370-5 PG 8 WC Orthopedics; Surgery SC Orthopedics; Surgery GA HU590 UT WOS:A1992HU59000032 PM 1613239 ER PT J AU GELBERMAN, RH AF GELBERMAN, RH TI FLEXOR SHEATH CONTINUITY - REPLY SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Letter RP GELBERMAN, RH (reprint author), MASSACHUSETTS GEN HOSP,WACC 527,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD MAY PY 1992 VL 17A IS 3 BP 582 EP 583 DI 10.1016/0363-5023(92)90378-3 PG 2 WC Orthopedics; Surgery SC Orthopedics; Surgery GA HU590 UT WOS:A1992HU59000040 ER PT J AU DUSTIN, ML CARPEN, O SPRINGER, TA AF DUSTIN, ML CARPEN, O SPRINGER, TA TI REGULATION OF LOCOMOTION AND CELL-CELL CONTACT AREA BY THE LFA-1 AND ICAM-1 ADHESION RECEPTORS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID FUNCTION-ASSOCIATED ANTIGEN-1; T-CELL; MOLECULE-1 ICAM-1; LEUKOCYTE DIFFERENTIATION; ENDOTHELIAL-CELLS; BETA-SUBUNIT; DISTINCT; MEMBRANE; BINDING; PROTEIN AB We demonstrate complementary differences in the behavior of B lymphoblastoid cells adhering to LFA-1 or its counter-receptor ICAM-1. The interaction of B lymphoblastoid cells with glass-supported planar bilayers bearing LFA-1 or ICAM-1 was observed by time-lapse video microscopy, and the distribution of adhesion receptors on cells interacting with the planar bilayers was studied by immunofluorescence microscopy. B lymphoblasts formed a large contact area and crawled rapidly (up to 25-mu-m/min) on planar bilayers bearing ICAM-1. In contrast, these cells attached to planar bilayers bearing LFA-1 through a fixed point about which the cells actively pivoted, using a single stalk-like projection. Phorbol ester-stimulated lymphoblasts, which adhere more strongly to ICAM-1-bearing substrates than unstimulated lymphoblasts, were still capable of locomotion on ICAM-1. Phorbol ester stimulation of B lymphoblasts on planar bilayers bearing LFA-1 promoted a rapid conversion from "stalk" attachment to symmetrical spreading of the cell on the substrate. Cellular LFA-1 remained uniformly distributed on the cell surface during interaction with bilayers bearing purified ICAM-1 as determined by immunofluorescence. In contrast, ICAM-1 was concentrated in the stalk-like structure through which the unstimulated B lymphoblasts adhered to LFA-1 in planar bilayers, but ICAM-1 immunofluorescence became more uniformly distributed over the cell surface within minutes of phorbol ester addition. Neither LFA-1 or ICAM-1 colocalized with the prominent staining of filamentous actin in the ruffling membrane regions. Interaction through cell surface LFA-1 and ICAM-1, 2, or 3 promotes different cellular morphologies and behaviors, the correlation of which with previously observed patterns of lymphocyte interaction with different cell types is discussed. C1 CTR BLOOD RES,800 HUNTINGTON AVE,BOSTON,MA 02115. HARVARD UNIV,SCH MED,COMM CELL & DEV BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA31798] NR 50 TC 117 Z9 118 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 1 PY 1992 VL 148 IS 9 BP 2654 EP 2663 PG 10 WC Immunology SC Immunology GA HQ182 UT WOS:A1992HQ18200002 PM 1349320 ER PT J AU CHEN, CY SALLES, G SELDIN, MF KISTER, AE REINHERZ, EL SHIPP, MA AF CHEN, CY SALLES, G SELDIN, MF KISTER, AE REINHERZ, EL SHIPP, MA TI MURINE COMMON ACUTE LYMPHOBLASTIC-LEUKEMIA ANTIGEN (CD10 NEUTRAL ENDOPEPTIDASE-24.11) - MOLECULAR CHARACTERIZATION, CHROMOSOMAL LOCALIZATION, AND MODELING OF THE ACTIVE-SITE SO JOURNAL OF IMMUNOLOGY LA English DT Article ID AMINO-ACID SEQUENCE; CONSERVED LINKAGE GROUP; 24.11 ENKEPHALINASE; DIRECTED MUTAGENESIS; MOUSE CHROMOSOME-1; BINDING-SITE; BONE-MARROW; SUBSTANCE-P; CELLS; GENE AB To further analyze CD10/NEP, function in lymphoid and nonlymphoid cells using well characterized murine systems, we isolated the murine CD10/NEP homologue, determined its chromosomal location, and modeled the enzyme's active site. The murine CD10/NEP cDNA predicts a 750-amino acid (aa) type II integral membrane protein with 90% identity to the human CD10 sequence and 100% conservation of critical aa and functional motifs. The latter include the pentapeptide consensus sequence required for zinc binding and catalytic activity, additional aa associated with substrate binding, and the extracellular cysteines that participate in disulfide bonds required for enzymatic activity. Like its human homologue, murine CD10/NEP has multiple alternative 5'-untranslated region sequences. The gene is localized on the proximal half of murine chromosome 3. In Northern analysis, murine CD10/NEP transcripts are abundant in bone marrow stromal cells that support pre-B cell differentiation but are undetectable in representative Abelson transformed pre-B cell lines. The murine CD10/NEP active site was modeled by aligning critical conserved CD10/NEP residues with comparable residues in the active site of thermolysin, a bacterial metalloprotease with similar substrate specificity. The model predicts that the two enzymes have similar clefts that comprise the active site and permit zinc-dependent substrate interactions. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,IMMUNOBIOL LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. DUKE UNIV,SCH MED,DEPT MED,DURHAM,NC 27710. DUKE UNIV,SCH MED,DEPT MICROBIOL,DURHAM,NC 27710. FU NCI NIH HHS [CA49232]; NHGRI NIH HHS [HG-00101] NR 57 TC 41 Z9 42 U1 0 U2 2 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD MAY 1 PY 1992 VL 148 IS 9 BP 2817 EP 2825 PG 9 WC Immunology SC Immunology GA HQ182 UT WOS:A1992HQ18200022 PM 1374101 ER PT J AU ZHANG, XQ YANG, L HO, DD KURITZKES, DR CHEN, ISY CHING, WTW CHEN, YMA SCHOOLEY, RT AF ZHANG, XQ YANG, L HO, DD KURITZKES, DR CHEN, ISY CHING, WTW CHEN, YMA SCHOOLEY, RT TI HUMAN T-LYMPHOTROPIC VIRUS TYPE-I-SPECIFIC AND TYPE-II-SPECIFIC ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY - STRAIN SPECIFICITY AND EPITOPE MAPPING SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID HUMAN IMMUNODEFICIENCY VIRUS; MEDIATED CYTO-TOXICITY; LEUKEMIA-VIRUS; HTLV-I; CELLS; INFECTION; RECIPIENTS; DISEASE; REGIONS AB Antibody-dependent cellular cytotoxicity (ADCC) against human T lymphotropic virus (HTLV) types I and II was investigated using sera obtained from infected individuals or from rabbits immunized with HTLV-1 or -II envelope peptides. Target cells included an HTLV-I-transformed cell line (C91/PL), an HTLV-II-transformed cell line (729pH6neo), and Epstein Barr virus (EBV)-transformed B lymphocytes expressing HTLV-I or -II env or gag gene products after infection with vaccinia/HTLV recombinants. ADCC activity was directed at HTLV-I and -II envelope glycoproteins but not against core (gag) components. In contrast to the human immunodeficiency virus system, significant cross-reactivity between HTLV-I- and -II-directed ADCC activity was observed. Epitope mapping studies using sera from rabbits that had been immunized with HTLV-I or -II envelope peptides suggested that the critical epitopes for ADCC activity are located primarily in hydrophilic regions of the exterior (gp46) part of the envelope glycoprotein. C1 UNIV COLORADO,HLTH SCI CTR,DIV INFECT DIS,BOX B-168,4200 E 9TH AVE,DENVER,CO 80262. VET ADM MED CTR,DENVER,CO 80220. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,INFECT DIS UNIT,BOSTON,MA 02114. UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,LOS ANGELES,CA 90024. NYU,AARON DIAMOND CTR AIDS RES,NEW YORK,NY 10003. NR 28 TC 4 Z9 4 U1 0 U2 1 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 MAY PY 1992 VL 165 IS 5 BP 805 EP 812 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HQ275 UT WOS:A1992HQ27500003 PM 1373751 ER PT J AU PENACRUZ, V BRONSON, RT REISS, CS MCINTOSH, K AF PENACRUZ, V BRONSON, RT REISS, CS MCINTOSH, K TI ALTERED HISTOPATHOLOGY IN PROTEIN-DEPRIVED MICE DURING SENDAI VIRUS PNEUMONIA - EVIDENCE FOR DELAYED INFLAMMATORY RESPONSE AND RECOVERY SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID INFECTION; CELLS AB The morphology of the lungs and airway during the course of respiratory infection caused by Sendai virus was examined in normal (20% protein diet) and malnourished (2% protein diet) BALB/c mice. Mortality in normal Sendai-infected mice was 0 compared with 71% in the infected malnourished group. Virus was isolated until day 6 in normally fed mice and until day 9 in the malnourished group. Pulmonary inflammation was largely mononuclear and began in the normally nourished animals on day 3, peaked at day 6, and reverted almost to normal by 30 days. In the malnourished group, inflammation was delayed by about 1 day and fell further behind during the first week. It peaked 10-13 days after infection and was still present with little resolution by day 30. These findings may have relevance to the high mortality of acute respiratory diseases in children of the developing world. C1 CHILDRENS HOSP MED CTR,DIV INFECT DIS,300 LONGWOOD AVE,BOSTON,MA 02115. TUFTS UNIV,SCH VET MED & MED,DEPT PATHOL,BOSTON,MA 02111. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. OI Reiss, Carol/0000-0003-4353-8882 FU NCI NIH HHS [P30 CA-06516]; NCRR NIH HHS [SO7 RR-05526]; NIAID NIH HHS [AI-18083] NR 19 TC 4 Z9 4 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 MAY PY 1992 VL 165 IS 5 BP 846 EP 851 PG 6 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HQ275 UT WOS:A1992HQ27500009 PM 1314870 ER PT J AU SAMORE, MH SIBER, GR AF SAMORE, MH SIBER, GR TI EFFECT OF PERTUSSIS TOXIN ON SUSCEPTIBILITY OF INFANT RATS TO HAEMOPHILUS-INFLUENZAE TYPE-B SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID BORDETELLA-PERTUSSIS; INHIBITION; VACCINES AB Pertussis toxin is an important virulence factor of Bordetella pertussis that may also contribute to the toxicity of pertussis vaccines. The effect of low doses of pertussis toxin on response to Haemophilus influenzae type b (Hib) infection was examined in infant rats. Pretreatment of rats with 10 or 100 ng of pertussis toxin increased blood bacterial concentration (P < .01), serum endotoxin levels (P < .01), and mortality (P < .05) relative to saline pretreated controls challenged with 4 x 10(3) Hib intraperitoneally. The 100-ng dose of pertussis toxin, but not the 10-ng dose, increased the leukocyte count. Thus, doses of pertussis toxin less than the threshold dose for inducing leukocytosis may enhance the susceptibility of infant rats to Hib infections. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,INFECT DIS LAB,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. STATE LAB INST,MASSACHUSETTS PUBL HLTH BIOL LABS,BOSTON,MA. FU NIAID NIH HHS [AI-18125, AI-07061] NR 15 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 MAY PY 1992 VL 165 IS 5 BP 945 EP 948 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HQ275 UT WOS:A1992HQ27500028 PM 1533239 ER PT J AU HERWALDT, BL KAYE, ET LEPORE, TJ BERMAN, JD BADEN, HP AF HERWALDT, BL KAYE, ET LEPORE, TJ BERMAN, JD BADEN, HP TI SODIUM STIBOGLUCONATE (PENTOSTAM) OVERDOSE DURING TREATMENT OF AMERICAN CUTANEOUS LEISHMANIASIS SO JOURNAL OF INFECTIOUS DISEASES LA English DT Note ID MUCOSAL LEISHMANIASIS; ANTIMONY; EFFICACY AB A 27-year-old woman who acquired cutaneous leishmaniasis in Central America was inadvertently treated with 10 times the intended daily dose of the pentavalent antimonial compound sodium stibogluconate (Pentostam): 8500 mg (143 mg/kg) instead of 850 mg. The patient felt "wiped out" during the 4-h infusion of the drug. After the mistake in dosing was discovered, she was vigorously hydrated and carefully monitored in an intensive care unit for > 48 h. Her vital signs were stable, and no arrhythmias were noted. Her alanine aminotransferase level rose briefly to 2.4 times the upper limit of normal, and her white blood cell count briefly fell 43% to a low of 3700/mu-l. Her skin lesions subsequently healed without further therapy. Although sodium stibogluconate has been associated with a variety of side effects, in this case, a single high dose of the drug was tolerated without serious toxicity. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. WALTER REED ARMY MED CTR,WASHINGTON,DC 20307. NANTUCKET COTTAGE HOSP,NANTUCKET,MA. RP HERWALDT, BL (reprint author), CTR DIS CONTROL,NATL CTR INFECT DIS,DIV PARASIT DIS,MAILSTOP F-13,1600 CLIFTON RD,ATLANTA,GA 30333, USA. NR 15 TC 9 Z9 9 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 MAY PY 1992 VL 165 IS 5 BP 968 EP 971 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA HQ275 UT WOS:A1992HQ27500034 PM 1314873 ER PT J AU WEINSTOCK, MA STAMPFER, MJ LEW, RA WILLETT, WC SOBER, AJ AF WEINSTOCK, MA STAMPFER, MJ LEW, RA WILLETT, WC SOBER, AJ TI CASE-CONTROL STUDY OF MELANOMA AND DIETARY VITAMIN-D - IMPLICATIONS FOR ADVOCACY OF SUN PROTECTION AND SUNSCREEN USE SO JOURNAL OF INVESTIGATIVE DERMATOLOGY LA English DT Note ID MALIGNANT-MELANOMA; HUMAN MELANOCYTES; CELL-GROWTH; EXPOSURE; 1,25-DIHYDROXYVITAMIN-D3; METABOLITES; INHIBITION; WOMEN; RISK AB The rapid increase in melanoma incidence and mortality has given rise to nationwide and international campaigns that encourage the public to protect themselves from solar radiation with clothing, sunscreens, and other measures. The basis of these campaigns has been challenged by proponents of the theory that vitamin D, which is generated in the skin by ultraviolet BY radiation, inhibits the development of melanoma. The present investigation tests this theory by examining the relation between dietary vitamin D and melanoma risk in a case-control study. Vitamin D intake was assessed by a food-frequency questionnaire in 165 melanoma patients and 209 controls. After controlling for age, hair color, and family history of melanoma, there was no association of melanoma risk with total vitamin D intake, calorie-adjusted vitamin D intake, vitamin D intake from foods, or consumption of milk or vitamin D supplements. We find no evidence to suggest that vitamin D protects against melanoma, and therefore continue to support the ongoing public health campaigns aimed at reducing sun exposure for the prevention of melanoma. C1 VET ADM MED CTR,DEPT MED,PROVIDENCE,RI 02908. BROWN UNIV,PROVIDENCE,RI 02912. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. ROGER WILLIAMS MED CTR,PROVIDENCE,RI. BRIGHAM & WOMENS HOSP,CHANNING LAB,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV MASSACHUSETTS,DEPT PHARMACOL,WORCESTER,MA 01605. MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. RP WEINSTOCK, MA (reprint author), VET ADM MED CTR,DERMATOEPIDEMIOL UNIT 111,830 CHALKSTONE AVE,PROVIDENCE,RI 02908, USA. FU PHS HHS [35837, 49531] NR 29 TC 58 Z9 58 U1 0 U2 2 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0022-202X J9 J INVEST DERMATOL JI J. Invest. Dermatol. PD MAY PY 1992 VL 98 IS 5 BP 809 EP 811 DI 10.1111/1523-1747.ep12499962 PG 3 WC Dermatology SC Dermatology GA HR030 UT WOS:A1992HR03000025 PM 1569330 ER PT J AU ROSOWSKY, A FORSCH, RA REICH, VE FREISHEIM, JH MORAN, RG AF ROSOWSKY, A FORSCH, RA REICH, VE FREISHEIM, JH MORAN, RG TI 1ST USE OF THE TAYLOR PTERIDINE SYNTHESIS AS A ROUTE TO POLYGLUTAMATE DERIVATIVES OF ANTIFOLATES .46. SIDE-CHAIN MODIFIED 5-DEAZAFOLATE AND 5-DEAZATETRAHYDROFOLATE ANALOGS AS MAMMALIAN FOLYLPOLYGLUTAMATE SYNTHETASE AND GLYCINAMIDE RIBONUCLEOTIDE FORMYLTRANSFERASE INHIBITORS - SYNTHESIS AND INVITRO BIOLOGICAL EVALUATION SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID FOLYL POLYGLUTAMATE SYNTHETASE; HUMAN DIHYDROFOLATE-REDUCTASE; GAMMA-CARBOXYL REPLACEMENT; DENOVO PURINE SYNTHESIS; CELL-GROWTH INHIBITION; METHOTREXATE ANALOGS; ANTITUMOR-ACTIVITY; FOLIC-ACID; 2,OMEGA-DIAMINOALKANOIC ACIDS; GLUTAMATE SYNTHETASE AB 5-Deazafolate and 5-deazatetrahydrofolate (DATHF) analogues with the glutamic acid side chain replaced by homocysteic aicd (HCysA), 2-amino-4-phosphonobutanoic acid (APBA), and ornithine (Orn) were synthesized as part of a larger program directed toward inhibitors of folylpolyglutamate synthetase (FPGS) as probes of the FPGS active site and as potential therapeutic agents. The tetrahydro compounds were also of interest as non-polyglutamatable inhibitors of the purine biosynthetic enzyme glycinamide ribonucleotide formyltransferase (GARFT). Reductive coupling of N2-acetamido-6-formylpyrido[2,3-d]pyrimidin-4(3H)-one with 4-aminobenzoic acid, followed by N-10-formylation, mixed anhydride condensation of the resultant N2-acetyl-N-10-formyl-5-deazapteroic acid with L-homocysteic acid, and removal of the N2-acetyl and N-10-formyl groups with NaOH, afforded N-(5-deazapteroyl)-L-homocysteic acid (5-dPteHCysA). Mixed anhydride condensation of N2-acetyl-N-10-formyl-5-deazapteroic acid with methyl D,L-2-amino-4-(diethoxyphosphinyl)butanoic acid, followed by consecutive treatment with Me3SiBr and NaOH, yielded D,L-2-[(5-deazapteroyl)amino]-4-phosphonobutanoic acid (5-dPteAPBA). Treatment with NaOH alone led to retention of one ethyl ester group on the phosphonate moiety. Catalytic hydrogenation of N2-acetyl-N-10-formyl-5-deazapteroic acid followed by mixed anhydride condensation with methyl L-homocysteate and deprotection with NaOH afforded N-(5,6,7,8-tetrahydro-5-deazapteroyl)-L-homocysteic acid (5-dH4PteHCysA). Similar chemistry starting from methyl D,L-2-amino-4-(diethoxyphosphinyl)butanoic acid and methyl N-delta-(benzyloxycarbonyl)-L-ornithinate yielded D,L-2-[(5-deaza-5,6,7,8-tetrahydropteroyl)amino]-4-phosphonobutanoic acid (5-dH4Pte-APBA) and N(alpha)-(5-deaza-5, 6,7,8-tetrahydropteroyl)-L-ornithine (5-dH4PteOrn), respectively. The 5-deazafolate analogues were inhibitors of mouse liver FPGS, and the DATHF analogues inhibited both mouse FPGS and mouse leukemic cell GARFT. Analogues with HCysA and monoethyl APBA side chains were less active as FPGS inhibitors than those containing an unesterified gamma-PO(OH)2 group, and their interaction with the enzyme was noncompetitive against variable folyl substrate. In contrast, Orn and APBA analogues obeyed competitive inhibition kinetics and were more potent, with K(i) values as low as 30 nM. Comparison of the DATHF analogues as GARFT inhibitors indicated that the Orn side chain diminished activity relative to DATHF, but that the compounds with gamma-sulfonate or gamma-phosphonate substitution retained activity, with K(i) values in the submicromolar range. The best GARFT inhibitor was the 5-dH4PteAPBA diastereomer mixture, with a K(i) of 47 nM versus 65 nM for DATHF. None of the compounds showed activity against cultured WI-L2 or CEM human leukemic lymphoblasts at concentrations of up to 100-mu-M. We conclude that linking the 5-deazapteroyl moiety to these amino acid side chains previously found inhibitory to FPGS enhances binding to FPGS, and that negatively charged groups at the gamma-position of the DATHF analogues allow maintenance of GARFT inhibition. However, inefficient cellular uptake is an obstacle to the use of these potential dual inhibitors of FPGS and GARFT as therapeutic agents. C1 UNIV SO CALIF, NORRIS COMPREHENS CANC CTR, LOS ANGELES, CA 90033 USA. UNIV SO CALIF, DEPT BIOCHEM, LOS ANGELES, CA 90033 USA. MED COLL OHIO, DEPT BIOCHEM & MOLEC BIOL, TOLEDO, OH 43699 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. RP ROSOWSKY, A (reprint author), HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA. FU NCI NIH HHS [CA39867, CA41461] NR 49 TC 14 Z9 14 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 MAY 1 PY 1992 VL 35 IS 9 BP 1578 EP 1588 DI 10.1021/jm00087a012 PG 11 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA HT158 UT WOS:A1992HT15800012 PM 1578484 ER PT J AU WANG, R CHEN, L COTTER, RJ QURESHI, N TAKAYAMA, K AF WANG, R CHEN, L COTTER, RJ QURESHI, N TAKAYAMA, K TI FRAGMENTATION OF LIPOPOLYSACCHARIDE ANCHORS IN PLASMA DESORPTION MASS-SPECTROMETRY SO JOURNAL OF MICROBIOLOGICAL METHODS LA English DT Article; Proceedings Paper CT 2ND INTERNATIONAL SYMP ON THE INTERFACE BETWEEN ANALYTICAL CHEMISTRY AND MICROBIOLOGY : CHROMATOGRAPHY AND MASS SPECTROMETRY IN MICROBIOLOGY CY JUN 10-13, 1991 CL LUND UNIV, LUND, SWEDEN HO LUND UNIV DE LIPID-A; LIPOPOLYSACCHARIDE; PLASMA DESORPTION MASS SPECTROMETRY; STRUCTURAL ANALYSIS ID PERFORMANCE LIQUID-CHROMATOGRAPHY; LIPID-A BACKBONE; LASER DESORPTION; SALMONELLA-TYPHIMURIUM; STRUCTURAL-ANALYSIS; ESCHERICHIA-COLI; DEFICIENT MUTANT; OLIGOSACCHARIDES; SPECTROSCOPY; DERIVATIVES AB Plasma desorption mass spectrometry (PD-MS) was employed for the structural analysis of lipid A's derived from the lipopolysaccharides (LPS) of Escherichia coli D31m4, Rhodopseudomonas sphaeroides ATCC 17023, and Rhodopseudomonas capsulata ATCC 23782. The deep rough chemotype LPS (ReLPS) of E. coli D31m4, a lipid A containing two 2-keto-3-deoxyoctonate (KDO) units, was also analyzed. Several forms were examined, including the mono- and di-phosphoryl lipid A's, and lipid A's methylated at the phosphate group. Positive ion PD-MS gave molecular ions, ions corresponding to the loss of ester-linked fatty acyl and glycosidic phosphate groups, oxonium ions formed by the cleavage of the distal sugar, and ions resulting from the two-bond cleavage of the reducing-end sugar. Negative ion PD-MS gave molecular ions and fragmentation products of the phosphate group and fatty acyl anions in the low mass region. The presence of the KDO group on the lipid A structure had little effect on the fragmentation pattern of the rest of the molecule of ReLPS. PD-MS of lipid A has allowed us to determine the molecular weight, the distribution of the fatty acyl groups in both the distal and reducing-end sugars, the nature of the O-linked fatty acyl groups, and the presence of a glycosidic-linked phosphate. In combination with proton nuclear magnetic resonance spectroscopy, PD-MS allows one to determine the complete structure of lipid A. C1 JOHNS HOPKINS UNIV,SCH MED,DEPT PHARMACOL & MOLEC SCI,MIDDLE ATLANTIC MASS SPECT FACIL,BALTIMORE,MD 21205. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MYCOBACTERIOL RES LAB,MADISON,WI 53705. UNIV WISCONSIN,DEPT BACTERIOL,MADISON,WI 53706. RI Wang, Rong/A-8721-2009 NR 25 TC 11 Z9 11 U1 1 U2 3 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-7012 J9 J MICROBIOL METH JI J. Microbiol. Methods PD MAY PY 1992 VL 15 IS 3 BP 151 EP 166 DI 10.1016/0167-7012(92)90037-5 PG 16 WC Biochemical Research Methods; Microbiology SC Biochemistry & Molecular Biology; Microbiology GA HW410 UT WOS:A1992HW41000003 ER PT J AU GOFF, DC OLIN, JA JENIKE, MA BAER, L BUTTOLPH, ML AF GOFF, DC OLIN, JA JENIKE, MA BAER, L BUTTOLPH, ML TI DISSOCIATIVE SYMPTOMS IN PATIENTS WITH OBSESSIVE-COMPULSIVE DISORDER SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID MULTIPLE PERSONALITY-DISORDER; STRUCTURED INTERVIEW; DEPERSONALIZATION; SCALE; RELIABILITY; BORDERLINE; VALIDITY; OVERLAP AB To clarify the relationship between dissociative symptoms and obsessive-compulsive disorder (OCD), 100 patients with OCD were assessed with standardized instruments measuring symptoms of OCD, dissociation, and depression. Diagnoses of personality disorders and dissociative disorders were made using structured interviews. Compared with a previous study, OCD patients had dissociation scores slightly higher than normal controls and comparable to patients with other anxiety disorders. Patients with elevated dissociation scores had more severe OCD symptoms, were more depressed, and were more likely to have a personality disorder than patients with low dissociation scores. Although dissociative symptoms were frequently reported by OCD patients, symptoms of OCD may also mimic dissociation in some patients. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,BOSTON,MA 02114. NR 29 TC 53 Z9 53 U1 1 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3018 J9 J NERV MENT DIS JI J. Nerv. Ment. Dis. PD MAY PY 1992 VL 180 IS 5 BP 332 EP 337 DI 10.1097/00005053-199205000-00008 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA HU602 UT WOS:A1992HU60200008 PM 1583477 ER PT J AU STOREY, E HYMAN, BT JENKINS, B BROUILLET, E MILLER, JM ROSEN, BR BEAL, MF AF STOREY, E HYMAN, BT JENKINS, B BROUILLET, E MILLER, JM ROSEN, BR BEAL, MF TI 1-METHYL-4-PHENYLPYRIDINIUM PRODUCES EXCITOTOXIC LESIONS IN RAT STRIATUM AS A RESULT OF IMPAIRMENT OF OXIDATIVE-METABOLISM SO JOURNAL OF NEUROCHEMISTRY LA English DT Note DE HUNTINGTONS DISEASE; PARKINSONS DISEASE; MITOCHONDRIA; 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; EXCITOTOXIN; MAGNETIC RESONANCE IMAGING ID GLUTAMATE; RECEPTOR; NEURONS; DISEASE AB The effects of 1-methyl-4-phenylpyridinium (MPP+) were studied in rat striatum. Using freeze-clamp, microwave, and water-suppressed proton chemical shift magnetic resonance imaging techniques, MPP+ resulted in marked increases in lactate and a depletion of ATP for up to 48 h after the injections. MPP+ produced dose-dependent depletions of dopamine, serotonin, gamma-aminobutyric acid, and substance P that were partially blocked at 1 week by prior decortication or completely blocked by MK-801 at 24 h. The lesions showed relative sparing of somatostatin-neuropeptide Y neurons, consistent with N-methyl-D-aspartate (NMDA) excitotoxicity. MPP+ produces impairment of oxidative phosphorylation in vivo, which may result in membrane depolarization with persistent activation of NMDA receptors and excitotoxic neuronal degeneration. An impairment of energy metabolism may therefore underlie slow excitotoxic neuronal death in neurodegenerative diseases. C1 MASSACHUSETTS GEN HOSP,NEUROL SERV,NEUROCHEM LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NMR CTR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Storey, Elsdon/A-9889-2013; Brouillet, Emmanuel/B-4784-2014 OI Brouillet, Emmanuel/0000-0001-6322-7403 FU NINDS NIH HHS [NS10828]; PHS HHS [16367] NR 20 TC 151 Z9 152 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD MAY PY 1992 VL 58 IS 5 BP 1975 EP 1978 DI 10.1111/j.1471-4159.1992.tb10080.x PG 4 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA HN274 UT WOS:A1992HN27400051 PM 1560246 ER PT J AU DELAMONTE, SM WANDS, JR AF DELAMONTE, SM WANDS, JR TI NEURONAL THREAD PROTEIN OVER-EXPRESSION IN BRAINS WITH ALZHEIMERS-DISEASE LESIONS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 319 EP 319 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200028 ER PT J AU LEE, JM WEINSTEIN, DA AF LEE, JM WEINSTEIN, DA TI FUNCTIONAL UNCOUPLING OF FRONTAL-CORTEX LOW AFFINITY 5-HT1A RECEPTORS IN ALZHEIMERS-DISEASE - IMPACT ON PHARMACOLOGICAL THERAPIES SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 320 EP 320 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200029 ER PT J AU NIHEI, K MCKEE, AC KOWALL, NW AF NIHEI, K MCKEE, AC KOWALL, NW TI DEGENERATION OF NONPYRAMIDAL LOCAL CIRCUIT NEURONS IN THE MOTOR CORTEX OF AMYOTROPHIC-LATERAL-SCLEROSIS PATIENTS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 5 Z9 5 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 322 EP 322 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200039 ER PT J AU HARRINGTON, KM LU, C MCKEE, AC KOWALL, NW AF HARRINGTON, KM LU, C MCKEE, AC KOWALL, NW TI PP60C-SRC IMMUNOREACTIVITY IS INCREASED IN SENILE PLAQUE NEURITES IN ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 328 EP 328 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200063 ER PT J AU HYMAN, BT MARZLOFF, K WENNINGER, JJ DAWSON, TM SNYDER, SH AF HYMAN, BT MARZLOFF, K WENNINGER, JJ DAWSON, TM SNYDER, SH TI SPARING OF NITRIC-OXIDE SYNTHASE CONTAINING NEURONS IN THE HIPPOCAMPAL-FORMATION IN ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 328 EP 328 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200060 ER PT J AU KOWALL, NW BEAL, MF MCKEE, AC FERRANTE, RJ AF KOWALL, NW BEAL, MF MCKEE, AC FERRANTE, RJ TI ELECTRON-TRANSPORT CHAIN ENZYMES ARE HETEROGENEOUSLY DISTRIBUTED IN HUMAN STRIATUM SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 329 EP 329 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200065 ER PT J AU HSU, DW HAKIM, F BILLER, BMK KLIBANSKI, A ZERVAS, NT HEDLEYWHYTE, ET AF HSU, DW HAKIM, F BILLER, BMK KLIBANSKI, A ZERVAS, NT HEDLEYWHYTE, ET TI PROLIFERATING CELL NUCLEAR ANTIGEN (PCNA) IN RECURRENT PITUITARY-ADENOMAS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 330 EP 330 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200070 ER PT J AU LOUIS, DN VONDEIMLING, A SEIZINGER, BR AF LOUIS, DN VONDEIMLING, A SEIZINGER, BR TI A RAPID ASSAY FOR DETECTION OF ALLELIC CHROMOSOMAL LOSS IN SMALL OR ARCHIVAL BRAIN-TUMOR SPECIMENS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 332 EP 332 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200079 ER PT J AU GOLDEN, JA SCHOENE, WC AF GOLDEN, JA SCHOENE, WC TI NEUROPATHOLOGY OF TRISOMY 9 AND COMPARISON WITH THE DANDY-WALKER MALFORMATION SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 340 EP 340 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200108 ER PT J AU MCKEE, AC YANKNER, BA KOWALL, NW SCHUMACHER, J BEAL, MF AF MCKEE, AC YANKNER, BA KOWALL, NW SCHUMACHER, J BEAL, MF TI THE NEUROTOXICITY OF BETA AMYLOID PROTEIN IN PRIMATES SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CHILDRENS HOSP MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RI Kowall, Neil/G-6364-2012 OI Kowall, Neil/0000-0002-6624-0213 NR 0 TC 2 Z9 2 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 359 EP 359 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200185 ER PT J AU SOBEL, RA WANG, Y AF SOBEL, RA WANG, Y TI VESTIBULAR (ACOUSTIC) SCHWANNOMAS - HISTOLOGIC FEATURES IN NEUROFIBROMATOSIS-2 (NF-2) AND UNILATERAL CASES SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ASSN NEUROPATHOLOGISTS INC PI LAWRENCE PA 1041 NEW HAMPSHIRE ST, LAWRENCE, KS 66044 SN 0022-3069 J9 J NEUROPATH EXP NEUR JI J. Neuropathol. Exp. Neurol. PD MAY PY 1992 VL 51 IS 3 BP 366 EP 366 PG 1 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA HT972 UT WOS:A1992HT97200210 ER PT J AU GLASS, J HOCHBERG, FH GRUBER, ML LOUIS, DN SMITH, D RATTNER, B AF GLASS, J HOCHBERG, FH GRUBER, ML LOUIS, DN SMITH, D RATTNER, B TI THE TREATMENT OF OLIGODENDROGLIOMAS AND MIXED OLIGODENDROGLIOMA-ASTROCYTOMAS WITH PCV CHEMOTHERAPY SO JOURNAL OF NEUROSURGERY LA English DT Article DE OLIGODENDROGLIOMA; MIXED GLIOMA; PROCARBAZINE; CCNU; VINCRISTINE ID MALIGNANT BRAIN-TUMORS; GLIOMAS; PROCARBAZINE; RADIOTHERAPY; COMBINATION; CCNU AB Malignant oligodendrogliomas have been shown to be responsive to chemotherapy. The authors administered systemic chemotherapy to seven patients with oligodendroglioma or anaplastic oligodendroglioma, and to 14 with mixed oligodendroglioma-astrocytoma. Fourteen patients underwent chemotherapy before and seven after irradiation. The PCV (procarbazine, methyl- 1 -(2-chloroethyl)- 1 -nitrosourea (CCNU), and vincristine) chemlotherapy was administered every 6 weeks (42-day cycles) for two to five cycles as follows: CCNU, 110 mg/sq m on Day 1; procarbazine, 60 mg/sq m/day on Days 8 to 21; and vincristine, 1.4 mg/sq m/day on Days 8 and 29. Complete or partial (> 50% reduction in tumor mass) responses at 20 to 100+ weeks after treatment were noted in 11 (79%) of the 14 patients treated before irradiation, including two with anaplastic oligodendroglioma and nine with mixed tumors. Complete responses were seen in two patients, one with anaplastic oligodendroglioma and one with a mixed tumor. Partial responses were seen in three of seven patients treated after radiotherapy. Stabilization of tumor growth followed PCV chemotherapy in four patients (two treated before and two after radiotherapy). Tumor growth progressed in two patients during therapy despite an initial response and in two patients despite therapy. The authors conclude that mixed oligodendroglial tumors as well as anaplastic oligodendrogliomas are responsive to PCV chemotherapy. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MED HEMATOL ONCOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 20 TC 154 Z9 155 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAY PY 1992 VL 76 IS 5 BP 741 EP 745 DI 10.3171/jns.1992.76.5.0741 PG 5 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HQ269 UT WOS:A1992HQ26900003 PM 1564535 ER PT J AU MAXWELL, M GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN AF MAXWELL, M GALANOPOULOS, T NEVILLEGOLDEN, J ANTONIADES, HN TI EFFECT OF THE EXPRESSION OF TRANSFORMING GROWTH-FACTOR-BETA-2 IN PRIMARY HUMAN GLIOBLASTOMAS ON IMMUNOSUPPRESSION AND LOSS OF IMMUNE SURVEILLANCE SO JOURNAL OF NEUROSURGERY LA English DT Article DE GLIOBLASTOMA; TRANSFORMING GROWTH FACTOR-BETA; ONCOGENE; INSITU HYBRIDIZATION ID CELL SUPPRESSOR FACTOR; FACTOR-BETA; HUMAN GLIOMAS; PROTEIN; LYMPHOCYTES; INHIBITION; TUMORS; SEQUENCE; INVITRO; CDNA AB Glioblastomas are malignant brain tumors that are attended by an immunosuppressed state. The authors have studied the expression of transforming growth factor-beta-2, which is known to have potent immunosuppressive and angiogenic properties. Transforming growth factor-beta-2 messenger ribonucleic acid and its protein product are both found to be greatly overexpressed in these tumors and are absent from normal brain tissue. The overexpression of this growth factor may contribute to the escape of neoplastic astrocytes from immune surveillance and, furthermore, to the immunosuppressed state that is characteristic of many of these patients. C1 MASSACHUSETTS GEN HOSP,CTR BLOOD RES,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. RADCLIFFE INFIRM,DEPT NEUROPATHOL,OXFORD OX2 6HE,ENGLAND. UNIV OXFORD,DEPT CLIN NEUROL,OXFORD,ENGLAND. FU NCI NIH HHS [CA-30101, CA-09382]; NHLBI NIH HHS [HL-29583] NR 37 TC 89 Z9 92 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI CHARLOTTESVILLE PA UNIV VIRGINIA, 1224 WEST MAIN ST, STE 450, CHARLOTTESVILLE, VA 22903 SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD MAY PY 1992 VL 76 IS 5 BP 799 EP 804 DI 10.3171/jns.1992.76.5.0799 PG 6 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA HQ269 UT WOS:A1992HQ26900011 PM 1373442 ER PT J AU JOHNSON, KA SPERLING, RA HOLMAN, BL NAGEL, JS GROWDON, JH AF JOHNSON, KA SPERLING, RA HOLMAN, BL NAGEL, JS GROWDON, JH TI CEREBRAL PERFUSION IN PROGRESSIVE SUPRANUCLEAR PALSY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article ID EMISSION COMPUTED-TOMOGRAPHY; ALZHEIMERS-DISEASE; POSITRON TOMOGRAPHY; DEMENTIA; HYPOMETABOLISM; DIAGNOSIS AB Progressive supranuclear palsy (PSP) is a neurodegenerative disorder in which structurally preserved cerebral cortex is thought to be functionally disconnected by subcortical lesions. To assess brain functional activity in patients with PSP, we measured regional cerebral perfusion, as estimated by [I-123] iofetamine (IMP) and single-photon emission computed tomography (SPECT), in 11 patients with a clinical diagnosis of PSP and 10 healthy control subjects. IMP uptake was measured in 2 basal ganglia and 24 cortical regions. Neuropsychological tests were administered to assess cognitive function. Compared to age-matched normal control subjects, relative IMP uptake was significantly reduced in PSP patients in basal ganglia (21%), superior frontal (25%), anterior parietal (19%), and inferior frontal (18%) regions. Cognitive performance was most abnormal on tests thought to be subserved predominantly by frontal lobes. Our study demonstrates that IMP-SPECT detects physiological abnormalities in the cortex that parallel behavioral impairments in PSP. C1 BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP JOHNSON, KA (reprint author), BRIGHAM & WOMENS HOSP,DEPT RADIOL,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NIA NIH HHS [P01 AG04953, P50 AG05134] NR 33 TC 38 Z9 38 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 MAY PY 1992 VL 33 IS 5 BP 704 EP 709 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HT117 UT WOS:A1992HT11700016 PM 1569479 ER PT J AU WOODROW, D MOSS, J SHORE, I SPIRO, RG AF WOODROW, D MOSS, J SHORE, I SPIRO, RG TI DIABETIC GLOMERULOSCLEROSIS - IMMUNOGOLD ULTRASTRUCTURAL STUDIES ON THE GLOMERULAR DISTRIBUTION OF TYPE-IV COLLAGEN AND HEPARAN-SULFATE PROTEOGLYCAN SO JOURNAL OF PATHOLOGY LA English DT Article DE IMMUNOGOLD; ULTRASTRUCTURE; GLOMERULAR BASEMENT MEMBRANE; DIABETES-MELLITUS; HEPARAN SULFATE PROTEOGLYCAN; TYPE-IV COLLAGEN ID BASEMENT-MEMBRANE COMPONENTS; SULFATE PROTEOGLYCAN; AMINONUCLEOSIDE NEPHROSIS; LAMININ; NEPHROPATHY; NEPHRITIS; PROTEINS; MATRIX; LIGHT AB We have undertaken an ultrastructural immunogold investigation of the distribution of type IV collagen and heparan sulphate proteoglycan (HSPG) in glomeruli from the kidneys of one normal control and three patients with diabetes mellitus and proteinuria. The sample included both diffuse and nodular diabetic glomerulosclerosis. In the control and diabetic kidneys, the type IV collagen was present predominantly on the endothelial aspect of the glomerular basement membrane (GBM), and by contrast the HSPG was found mainly on the epithelial side. In the mesangium in both control and diabetic glomeruli, type IV collagen was found predominantly in the central regions, while HSPG was mostly restricted to the region beneath the epithelial cells. Consequently, where there is a marked increase in mesangial matrix with nodule formation in diabetics there is a corresponding increase in the amount of type IV collagen but not of HSPG. Although the three diabetic patients were proteinuric, the HSPG was not decreased in the thickened GBMs. C1 HARVARD UNIV,SCH MED,CHANNING LAB,ELLIOTT P JOSLIN RES LAB,BOSTON,MA 02115. RP WOODROW, D (reprint author), CHARING CROSS & WESTMINSTER MED SCH,DEPT HISTOPATHOL,FULHAM PL RD,LONDON W6 8RF,ENGLAND. NR 26 TC 26 Z9 27 U1 0 U2 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX, ENGLAND PO19 1UD SN 0022-3417 J9 J PATHOL JI J. Pathol. PD MAY PY 1992 VL 167 IS 1 BP 49 EP 58 DI 10.1002/path.1711670109 PG 10 WC Oncology; Pathology SC Oncology; Pathology GA HW177 UT WOS:A1992HW17700008 PM 1625058 ER PT J AU BRAMSON, RT BLICKMAN, JG AF BRAMSON, RT BLICKMAN, JG TI PERFORATION DURING HYDROSTATIC REDUCTION OF INTUSSUSCEPTION - PROPOSED MECHANISM AND REVIEW OF THE LITERATURE SO JOURNAL OF PEDIATRIC SURGERY LA English DT Article DE INTUSSUSCEPTION; PERFORATION; HYDROSTATIC REDUCTION ID CHILDREN C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV PEDIAT RADIOL,BOSTON,MA 02114. TAMPA GEN HOSP,DEPT RADIOL,TAMPA,FL 33606. NR 25 TC 18 Z9 18 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0022-3468 J9 J PEDIATR SURG JI J. Pediatr. Surg. PD MAY PY 1992 VL 27 IS 5 BP 589 EP 591 DI 10.1016/0022-3468(92)90454-F PG 3 WC Pediatrics; Surgery SC Pediatrics; Surgery GA HT460 UT WOS:A1992HT46000014 PM 1625128 ER PT J AU PERKELL, J LANE, H SVIRSKY, M WEBSTER, J AF PERKELL, J LANE, H SVIRSKY, M WEBSTER, J TI SPEECH OF COCHLEAR IMPLANT PATIENTS - A LONGITUDINAL-STUDY OF VOWEL PRODUCTION SO JOURNAL OF THE ACOUSTICAL SOCIETY OF AMERICA LA English DT Article ID PERCEPTION AB Acoustic parameters were measured for vowels spoken in /hVd/ context by four postlingually deafened recipients of multichannel (Ineraid) cochlear implants. Three of the subjects became totally deaf in adulthood after varying periods of partial hearing loss; the fourth became totally deaf at age four. The subjects received different degrees of perceptual benefit from the prosthesis. Recordings were made before, and at intervals following speech processor activation. The measured parameters included F1, F2, F0, SPL, duration, and amplitude difference between the first two harmonic peaks in the log magnitude spectrum (H1-H2). Numerous changes in parameter values were observed from pre- to post-implant, with differences among subjects. Many changes, but not all, were in the direction of normative data, and most changes were consistent with hypotheses about relations among the parameters. Some of the changes tended to enhance phonemic contrasts; others had the opposite effect. For three subjects, H1-H2 changed in a direction consistent with measurements of their average air flow when reading; that relation was more complex for the fourth subject. The results are interpreted with respect to: characteristics of the individual subjects, including vowel identification scores; mechanical interactions among glottal and supraglottal articulations; and hypotheses about the role of auditory feedback in the control of speech production. Almost all the observed differences could be attributed to changes in the average settings of speaking rate, F0 and SPL, which presumably can be perceived without the need for spectral place information. Some observed F2 realignment may be attributable to the reception of spectral cues. C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,BOSTON,MA 02114. NORTHEASTERN UNIV,BOSTON,MA 02115. RP PERKELL, J (reprint author), MIT,ELECTR RES LAB,ROOM 36-511,50 VASSAR ST,CAMBRIDGE,MA 02139, USA. RI Svirsky, Mario/A-4160-2008 OI Svirsky, Mario/0000-0002-9238-0682 FU NIDCD NIH HHS [DC00361] NR 38 TC 55 Z9 55 U1 0 U2 7 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0001-4966 J9 J ACOUST SOC AM JI J. Acoust. Soc. Am. PD MAY PY 1992 VL 91 IS 5 BP 2961 EP 2978 DI 10.1121/1.402932 PG 18 WC Acoustics; Audiology & Speech-Language Pathology SC Acoustics; Audiology & Speech-Language Pathology GA HT688 UT WOS:A1992HT68800051 PM 1629489 ER PT J AU SEMRUDCLIKEMAN, M BIEDERMAN, J SPRICHBUCKMINSTER, S LEHMAN, BK FARAONE, SV NORMAN, D AF SEMRUDCLIKEMAN, M BIEDERMAN, J SPRICHBUCKMINSTER, S LEHMAN, BK FARAONE, SV NORMAN, D TI COMORBIDITY BETWEEN ADDH AND LEARNING-DISABILITY - A REVIEW AND REPORT IN A CLINICALLY REFERRED SAMPLE SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE LEARNING DISABILITY; ATTENTION DEFICIT; DISORDER; ATTENTION-DEFICIT HYPERACTIVITY DISORDER; COMORBIDITY ID ATTENTION DEFICIT DISORDER; HYPERACTIVE-CHILDREN; FOLLOW-UP; PSYCHIATRIC STATUS; BOYS; ADOLESCENTS; PREVALENCE; ADULTS AB A widely variable overlap ranging from 10 to 92% has been reported in the literature between attention deficit disorder with hyperactivity (ADDH) and learning disability (LD), most likely a result of inconsistencies in the criteria used to define LD in different studies. The following study seeks to more accurately determine rates of LD in clinically referred children. Using a psychometrically reliable methodological approach, it was expected that the rate of LD in ADDH children would be far more modest than previously reported. Subjects were referred children with ADDH (N = 60), children with academic problems (N = 30), and normal controls (N = 36) of both sexes with available psychological and achievement testing. Using a liberal definition of LD, significant differences were found between the groups (ADDH = 38% versus academic problems = 43% versus normals = 8%; p = 0.002). In contrast, more modest rates were found using two more stringent methods of assessment (23 and 17%; 10 and 3%; 2 and 0%, respectively; p = 0.02). Arithmetic-based LD appears to be equally identified by both stringent methods, whereas the liberal definition overidentified children in all three groups. These findings show that a liberal definition of LD overidentifies LD not only in ADDH children but also in normal children. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. FU NIMH NIH HHS [R01 MH-41314-01A2] NR 60 TC 279 Z9 284 U1 4 U2 17 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1992 VL 31 IS 3 BP 439 EP 448 DI 10.1097/00004583-199205000-00009 PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA HT110 UT WOS:A1992HT11000010 PM 1592775 ER PT J AU STEINGARD, R BIEDERMAN, J DOYLE, A SPRICHBUCKMINSTER, S AF STEINGARD, R BIEDERMAN, J DOYLE, A SPRICHBUCKMINSTER, S TI PSYCHIATRIC COMORBIDITY IN ATTENTION-DEFICIT DISORDER - IMPACT ON THE INTERPRETATION OF CHILD-BEHAVIOR CHECKLIST RESULTS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE CHILD BEHAVIOR CHECKLIST; ATTENTION DEFICIT DISORDER; COMORBIDITY ID DSM-III DISORDERS; GENERAL-POPULATION; LARGE SAMPLE; RISK-FACTORS; PREADOLESCENT CHILDREN; HYPERACTIVE BOYS; PREVALENCE; CONVERGENCE; DIAGNOSES; FAMILY AB Studies have investigated associations between the Child Behavior Checklist (CBCL) and clinical diagnoses without assessing the impact of comorbidity on these results. This study evaluates associations between parental reports from the CBCL and a structured diagnostic interview in children with attention deficit disorder with hyperactivity (ADDH) stratified by the presence (ADDH+) or absence (ADDH-) of psychiatric comorbidity. Interview-defined ADDH children scored significantly worse on all scales of the CBCL compared with scores from interview-defined non-ill comparisons. However, these findings were accounted for by the subgroup of children with ADDH+. The results indicate a good correspondence between CBCL-based ratings and interview-defined diagnoses. These findings also suggest that the CBCL may be a good screening instrument, not only for ADDH but also for comorbid psychiatric disorders. C1 MASSACHUSETTS GEN HOSP,PSYCHOPHARMACOL UNIT,ACC725,15 PARKMAN ST,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 28 TC 66 Z9 66 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1992 VL 31 IS 3 BP 449 EP 454 DI 10.1097/00004583-199205000-00010 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA HT110 UT WOS:A1992HT11000011 PM 1592776 ER PT J AU BLOOMBERG, J WOZNIAK, J FOST, N MEDEARIS, DN HERZOG, DB AF BLOOMBERG, J WOZNIAK, J FOST, N MEDEARIS, DN HERZOG, DB TI ETHICAL DILEMMAS IN CHILD AND ADOLESCENT CONSULTATION PSYCHIATRY SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE CHILD AND ADOLESCENT PSYCHIATRY; CONSULTATION; ETHICS AB Ethical issues in child and adolescent psychiatry consultation arise frequently but seldom are discussed in a public setting. This case of an adolescent victim of a surgical accident illustrates many aspects of consultation psychiatry. The consult question itself, of behavior management, is not unusual, although in this case the question is complicated by the sequelae of trauma, psychosocial chaos, and the staff's angry feelings toward the patient. In addition, potential surgical wrongdoing at the referring hospital brings up the more difficult ethical questions of the consultant's responsibilities, which must be to the patient and his family, as well as to the attending and referring physicians. C1 UNIV WISCONSIN,SCH MED,DEPT PEDIAT,MADISON,WI 53706. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILD PSYCHIAT CONSULTAT LIAISON SERV,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CHILDRENS SERV,BOSTON,MA 02114. RP BLOOMBERG, J (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT CHILD PSYCHIAT,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1992 VL 31 IS 3 BP 557 EP 561 DI 10.1097/00004583-199205000-00025 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA HT110 UT WOS:A1992HT11000026 PM 1592791 ER PT J AU SUGAR, JA HERZOG, DB AF SUGAR, JA HERZOG, DB TI HOSPITALS AND LOS SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP SUGAR, JA (reprint author), UNIV MICHIGAN,MED CTR,ANN ARBOR,MI 48109, USA. NR 3 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 1992 VL 31 IS 3 BP 566 EP 567 DI 10.1097/00004583-199205000-00034 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA HT110 UT WOS:A1992HT11000036 PM 1592796 ER PT J AU DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC ROBINS, P SEBBEN, JE SMITH, JG AF DRAKE, LA CEILLEY, RI CORNELISON, RL DOBES, WA DORNER, W GOLTZ, RW LEWIS, CW SALASCHE, SJ TURNER, MLC ROBINS, P SEBBEN, JE SMITH, JG TI GUIDELINES OF CARE FOR OFFICE SURGICAL FACILITIES .1. SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID STERILE TECHNIQUE; WOUND-INFECTION; SURGERY; PREVENTION RP DRAKE, LA (reprint author), MASSACHUSETTS GEN HOSP,WELLMAN 2,BOSTON,MA 02114, USA. NR 31 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 0190-9622 J9 J AM ACAD DERMATOL JI J. Am. Acad. Dermatol. PD MAY PY 1992 VL 26 IS 5 BP 763 EP 765 PN 1 PG 3 WC Dermatology SC Dermatology GA HR213 UT WOS:A1992HR21300017 ER PT J AU LARSEN, GC MANOLIS, AS SONNENBERG, FA BESHANSKY, JR ESTES, NAM PAUKER, SG AF LARSEN, GC MANOLIS, AS SONNENBERG, FA BESHANSKY, JR ESTES, NAM PAUKER, SG TI COST-EFFECTIVENESS OF THE IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR - EFFECT OF IMPROVED BATTERY LIFE AND COMPARISON WITH AMIODARONE THERAPY SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Review ID CORONARY-ARTERY DISEASE; REFRACTORY VENTRICULAR-TACHYCARDIA; HOSPITAL CARDIAC-ARREST; SUDDEN-DEATH; FOLLOW-UP; FIBRILLATION; SURVIVAL; ARRHYTHMIAS; TACHYARRHYTHMIAS; RESUSCITATION AB The implantable cardioverter-defibrillator (ICD) greatly reduces the incidence of sudden cardiac death among patients with recurrent sustained ventricular tachycardia and fibrillation who do not respond to conventional antiarrhythmic therapy. A cost-effectiveness analysis was performed, comparing the ICD, amiodarone and conventional agents. Actual variable costs of hospitalization and follow-up care were used for 21 ICD- and 43 amiodarone-treated patients. Life expectancy and total variable costs were predicted with use of a Markov decision analytic model. Clinical event rates and probabilities were based on published reports or expert opinion. Life expectancy with an ICD (6.1 years) was 50% greater than that associated with treatment with amiodarone (3.9 years) and 2.5 times that associated with conventional treatment (2.5 years). Assuming replacement every 24 months, ICD lifetime treatment costs (in 1989 dollars) for a 55-year old patient are expected to be $89,600 compared with $24,800 for amiodarone and $16,100 for conventional therapy, yielding a marginal cost/effectiveness ratio for ICD versus amiodarone therapy of $29,200/year of life saved, which is comparable to that of other accepted medical treatments. If technologic improvements extend average battery life to 36 months, the marginal cost/effectiveness ratio would be $21,800/year of life saved, and at 96 months it would be $13,800/year of life saved. Patient age at implantation did not significantly affect these results, If quality of life on amiodarone therapy is 30% lower than that with the ICD, the marginal cost/effectiveness ratio decreases by 35%. If the quality of life for patients receiving drugs is 40% lower than that of patients treated with an ICD, use of the defibrillator becomes the dominant strategy. C1 NEW ENGLAND MED CTR HOSP,DIV CLIN DECIS MAKING,BOSTON,MA 02111. NEW ENGLAND MED CTR HOSP,DEPT MED,DIV CARDIOL,ELECTROPHYSIOL SERV,BOSTON,MA 02111. TUFTS UNIV,SCH MED,BOSTON,MA 02111. OREGON HLTH SCI UNIV,PORTLAND,OR 97201. RP LARSEN, GC (reprint author), PORTLAND VET AFFAIRS MED CTR,DIV CARDIOL 111B,PORTLAND,OR 97201, USA. RI Manolis, Antonis/F-5003-2014 FU NLM NIH HHS [LM 7044, LM 4493] NR 45 TC 93 Z9 93 U1 1 U2 2 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAY PY 1992 VL 19 IS 6 BP 1323 EP 1334 PG 12 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HR084 UT WOS:A1992HR08400029 PM 1564234 ER PT J AU HUTTER, AM AF HUTTER, AM TI THE ACC AND HEALTH-CARE POLICY - A TIME FOR UNITY AND ACTION SO JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY LA English DT Editorial Material RP HUTTER, AM (reprint author), MASSACHUSETTS GEN HOSP,ACC BLDG,SUITE 467,15 PARKMAN ST,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0735-1097 J9 J AM COLL CARDIOL JI J. Am. Coll. Cardiol. PD MAY PY 1992 VL 19 IS 6 BP 1364 EP 1364 PG 1 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA HR084 UT WOS:A1992HR08400035 PM 1564239 ER PT J AU ALBERT, M COHEN, C AF ALBERT, M COHEN, C TI THE TEST FOR SEVERE IMPAIRMENT - AN INSTRUMENT FOR THE ASSESSMENT OF PATIENTS WITH SEVERE COGNITIVE DYSFUNCTION SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ALZHEIMERS-DISEASE AB Objective: To develop a reliable and valid test of cognitive function suitable for patients with severe cognitive impairment. Design: Administration of a test; test-retest reliability; comparison to traditional test. Setting: Chronic long-term-care facility. Patients or Other Participants: The participants were 40 elderly residents with severe cognitive impairment. Main Outcome Measures: Results of the Test for Severe Impairment (TSI) and its subsections (language, memory, executive function, and motor performance); correlation of test and retest scores; correlation of TSI with Mini-Mental State Exam. Results: The TSI was significantly correlated with the Mini-Mental State Exam (r = 0.83, P less-than-or-equal-to 0.0001). Test-retest reliability was high (r = 0.96, P < 0.0001). The internal reliability of the test was also good (alpha = 0.90). Preliminary result of a factor analysis suggests that factor scores may be derived that relate to memory, language production, and knowledge of body parts. Conclusions: The TSI is a valid and reliable test of cognitive function in patients with severe cognitive impairment. It is appropriate to use it as a unified scale. C1 HEBREW REHABIL CTR AGED,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA 02115. RP ALBERT, M (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CNY-9,BOSTON,MA 02114, USA. FU NIA NIH HHS [P01-AG04390] NR 7 TC 165 Z9 167 U1 0 U2 1 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 MAY PY 1992 VL 40 IS 5 BP 449 EP 453 PG 5 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HT856 UT WOS:A1992HT85600003 PM 1634695 ER PT J AU HAGENCOENEN, J DRINKA, PJ SIEWERT, M AF HAGENCOENEN, J DRINKA, PJ SIEWERT, M TI TETANUS-DIPHTHERIA VACCINATIONS IN A VETERANS NURSING-HOME SO JOURNAL OF THE AMERICAN GERIATRICS SOCIETY LA English DT Article ID ADULTS; IMMUNITY; IMMUNIZATION C1 WISCONSIN VET HOME,KING,WI 54946. UNIV WISCONSIN,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. NR 20 TC 2 Z9 2 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 MAY PY 1992 VL 40 IS 5 BP 513 EP 514 PG 2 WC Geriatrics & Gerontology; Gerontology SC Geriatrics & Gerontology GA HT856 UT WOS:A1992HT85600016 PM 1634708 ER PT J AU REGAS, FC EHRLICH, HP AF REGAS, FC EHRLICH, HP TI ELUCIDATING THE VASCULAR-RESPONSE TO BURNS WITH A NEW RAT MODEL SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article ID IBUPROFEN; INJURY AB Burn injury causes acute thrombosis and occlusion of vessels in the dermis directly killed by thermal energy. A vascular response also occurs in the uninjured dermis bordering the site of injury. Diminished blood flow leads to progressive ischemia and necrosis in the dermis beneath and surrounding the burn. If blood flow is maintained or restored in this area, the tissue survives. A noninvasive technique for studying dynamic changes in blood flow in this transitional dermis in rats is presented. A rectangular brass bar 19 mm wide with 5-mm transverse notches was heated in boiling water and applied to the skin surface for 20 seconds, making a "comb" burn composed of a row of four rectangular 10 x 19-mm full-thickness burns. Between the burns were 5 x 19-mm bands of uninjured skin, called "interspaces." After burning, blood flow near the surface of both the burn sites and the interspaces was monitored with a laser Doppler perfusion monitor for 24 hours. The vascular patency of blood vessels was directly visualized by latex vascular casts made 24 hours after burn. The possible prevention of progressive ischemia by injecting systemic ibuprofen was examined in this new model. Normal skin has a surface blood flow reading of 80 +/- 16 mV, burn sites have a reading of 11 +/- 4 mV, and interspaces have a reading of 21 +/- 4 mV at 24 hours postburn in untreated rats. Systemic ibuprofen given IM immediately postburn at 12.5 mg/kg increased blood flow to 80 +/- 28 mV within the interspaces, to 17 +/- 12 mV in the burn site, and to 80 +/- 9 mV in normal skin. The vascular casts showed an absence of patent vessels within both the burn sites and interspaces in untreated rats. The four individual burn sites had generated into a larger single full-thickness injury. In treated rats patent vessels were present in the interspaces but not in the burn sites. Four individual wounds were evident at 24 hours. Histologic preparations of vascular casts showed the absence of latex-filled vessels and thrombus-filled vessels in the burn sites and the interspaces of untreated rats. With ibuprofen therapy, latex-filled vessels were evident within the interspaces and dermis as were thrombus-filled vessels within the burn sites. C1 SHRINERS BURN INST,WOUND HEALING LAB,51 BLOSSOM ST,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. NR 16 TC 64 Z9 64 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1079-6061 J9 J TRAUMA JI J. Trauma-Injury Infect. Crit. Care PD MAY PY 1992 VL 32 IS 5 BP 557 EP 563 DI 10.1097/00005373-199205000-00004 PG 7 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA HW811 UT WOS:A1992HW81100004 PM 1588642 ER PT J AU MCDOUGAL, WS AF MCDOUGAL, WS TI METABOLIC COMPLICATIONS OF URINARY INTESTINAL DIVERSION SO JOURNAL OF UROLOGY LA English DT Editorial Material DE URINARY DIVERSION; METABOLISM ID ILEAL CONDUIT; HYPERAMMONEMIC ENCEPHALOPATHY; PATHO-PHYSIOLOGY; ACID-SECRETION; RENAL-FUNCTION; URETEROSIGMOIDOSTOMY; SEGMENTS; BLADDER; CARCINOMA; COLON C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP MCDOUGAL, WS (reprint author), MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114, USA. NR 87 TC 300 Z9 307 U1 0 U2 4 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAY PY 1992 VL 147 IS 5 BP 1199 EP 1208 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA HR463 UT WOS:A1992HR46300001 PM 1569649 ER PT J AU KOCH, MO MCDOUGAL, WS HALL, MC HILL, DE BRAREN, HV DONOFRIO, MN AF KOCH, MO MCDOUGAL, WS HALL, MC HILL, DE BRAREN, HV DONOFRIO, MN TI LONG-TERM METABOLIC EFFECTS OF URINARY-DIVERSION - A COMPARISON OF MYELOMENINGOCELE PATIENTS MANAGED BY CLEAN INTERMITTENT CATHETERIZATION AND URINARY-DIVERSION SO JOURNAL OF UROLOGY LA English DT Article DE URINARY DIVERSION; CATHETERIZATION; BONE DENSITY; MINERAL ID INTESTINAL SEGMENTS; FOLLOW-UP; ACIDOSIS; ILEAL; CHILDREN; BONE; CALCIUM; COMPLICATIONS; REPLACEMENT; BLADDER AB We previously reported that chronic urinary diversion through intestinal segments may have adverse effects on bone and mineral metabolism. This study examined the long-term health of patients managed by urinary diversion (94% by ileal conduit) for neuropathic bladders secondary to myelomeningocele defects and compared them to a control population of myelomeningocele patients managed by intermittent catheterization. Of the patients 93 were studied by personal interview, chart review, morphometric analysis, serum studies and dual-photon bone density determination. Average followup was 23 +/- 6 years in the urinary diversion group and 17 +/- 5 years in the intermittent catheterization group. Fractures occurred in 40% of the patients in both groups. Patients with a urinary diversion had an increased need for surgery to correct spinal curvature (57% versus 40%) and a significantly increased incidence of complications resulting from orthopedic procedures (17% versus 3%, p less-than-or-equal-to 0.05). There was also an adverse effect on renal function. The urinary diversion group had an increased incidence of radiographic renal deterioration (57% versus 8%, p < 0.001), nephrolithiasis (43% versus 2%, p < 0.001), pyelonephritis (60% versus 21%, p < 0.001) and intermittent metabolic acidosis (20% versus 5%, p = 0.05). Surgery was required in 37% for stomal complications and in 17% for ureterointestinal stricture. Linear growth was adversely affected by urinary diversion. Patients with urinary diversion had decreased lengths for all morphometric parameters and a greater percentage of them were at or below the 10th percentile standards. Serum electrolytes, liver function studies, vitamin D3 and parahormone showed no differences in the 2 groups. No patient had a significant metabolic acidosis at the time of study. Bone densities were significantly diminished in both groups and not significantly different. This study strongly suggests that urinary diversion through intestinal segments is associated with adverse effects on bone health. C1 VANDERBILT UNIV,MED CTR,DEPT UROL,NASHVILLE,TN 37240. MASSACHUSETTS GEN HOSP,DEPT UROL,BOSTON,MA 02114. NR 32 TC 65 Z9 65 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAY PY 1992 VL 147 IS 5 BP 1343 EP 1347 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA HR463 UT WOS:A1992HR46300051 PM 1569680 ER PT J AU BACHOR, R FLOTTE, TJ SCHOLZ, M DRETLER, S HASAN, T AF BACHOR, R FLOTTE, TJ SCHOLZ, M DRETLER, S HASAN, T TI COMPARISON OF INTRAVENOUS AND INTRAVESICAL ADMINISTRATION OF CHLOROALUMINUM SULFONATED PHTHALOCYANINE FOR PHOTODYNAMIC TREATMENT IN A RAT BLADDER-CANCER MODEL SO JOURNAL OF UROLOGY LA English DT Article DE BLADDER NEOPLASMS; PHOTOTHERAPY ID INTRATUMOR INJECTION; THERAPY; CARCINOMA; TUMORS; PHOTOSENSITIZERS AB Photodynamic therapy is an experimental treatment of superficial bladder tumors. Photofrin, a mixture of porphyrins, is the only photosensitizer in clinical use in the U.S.A. and its major side effect is prolonged cutaneous phototoxicity. In order to circumvent this problem of phototoxicity, new photosensitizers are being examined. Cutaneous phototoxicity may also be minimized by local administration of photosensitizer. Therefore, in this study, we investigated the photosensitizer chloro-aluminum sulfonated phthalocyanine (CASPc) in vivo in a rat bladder carcinoma model, and compared two different routes of CASPc administration. AY-27 rat bladder carcinoma cells were transplanted into rat bladders. Eight days after tumor transplantation the biodistribution of CASPc in bladder, skin, muscle and bladder tumor was determined by fluorescence measurements after dye extraction. Photosensitizer administered by intravenous injection and intravesical instillation, were compared. The concentration of CASPc in bladder and bladder tumor after intravenous injection and intravesical instillation was similar. The ratio of dye uptake between tumor and normal bladder after either administration was approximately two. Although no systemic absorption of the photosensitizer was observed after intravesical instillation, there was no reduction in tumor uptake or in the ratio between tumor to normal surrounding tissue. Therefore, no systemic side effects or skin phototoxicity are expected upon intravesical instillation. The microscopic biodistribution of CASPc after intravenous injection and intravesical instillation was also compared. After intravenous injection, the photosensitizer was distributed within the whole tumor with increased fluorescence around the microvasculature. In the normal bladder wall, weak fluorescence was seen in the area of the vasculature in the submucosa and the muscularis. After intravesical instillation, strong fluorescence was detected only at the tumor surface and in normal urothelium; no fluorescence was found in other areas of the tumor or in submucosa or muscularis. A comparison of the photodynamic treatment of model bladder tumors showed that tumor destruction after either method was similar but that there were less side effects to normal bladder wall after intravesical instillation of the CASPc. Intravesical administration of photosensitizers may, therefore, be a viable alternative to intravenous injection with potential for reduced systemic and normal tissue toxicity. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,DEPT UROL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. FU NIAMS NIH HHS [GMA-1,2 R01-AR 23595] NR 19 TC 20 Z9 23 U1 1 U2 3 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-5347 J9 J UROLOGY JI J. Urol. PD MAY PY 1992 VL 147 IS 5 BP 1404 EP 1410 PG 7 WC Urology & Nephrology SC Urology & Nephrology GA HR463 UT WOS:A1992HR46300074 PM 1569696 ER PT J AU JIN, XW SPECK, SH AF JIN, XW SPECK, SH TI IDENTIFICATION OF CRITICAL CIS ELEMENTS INVOLVED IN MEDIATING EPSTEIN-BARR-VIRUS NUCLEAR ANTIGEN 2-DEPENDENT ACTIVITY OF AN ENHANCER LOCATED UPSTREAM OF THE VIRAL BAMHI C-PROMOTER SO JOURNAL OF VIROLOGY LA English DT Article ID LATENT MEMBRANE-PROTEIN; LYMPHOCYTES-B; RNA; TRANSACTIVATION; EXPRESSION; TRANSCRIPT AB The six genes encoding the Epstein-Barr virus nuclear antigens (EBNAs) are transcribed from one of two promoters, BamHI C promoter (Cp) or BamHI W promoter (Wp), located near the left end of the viral genome. During the establishment of viral latency in B lymphocytes, Wp is used exclusively before a switch to Cp usage. We and others have previously identified an enhancer in the region upstream of Cp which requires EBNA 2 for activity (M. Woisetschlaeger, X. W. Jin, C. N. Yandava, L. A. Furmanski, J. L. Strominger, and S. H. Speck, Proc. Natl. Acad. Sci. USA 88:3942-3946, 1991; N. S. Sung, S. Kenney, D. Gutsch, and J. S. Pagano, J. Virol. 65:2164-2169, 1991). Infection of B lymphocytes with a mutant virus lacking the EBNA 2 gene results in prolonged usage of Wp and failure to switch to Cp usage, indicating that EBNA 2 transactivation of the enhancer upstream of Cp may be critical for promoter switching. In this study, we have defined the minimal EBNA 2-dependent enhancer by using a series of deletion mutants. The results of site-directed mutagenesis revealed that there are three regions of the enhancer that are important for activity, two of which appear to bind B-lymphocyte-specific factors. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA43143] NR 37 TC 82 Z9 82 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAY PY 1992 VL 66 IS 5 BP 2846 EP 2852 PG 7 WC Virology SC Virology GA HP817 UT WOS:A1992HP81700031 PM 1313905 ER PT J AU CAI, WZ SCHAFFER, PA AF CAI, WZ SCHAFFER, PA TI HERPES-SIMPLEX VIRUS TYPE-1 ICP0 REGULATES EXPRESSION OF IMMEDIATE-EARLY, EARLY, AND LATE GENES IN PRODUCTIVELY INFECTED-CELLS SO JOURNAL OF VIROLOGY LA English DT Article ID TEMPERATURE-SENSITIVE MUTANTS; HUMAN IMMUNODEFICIENCY VIRUS; COMPLETE DNA-SEQUENCE; LONG UNIQUE REGION; MACROMOLECULAR-SYNTHESIS; DELETION MUTANTS; MONOCLONAL-ANTIBODIES; BINDING PROTEIN; VIRAL-PROTEINS; MESSENGER-RNA AB The herpes simplex virus type 1 protein, ICP0, can activate expression of all kinetic classes of viral promoters in transient expression assays. To examine the role of ICP0 in the regulation of viral gene expression during productive infection, we characterized the wild-type virus, an ICP0 null mutant (7134), and several ICP0 nonsense mutant viruses with regard to virus replication and protein synthesis in Vero cells. Relative to wild-type virus, 7134 was severely deficient in viral growth and protein synthesis at low multiplicities of infection but exhibited a nearly wild-type phenotype at high multiplicities. The phenotypes of the ICP0 nonsense mutants were intermediate between those of the wild-type virus and 7134 in that the more ICP0-coding sequence expressed by a given nonsense mutant, the more wild type-like was its phenotype. The location of the ICP0 domain responsible for transactivation during productive infection was confirmed to be within the N-terminal portion of the protein, as previously shown in transient expression assays. Immunoprecipitation and immunofluorescence tests were used to detect low-level expression of selected immediate-early (IE), early (E), and late (L) proteins by mutant and wild-type viruses following low-multiplicity infection. The 7134 deletion mutant and several nonsense mutants expressed markedly reduced levels of E and L proteins but wild-type levels of the IE protein, ICP4. Because the latency-associated transcripts (LATs) are specified by the strand opposite that which encodes ICP0, the ICP0 deletion and nonsense mutants are by definition ICP0-LAT double mutants. The ability of a LAT-ICP0+ mutant to replicate as efficiently as wild-type virus at low multiplicities and the ability of ICP0-expressing 0-28 cells to complement the defects of the mutants in E and L protein synthesis indicates that the phenotypes of the mutants are caused by mutations in ICP0 and not the LATs. Thus, we conclude that ICP0 up-regulates E and L but not necessarily IE gene expression during productive infection. The activation of IE gene expression by ICP0 during productive infection is likely overshadowed by the activity of the virion-associated protein, VP16. This hypothesis was tested by transfection of Vero cells with infectious mutant and wild-type viral DNAs. In such tests, no VP16 is present at early times posttransfection. Significantly fewer cells transfected with infectious 7134 DNA expressed ICP4 than cells transfected with KOS DNA. This reduction was fully reversed by cotransfection with an ICP0-expressing plasmid. Therefore, ICP0 up-regulates ICP4 expression in the absence of virion-associated proteins during productive infection following transfection of infectious viral DNA. Taken together, these findings demonstrate a role for ICP0 in the induction of E and L gene expression during productive infection and suggest a role for ICP0 in the induction of IE gene expression during the early stage of reactivation from latency which proceeds in the absence of virion-associated proteins. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,TUMOR VIRUS GENET LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MICROBIOL & MOLEC GENET,BOSTON,MA 02115. FU NCI NIH HHS [R37 CA20260]; NIAID NIH HHS [P01 AI24010] NR 74 TC 191 Z9 194 U1 1 U2 3 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD MAY PY 1992 VL 66 IS 5 BP 2904 EP 2915 PG 12 WC Virology SC Virology GA HP817 UT WOS:A1992HP81700038 PM 1313909 ER PT J AU PEI, Y HERCZ, G GREENWOOD, C SHERRARD, D SEGRE, G MANUEL, A SAIPHOO, C FENTON, S AF PEI, Y HERCZ, G GREENWOOD, C SHERRARD, D SEGRE, G MANUEL, A SAIPHOO, C FENTON, S TI NONINVASIVE PREDICTION OF ALUMINUM BONE-DISEASE IN HEMOTONEAL AND PERITONEAL-DIALYSIS PATIENTS SO KIDNEY INTERNATIONAL LA English DT Article ID DEFEROXAMINE; OSTEODYSTROPHY; ACCUMULATION AB Between October 1987 and October of 1989, we conducted a prospective study to evaluate non-invasive test strategies for predicting aluminum bone disease (ABD) in a group of largely unselected dialysis patients based on their deferoxamine (DFO) test alone, or the combined results of their DFO test and intact 1-84 parathyroid hormone (PTH) levels. These test parameters were evaluated against the pathological diagnosis of ABD based on bone biopsy ("gold standard"). A total of 445 patients in three dialysis centers in Toronto were serially followed for their clinical, laboratory and risk parameters for renal osteodystrophy during the study, and 259 (142 PD and 117 HD) patients underwent a series of investigations which included the DFO test, measurement of intact 1-84 PTH levels, and an iliac crest bone biopsy. Serum aluminum ([Al]) level greater-than-or-equal-to 3700 nM (or 100-mu-g/liter) had a positive predictive value (PPV) of 75% for ABD in our PD and 88% in our HD patients, but its sensitivity was low (10 and 37%). Delta [Al] (that is, incremental rise of serum [Al] from baseline post-DFO) was useful in predicting ABD in our PD but not HD patients. Test combination based on delta [Al] greater-than-or-equal-to 5550 nM (or 150-mu-g/liter) and PTH level < 20 pM (or 200 pg/ml) yielded the best PPV greater-than-or-equal-to 95% for ABD in both PD and HD patients. This test cut-off would remain highly predictive of ABD even if the prevalence of ABD decreases to as low as 5% for the PD patients and 10% for the HD patients. However, for patients who have discontinued their aluminum gels for greater-than-or-equal-to 6 months these test strategies would not be useful due to a very high frequency of false-negative cases (or low sensitivity). Thus, the main utility of these non-invasive strategies will be in those patients who continue to require treatment of aluminum gels for their phosphate control. C1 UNIV TORONTO,DEPT MED,TORONTO M5S 1A1,ONTARIO,CANADA. MT SINAI HOSP,SAMUEL LUNENFELD RES INST,CLIN EPIDEMIOL UNIT,TORONTO M5G 1X5,ONTARIO,CANADA. UNIV WASHINGTON,SEATTLE,WA 98195. VET ADM MED CTR,SEATTLE,WA. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 18 TC 80 Z9 82 U1 0 U2 0 PU BLACKWELL SCIENCE INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD MAY PY 1992 VL 41 IS 5 BP 1374 EP 1382 DI 10.1038/ki.1992.202 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA HQ647 UT WOS:A1992HQ64700031 PM 1614052 ER PT J AU ACKERMAN, JL RALEIGH, DP GLIMCHER, MJ AF ACKERMAN, JL RALEIGH, DP GLIMCHER, MJ TI P-31 MAGNETIC-RESONANCE-IMAGING OF HYDROXYAPATITE - A MODEL FOR BONE IMAGING SO MAGNETIC RESONANCE IN MEDICINE LA English DT Article ID SOLID-STATE; CHEMICAL-SHIFT; CALCIUM PHOSPHATES; CROSS-POLARIZATION; SELF-DIFFUSION; MAS-NMR; P-31; SPECTROSCOPY; RELAXATION; GRADIENTS C1 HARVARD UNIV,SCH MED,CTR NMR,BOSTON,MA 02129. MIT,DEPT CHEM,CAMBRIDGE,MA 02139. HARVARD UNIV,CHILDRENS HOSP,SCH MED,MED CTR,DEPT ORTHOPAED SURG,BOSTON,MA 02115. RP ACKERMAN, JL (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,149 13TH ST,BOSTON,MA 02129, USA. RI Ackerman, Jerome/E-2646-2015 OI Ackerman, Jerome/0000-0001-5176-7496 FU NCRR NIH HHS [RR00995]; NIAMS NIH HHS [AR34078]; NIGMS NIH HHS [GM23403] NR 51 TC 21 Z9 22 U1 0 U2 2 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0740-3194 J9 MAGNET RESON MED JI Magn.Reson.Med. PD MAY PY 1992 VL 25 IS 1 BP 1 EP 11 DI 10.1002/mrm.1910250102 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HT491 UT WOS:A1992HT49100001 PM 1317501 ER PT J AU BERGNER, M BARRY, MJ BOWMAN, MA DOYLE, MA GUESS, HA NUTTING, PA AF BERGNER, M BARRY, MJ BOWMAN, MA DOYLE, MA GUESS, HA NUTTING, PA TI WHERE DO WE GO FROM HERE - OPPORTUNITIES FOR APPLYING HEALTH-STATUS ASSESSMENT MEASURES IN CLINICAL SETTINGS SO MEDICAL CARE LA English DT Article; Proceedings Paper CT 3RD CONF ON ADVANCES IN HEALTH STATUS ASSESSMENT CY SEP 12-14, 1991 CL GEORGETOWN UNIV CONF CTR, WASHINGTON, DC SP NATL ACAD SCI, INST MED, AGCY HLTH CARE POLICY & RES, CTR DIS CONTROL, NIH, ELI LILLY, GLAXO, PFIZER HO GEORGETOWN UNIV CONF CTR C1 MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02114. PK NICOLLET MED FDN,MINNEAPOLIS,MN. MERCK SHARP & DOHME LTD,CHAPEL HILL,NC. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,DEPT FAMILY & COMMUNITY MED,WINSTON SALEM,NC 27103. UNIV N CAROLINA,CHAPEL HILL,NC 27514. US DEPT HHS,AGCY HLTH CARE POLICY & RES,CTR GEN HLTH SERV RES,ROCKVILLE,MD 20852. RP BERGNER, M (reprint author), JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DIV HLTH POLICY & MANAGEMENT,ROOM 606,HAMPTON HOUSE,BALTIMORE,MD 21205, USA. RI bowman, marjorie/F-7235-2013 OI bowman, marjorie/0000-0002-1945-9212 NR 6 TC 9 Z9 9 U1 0 U2 1 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD MAY PY 1992 VL 30 IS 5 SU S BP MS219 EP MS230 PG 12 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA HU834 UT WOS:A1992HU83400022 ER PT J AU LO, YC AF LO, YC TI ALBEDOS FOR 4-MV, 10-MV, AND 18-MV BREMSSTRAHLUNG X-RAY-BEAMS ON CONCRETE, IRON, AND LEAD NORMALLY INCIDENT SO MEDICAL PHYSICS LA English DT Article DE ACCELERATORS; BREMSSTRAHLUNG; MONTE-CARLO; SHIELDING ID DISTRIBUTIONS AB Backscattering of radiation incident on a solid medium has been treated with some success as a reflection phenomenon. The concept of albedo has been used in the literature to deal with this problem. A Monte Carlo program has been used in this study to simulate the generation of bremsstrahlung beams from medical linear accelerators. The accuracy of the calculated spectra have been checked indirectly by calculating TPRs and comparing them with measured values. The dose albedos for Co-60 and Cs-137 beams normally incident on concrete have been calculated and compared with experimentally determined values in the literature. The generated energy spectra are then used to calculate the albedo factors for 4-, 10-, and 18-MV bremsstrahlung x-ray beams normally incident on concrete, iron, and lead. The number albedo decreases with increase in the atomic number of the reflecting medium. However, for high-energy photons, the dose albedo increases with increase in the atomic number of the medium. This is an important factor that needs to be considered in the design of shielding. The calculated energy spectra can be used in other problems and the albedo factors can be applied in practical shielding design for medical linear accelerators. RP LO, YC (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. NR 23 TC 5 Z9 5 U1 0 U2 0 PU AMER INST PHYSICS PI WOODBURY PA CIRCULATION FULFILLMENT DIV, 500 SUNNYSIDE BLVD, WOODBURY, NY 11797-2999 SN 0094-2405 J9 MED PHYS JI Med. Phys. PD MAY-JUN PY 1992 VL 19 IS 3 BP 659 EP 666 DI 10.1118/1.596914 PG 8 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA HZ958 UT WOS:A1992HZ95800020 PM 1324391 ER PT J AU LOPESVIRELLA, MF VIRELLA, G AF LOPESVIRELLA, MF VIRELLA, G TI LIPOPROTEINS AND IMMUNE-RESPONSES IN THE VASCULAR WALL AND THEIR CONTRIBUTION TO ATHEROSCLEROSIS IN DIABETES SO METABOLISM-CLINICAL AND EXPERIMENTAL LA English DT Article; Proceedings Paper CT INTERNATIONAL SYMP ON DIABETES, VASCULAR RISKS, AND GLICLAZIDE ( DIAMICRON ) CY JUN 28, 1991 CL WASHINGTON, DC SP SERVIER INT RES INST ID LOW-DENSITY LIPOPROTEIN; MONOCYTE-DERIVED MACROPHAGES; SMOOTH-MUSCLE CELLS; CHOLESTERYL ESTER SYNTHESIS; HUMAN-ENDOTHELIAL CELLS; POLYMORPHONUCLEAR LEUKOCYTES; INTERLEUKIN-1; RELEASE; MECHANISM; COMPLEXES C1 MED UNIV S CAROLINA,DEPT MED,DIV ENDOCRINOL METAB NUTR,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MICROBIOL & IMMUNOL,CHARLESTON,SC 29425. RP LOPESVIRELLA, MF (reprint author), RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,109 BEE ST,CHARLESTON,SC 29403, USA. NR 41 TC 8 Z9 8 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0026-0495 J9 METABOLISM JI Metab.-Clin. Exp. PD MAY PY 1992 VL 41 IS 5 SU 1 BP 11 EP 15 DI 10.1016/0026-0495(92)90087-Q PG 5 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HU840 UT WOS:A1992HU84000004 PM 1574007 ER PT J AU RUBIN, DH WEINER, DB DWORKIN, C GREENE, MI MAUL, GG WILLIAMS, WV AF RUBIN, DH WEINER, DB DWORKIN, C GREENE, MI MAUL, GG WILLIAMS, WV TI RECEPTOR UTILIZATION BY REOVIRUS TYPE-3 - DISTINCT BINDING-SITES ON THYMOMA AND FIBROBLAST CELL-LINES RESULT IN DIFFERENTIAL COMPARTMENTALIZATION OF VIRIONS SO MICROBIAL PATHOGENESIS LA English DT Article DE REOVIRUS; HEMAGGLUTININ; ANTIIDIOTYPE; CELLULAR RECEPTORS; VIRUS ATTACHMENT POLYPEPTIDE ID MAMMALIAN REOVIRUS; ATTACHMENT PROTEIN; SURFACE RECEPTOR; MOLECULAR-BASIS; HEMAGGLUTININ; ANTIBODY; VIRULENCE; MEMBRANE; GLYCOPROTEINS; IDIOTYPE C1 NASHVILLE VET AFFAIRS MED CTR,DEPT MICROBIOL,NASHVILLE,TN 37212. WISTAR INST,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,RHEUMATOL SECT,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,DEPT RES MED,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PATHOL & LAB MED,IMMUNOBIOL SECT,PHILADELPHIA,PA 19104. RP RUBIN, DH (reprint author), NASHVILLE VET AFFAIRS MED CTR,DEPT MED,1310 24TH AVE S,NASHVILLE,TN 37212, USA. RI Weiner, David/H-8579-2014 NR 47 TC 33 Z9 34 U1 0 U2 1 PU ACADEMIC PRESS LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0882-4010 J9 MICROB PATHOGENESIS JI Microb. Pathog. PD MAY PY 1992 VL 12 IS 5 BP 351 EP 365 DI 10.1016/0882-4010(92)90098-9 PG 15 WC Immunology; Microbiology SC Immunology; Microbiology GA JD037 UT WOS:A1992JD03700004 PM 1501574 ER PT J AU FLOTTE, TJ LAMBERTI, L AF FLOTTE, TJ LAMBERTI, L TI ASYMMETRY IN MELANOCYTIC LESIONS - A MORPHOMETRIC ANALYSIS SO MODERN PATHOLOGY LA English DT Article DE MELANOMA; COMPUTER; ASYMMETRY; NEVUS; MORPHOMETRY ID CUTANEOUS MALIGNANT MELANOMAS; SPITZ EPITHELOID NAEVI; PROLIFERATIVE ACTIVITY; DNA-CYTOPHOTOMETRY; BENIGN COMPOUND; IMAGE-ANALYSIS; SKIN TUMORS; DIAGNOSIS; PROGNOSIS; NEVI AB The purpose of this study was to establish a morphometric technique that would approximate the subjective histological criteria of asymmetry in the diagnosis of malignant melanoma. The dermal and epidermal outlines of 52 consecutive malignant melanomas and 56 consecutive melanocytic nevi were digitized and analyzed for morphometric parameters of size, coordinates, and shape. The two parameters that showed the most significant discriminatory functions were the differences in the center of masses of the epidermal and dermal components in the horizontal dimension and the length of the longest segment in the lesion. C1 MASSACHUSETTS GEN HOSP,DEPT DERMATOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 31 TC 2 Z9 2 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0893-3952 J9 MODERN PATHOL JI Mod. Pathol. PD MAY PY 1992 VL 5 IS 3 BP 333 EP 336 PG 4 WC Pathology SC Pathology GA HV524 UT WOS:A1992HV52400022 PM 1495938 ER PT J AU ZINKEL, SS PAL, SK SZEBERENYI, J COOPER, GM AF ZINKEL, SS PAL, SK SZEBERENYI, J COOPER, GM TI IDENTIFICATION OF A NEGATIVE REGULATORY ELEMENT THAT INHIBITS C-MOS TRANSCRIPTION IN SOMATIC-CELLS SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID PROTO-ONCOGENE PRODUCT; MOUSE-TISSUES; EXPRESSION; GENE AB We have used transient expression assays to identify a cis-acting region in the 5' flanking sequence of murine c-mos which, when deleted, allows expression from the c-mos promoter in NIH 3T3 cells. This negative regulatory sequence, located 400 to 500 nucleotides upstream of the c-mos ATG, also inhibited expression from a heterologous promoter. In addition to NIH 3T3 cells, the c-mos negative regulatory sequence was active in BALB/3T3 cells, PC12 rat pheochromocytoma cells, and A549 human lung carcinoma cells. Site-specific mutagenesis identified three possibly interacting regions that were involved in negative regulatory activity, located around -460, -425, and -405 with respect to the ATG. RNase protection analysis indicated that once the negative regulatory sequences were deleted, transcription in NIH 3T3 cells initiated from the same transcription initiation sites normally utilized in spermatocytes, approximately 280 nucleotides upstream of the ATG. Deletions beyond the spermatocyte promoter, however, allowed transcription initiation from progressively downstream c-mos sequences. Deletion or mutation of sequences surrounding the oocyte promoter at - 53 also had little effect on expression of c-mos constructs in NIH 3T3 cells. Therefore, the major determinant of c-mos expression in NIH 3T3 cells was removal of the negative regulatory sequence rather than the utilization of a unique promoter. The c-mos negative regulatory sequences thus appear to play a significant role in tissue-specific c-mos expression by inhibiting transcription in somatic cells. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA08667]; NICHD NIH HHS [HD26594] NR 23 TC 17 Z9 18 U1 1 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1992 VL 12 IS 5 BP 2029 EP 2036 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HQ338 UT WOS:A1992HQ33800014 PM 1533271 ER PT J AU STRAUSS, EC ANDREWS, NC HIGGS, DR ORKIN, SH AF STRAUSS, EC ANDREWS, NC HIGGS, DR ORKIN, SH TI INVIVO FOOTPRINTING OF THE HUMAN ALPHA-GLOBIN LOCUS UPSTREAM REGULATORY ELEMENT BY GUANINE AND ADENINE LIGATION-MEDIATED POLYMERASE CHAIN-REACTION SO MOLECULAR AND CELLULAR BIOLOGY LA English DT Article ID DOMINANT CONTROL REGION; PORPHOBILINOGEN DEAMINASE GENE; TRANSGENIC MICE; ERYTHROID-CELLS; DNA-BINDING; EXPRESSION; ENHANCER; ACTIVATION; PROMOTER; PROTEIN AB A major regulatory element required for expression of the human alpha-globin genes is located 40 kb upstream of the embryonic zeta-globin gene. To understand how this and other locus control region (LCR) elements contribute to high-level expression in erythroid cells, we have performed high-resolution, in vivo dimethyl sulfate footprinting. In addition, we have modified the dimethyl sulfate-based ligation-mediated polymerase chain reaction in vivo footprinting procedure to permit the assessment of interactions at guanine and adenine residues, rather than guanines alone. In vivo footprinting of the human alpha-LCR element carried on chromosome 16 in a mouse erythroleukemia cell environment revealed protein occupancy at GATA-1, AP-1/NF-E2, and CACC/GGTGG motifs, specific differences compared with in vitro protein binding, and distinct changes in one region upon dimethyl sulfoxide-induced cellular maturation. No protein contacts were detected in nonexpressing hepatoma cells. In addition, we have demonstrated that two AP-1 motifs in the alpha-LCR element which are occupied in vivo bind purified mouse NF-E2 protein in vitro. Our data suggest that three proteins, GATA-1, NF-E2, and unknown CACC/GGTGG factors, are minimally required as DNA-binding proteins for the function of LCR-like elements. The juxtaposition and interaction of these factors with each other, and with accessory proteins not directly in contact with DNA, are likely to account for the relative position independence of the upstream globin regulatory elements. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,MIT,DIV HLTH SCI & TECHNOL,CAMBRIDGE,MA 02138. HOWARD HUGHES MED INST,BOSTON,MA 02115. JOHN RADCLIFFE HOSP,INST MOLEC MED,MRC,MOLEC HAEMATOL UNIT,OXFORD OX3 9DU,ENGLAND. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. OI Andrews, Nancy/0000-0003-0243-4462 NR 42 TC 90 Z9 91 U1 0 U2 0 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0270-7306 J9 MOL CELL BIOL JI Mol. Cell. Biol. PD MAY PY 1992 VL 12 IS 5 BP 2135 EP 2142 PG 8 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA HQ338 UT WOS:A1992HQ33800026 PM 1569944 ER PT J AU DATTA, S MAGGE, SN MADISON, LD JAMESON, JL AF DATTA, S MAGGE, SN MADISON, LD JAMESON, JL TI THYROID-HORMONE RECEPTOR MEDIATES TRANSCRIPTIONAL ACTIVATION AND REPRESSION OF DIFFERENT PROMOTERS INVITRO SO MOLECULAR ENDOCRINOLOGY LA English DT Article ID ALPHA-SUBUNIT GENE; RAT GROWTH-HORMONE; PROGESTERONE-RECEPTOR; RESPONSE ELEMENTS; GLUCOCORTICOID RECEPTOR; VITELLOGENIN PROMOTER; TATA BOX; BINDING; BETA; EXPRESSION AB The thyroid hormone receptor (TR) has the dual ability to activate or repress transcription of specific genes. A cell-free transcription system was used to study the effects of TR on transcription by positively (TREpMLP) and negatively (TSH-alpha) regulated promoters. Receptor-deficient HeLa cell extracts were complemented with baculovirus-produced TR. TR stimulated transcription from the TREpMLP promoter by 3-fold, and trans-activation did not require hormone. Transcriptional stimulation by TR required the presence of the TRE sequence and was diminished by the addition of competitor TRE binding sites. Baculovirus-produced TR repressed transcription in vitro from the TSH-alpha promoter by 30-50%, also in a hormone-independent manner. Transcription from a control adenovirus 2 major late promoter was unaffected by added TR. Receptor-specific antisera and competition with TRE binding sites impaired TR-mediated repression of the TSH-alpha promoter. Unlike transcriptional stimulation, which was optimal when TR and HeLa extracts were added concomitantly, transcriptional repression by the TR was most effective when the receptor was preincubated with the alpha-promoter, suggesting that receptor binding to the promoter may block access of other proteins to cause transcriptional repression. These results indicate that baculovirus-expressed TR mediates transcriptional activation and repression in a promoter-specific manner in vitro. This system provides a valuable model for examining transcriptional control by the TR. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,THYROID UNIT, JACKSON 1021, BOSTON, MA 02114 USA. OI Jameson, James/0000-0001-9538-4059 FU NICHD NIH HHS [HD-28138]; NIDDK NIH HHS [DK-42144] NR 48 TC 14 Z9 14 U1 0 U2 0 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 MAY PY 1992 VL 6 IS 5 BP 815 EP 825 DI 10.1210/me.6.5.815 PG 11 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA HV306 UT WOS:A1992HV30600015 PM 1603088 ER PT J AU CROS, D GOMINAK, S SHAHANI, B FANG, JJ DAY, B AF CROS, D GOMINAK, S SHAHANI, B FANG, JJ DAY, B TI COMPARISON OF ELECTRIC AND MAGNETIC COIL STIMULATION IN THE SUPRACLAVICULAR REGION SO MUSCLE & NERVE LA English DT Article DE SUPRACLAVICULAR STIMULATION; COMPOUND MOTOR ACTION POTENTIALS; MAGNETIC COIL STIMULATION ID PERSISTENT CONDUCTION BLOCK; DEMYELINATING NEUROPATHY AB We compared the compound motor action potentials (CMAPs) evoked in the biceps, triceps, and abductor digiti minimi (ADM) muscles by conventional electrical stimulation at Erb's point (EP), and by magnetic coil stimulation of the supraclavicular region in 11 normal subjects. We found that magnetic coil stimulation was less effective than conventional stimulation in activating motor fibers in the brachial plexus in 45% of the recordings analyzed. CMAP amplitudes greater than those obtained with EP electrical stimulation were seen in 16% of recordings with supraclavicular magnetic stimulation, and in 33% of recordings with cervical magnetic stimulation, indicating that EP electrical stimulation is submaximal in a large proportion of cases. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP CROS, D (reprint author), MASSACHUSETTS GEN HOSP,CLIN NEUROPHYSIOL LABS,BIGELOW 12,BOSTON,MA 02114, USA. NR 11 TC 9 Z9 9 U1 0 U2 0 PU JOHN WILEY & SONS INC PI NEW YORK PA 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0148-639X J9 MUSCLE NERVE JI Muscle Nerve PD MAY PY 1992 VL 15 IS 5 BP 587 EP 590 DI 10.1002/mus.880150509 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA HP589 UT WOS:A1992HP58900008 PM 1584250 ER PT J AU SIMON, MC PEVNY, L WILES, MV KELLER, G COSTANTINI, F ORKIN, SH AF SIMON, MC PEVNY, L WILES, MV KELLER, G COSTANTINI, F ORKIN, SH TI RESCUE OF ERYTHROID DEVELOPMENT IN GENE TARGETED GATA-1- MOUSE EMBRYONIC STEM-CELLS SO NATURE GENETICS LA English DT Article ID DOMINANT CONTROL REGION; DNA-BINDING FACTOR; BETA-GLOBIN GENE; TRANSCRIPTION FACTOR; HOMOLOGOUS RECOMBINATION; TRANSGENIC MICE; GAMMA-GLOBIN; FACTOR NF-E1; EXPRESSION; PROTEIN AB Development of definitive (fetal liver-derived) red cells is blocked by a targeted mutation in the gene encoding the transcription factor GATA-1. We used in vitro differentiation of GATA-1- mouse embryonic stem (ES) cells to reveal a requirement for GATA-1 during primitive (yolk sac-derived) erythropoiesis and to establish a rescue assay. We show that the block to development includes primitive, as well as definitive, erythroid cells and is complete at the level of globin RNA expression; that the introduction of a normal GATA-1 gene restores developmental potential both in vivo and in vitro; and that efficient rescue is dependent on a putative autoregulatory GATA-motif in the distal promoter. Use of in vitro differentiated ES cells bridges a gap between conventional approaches to gene function in cell lines and analysis of loss of function mutations in the whole animal. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. NATL JEWISH CTR IMMUNOL,DENVER,CO 80206. COLUMBIA UNIV COLL PHYS & SURG,DEPT GENET & DEV,NEW YORK,NY 10032. BASEL INST IMMUNOL,CH-4005 BASEL,SWITZERLAND. RI Brugnara, Carlo/A-8041-2010 OI Brugnara, Carlo/0000-0001-8192-8713 NR 46 TC 204 Z9 207 U1 0 U2 2 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 MAY PY 1992 VL 1 IS 2 BP 92 EP 98 DI 10.1038/ng0592-92 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA JC980 UT WOS:A1992JC98000006 PM 1302015 ER PT J AU MACDONALD, ME NOVELLETTO, A LIN, C TAGLE, D BARNES, G BATES, G TAYLOR, S ALLITTO, B ALTHERR, M MYERS, R LEHRACH, H COLLINS, FS WASMUTH, JJ FRONTALI, M GUSELLA, JF AF MACDONALD, ME NOVELLETTO, A LIN, C TAGLE, D BARNES, G BATES, G TAYLOR, S ALLITTO, B ALTHERR, M MYERS, R LEHRACH, H COLLINS, FS WASMUTH, JJ FRONTALI, M GUSELLA, JF TI THE HUNTINGTONS-DISEASE CANDIDATE REGION EXHIBITS MANY DIFFERENT HAPLOTYPES SO NATURE GENETICS LA English DT Article ID GENE; LOCALIZATION AB Analysis of 78 Huntington's disease (HD) chromosomes with multi-allele markers revealed 26 different haplotypes, suggesting a variety of independent HD mutations. The most frequent haplotype, accounting for about one third of disease chromosomes, suggests that the disease gene is between D4S182 and D4S180. However, the paucity of an expected class of chromosomes that can be related to this major haplotype by assuming single crossovers may reflect the operation of other mechanisms in creating haplotype diverstiy. Some of these mechanisms sustain alternative scenarios that do not require a multiple mutational origin for HD and/or its positioning between D4S182 and DAS180. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV MICHIGAN,HOWARD HUGHES MED INST,ANN ARBOR,MI 48109. UNIV MICHIGAN,DEPT INTERNAL MED & HUMAN GENET,DEARBORN,MI 48128. UNIV TOR VERGATA ROMA,DIPARTIMENTO BIOL,ROME,ITALY. CNR,IST MED SPERIMENTALE,ROME,ITALY. BOSTON UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02118. IMPERIAL CANC RES FUND,LONDON WC2A 3PX,ENGLAND. UNIV CALIF IRVINE,DEPT BIOL CHEM,IRVINE,CA 92717. RP MACDONALD, ME (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROGENET LAB,BOSTON,MA 02114, USA. RI Bates, Gillian/E-1146-2012; OI Bates, Gillian/0000-0002-4041-6305; Novelletto, Andrea/0000-0002-1146-7680 NR 22 TC 120 Z9 121 U1 0 U2 4 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 MAY PY 1992 VL 1 IS 2 BP 99 EP 103 DI 10.1038/ng0592-99 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA JC980 UT WOS:A1992JC98000007 PM 1302016 ER PT J AU HARDIMAN, O BROWN, RH BEGGS, AH SPECHT, L SKLAR, RM AF HARDIMAN, O BROWN, RH BEGGS, AH SPECHT, L SKLAR, RM TI DIFFERENTIAL GLUCOCORTICOID EFFECTS ON THE FUSION OF DUCHENNE BECKER AND CONTROL MUSCLE CULTURES - PHARMACOLOGICAL DETECTION OF ACCELERATED AGING IN DYSTROPHIC MUSCLE SO NEUROLOGY LA English DT Article ID SERUM-FREE MEDIUM; SKELETAL-MUSCLE; MUSCULAR-DYSTROPHY; SATELLITE CELLS; GROWTH; MYOBLASTS; INSULIN AB We report that the glucocorticoid methylprednisolone (Mepd) enhanced myogenesis in normal primary human muscle cultures, but inhibited myogenesis of most Duchenne/Becker muscle cultures. A decline in the magnitude of myogenic stimulation by Mepd correlated with age in a random group of control patients, including some with neurologic diseases other than Duchenne/Becker dystrophy. A case of Duchenne muscular dystrophy from an exceptionally young patient yielded a muscle culture that was myogenically stimulated by Mepd. These results suggest that continuous cycles of degeneration and regeneration of dystrophic muscle in vivo may result in a change of the glucocorticoid response of the muscle progenitor cells. The glucocorticoid effects suggest caution in the long-term clinical use of these agents for muscle disease such as Duchenne muscular dystrophy. C1 MASSACHUSETTS GEN HOSP,CECIL B DAY NEUROMUSCULAR RES LABS,149 13TH ST,NAVY YARD,BOSTON,MA 02129. CHILDRENS HOSP MED CTR,DEPT GENET,BOSTON,MA 02115. CHILDRENS HOSP MED CTR,DEPT NEUROL,BOSTON,MA 02115. FU NINDS NIH HHS [R01 NS 00787-05] NR 27 TC 14 Z9 14 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 MAY PY 1992 VL 42 IS 5 BP 1085 EP 1091 PG 7 WC Clinical Neurology SC Neurosciences & Neurology GA HT665 UT WOS:A1992HT66500029 PM 1579232 ER PT J AU DIMITRIADOU, V BUZZI, MG THEOHARIDES, TC MOSKOWITZ, MA AF DIMITRIADOU, V BUZZI, MG THEOHARIDES, TC MOSKOWITZ, MA TI ULTRASTRUCTURAL EVIDENCE FOR NEUROGENICALLY MEDIATED CHANGES IN BLOOD-VESSELS OF THE RAT DURA-MATER AND TONGUE FOLLOWING ANTIDROMIC TRIGEMINAL STIMULATION SO NEUROSCIENCE LA English DT Article ID PLATELET-ACTIVATING FACTOR; GENE-RELATED PEPTIDE; SUBSTANCE-P; MAST-CELLS; ENDOTHELIAL-CELLS; VASCULAR-PERMEABILITY; PLASMA EXTRAVASATION; NERVE-FIBERS; GUINEA-PIG; 5-HYDROXYTRYPTAMINE RELEASE AB We investigated the effects of unilateral electrical trigeminal ganglion stimulation (0.1 or 1.0 mA, 5 Hz, 5 ms, 5 min) on the morphology of blood vessels within the rat dura mater and tongue using light and transmission electron microscopy. Stimulation at both intensities caused changes which were confined to the ipsilateral post-capillary venules except in the tongue where arterioles were affected as well. Changes were more marked after 1.0 mA. Dramatic increases in the numbers of endothelial pinocytotic vesicles were found along the luminal and abluminal surfaces ipsilateral to the stimulation. Tight junctions remained largely intact, except that injected ferritin particles were occasionally trapped inside these junctions. Cytoplasmic microvilli and endothelial blebs were sometimes present as well. Approximately 80% of the examined dural post-capillary venules showed one or more of these endothelial changes. Horseradish peroxidase injected intravenously 5 min prior to stimulation was detected in the extracellular space surrounding dural blood vessels and within pinocytotic vesicles. Ferritin injected similarly, was also localized in post-capillary venule walls, interstitial spaces, intraendothelial vesicles and in vacuoles. Platelet accumulation and aggregation were present in approximately 10% of post-capillary venules in dura and tongue. These changes were associated with mast cell secretion, but neither vascular nor mast cell activation was observed in adult rats in whom C-fibers were destroyed during the neonatal period with capsaicin. The present observations provide morphological evidence which supports findings from previously reported albumin tracer studies suggesting enhanced transport and endothelial activation following electrical stimulation of small caliber afferent fibers. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,STROKE RES LAB,32 FRUIT ST,BOSTON,MA 02114. TUFTS UNIV,SCH MED,DEPT PHARMACOL & EXPTL THERAPEUT,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Theoharides, Theoharis/E-5596-2010 FU NINDS NIH HHS [NS21558] NR 98 TC 115 Z9 117 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0306-4522 J9 NEUROSCIENCE JI Neuroscience PD MAY PY 1992 VL 48 IS 1 BP 187 EP 203 DI 10.1016/0306-4522(92)90348-6 PG 17 WC Neurosciences SC Neurosciences & Neurology GA HN141 UT WOS:A1992HN14100015 PM 1374861 ER PT J AU HENDRICKS, KM BADRUDDIN, SH AF HENDRICKS, KM BADRUDDIN, SH TI WEANING RECOMMENDATIONS - THE SCIENTIFIC BASIS SO NUTRITION REVIEWS LA English DT Review ID BREAST-FED INFANTS; GASTROINTESTINAL-TRACT; HOT CLIMATE; COWS MILK; CHILDREN; MALNUTRITION; REQUIREMENTS; PROTECTION; COUNTRIES; DIGESTION AB Current weaning recommendations are based on nutritional need, physiologic maturation, and the behavioral and developmental aspects of infant feeding. Inadequate energy and protein intake and deficiencies of iron, zinc, vitamin A, and vitamin D are the most commonly observed nutrient deficiencies during infancy and weaning recommendations have focused on their prevention. This article reviews the data and summarizes implications for infant weaning in both developed and developing countries. Current published recommendations for infant feeding are outlined and major concerns are highlighted. C1 AGA KHAN UNIV,DEPT MEDI,KARACHI,PAKISTAN. AGA KHAN UNIV,DEPT COMMUNITY HLTH SCI,KARACHI,PAKISTAN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,COMBINED PROGRAM PEDIAT & NUTR,BOSTON,MA 02114. RP HENDRICKS, KM (reprint author), BOSTON UNIV,SARGENT COLL ALLIED HLTH PROFESS,DEPT HLTH SCI,BOSTON,MA 02215, USA. NR 77 TC 35 Z9 40 U1 0 U2 2 PU INT LIFE SCIENCES INST PI LAWRENCE PA 810 EAST 10TH ST SUBSCRIPTION OFFICE, LAWRENCE, KS 66044 SN 0029-6643 J9 NUTR REV JI Nutr. Rev. PD MAY PY 1992 VL 50 IS 5 BP 125 EP 133 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA HY998 UT WOS:A1992HY99800001 PM 1630717 ER PT J AU MUNTZ, HG GOFF, BA THOR, AD TARRAZA, HM AF MUNTZ, HG GOFF, BA THOR, AD TARRAZA, HM TI POST-HYSTERECTOMY CARCINOMA OF THE FALLOPIAN-TUBE MIMICKING A VESICOVAGINAL FISTULA SO OBSTETRICS AND GYNECOLOGY LA English DT Article ID ADENOCARCINOMA AB A 49-year-old woman presented with a profuse watery vaginal discharge 16 years after a vaginal hysterectomy. Pelvic examination revealed clear fluid leaking from the vaginal apex. Cytologic evaluation of the draining fluid was normal, as was a biopsy of the vaginal apex. A vesicovaginal fistula was suspected. Intravenous pyelogram and cystogram did not reveal communication of the urinary tract with the fistula. Injection of radiopaque dye through the fistula tract demonstrated a 5-7-cm enclosed cystic space with a 4-cm pedunculated mass within the cyst lumen. Exploratory surgery revealed fallopian tube carcinoma involving the right tube. The tumor mass was completely excised, and there was no evidence of spread beyond the encapsulated cystic fallopian tube. The woman was treated with six cycles of cisplatin combination chemotherapy, and after 5 years remains free of disease. C1 MASSACHUSETTS GEN HOSP,VINCENT MEM GYNECOL SERV,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. NR 16 TC 12 Z9 12 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 MAY PY 1992 VL 79 IS 5 BP 853 EP 856 PN 2 PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA HQ292 UT WOS:A1992HQ29200023 PM 1565386 ER PT J AU PORIES, S JAROS, K STEELE, G PAULEY, A SUMMERHAYES, IC AF PORIES, S JAROS, K STEELE, G PAULEY, A SUMMERHAYES, IC TI ONCOGENE-MEDIATED TRANSFORMATION OF FETAL-RAT COLON INVITRO SO ONCOGENE LA English DT Article ID PP60C-SRC PROTEIN-KINASE; INTESTINAL EPITHELIAL-CELLS; C-MYC ONCOGENES; SUCRASE-ISOMALTASE; COLORECTAL CANCERS; MONOLAYER-CULTURE; GENE-MUTATIONS; HA-RAS; V-MYC; LINES AB Short-term maintenance of fetal rat colonic tissue in vitro has been demonstrated using a collagen matrix organ culture system. The introduction of single (v-myc, v-ras(H), v-src) oncogenes or combinations of oncogenes (v-myc/ras(H), v-myc/src) into normal colon mucosal elements was established using retroviral vectors, resulting in enhanced proliferation and migration of epithelial cells from the lumen of tissue implants. Expression of a single oncogene in normal colon epithelium did not result in the establishment of cell lines. In contrast, expression of cooperating oncogenic elements resulted in cell lines in > 80% of experiments, revealing different morphological characteristics dependent upon the oncogene combination used. Confirmation of the expression of viral transcripts was determined using Northern blot analysis and viral oncoprotein expression using Western blot analysis (p21) and an immunoprecipitation kinase assay (src). Expression of keratin filaments was lost following passaging of cell lines but could be induced by the myc/ras transformants by growth on Rat-1 feeder layers. This induction phenomenon was not observed with myc/src lines, and although these expressed high levels of surcase isomaltase the epithelial origin of these cells is unclear. Karyotypic analysis performed on three myc/ras-transformed cell lines revealed a normal chromosome complement associated with transformation. In this report we describe a novel in vitro transformation system for normal rat colonic epithelium mediated by the introduction of oncogene elements using different retroviral vector constructs. The potential to generate cell lines representing different stages of neoplastic progression using relevant genetic components presents significant advantages for the study of cellular and molecular interactions underlying colon neoplastic progression. C1 HARVARD UNIV,NEW ENGLAND DEACONESS HOSP,SCH MED,CANC BIOL LAB,50 BINNEY ST,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CYTOGENET LAB,BOSTON,MA 02115. FU NCI NIH HHS [CA44704, CA42944] NR 53 TC 8 Z9 9 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1992 VL 7 IS 5 BP 885 EP 893 PG 9 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HP642 UT WOS:A1992HP64200007 PM 1373876 ER PT J AU LIU, E THOR, A HE, M BARCOS, M LJUNG, BM BENZ, C AF LIU, E THOR, A HE, M BARCOS, M LJUNG, BM BENZ, C TI THE HER2 (C-ERBB-2) ONCOGENE IS FREQUENTLY AMPLIFIED IN INSITU CARCINOMAS OF THE BREAST SO ONCOGENE LA English DT Note ID SURGICAL ADJUVANT BREAST; PROTEIN OVEREXPRESSION; CANCER; AMPLIFICATION; EXPRESSION; SURVIVAL; PROJECT; GENE AB Amplification and overexpression of the HER2 (c-erbB-2) oncogene was assessed in paraffin-embedded specimens from 27 in situ carcinomas of the breast and from 122 stage II breast cancers. Gene amplification detected in these archival tissues by differential polymerase chain reaction (PCR) was found in 48% of in situ carcinomas and in 21% of stage II lesions (chi(2) = 7.62, p less-than-or-equal-to 0.01). In addition, the level of gene amplification correlated with the level of HER2 oncoprotein expression as measured by immunohistochemistry for both in situ cancers (p less-than-or-equal-to 0.025) and stage II cancers (p less-than-or-equal-to 0.0005). This high incidence of HER2 gene amplification with accompanying overexpression in non-invasive breast tumors suggests that perturbations of the HER2 oncogene are among the earliest and most common genetic lesions in human breast cancer. C1 UNIV CALIF SAN FRANCISCO,CANC RES INST,M-1283,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PATHOL,SAN FRANCISCO,CA 94143. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV N CAROLINA,DEPT MED,CURRICULUM GENET,CHAPEL HILL,NC 27599. ROSWELL PK CANC INST,DEPT PATHOL,BUFFALO,NY. UNIV N CAROLINA,LINEBERGER CANC RES CTR,CHAPEL HILL,NC 27599. RI Liu, Edison/C-4141-2008 FU NCI NIH HHS [P01 CA 44768, 5U10-CA31946-08, 5U10-CA37055-08] NR 24 TC 188 Z9 193 U1 0 U2 3 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HAMPSHIRE, ENGLAND RG21 6XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD MAY PY 1992 VL 7 IS 5 BP 1027 EP 1032 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA HP642 UT WOS:A1992HP64200026 PM 1349163 ER PT J AU GRAGOUDAS, ES EGAN, KM SEDDON, JM WALSH, SM MUNZENRIDER, JE AF GRAGOUDAS, ES EGAN, KM SEDDON, JM WALSH, SM MUNZENRIDER, JE TI INTRAOCULAR RECURRENCE OF UVEAL MELANOMA AFTER PROTON-BEAM IRRADIATION SO OPHTHALMOLOGY LA English DT Article; Proceedings Paper CT 1991 ANNUAL MEETING OF THE AMERICAN ACADEMY OF OPHTHALMOLOGY CY OCT, 1991 CL ANAHEIM, CA SP AMER ACAD OPHTHALMOL ID CHOROIDAL MELANOMA; ENUCLEATION; SURVIVAL; THERAPY; METASTASIS; REGRESSION; RADIATION; PLAQUE AB The authors evaluated tumor recurrence as an end point in 1077 uveal melanoma patients treated by proton beam irradiation between 1975 and 1987, with a mean follow-up of 4.0 years. Twenty tumors (1.9%) exhibited definitive growth between 4 months and 66 months after irradiation (median, 19 months): 10 were marginal recurrences, 5 were ring melanomas, 3 were uncontrolled tumors, and 2 were extrascleral extensions. Ten of these eyes were enucleated without further intervention, 2 patients died of metastases soon after the growth was detected, and 8 patients had further conservative therapy. In 5 other patients, tumor growth was suspected but unconfirmed and the eye was enucleated elsewhere; the 5-year probability of local tumor control based on 25 recurrences was 97% +/- 1%. There was a nonsignificant increase in the rate of metastases among patients with documented tumor recurrence (adjusted relative risk, 1.5; 95% confidence interval, 0.66 to 3.4). Results suggest that recurrence of uveal melanomas treated by proton beam therapy is uncommon, but that treatment failure may increase risk of death from metastasis. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,EPIDEMIOL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT MED,BOSTON,MA 02114. RP GRAGOUDAS, ES (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,RETINA SERV,243 CHARLES ST,BOSTON,MA 02114, USA. NR 25 TC 76 Z9 76 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD MAY PY 1992 VL 99 IS 5 BP 760 EP 766 PG 7 WC Ophthalmology SC Ophthalmology GA HU975 UT WOS:A1992HU97500029 PM 1594223 ER PT J AU FERNANDEZDELCASTILLO, C SCHMIDT, J RATTNER, DW LEWANDROWSKI, K COMPTON, CC JEHANLI, A PATEL, G HERMONTAYLOR, J WARSHAW, AL AF FERNANDEZDELCASTILLO, C SCHMIDT, J RATTNER, DW LEWANDROWSKI, K COMPTON, CC JEHANLI, A PATEL, G HERMONTAYLOR, J WARSHAW, AL TI GENERATION AND POSSIBLE SIGNIFICANCE OF TRYPSINOGEN ACTIVATION PEPTIDES IN EXPERIMENTAL ACUTE-PANCREATITIS IN THE RAT SO PANCREAS LA English DT Article DE ACUTE PANCREATITIS; CERULEIN; EXPERIMENTAL PANCREATITIS; TAP; TRYPSIN; TRYPSINOGEN AB Trypsinogen activation peptides (TAP) were quantified by radioimmunoassay in blood, urine, and peritoneal exudate of rats with experimental pancreatitis. Forty-four animals were studied, comprising a control group and four different induction techniques (cerulein, cerulein plus either 2- or 10-min intraductal glycodeoxycholic acid [GDOC] infusion, and cerulein plus intraductal GDOC with enterokinase [EK]). Significantly higher TAP concentrations were found at 6 h (or at death) in plasma and ascites of all pancreatitis groups compared with controls. TAP quantitation in hourly urine samples demonstrated significantly higher concentrations from the third hour onward in the most severe groups and from the fourth hour onward in the cerulein-treated rats. All nonsurviving rats had a plasma TAP of > 2.5 nM/L, whereas only 1 of 34 surviving animals had such a concentration (p < 0.001). A significant stepwise increase in total TAP in ascites was found when comparing the cerulein group, the two GDOC groups, and the EK group (p < 0.001). Chromatography of samples with a high TAP content demonstrated comigration with synthetic TAP. We conclude that free TAP are present in blood, urine, and peritoneal exudate of rats with experimental pancreatitis of different pathogenesis and that the amount of TAP may be indicative of the severity of the disease process. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,ACC 336,15 PARKMAN ST,BOSTON,MA 02114. NR 0 TC 35 Z9 35 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0885-3177 J9 PANCREAS JI Pancreas PD MAY PY 1992 VL 7 IS 3 BP 263 EP 270 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA HN237 UT WOS:A1992HN23700001 PM 1375747 ER PT J AU MENY, R KELLY, DH AF MENY, R KELLY, DH TI ON SUDDEN SEVERE BRADYCARDIA IN INFANCY - REPLY SO PEDIATRIC PULMONOLOGY LA English DT Letter RP MENY, R (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 8755-6863 J9 PEDIATR PULM JI Pediatr. Pulmonol. PD MAY PY 1992 VL 13 IS 1 BP 63 EP 63 PG 1 WC Pediatrics; Respiratory System SC Pediatrics; Respiratory System GA HT897 UT WOS:A1992HT89700017 ER PT J AU JELLINEK, MS AF JELLINEK, MS TI FACING TRAGIC DECISIONS WITH PARENTS IN THE NICU - CLINICAL PERSPECTIVES - REPLY SO PEDIATRICS LA English DT Letter RP JELLINEK, MS (reprint author), MASSACHUSETTS GEN HOSP,CHILD PSYCHIAT SERV,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD, ELK GROVE VILLAGE, IL 60007-1098 SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD MAY PY 1992 VL 89 IS 5 BP 981 EP 981 PN 1 PG 1 WC Pediatrics SC Pediatrics GA HT168 UT WOS:A1992HT16800053 ER PT J AU JONES, MM SINGH, PK GALE, GR SMITH, AB ATKINS, LM AF JONES, MM SINGH, PK GALE, GR SMITH, AB ATKINS, LM TI CADMIUM MOBILIZATION INVIVO BY INTRAPERITONEAL OR ORAL-ADMINISTRATION OF MONOALKYL ESTERS OF MESO-2,3-DIMERCAPTOSUCCINIC ACID IN THE MOUSE SO PHARMACOLOGY & TOXICOLOGY LA English DT Article ID CHELATING-AGENTS; EXCRETION; DIMERCAPTOSUCCINATE; METALLOTHIONEIN; TOXICITY; DEPOSITS AB The relative activities of a series of nine monoalkyl esters of meso-2,3-dimercaptosuccinic acid have been examined as agents for the mobilization of cadmium from mice one week after intraperitoneal administration of cadmium chloride. Eight of these are newly synthetized; all are of the type ROOCCH(SH)CH(SH)COOH, were R=Me, MMDMS; R=C2H5, MEDMS; R=(CH2)2CH3, Mn-PDMS; R=CHMe2, Mi-PDMS; R=(CH2)3CH3, Mn-BDMS; R=CH2CHMe2, Mi-BDMS; R=(CH2)4CH3, Mn-ADMS; R=(CH2)2CHMe2, Mi-ADMS; and R=(CH2)5CH3, Mn-HDMS. All are soluble in dilute sodium bicarbonate solutions and can be administered as aqueous solutions. Cadmium mobilization data were collected on each compound using mice previously loaded with cadmium; the monoesters were administered at a level of 0.40 mmol/kg intraperitoneally daily for five days. Data on whole body cadmium mobilization indicated that the monoester with the isoamyl group was the most effective under the conditions used. The relative whole body cadmium mobilization increased with the number of carbon atoms in the alkyl group of the monoester up to C5 and then decreased for the C6 compound. Cadmium removal from the kidneys and liver was also measured. It was found that the monoisoamyl ester was the most effective in removing cadmium from both the liver and the kidneys. The monoisoamyl ester also proved to be very effective in mobilizing cadmium from both the liver and the kidneys when given orally. This is the first compound which is reported capable of mobilizing cadmium in vivo from aged deposits after oral administration. C1 VANDERBILT UNIV,CTR MOLEC TOXICOL,NASHVILLE,TN 37235. VET ADM MED CTR,RALPH H JOHNSON DEPT,CHARLESTON,SC 29403. MED UNIV S CAROLINA,DEPT PHARMACOL,CHARLESTON,SC 29425. RP JONES, MM (reprint author), VANDERBILT UNIV,DEPT CHEM,BOX 1583,STN B,NASHVILLE,TN 37235, USA. FU NIEHS NIH HHS [ES 02683-10] NR 23 TC 86 Z9 89 U1 0 U2 1 PU MUNKSGAARD INT PUBL LTD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0901-9928 J9 PHARMACOL TOXICOL JI Pharmacol. Toxicol. PD MAY PY 1992 VL 70 IS 5 BP 336 EP 343 PN 1 PG 8 WC Pharmacology & Pharmacy; Toxicology SC Pharmacology & Pharmacy; Toxicology GA HY281 UT WOS:A1992HY28100004 PM 1319053 ER PT J AU Oda, K Yamato, K Ohta, E Nakamura, Y Takemura, M Nozato, N Akashi, K Kanegae, T Ogura, Y Kohchi, T Ohyama, K AF Oda, Kenji Yamato, Katsuyuki Ohta, Eiji Nakamura, Yasukazu Takemura, Miho Nozato, Naoko Akashi, Kinya Kanegae, Takeshi Ogura, Yutaka Kohchi, Takayuki Ohyama, Kanji TI Complete Nucleotide Sequence of the Mitochondrial DNA from a Liverwort, Marchantia polymorpha SO PLANT MOLECULAR BIOLOGY REPORTER LA English DT Article DE Liverwort; mitochondrial DNA; complete nucleotide sequence AB Libraries of cosmid and plasmid clones covering the entire region of mtDNA from the liverwort Marchantia polymorpha were constructed. These clones were used for the determination of the complete nucleotide sequence of the liverwort mtDNA totally 186,608 bp (GenBank no. M68929) and including genes for 3 species of ribosomal RNAs, 29 genes for 27 species of transfer RNAs, and 30 genes for functionally known proteins ( 16 ribosomal proteins, 3 subunits of cytochrome coxidase, apocytochrome b protein, 3 subunits of H*-ATPase, and 7 subunits of NADH ubiquinone oxidoreductase). The genome also contains 32 unidentified open reading frames. Thus the complete nucleotide sequences from both chloroplast and mitochondrial genomes have been determined in the same organism. Plasmid clones are available upon the request. C1 [Oda, Kenji; Yamato, Katsuyuki; Ohta, Eiji; Nakamura, Yasukazu; Takemura, Miho; Nozato, Naoko; Akashi, Kinya; Kanegae, Takeshi; Ohyama, Kanji] Kyoto Univ, Dept Agr Chem, Fac Agr, Kyoto 60601, Japan. [Ogura, Yutaka] Okayama Univ, Bioresources Res Inst, Kurashiki, Okayama 710, Japan. [Kohchi, Takayuki] Massachusetts Gen Hosp, Dept Mol Biol, Boston, MA 02114 USA. RP Ohyama, K (reprint author), Kyoto Univ, Dept Agr Chem, Fac Agr, Kyoto 60601, Japan. RI YAMATO, Katsuyuki/Q-7263-2016; OI Nakamura, Yasukazu/0000-0002-6782-5715 FU Ministry of Education, Science and Culture, Japan; Yamada Science Foundation FX This work was supported in part by a Grant-in-Aid for Scientific Research in Priority Area from the Ministry of Education, Science and Culture, Japan, and the Yamada Science Foundation. NR 11 TC 21 Z9 21 U1 0 U2 2 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0735-9640 EI 1572-9818 J9 PLANT MOL BIOL REP JI Plant Mol. Biol. Rep. PD MAY PY 1992 VL 10 IS 2 BP 105 EP 163 DI 10.1007/BF02668342 PG 59 WC Biochemical Research Methods; Plant Sciences SC Biochemistry & Molecular Biology; Plant Sciences GA V41EC UT WOS:000209528500004 ER PT J AU FRUMAN, DA KLEE, CB BIERER, BE BURAKOFF, SJ AF FRUMAN, DA KLEE, CB BIERER, BE BURAKOFF, SJ TI CALCINEURIN PHOSPHATASE-ACTIVITY IN LYMPHOCYTES-T IS INHIBITED BY FK-506 AND CYCLOSPORINE-A SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE IMMUNOPHILINS; IMMUNOSUPPRESSION ID CELL ACTIVATION; PROTEIN PHOSPHATASES; LIMITED PROTEOLYSIS; MACROLIDES FK-506; RAPAMYCIN; FK506; IMMUNOPHILIN; SPECIFICITY; EXPRESSION; MECHANISMS AB The immunosuppressive agents cyclosporin A (CsA) and FK 506 bind to distinct families of intracellular proteins (immunophilins) termed cyclophilins and FK 506-binding proteins (FKBPs). Recently, it has been shown that, in vitro, the complexes of CsA-cyclophilin and FK 506-FKBP-12 bind to and inhibit the activity of calcineurin, a calcium-dependent serine/threonine phosphatase. We have investigated the effects of drug treatment on phosphatase activity in T lymphocytes. Calcineurin is expressed in T cells, and its activity can be measured in cell lysates. Both CsA and FK 506 specifically inhibit cellular calcineurin at drug concentrations that inhibit interleukin 2 production in activated T cells. Rapamycin, which binds to FKBPs but exhibits different biological activities than FK 506, has no effect on calcineurin activity. Furthermore, excess concentrations of rapamycin prevent the effects of FK 506, apparently by displacing FK 506 from FKBPs. These results show that calcineurin is a target of drug-immunophilin complexes in vivo and establish a physiological role for calcineurin in T-cell activation. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DIV MED SCI,COMM IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. NCI,BIOCHEM LAB,BETHESDA,MD 20892. BRIGHAM & WOMENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [CA39542] NR 31 TC 679 Z9 687 U1 4 U2 10 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 MAY 1 PY 1992 VL 89 IS 9 BP 3686 EP 3690 DI 10.1073/pnas.89.9.3686 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR853 UT WOS:A1992HR85300004 PM 1373887 ER PT J AU REDHEAD, CR EDELMAN, AE BROWN, D LANDRY, DW ALAWQATI, Q AF REDHEAD, CR EDELMAN, AE BROWN, D LANDRY, DW ALAWQATI, Q TI A UBIQUITOUS 64-KDA PROTEIN IS A COMPONENT OF A CHLORIDE CHANNEL OF PLASMA AND INTRACELLULAR MEMBRANES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID AIRWAY EPITHELIUM; XENOPUS OOCYTES; SHAKER LOCUS; CELL-LINE; KINASE-C; DROSOPHILA; TRANSPORT; CONDUCTANCE; CAMP AB Chloride channels are present in the plasma and intracellular membranes of most cells. Previously, using the ligand indanyloxyacetic acid (IAA), we purified four major proteins from bovine kidney cortex membrane vesicles. These proteins gave rise to chloride channel activity when reconstituted into phospholipid vesicles. Two of these proteins (97 and 27 kDa) were found to be drug-binding proteins by N-terminal sequence analysis. Antibodies raised to the 64-kDa protein stained only this protein on immunoblots, and only this protein was present after purification on an immunoaffinity column. In addition, these same antibodies were able to deplete IAA-94 inhibitable chloride channel activity from solubilized kidney membranes. Of fractions obtained from the gel filtration of solubilized kidney membranes, only those containing this 64-kDa protein exhibited measurable chloride channel activity. Immunoblots of a variety of species and cell types, both epithelial and nonepithelial, revealed that this protein is ubiquitous and highly conserved. Immunocytochemistry in CFPAC-1 cells revealed staining for this protein on the apical plasma membrane and in the membranes of intracellular organelles. These results demonstrate that the integral membrane protein p64 is a component of chloride channels present in both epithelial plasma membrane and the membranes of intracellular organelles. C1 MASSACHUSETTS GEN HOSP, RENAL UNIT, BOSTON, MA 02114 USA. RP REDHEAD, CR (reprint author), COLUMBIA UNIV COLL PHYS & SURG, DEPT MED, 630 W 168TH ST, NEW YORK, NY 10032 USA. RI Al-Awqati, Qais/B-2465-2009; OI Al-Awqati, Qais/0000-0001-7141-1040 FU NIDDK NIH HHS [DK39532, DK41146] NR 38 TC 61 Z9 62 U1 0 U2 2 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1992 VL 89 IS 9 BP 3716 EP 3720 DI 10.1073/pnas.89.9.3716 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR853 UT WOS:A1992HR85300010 PM 1315034 ER PT J AU COLONNA, M BRESNAHAN, M BAHRAM, S STROMINGER, JL SPIES, T AF COLONNA, M BRESNAHAN, M BAHRAM, S STROMINGER, JL SPIES, T TI ALLELIC VARIANTS OF THE HUMAN PUTATIVE PEPTIDE TRANSPORTER INVOLVED IN ANTIGEN PROCESSING SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE MAJOR HISTOCOMPATIBILITY COMPLEX; TRANSPORTER POLYMORPHISM; ANKYLOSING SPONDYLITIS; DIABETES; CELIAC DISEASE ID MAJOR HISTOCOMPATIBILITY COMPLEX; CLASS-II REGION; DEPENDENT DIABETES-MELLITUS; ANKYLOSING-SPONDYLITIS; CELIAC-DISEASE; HLA; GENE; MHC; SUSCEPTIBILITY; RESISTANCE AB Antigen processing for presentation of peptide epitopes by major histocompatibility complex (MHC) class I molecules involves genes in the MHC class II region. Among these, PSF1 and PSF2 encode subunits of a transporter, which presumably delivers cytosolic peptides across the endoplasmic reticulum membrane to class I molecules. This close functional relationship of the transporter and class I heavy chain genes and their linkage within the MHC raise the question of whether PSF1 and PSF2, like most class I genes, are polymorphic. By single-strand conformation polymorphism analysis and DNA sequencing, a small number of amino acid sequence variants of both PSF1 and PSF2 was identified in a panel of cell lines. This limited polymorphism may contribute to a higher degree of variability at the level of the functional transporter, in which different alleles of the PSF1 and PSF2 subunits may be combined. A possible involvement of the PSF1 and PSF2 genes in susceptibility to MHC-associated diseases was examined in a preliminary assessment in patients with ankylosing spondylitis, insulin-dependent diabetes mellitus, or celiac disease. C1 IST NAZL RIC CANC,GENOA,ITALY. RP COLONNA, M (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR VIROL,44 BINNEY ST,BOSTON,MA 02115, USA. OI Colonna, Marco/0000-0001-5222-4987 FU NIAID NIH HHS [AI-30581]; NIDDK NIH HHS [DK-30241] NR 44 TC 235 Z9 241 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 MAY 1 PY 1992 VL 89 IS 9 BP 3932 EP 3936 DI 10.1073/pnas.89.9.3932 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR853 UT WOS:A1992HR85300054 PM 1570316 ER PT J AU LEARY, AG ZENG, HQ CLARK, SC OGAWA, M AF LEARY, AG ZENG, HQ CLARK, SC OGAWA, M TI GROWTH-FACTOR REQUIREMENTS FOR SURVIVAL IN G0 AND ENTRY INTO THE CELL-CYCLE OF PRIMITIVE HUMAN HEMATOPOIETIC PROGENITORS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE HEMATOPOIETIC STEM CELLS; INTERLEUKINS ID MULTIPOTENTIAL HEMATOPOIETIC PROGENITORS; COLONY-STIMULATING FACTOR; BLAST CELL; STEM-CELLS; INTERLEUKIN-3-DEPENDENT PROLIFERATION; BONE-MARROW; CULTURE; DIFFERENTIATION; IDENTIFICATION; INVITRO AB In this study we have isolated populations of dormant human hemopoietic progenitors by two different approaches. First CD34+ cells isolated by panning were further separated on the basis of absence of HLA-DR expression by using fluorescence-activated cell sorting. Second, CD34+ HLA-DR- cells were isolated by nonadherence to soybean agglutinin, negative immunomagnetic bead selection with lineage-specific antibodies, and two-color cell sorting. Progenitors in either cell population were unable to form colonies in the presence of interleukin (IL)-3 alone but yielded a substantial number of colonies, including multilineage colonies, in the presence of combinations of IL-3 and IL-6. Similarly, IL-3 plus any one of the other synergistic factors, including granulocyte colony-stimulating factor, IL-11, leukemia inhibitory factor, and steel factor, effectively supported colony formation from CD34+ HLA-DR- progenitors. Sequential observation of colony formation from single CD34+ HLA-DR- cells provided definitive evidence that the synergistic factors trigger cell divisions of dormant cells. Studies with delayed addition of factors to the cultures provided evidence that this population of cells also requires IL-3 or granulocyte/macrophage colony-stimulating factor (GM-CSF) to survive even while dormant. In contrast, none of the synergistic factors were able to replace IL-3 or GM-CSF in this function. These findings confirm and extend the model that multiple factors with overlapping functions operate both independently and in combination to regulate early stages of hemopoiesis. C1 RALPH H JOHNSON DEPT VET AFFAIRS MED CTR,CHARLESTON,SC 29403. GENET INST,CAMBRIDGE,MA 02140. MED UNIV S CAROLINA,DEPT MED,CHARLESTON,SC 29425. FU NIDDK NIH HHS [DK32294] NR 22 TC 223 Z9 223 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 MAY 1 PY 1992 VL 89 IS 9 BP 4013 EP 4017 DI 10.1073/pnas.89.9.4013 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR853 UT WOS:A1992HR85300071 PM 1373892 ER PT J AU RAZIWOLF, Z FREEMAN, GJ GALVIN, F BENACERRAF, B NADLER, L REISER, H AF RAZIWOLF, Z FREEMAN, GJ GALVIN, F BENACERRAF, B NADLER, L REISER, H TI EXPRESSION AND FUNCTION OF THE MURINE-B7 ANTIGEN, THE MAJOR COSTIMULATORY MOLECULE EXPRESSED BY PERITONEAL-EXUDATE CELLS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID HUMAN LYMPHOCYTES-T; MONOCLONAL-ANTIBODY; PRESENTING CELLS; B-CELLS; ACTIVATION; RECEPTOR; DETERMINANT; COMPLEX; CONSTRUCTION; INDUCTION AB The murine B7 (mB7) protein is a potent costimulatory molecule for the T-cell receptor (TCR)-mediated activation of murine CD4+ T cells. We have previously shown that stable mB7-transfected Chinese hamster ovary (CHO) cells but not vector-transfected controls synergize with either anti-CD3 monoclonal antibody-induced or concanavalin A-induced T-cell activation, resulting ultimately in lymphokine production and proliferation. We now have generated a hamster anti-mB7 monoclonal antibody. This reagent recognizes a protein with an apparent molecular mass of 50-60 kDa. The mB7 antigen is expressed on activated B cells and on peritoneal exudate cells (PECs). Antibody blocking experiments demonstrate that mB7 is the major costimulatory molecule expressed by PECs for the activation of murine CD4+ T cells. This suggests an important role for mB7 during immune-cell interactions. We have also surveyed a panel of murine cell lines capable of providing costimulatory activity. Our results indicate that mB7 is the major costimulatory molecule on some but not all cell lines and that there may be additional molecules besides mB7 that can costimulate the activation of murine CD4+ T cells. C1 HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. FU NCI NIH HHS [CA-46967, CA-40216]; NIAID NIH HHS [AI-30169] NR 34 TC 240 Z9 240 U1 0 U2 2 PU NATL ACAD PRESS PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD MAY 1 PY 1992 VL 89 IS 9 BP 4210 EP 4214 DI 10.1073/pnas.89.9.4210 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA HR853 UT WOS:A1992HR85300112 PM 1373896 ER PT J AU MANSCHRECK, TC AF MANSCHRECK, TC TI AN OVERVIEW OF DELUSIONS AND DELUSIONAL DISORDERS - CONTEMPORARY PSYCHOPATHOLOGY SO PSYCHIATRIC ANNALS LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,PSYCHIAT,HANOVER,NH 03756. RP MANSCHRECK, TC (reprint author), NEW HAMPSHIRE HOSP,DARTMOUTH MED SCH,105 PLEASANT ST,CONCORD,NH 03301, USA. NR 5 TC 1 Z9 1 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD MAY PY 1992 VL 22 IS 5 BP 229 EP 231 PG 3 WC Psychiatry SC Psychiatry GA HT714 UT WOS:A1992HT71400003 ER PT J AU MANSCHRECK, TC AF MANSCHRECK, TC TI DELUSIONAL DISORDERS - CLINICAL CONCEPTS AND DIAGNOSTIC STRATEGIES SO PSYCHIATRIC ANNALS LA English DT Article C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. DARTMOUTH COLL,HITCHCOCK MED CTR,DARTMOUTH MED SCH,PSYCHIAT,HANOVER,NH 03756. RP MANSCHRECK, TC (reprint author), NEW HAMPSHIRE HOSP,RES,105 PLEASANT ST,CONCORD,NH 03301, USA. NR 20 TC 7 Z9 8 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0048-5713 J9 PSYCHIAT ANN JI Psychiatr. Ann. PD MAY PY 1992 VL 22 IS 5 BP 241 EP 251 PG 11 WC Psychiatry SC Psychiatry GA HT714 UT WOS:A1992HT71400005 ER PT J AU SILVA, JA LEONG, GB AF SILVA, JA LEONG, GB TI THE CAPGRAS SYNDROME IN PARANOID SCHIZOPHRENIA SO PSYCHOPATHOLOGY LA English DT Article ID SUBJECTIVE DOUBLES; INTERMETAMORPHOSIS; DELUSION; SYSTEM AB Capgras syndrome is characterized by a delusion of impostors who are thought to be physically similar but psychologically distinct from the misidentified person. This syndrome is generally thought to be relatively rare. Most of our knowledge about Capgras syndrome derives from single case studies and small series of cases usually from diagnostically heterogeneous groups. In this article, a series of 31 patients suffering from both paranoid schizophrenia and Capgras syndrome is described. Issues pertaining to the phenomenology of Capgras syndrome, the possible relation between Capgras syndrome and other delusional misidentification syndromes, and a neurobiological hypothesis aimed at explaining Capgras syndrome are discussed. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,PSYCHIAT SERV,LOS ANGELES,CA. NR 35 TC 33 Z9 33 U1 2 U2 7 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PD MAY-JUN PY 1992 VL 25 IS 3 BP 147 EP 153 PG 7 WC Psychiatry SC Psychiatry GA JV420 UT WOS:A1992JV42000005 PM 1448540 ER EF