FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Cooke, KR Martin, TR Kobzik, L Delmonte, J Ferrara, JLM AF Cooke, KR Martin, TR Kobzik, L Delmonte, J Ferrara, JLM TI A murine model for idiopathic pneumonia syndrome: The role of alloreactivity and endotoxin in lung injury after bone marrow transplantation SO BLOOD LA English DT Meeting Abstract C1 CHILDRENS HOSP,DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH PUBL HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2287 EP 2287 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002288 ER PT J AU Boussiotis, VA Barber, DL Freeman, GJ Lee, BY Gribben, JG Nadler, LM AF Boussiotis, VA Barber, DL Freeman, GJ Lee, BY Gribben, JG Nadler, LM TI Anergic T cell clones do not respond to IL-12: Evidence that alloantigen specific anergy might not be reversed in vivo by IL-12 SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2288 EP 2288 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002289 ER PT J AU Manie, S Sattler, M Astier, A Phifer, J Salgia, R Griffin, JD Freedman, A AF Manie, S Sattler, M Astier, A Phifer, J Salgia, R Griffin, JD Freedman, A TI beta integrin ligation induces tyrosine phosphorylation of the proto-oncogene product p120(Cbl) and association with the p85 phosphatidylinositol-3' kinase subunit. SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. RI Astier, Anne/A-1641-2008 OI Astier, Anne/0000-0002-0144-3431 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2364 EP 2364 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002365 ER PT J AU Ganju, RK Shpektor, R Shipp, MA AF Ganju, RK Shpektor, R Shipp, MA TI CD10 neutral endopeptidase 24.11 is phosphorylated by casein kinase II and co-associates with other phosphoproteins including the lyn src-related kinase SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2367 EP 2367 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002368 ER PT J AU Golub, T McLean, T Stegmaier, K Ritz, J Sallan, S Neuberg, D Gilliland, DG AF Golub, T McLean, T Stegmaier, K Ritz, J Sallan, S Neuberg, D Gilliland, DG TI TEL-AML1: The most common gene rearrangement in childhood ALL SO BLOOD LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2377 EP 2377 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002378 ER PT J AU Liu, ET Dodge, R Myer, A Zhang, XX Schiffer, C Mayer, R Bloomfield, CD AF Liu, ET Dodge, R Myer, A Zhang, XX Schiffer, C Mayer, R Bloomfield, CD TI De novo acute myeloid leukemias harboring ras mutations exhibit preferential sensitivity to dose intensive cytarabine as consolidation therapy. SO BLOOD LA English DT Meeting Abstract C1 UNIV N CAROLINA,CHAPEL HILL,NC. DUKE UNIV,DURHAM,NC. UNIV MARYLAND,BALTIMORE,MD 21201. DANA FARBER CANC INST,BOSTON,MA 02115. ROSWELL PK CANC INST,BUFFALO,NY. CALGB,CHICAGO,IL. NR 0 TC 2 Z9 2 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2380 EP 2380 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002381 ER PT J AU Wang, DK Ritz, J Robertson, MJ AF Wang, DK Ritz, J Robertson, MJ TI Expression and function of CD95 (APO-1/Fas) antigen on B-cell malignancies stimulated by CD40 ligand SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2396 EP 2396 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002397 ER PT J AU Schultze, JL Cardoso, AA Seamon, MJ Gribben, JG Nadler, LM AF Schultze, JL Cardoso, AA Seamon, MJ Gribben, JG Nadler, LM TI Induction and amplification of anti-follicular lymphoma specific cytolytic T cells in vitro: Potential for adoptive transfer SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. RI Schultze, Joachim/D-7794-2011 OI Schultze, Joachim/0000-0003-2812-9853 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2398 EP 2398 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002399 ER PT J AU Federowicz, I Barrett, B Andersen, J Urashima, M Popovsky, M Anderson, K AF Federowicz, I Barrett, B Andersen, J Urashima, M Popovsky, M Anderson, K TI Characterization of reactions after transfusion of prestorage leukoreduced cellular blood components. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BLOOD COMPONENT LAB,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. AMER RED CROSS,BLOOD SERV NEW ENGLAND REG,DEDHAM,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2421 EP 2421 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002422 ER PT J AU Soiffer, R Mauch, P Alyea, E Anderson, K BartlettPandite, L Fisher, D Freedman, A Robertson, M Murray, C Freeman, A Marcus, K Nadler, L Ritz, J AF Soiffer, R Mauch, P Alyea, E Anderson, K BartlettPandite, L Fisher, D Freedman, A Robertson, M Murray, C Freeman, A Marcus, K Nadler, L Ritz, J TI CD6 depleted allogeneic bone marrow transplantation (BMT) from HLA mismatched related donors. SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. JOINT CTR RADIAT THERAPY,DEPT RADIAT THERAPY,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2468 EP 2468 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002469 ER PT J AU Boussiotis, VA Freeman, GJ Lee, BY Gribben, JG Nadler, LM AF Boussiotis, VA Freeman, GJ Lee, BY Gribben, JG Nadler, LM TI Cell clonal anergy results in upregulation of anti-apoptosis survival proteins and absence of Fas expression SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2476 EP 2476 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002477 ER PT J AU Dey, B Pearson, DA Szot, GL Sykes, M AF Dey, B Pearson, DA Szot, GL Sykes, M TI Mechanisms of inhibition of acute graft-vs-host disease in mice by interleukin-12 SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,TRANSPLANTAT BIOL RES CTR,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2477 EP 2477 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002478 ER PT J AU Ke, XY Boussiotis, VA Gimmi, C Freeman, GJ Nadler, LM Gribben, JG AF Ke, XY Boussiotis, VA Gimmi, C Freeman, GJ Nadler, LM Gribben, JG TI Mechanistic characterization of signals that induce and prevent the induction of T cell anergy SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2478 EP 2478 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002479 ER PT J AU Pan, L Delmonte, J Jalonen, CK Ferrara, JLM AF Pan, L Delmonte, J Jalonen, CK Ferrara, JLM TI Pretreatment of donor mice with granulocyte colony-stimulating factor (G-CSF) polarizes donor T lymphocytes toward type 2 cytokine production and reduces severity of experimental graft vs host disease SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2481 EP 2481 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002482 ER PT J AU Krenger, W Snyder, KM Delmonte, J Byon, JCH Falzarano, G Ferrara, JLM AF Krenger, W Snyder, KM Delmonte, J Byon, JCH Falzarano, G Ferrara, JLM TI Interferon-gamma end tumor necrosis factor-alpha mediate immunodeficiency after allogeneic bone marrow transplantation through induction of the nitric oxide pathway. SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. CHILDRENS HOSP,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2483 EP 2483 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002484 ER PT J AU Friedrich, C Webb, IJ GutierrezRamos, JC AF Friedrich, C Webb, IJ GutierrezRamos, JC TI Stromal cell line derived factors affect the growth of stromal cells in vitro and the recovery of the microenvironment of the bone marrow after chemotherapy in vivo. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT GENET,BOSTON,MA 02115. NR 1 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2642 EP 2642 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002643 ER PT J AU Kharbanda, S Pandey, P Ren, R Zon, L Kufe, D AF Kharbanda, S Pandey, P Ren, R Zon, L Kufe, D TI c-ABL activation regulates induction of the SEK1/stress-activated protein kinase pathway in the cellular response to 1-beta-D-arabinosyl-cytosine. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. BRANDEIS UNIV,ROSENSTIEL BASIC MED SCI RES CTR,DEPT BIOL,WALTHAM,MA 02254. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2664 EP 2664 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002665 ER PT J AU Teicher, BA Holden, SA Chen, YN Menon, K AF Teicher, BA Holden, SA Chen, YN Menon, K TI Interaction of recombinant human interleukin eleven with cytotoxic cancer therapies in vitro and in vivo. SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2806 EP 2806 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002807 ER PT J AU Gerwin, N Xu, H Springer, TA GutierrezRamos, JC AF Gerwin, N Xu, H Springer, TA GutierrezRamos, JC TI Analysis of intercellular adhesion molecule-2 deficient mice SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES INC,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT GENET & PATHOL,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2849 EP 2849 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002850 ER PT J AU Jia, GQ Gonzalo, JA Kopf, M Lichtman, A GuterrezRamos, JC AF Jia, GQ Gonzalo, JA Kopf, M Lichtman, A GuterrezRamos, JC TI The mRNA expression of mouse eotaxin is not restricted to the development of a Th2-type response in vitro or in vivo. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,CTR BLOOD RES INC,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2853 EP 2853 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002854 ER PT J AU Delabesse, E Bernard, M Meyer, V Smit, L Valensi, F Ritz, J Strominger, JL Macintyre, E AF Delabesse, E Bernard, M Meyer, V Smit, L Valensi, F Ritz, J Strominger, JL Macintyre, E TI Comparative expression of TAL-1, RBTN-1/2 and GATA 1/3 in T-ALL. SO BLOOD LA English DT Meeting Abstract C1 CHU NECKER ENFANTS MALAD,DEPT HEMATOL,PARIS,FRANCE. CHU NECKER ENFANTS MALAD,CNRS,URA 1461,PARIS,FRANCE. HARVARD UNIV,DANA FARBER CANC INST,CAMBRIDGE,MA 02138. NR 0 TC 0 Z9 0 U1 1 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 NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 2895 EP 2895 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91002896 ER PT J AU Legare, RD Ho, CY Otterud, B Varvil, T Gallagher, M Li, F Leppert, M Gilliland, DG AF Legare, RD Ho, CY Otterud, B Varvil, T Gallagher, M Li, F Leppert, M Gilliland, DG TI A familial platelet disorder with propensity to develop acute myeloid leukemia is linked to human chromosome 21q22.1-22.2. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT. UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3056 EP 3056 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003057 ER PT J AU Stone, RM Piro, ID Saven, A Berg, DT Bryan, WJ Fay, JW Herzig, GP Herzig, RH Shields, AF Coleman, BS Lee, EJ AF Stone, RM Piro, ID Saven, A Berg, DT Bryan, WJ Fay, JW Herzig, GP Herzig, RH Shields, AF Coleman, BS Lee, EJ TI A phase I novel alkylating agent (AA), adozelesin patients (PTS) with refractory hematologic malignancies (HM) SO BLOOD LA English DT Meeting Abstract C1 DANA FARBER CANC INST, BOSTON, MA 02115 USA. Scripps Res Inst, DEPT CHEM, LA JOLLA, CA 92037 USA. UNIV MARYLAND, CTR CANC, BALTIMORE, MD 21201 USA. BAYLOR UNIV, MED CTR, DALLAS, TX USA. ROSWELL PK CANC INST, BUFFALO, NY USA. JEWISH GEN HOSP, CTR ONCOL, CINCINNATI, OH USA. VET ADM MED CTR, SEATTLE, WA 98108 USA. UPJOHN CO, KALAMAZOO, MI 49001 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3116 EP 3116 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003117 ER PT J AU Friedberg, RC Wang, S AF Friedberg, RC Wang, S TI The impact upon platelet utilization of guidelines coupled with an aggressive transfusion medicine clinical consultation service SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM VAMC,DEPT PATHOL,PATHOL & LAB MED SERV,BIRMINGHAM,AL. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3411 EP 3411 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003412 ER PT J AU Friedberg, RC Bell, WC Sinor, LT AF Friedberg, RC Bell, WC Sinor, LT TI Prevalence of platelet-directed antibodies in surgical patients: Implications for platelet transfusion protocols. SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM VAMC,DEPT PATHOL,PATHOL & LAB MED SERV,BIRMINGHAM,AL. IMMUCOR INC,NORCROSS,GA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3412 EP 3412 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003413 ER PT J AU Friedberg, RC Huang, ST AF Friedberg, RC Huang, ST TI Provision of blood products to a patient with documented anaphylaxis to corn-derived compounds including ACD and CPD. SO BLOOD LA English DT Meeting Abstract C1 UNIV ALABAMA,BIRMINGHAM VAMC,DEPT PATHOL,PATHOL & LAB MED SERV,BIRMINGHAM,AL. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3413 EP 3413 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003414 ER PT J AU Cruz, MA Bienkowski, J Liddington, R Wise, RJ Handin, RI AF Cruz, MA Bienkowski, J Liddington, R Wise, RJ Handin, RI TI A possible role for a metal ion-dependent adhesion sequence (MIDAS) in the vWF-A3 domain in its binding to collagen. SO BLOOD LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DEPT MED & BIOL CHEM,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MOLEC PHARMACOL,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3459 EP 3459 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003460 ER PT J AU Messmore, HL Farid, S Fabbrini, N AF Messmore, HL Farid, S Fabbrini, N TI The anticoagulant effect of heparin is altered by a pentasaccharide. SO BLOOD LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,HINES,IL 60141. LOYOLA UNIV,STRITCH SCH MED,MAYWOOD,IL 60153. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3514 EP 3514 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003515 ER PT J AU Messmore, HL Farid, S Fabbrini, N AF Messmore, HL Farid, S Fabbrini, N TI Effect of factor VIII levels on the calcium thrombin time (CATT) of heparinized normal plasma. SO BLOOD LA English DT Meeting Abstract C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,HINES,IL 60141. LOYOLA UNIV,STRITCH SCH MED,MAYWOOD,IL 60153. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3515 EP 3515 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003516 ER PT J AU Hitz, SL Kayiani, MD Schlerman, FJ Bree, AG Grupp, SA Goldman, SJ AF Hitz, SL Kayiani, MD Schlerman, FJ Bree, AG Grupp, SA Goldman, SJ TI The hematologic effects of recombinant human interleukin 11 in a myelosuppressed nonhuman primate model. SO BLOOD LA English DT Meeting Abstract C1 GENET INST INC,CAMBRIDGE,MA. DANA FARBER CANC INST,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3579 EP 3579 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003580 ER PT J AU Merkel, PA Pierangeli, SS Convery, K Chang, YC Harris, EN Polisson, RP AF Merkel, PA Pierangeli, SS Convery, K Chang, YC Harris, EN Polisson, RP TI Comparison between the standard anticardiolipin antibody test and a new phospholipid test in patients with a variety of connective tissue diseases. SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. UNIV LOUISVILLE,LOUISVILLE,KY 40292. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3669 EP 3669 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003669 ER PT J AU Dasgupta, A Rajagopal, C Efird, J McAfee, S Meehan, K Mazumder, A Spitzer, T AF Dasgupta, A Rajagopal, C Efird, J McAfee, S Meehan, K Mazumder, A Spitzer, T TI High dose cyclophosphamide (CY) carboplatin (Carbo) and autologous bone marrow transplantation (ABMT) peripheral blood stem cell transplantation (PBSCT) for metastatic breast cancer: An analysis of prognostic factors. SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GEORGETOWN UNIV,MED CTR,WASHINGTON,DC 20007. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3757 EP 3757 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003757 ER PT J AU Durie, BGM Gale, RP Dubois, R Naumov, IM Anderson, KC Audeh, WM Bergsagel, D Jagannath, S Kyle, RA Oken, MM Perlman, M Rifkin, RM Stone, MJ AF Durie, BGM Gale, RP Dubois, R Naumov, IM Anderson, KC Audeh, WM Bergsagel, D Jagannath, S Kyle, RA Oken, MM Perlman, M Rifkin, RM Stone, MJ TI Multiple myeloma: RAND-Delphi analysis of appropriateness of peripheral blood and bone marrow autotransplants, with comparisons using the analytic hierarchy decision process SO BLOOD LA English DT Meeting Abstract C1 CEDARS SINAI COMP CANC CTR,LOS ANGELES,CA. VALUE HLTH SCI,SANTA MONICA,CA. DANA FARBER CANC INST,BOSTON,MA 02115. UNIV TORONTO,TORONTO,ON,CANADA. UNIV ARKANSAS,FAYETTEVILLE,AR 72701. MAYO CLIN,ROCHESTER,MN. BAYLOR SAMMONS CANC CTR,DALLAS,TX. PIPER CANC INST MN,MOBILE,AL. PIPER CANC INST MN,DENVER,CO. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3763 EP 3763 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003763 ER PT J AU WANG, ZY ZHANG, Y KAMEN, D LEES, E RAVID, K AF WANG, ZY ZHANG, Y KAMEN, D LEES, E RAVID, K TI CYCLIN D3 IS ESSENTIAL FOR MEGAKARYOCYTOPOIESIS SO BLOOD LA English DT Article ID PLATELET FACTOR-IV; CELL-CYCLE; DNA-REPLICATION; MONOCLONAL-ANTIBODY; MITOTIC CONTROL; FISSION YEAST; LINE; PHASE; GENE; EXPRESSION AB A normal cell cycle in most eukaryotic cells consists of a tightly regulated sequence of phases including DNA synthesis (S) followed by a gap (G2), mitosis (M), and a gap (G1). In the megakaryocytic lineage, the cells undergo endomitosis, which involves DNA synthesis in the absence of mitosis, thus giving rise to polyploid cells. We aimed at defining whether the megakaryocytic cell cycle consists of a continuous S phase or of G1/S phases and at determining which cyclins are involved in this process, Studies were performed in primary cultures of mouse bone marrow cells. DNA synthesis in megakaryocytes was followed by determining incorporation of a DNA precursor, bromodeoxyuridine (BrdU), into the cells by in situ staining for BrdU, These experiments showed that no more than 15% of the recognizable megakaryocytes in normal bone marrow are in the process of endomitosis, including S phases interrupted by short gaps. Using immunohistochemistry, we showed that mature megakaryocytes express the G1 phase cyclin and cyclin D3, but not the mitotic cyclin, cyclin B1. Under culture conditions that selectively promote megakaryocytopoiesis, antisense oligonucleotides designed to suppress cyclin D3 expression, but not sense oligonucleotides or antisense oligonucleotides to cyclin B1, dramatically suppress endomitosis and abrogate megakaryocyte development. Our results indicate that endoreduplication in megakaryocytes is associated with low levels of or the absence of cyclin B1, whereas progression through this process depends on the G1 phase for which cyclin D3 is crucial. (C) 1995 by The American Society of Hematology. C1 BOSTON UNIV,SCH MED,CANC RES CTR,DEPT BIOCHEM,BOSTON,MA 02118. MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA. FU NHLBI NIH HHS [HL53080-02] NR 45 TC 94 Z9 98 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 NOV 15 PY 1995 VL 86 IS 10 BP 3783 EP 3788 PG 6 WC Hematology SC Hematology GA TE585 UT WOS:A1995TE58500019 PM 7579345 ER PT J AU CORZO, D YUNIS, JJ SALAZAR, M LIEBERMAN, JA HOWARD, A AWDEH, Z ALPER, CA YUNIS, EJ AF CORZO, D YUNIS, JJ SALAZAR, M LIEBERMAN, JA HOWARD, A AWDEH, Z ALPER, CA YUNIS, EJ TI THE MAJOR HISTOCOMPATIBILITY COMPLEX REGION MARKED BY HSP70-1 AND HSP70-2 VARIANTS IS ASSOCIATED WITH CLOZAPINE-INDUCED AGRANULOCYTOSIS IN 2 DIFFERENT ETHNIC-GROUPS SO BLOOD LA English DT Article ID HEAT-SHOCK PROTEIN; NECROSIS-FACTOR-ALPHA; JEWISH PATIENTS; RHEUMATOID-ARTHRITIS; POLYMORPHIC ANALYSIS; PEMPHIGUS-VULGARIS; ESCHERICHIA-COLI; GENES; EXPRESSION; INDUCTION AB Genes of the major histocompatibility complex (MHC) have been associated with susceptibility to drug-induced adverse reactions. We previously found that clozapine-induced agranulocytosis (CA) is associated with the HLA-DRB1*0402, DRB4*0101, DQB1*0302, DQA1*0301 haplotype in Ashkenazi Jewish patients and with the HLA-DRB1*1601, DRB5*02, DQB1*0502, DQA1*0102 haplotype in non-Jewish patients. In the present study, we tested the hypothesis that the variants of the heat-shock protein 70 (HSP-TID) encoded by the HSP-70 loci located within the MHC region and known to be involved in apoptosis and regulation of cell proliferation could play an important role in molecular mechanisms of CA. First, we analyzed HSP70-2 polymorphism in risk-associated haplotypes from HLA homozygous cells and normal individuals and confirmed that the HSP70-2 9-kb variant was associated invariably with DR4 (HLA-DRB1*0402, DQB1*0302) and DR2 (HLA-DRB1*01601, DQB1*0502, DQA1*0102 and HLA-DRB1*1501, DQB1*0602) haplotypes, which were the haplotypes found increased in Jewish and non-Jewish patients with CA, respectively. The 9.0-kb variant was also found to be associated with HLA-B44, DRB1*0401 and HLA-B44, DRB1*07 haplotypes. Second, in patients with CA (12 Ashkenazi Jewish and 20 non-Jewish patients), HSP70-1 A and HSP70-2 9.0-kb variants were associated with the MHC haplotypes found by us to be markers of susceptibility to CA. The clozapine-treated control group had an excess number of HSP70-1 C and HSP70-2 8.5-kb variants, consistent with genetic resistance to CA associated with those variants. This finding supports our hypothesis that a dominant gene within the MHC region (marked by HSP70-1 and HSP70-2), but not necessarily HLA, is associated with CA in two different ethnic groups. (C) 1995 by The American Society of Hematology. C1 DANA FARBER CANC INST, DIV IMMUNOGENET, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT PEDIAT, BOSTON, MA 02115 USA. LONG ISL JEWISH MED CTR, HILLSIDE HOSP, GLEN OAKS, NY 11004 USA. MONTEFIORE MED CTR, ALBERT EINSTEIN COLL MED, DEPT PSYCHIAT, BRONX, NY 10461 USA. CTR BLOOD RES, BOSTON, MA 02115 USA. MAIMONDIES MED CTR, DEPT PEDIAT, BROOKLYN, NY USA. FU NIMH NIH HHS [MH-00537, MH-47029] NR 48 TC 52 Z9 52 U1 0 U2 1 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 NOV 15 PY 1995 VL 86 IS 10 BP 3835 EP 3840 PG 6 WC Hematology SC Hematology GA TE585 UT WOS:A1995TE58500025 PM 7579351 ER PT J AU Tsai, T Goodman, S Schiller, G Adkins, D Callander, N Wolff, S Freytes, C AF Tsai, T Goodman, S Schiller, G Adkins, D Callander, N Wolff, S Freytes, C TI Allogeneic bone marrow transplantation (Allo BMT) for relapse after autologous bone marrow transplantation (Auto BMT) in lymphomas and acute leukemia SO BLOOD LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NASHVILLE VA MED CTR,NASHVILLE,TN. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA 90024. WASHINGTON UNIV,SCH MED,ST LOUIS,MO 63110. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3864 EP 3864 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003864 ER PT J AU Tsai, T Salzman, D Clark, G Castro, J Callander, N Boldt, D Roodman, GD SheridanLeos, N Wiesner, A Adkins, D Harris, K Rodriguez, T Gokmen, E LeMaistre, CF Freytes, CO AF Tsai, T Salzman, D Clark, G Castro, J Callander, N Boldt, D Roodman, GD SheridanLeos, N Wiesner, A Adkins, D Harris, K Rodriguez, T Gokmen, E LeMaistre, CF Freytes, CO TI Augmented cyclophosphamide (C), carmustine (B) and etoposide (V) +/- dacarbazine (D) with autologous bone marrow transplantation (bmt) for relapsed or refractory Hodgkin's disease: Lower peritransplant mortality and analysis of prognostic factors. SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,AUDIE L MURPHY MEM VET HOSP,SAN ANTONIO,TX 78284. S TEXAS CANC INST,SAN ANTONIO,TX. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3865 EP 3865 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003865 ER PT J AU Vose, JM Pandite, L Beveridge, RA Geller, RB Schuster, MW Anderson, JE LeMaistre, CF Lebsack, ME AF Vose, JM Pandite, L Beveridge, RA Geller, RB Schuster, MW Anderson, JE LeMaistre, CF Lebsack, ME TI Phase III study comparing pixy321 and GM-CSF following autologous bone marrow transplantation (ABMT) in patients with nonHodgkin's lymphoma (NHL) SO BLOOD LA English DT Meeting Abstract C1 UNIV NEBRASKA,MED CTR,OMAHA,NE 68105. DANA FARBER CANC INST,BOSTON,MA 02115. CORAM,FAIRFAX HOSP,FAIRFAX HEM ONC ASSOC,FAIRFAX,VA. EMORY UNIV,ATLANTA,GA 30322. N SHORE UNIV HOSP,MANHASSET,NY. FRED HUTCHINSON CANC RES CTR,SEATTLE,WA 98104. S TEXAS CANC INST,SAN ANTONIO,TX. IMMUNEX CORP,SEATTLE,WA. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3876 EP 3876 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003876 ER PT J AU ILARIA, RL VANETTEN, RA AF ILARIA, RL VANETTEN, RA TI THE SH2 DOMAIN OF P210(BCR/ABL) IS NOT REQUIRED FOR THE TRANSFORMATION OF HEMATOPOIETIC FACTOR-DEPENDENT CELLS SO BLOOD LA English DT Article ID CHRONIC MYELOGENOUS LEUKEMIA; ABL TYROSINE KINASE; POSITIVE HUMAN LEUKEMIAS; BCR-ABL; C-ABL; PHILADELPHIA-CHROMOSOME; V-ABL; SIGNAL TRANSDUCTION; MOLECULAR-CLONING; REGULATORY DOMAIN AB Src-homology region 2 (SH2) domains, by binding to tyrosine-phosphorylated sequences, mediate specific protein-protein interactions important in diverse signal transduction pathways, Previous studies have shown that activated forms of the Abl tyrosine kinase, including p210(BCR/ABL) Of human chronic myelogenous leukemia, require the SH2 domain for the transformation of fibroblasts. To determine whether SH2 is also required for Bcr/Abl to transform hematopoietic cells, we have studied two SH2 domain mutations in p210(BCR/ABL): a point mutation in the conserved FLVRES motif (P210/R1053K), which interferes with phosphotyrosine-binding by SH2, and a complete deletion of SH2 (P210/Delta SH2). Despite a negative effect on intrinsic Abl kinase activity, both P210 SH2 mutants were still able to transform the hematopoietic factor-dependent cell lines Ba/F3 and FDC-P1 to growth factor independence. Unexpectedly, both mutants showed greater transforming activity than wildtype P210 in a quantitative transformation assay, probably as a consequence of increased stability of the SH2 mutant proteins in vivo, Cells transformed by both P210 SH2 mutants were leukemogenic in syngeneic mice, and P210/R1053K mice exhibited a distinct disease phenotype, reminiscent of that induced by v-Abl. These results demonstrate that while the Abl SH2 domain is essential for BCR/ABL transformation of fibroblasts, it is dispensable for the transformation of hematopoietic factor-dependent cell lines. (C) 1995 by The American Society of Hematology. C1 HARVARD UNIV,SCH MED,CTR BLOOD RES,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,DIV HEMATOL ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [IU01 CA5771401]; NHLBI NIH HHS [5T32 HL07623] NR 53 TC 58 Z9 58 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 NOV 15 PY 1995 VL 86 IS 10 BP 3897 EP 3904 PG 8 WC Hematology SC Hematology GA TE585 UT WOS:A1995TE58500033 PM 7579359 ER PT J AU Kurzon, J Andrews, DM Stowell, CP McAfee, S Spitzer, T AF Kurzon, J Andrews, DM Stowell, CP McAfee, S Spitzer, T TI Increased post-mobilization WBC count correlates with reduced volume of processed blood during PBSC apheresis, without adversely affecting time to engraftment SO BLOOD LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BLOOD TRANSFUS SERV,BOSTON,MA. HARVARD UNIV,CTR CANC,BONE MARROW TRANSPLANT PROGRAM,BOSTON,MA 02115. 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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3931 EP 3931 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003931 ER PT J AU Jiang, CY Anderson, J Reedy, S Roodman, GD AF Jiang, CY Anderson, J Reedy, S Roodman, GD TI Construction of oncogene-containing retroviral expression vectors and their transforming capacity. SO BLOOD LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED HEMATOL,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,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 0006-4971 J9 BLOOD JI Blood PD NOV 15 PY 1995 VL 86 IS 10 SU 1 BP 3987 EP 3987 PG 1 WC Hematology SC Hematology GA TH910 UT WOS:A1995TH91003987 ER PT J AU MARTENSON, JA LIPSITZ, SR LEFKOPOULOU, M ENGSTROM, PF DAYAL, YY COBAU, CD OKEN, MM HALLER, DG AF MARTENSON, JA LIPSITZ, SR LEFKOPOULOU, M ENGSTROM, PF DAYAL, YY COBAU, CD OKEN, MM HALLER, DG TI RESULTS OF COMBINED-MODALITY THERAPY FOR PATIENTS WITH ANAL CANCER (E7283) - AN EASTERN-COOPERATIVE-ONCOLOGY-GROUP-STUDY SO CANCER LA English DT Article DE ANUS; CANCER; CHEMOTHERAPY; COMBINATION THERAPY; RADIATION THERAPY; SURVIVAL RATE ID SQUAMOUS-CELL CARCINOMA; RADIATION-THERAPY; CHEMOTHERAPY; RADIOTHERAPY; IRRADIATION; MANAGEMENT; ANUS AB Background. This prospective study assessed combined modality therapy of patients with International Union Against Cancer classification T1-4 NO MO anal cancer. Methods. Protocol therapy consisted of a dose of 4000 cGy to the pelvis, anus, and perineum, followed by a 1000-1300 cGy boost. Infusions of 5-fluorouracil and mitomycin-C were administered when radiation therapy began. A second infusion of 5-fluorouracil was administered 28 days later. Biopsy was performed 6-8 weeks after completion of treatment. Positive biopsy findings resulted in abdominal-perineal resection. Results. Survival at 7 years for 50 eligible patients was 58%. White patients and those with favorable performance status had significantly better survival. Of the 46 patients evaluable for response, 34 had a complete response, 11 had a partial response, and 1 had no response. Seven-year survival for partial responders was 53%. Freedom from locoregional progression was 80% at 7 years. Conclusion. Treatment with a combination of chemotherapy and radiation therapy is effective for patients with anal cancer. The investigation of methods of improving therapy is warranted. C1 DANA FARBER CANC INST,BOSTON,MA 02115. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. FLOWER MEM HOSP,SYLVANIA,OH. VIRGINIA PIPER CANC INST,MINNEAPOLIS,MN. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. RP MARTENSON, JA (reprint author), MAYO CLIN & MAYO FDN,200 1ST ST SW,ROCHESTER,MN 55905, USA. FU NCI NIH HHS [CA23318, CA13650, CA18281] NR 20 TC 28 Z9 29 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 NOV 15 PY 1995 VL 76 IS 10 BP 1731 EP 1736 DI 10.1002/1097-0142(19951115)76:10<1731::AID-CNCR2820761009>3.0.CO;2-H PG 6 WC Oncology SC Oncology GA TC718 UT WOS:A1995TC71800008 PM 8625041 ER PT J AU NETTI, PA BAXTER, LT BOUCHER, Y SKALAK, R JAIN, RK AF NETTI, PA BAXTER, LT BOUCHER, Y SKALAK, R JAIN, RK TI TIME-DEPENDENT BEHAVIOR OF INTERSTITIAL FLUID PRESSURE IN SOLID TUMORS - IMPLICATIONS FOR DRUG-DELIVERY SO CANCER RESEARCH LA English DT Article ID HUMAN ADENOCARCINOMA LS174T; ANGIOTENSIN-II; BLOOD-FLOW; MICROVASCULAR PERMEABILITY; ARTICULAR-CARTILAGE; NEOPLASTIC TISSUES; THEORETICAL-MODEL; SURFACE-AREA; WATER FLUX; SCID MICE AB Elevated interstitial fluid pressure (IFP) may constitute a significant physiological barrier to drug delivery in solid tumors. Strategies for overcoming this barrier have not been developed to date, To identify and characterize various mechanisms regulating IFP and to develop strategies for overcoming the IFP barrier, we modeled the tumor as a poroelastic solid, We used this model to simulate the effect of changes in microvascular pressure and tumor blood now (TBF) on IFP, To test model predictions, the effects of changes in arterial pressure and TBF on IFP were measured using a tissue-isolated tumor preparation. IFP in the center of an isolated tumor was predicted to follow variation of the arterial pressure with a time delay of the order of magnitude of 10 s, and this delay was found to be 11 +/- 6 s experimentally, Following a cessation of TBP, the time constant of the drop in IFP was predicted to be of the order of 1000 s and was found to be 1500 +/- 900 s experimentally, The former time scale is characteristic of transcapillary fluid exchange, and the latter of percolation of fluid through the interstitial matrix, Relying on the good agreement between theoretical predictions and experimental data, we estimated the effect of blood pressure modulation on macromolecular uptake in solid tumors, Our results show that no appreciable increase of macromolecular uptake should occur either by an acute or by a chronic increase of blood pressure. On the other hand, higher uptake would result from periodic modulation of blood pressure, Therefore, the effectiveness of a vasoconstrictor such as angiotensin II to increase macromolecular delivery should be significantly enhanced by periodic rather than bolus or continuous administration of the vasoactive agent. C1 HARVARD UNIV,SCH MED,BOSTON,MA. UNIV CALIF SAN DIEGO,DEPT BIOENGN,SAN DIEGO,CA 92093. RP NETTI, PA (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114, USA. OI NETTI, PAOLO/0000-0002-2435-7181 FU NCI NIH HHS [R35-CA-56591] NR 53 TC 158 Z9 162 U1 0 U2 12 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 NOV 15 PY 1995 VL 55 IS 22 BP 5451 EP 5458 PG 8 WC Oncology SC Oncology GA TD887 UT WOS:A1995TD88700057 PM 7585615 ER PT J AU LAHAM, LE WAY, M YIN, HL JANMEY, PA AF LAHAM, LE WAY, M YIN, HL JANMEY, PA TI IDENTIFICATION OF 2 SITES IN GELSOLIN WITH DIFFERENT SENSITIVITIES TO ADENINE-NUCLEOTIDES SO EUROPEAN JOURNAL OF BIOCHEMISTRY LA English DT Article DE GELSOLIN; ACTIN; NUCLEOTIDES; ATP ID ACTIN-BINDING-SITES; BOUND ADENOSINE 5'-TRIPHOSPHATE; CELLULAR OXIDANT INJURY; HUMAN-PLASMA GELSOLIN; F-ACTIN; ATP HYDROLYSIS; MUSCLE ACTIN; POLYMERIZATION; COMPLEX; FILAMENTS AB The affinity of monomeric actin for several actin-binding proteins, including gelsolin, depends on adenine nucleotides. Gelsolin binds faster and with higher affinity to ADP-actin than to ATP-actin. Here, we show that the C-terminal actin-binding domain of gelsolin, which is required for filament nucleating activity but not for filament severing activity, contains the site that distinguishes between ATP-actin and ADP-actin monomers. In contrast, actin binding to the N-terminal half of gelsolin depends on solution ATP concentrations, but not on the nucleotide (ATP or ADP) tightly bound in the cleft of the actin monomer. Binding is stronger in the absence of free nucleotide or in the presence of 0.5 mM ADP than in solutions containing 0.5 mM ATP. Complexes formed using different nucleotide concentrations differ in their filament-severing activities as well as in their abilities to increase the fluorescence of 4-chloro-7-nitrobenzeno-2-oxa-1,3-diazole-labeled actin monomers. These results suggest that, at physiologic concentrations of nucleotides, both free and actin-bound ATP may affect the binding of actin to its accessory proteins and that gelsolin, actin, or the gelsolin-actin complex, contains a low-affinity nucleotide-binding site. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02115. RP LAHAM, LE (reprint author), DANA FARBER CANC INST,DEPT CELLULAR & MOLEC BIOL,M-815,55 BINNEY ST,BOSTON,MA 02115, USA. FU NIAMS NIH HHS [AR38910] NR 81 TC 7 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-2956 J9 EUR J BIOCHEM JI Eur. J. Biochem. PD NOV 15 PY 1995 VL 234 IS 1 BP 1 EP 7 DI 10.1111/j.1432-1033.1995.001_c.x PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TG087 UT WOS:A1995TG08700001 PM 8529627 ER PT J AU FRANKEL, FR HEGDE, S LIEBERMAN, J PATERSON, Y AF FRANKEL, FR HEGDE, S LIEBERMAN, J PATERSON, Y TI INDUCTION OF CELL-MEDIATED IMMUNE-RESPONSES TO HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 GAG PROTEIN BY USING LISTERIA-MONOCYTOGENES AS A LIVE VACCINE VECTOR SO JOURNAL OF IMMUNOLOGY LA English DT Article ID CYTOTOXIC LYMPHOCYTES-T; CLASS-I MOLECULES; HIV-INFECTION; INTRACELLULAR BACTERIA; ANTIGEN PRESENTATION; CONSERVED EPITOPES; BACILLUS-SUBTILIS; SIV VACCINE; RECOMBINANT; SEQUENCE AB Cytolytic T cells, acting through cytokines or by direct lysis of infected target cells, have been shown to play a significant role in the control of viral infections and may be responsible for the prolonged asymptomatic phase following infection by HIV. Accordingly, methods that can generate strong cell-mediated immune responses may be useful in the development of prophylactic and therapeutic vaccines against HIV. Listeria monocytogenes is a Gram-positive intracellular microorganism that elicits strong cell-mediated immune responses against its own secreted proteins following infection. In this study we have modified the chromosome of L. monocytogenes so that it stably expresses and secretes the p55 HIV gag gene product and examined the cell-mediated immune response of BALB/c mice to infection with this recombinant organism. Infected animals were found to mount a specific, strong, long-lasting CD8(+) cytolytic T cell response against a predominant epitope contained within the p24 fragment of the HIV Gag protein. This epitope previously has been shown to be recognized by CTLs obtained from some HIV-infected humans. Our results suggest that chromosomally modified strains of L. monocytogenes may provide valuable vaccine vectors for use against HIV. C1 HARVARD UNIV, SCH MED, CTR BLOOD RES, BOSTON, MA 02115 USA. RP FRANKEL, FR (reprint author), UNIV PENN, SCH MED, DEPT MICROBIOL, 327 JOHNSON PAVILL, PHILADELPHIA, PA 19104 USA. RI Lieberman, Judy/A-2717-2015 FU NIAID NIH HHS [AI 36611] NR 67 TC 73 Z9 75 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 15 PY 1995 VL 155 IS 10 BP 4775 EP 4782 PG 8 WC Immunology SC Immunology GA TD888 UT WOS:A1995TD88800033 PM 7594479 ER PT J AU RUTLEDGE, BJ RAYBURN, H ROSENBERG, R NORTH, RJ GLADUE, RP CORLESS, CL ROLLINS, BJ AF RUTLEDGE, BJ RAYBURN, H ROSENBERG, R NORTH, RJ GLADUE, RP CORLESS, CL ROLLINS, BJ TI HIGH-LEVEL MONOCYTE CHEMOATTRACTANT PROTEIN-1 EXPRESSION IN TRANSGENIC MICE INCREASES THEIR SUSCEPTIBILITY TO INTRACELLULAR PATHOGENS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID HISTAMINE-RELEASING FACTOR; ACTIVATING FACTOR; CELL-LINE; JE; PURIFICATION; BASOPHILS; RESISTANT; INFECTION; RECEPTOR; PRODUCT AB We have constructed transgenic mice in which the mouse mammary tumor virus long terminal repeat controls the expression of murine monocyte chemoattractant protein-1 (MCP-1). Several independently derived lines of transgenic mice constitutively expressed MCP-1 protein in a variety of organs, Protein extracts from these organs had substantial in vitro monocyte chemoattractant activity that was neutralized by an anti-MCP-1 Ab, indicating that transgenic MCP-1 protein is biologically active, However, no transgenic mouse at any age displayed monocyte infiltrates in MCP-1-expressing organs, Two transgenic lines had circulating MCP-1 levels of 13 to 26 ng/ml, which is a concentration sufficient to induce maximal monocyte chemotaxis in vitro, These transgenic lines showed a 1 to 1.5 log greater sensitivity to infection with Listeria monocytogenes and Mycobacterium tuberculosis. A third transgenic line had lower serum levels of MCP-1 and was resistant to L. monocytogenes, The results suggest that this transgenic model is one of monocyte nonresponsiveness to locally produced MCP-1 due to either receptor desensitization or neutralization of a chemoattractant gradient by high systemic concentrations of MCP-1. Regardless of the mechanism, the data indicate that constitutively high levels of MCP-1 expression do not induce monocytic infiltrates, and that MCP-1 is involved in the host response to intracellular pathogens. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. TRUDEAU INST INC,SARANAC LAKE,NY 12983. PFIZER INC,PFIZER CENT RES,GROTON,CT 06340. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [CA53091] NR 35 TC 152 Z9 155 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 NOV 15 PY 1995 VL 155 IS 10 BP 4838 EP 4843 PG 6 WC Immunology SC Immunology GA TD888 UT WOS:A1995TD88800040 PM 7594486 ER PT J AU MORROW, M HARRIS, JR SCHNITT, SJ AF MORROW, M HARRIS, JR SCHNITT, SJ TI LOCAL-CONTROL FOLLOWING BREAST-CONSERVING SURGERY FOR INVASIVE CANCER - RESULTS OF CLINICAL-TRIALS SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Review ID RANDOMIZED TRIAL; STAGE-I; SEGMENTAL-MASTECTOMY; MAMMARY-CARCINOMA; RADIATION-THERAPY; RADIOTHERAPY; CONSERVATION; IRRADIATION; LUMPECTOMY; WOMEN AB Prospective, randomized clinical trials have demonstrated that the alternatives of mastectomy or conservative surgery plus radiation therapy provide equivalent survival for patients with invasive breast cancer, The identification of a subset of women who could undergo conservative surgery without radiotherapy would avoid the costs, inconvenience, and complications of radiotherapy and is an important research goal, Four randomized trials comparing conservative surgery alone with conservative surgery plus radiotherapy have demonstrated an average reduction in the risk of disease recurrence in the breast of 84% with the use of radiotherapy, No significant differences in survival have been observed, although the available studies lack sufficient numbers of patients to demonstrate a potential small, but clinically important, survival advantage for patients treated with radiotherapy, Subset analysis in the randomized trials and prospective studies of highly selected patients have failed to consistently identify a group of patients who do not benefit from radiation therapy, Any recurrence of breast cancer is psychologically devastating, and fewer than one half of the patients who have had disease recurrence after conservative surgery alone have undergone further breast-conserving treatment, At present, a group of patients who do not require radiotherapy has not been reproducibly identified, and radiotherapy should remain a part of breast-conserving therapy for invasive carcinoma. C1 NORTHWESTERN UNIV,SCH MED,DEPT SURG,CHICAGO,IL 60611. BETH ISRAEL HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. BETH ISRAEL HOSP,DEPT PATHOL,BOSTON,MA 02215. NR 35 TC 35 Z9 38 U1 0 U2 2 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 NOV 15 PY 1995 VL 87 IS 22 BP 1669 EP 1673 DI 10.1093/jnci/87.22.1669 PG 5 WC Oncology SC Oncology GA TD409 UT WOS:A1995TD40900009 PM 7473814 ER PT J AU HIRAYAMA, T MAEDA, T SAITO, H SHINOZAKI, K AF HIRAYAMA, T MAEDA, T SAITO, H SHINOZAKI, K TI CLONING AND CHARACTERIZATION OF 7 CDNAS FOR HYPEROSMOLARITY-RESPONSIVE (HOR) GENES OF SACCHAROMYCES-CEREVISIAE SO MOLECULAR AND GENERAL GENETICS LA English DT Article DE SACCHAROMYCES CEREVISIAE; HYPEROSMOTIC STRESS; SIGNAL TRANSDUCTION PATHWAY ID PROTEIN-KINASE; HEAT-SHOCK; IMPORTANT DETERMINANT; STRESS CONDITIONS; SALT TOLERANCE; CELL-CYCLE; YEAST; EXPRESSION; ATPASE; DEHYDROGENASE AB Yeast cells can respond and adapt to osmotic stress. In our attempt to clarify the molecular mechanisms of cellular responses to osmotic stress, we cloned seven cDNAs for hyperosmolarity-responsive (HOR) genes from Saccharomyces cerevisiae by a differential screening method. Structural analysis of the clones revealed that these designated HOR1, HOR3, HOR4, HOR5 and HOR6 encoded glycerol-3-phosphate dehydrogenase (Gpd1p), glucokinase (Glk1p), hexose transporter (Hxt1p), heat-shock protein 12 (Hsp12p) and Na+, K+, Li+-ATPase (Ena1p), respectively. HOR2 and HOR7 corresponded to novel genes. Gpd1p is a key enzyme in the synthesis of glycerol, which is a major osmoprotectant in S. cerevisiae. Cloning of HOR1/GPD1 as a HOR gene indicates that the accumulation of glycerol in yeast cells under hyperosmotic stress is, at least in part, caused by an increase in the level of GPDH protein. We performed a series of Northern blot analyses using HOR cDNAs as probes and RNAs prepared from cells grown under various conditions and from various mutant cells. The results suggested that all the HOR genes are regulated by common signal transduction pathways. However, the fact that they exhibited certain distinct responses indicated that they might also be regulated by specific pathways in addition to the common pathways. Ca2+ seemed to be involved in the signaling systems. In addition, Hog1p, one of the MAP kinases in yeast, appeared to be involved in the regulation of expression of HOR genes, although its function seemed to be insufficient for the overall regulation of expression of these genes. C1 RIKEN, INST PHYS & CHEM RES, TSUKUBA LIFE SCI CTR, PLANT MOLEC BIOL LAB, TSUKUBA, IBARAKI 305, JAPAN. HARVARD UNIV, SCH MED, DANA FARBER CANC INST, DIV TUMOR IMMUNOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. RI Shinozaki, Kazuo/G-4202-2013; HIRAYAMA, Takashi/B-2496-2011 OI HIRAYAMA, Takashi/0000-0002-3868-2380 NR 43 TC 80 Z9 84 U1 0 U2 5 PU SPRINGER PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0026-8925 J9 MOL GEN GENET JI Mol. Gen. Genet. PD NOV 15 PY 1995 VL 249 IS 2 BP 127 EP 138 DI 10.1007/BF00290358 PG 12 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA TG139 UT WOS:A1995TG13900001 PM 7500933 ER PT J AU SPITZER, M KWONG, KK KENNEDY, W ROSEN, BR BELLIVEAU, JW AF SPITZER, M KWONG, KK KENNEDY, W ROSEN, BR BELLIVEAU, JW TI CATEGORY-SPECIFIC BRAIN ACTIVATION IN FMRI DURING PICTURE NAMING SO NEUROREPORT LA English DT Article DE FUNCTIONAL MAGNETIC RESONANCE IMAGING (FMRI); CATEGORY-SPECIFIC NAMING; SEMANTIC MEMORY; CORTICAL ACTIVATION ID BODY PARTS; IMPAIRMENT; KNOWLEDGE; DEFICIT AB NEUROPSYCHOLOGICAL, computational, and psycholinguistic data suggest the existence of semantic maps, i.e. localized representations of semantic information in the brain. Using functional magnetic resonance imaging, this hypothesis was directly tested with a picture naming task involving items from four different semantic categories. Small left lateralized fronto-temporal cortical sites of category-specific activation were found when brain activation signals were averaged. Data suggest the existence of multiple maps coding high-level representations of objects, such that meaningful distinctions, at least in part, govern the physical distribution of cortical semantic storage. C1 MASSACHUSETTS GEN HOSP,NMR CTR,BOSTON,MA 02129. RP SPITZER, M (reprint author), UNIV HEIDELBERG,HOSP PSYCHIAT,VOSS STR 4,D-69115 HEIDELBERG,GERMANY. NR 25 TC 71 Z9 72 U1 0 U2 3 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 13 PY 1995 VL 6 IS 16 BP 2109 EP 2112 DI 10.1097/00001756-199511000-00003 PG 4 WC Neurosciences SC Neurosciences & Neurology GA TH461 UT WOS:A1995TH46100002 PM 8595181 ER PT J AU FEIGIN, AM ARONOV, EV BRYANT, BP TEETER, JH BRAND, JG AF FEIGIN, AM ARONOV, EV BRYANT, BP TEETER, JH BRAND, JG TI CAPSAICIN AND ITS ANALOGS INDUCE ION CHANNELS IN PLANAR LIPID BILAYERS SO NEUROREPORT LA English DT Article DE CAPSAICIN; ION CHANNELS; LIPID BILAYER ID ANALGESIC AGENTS; AGONIST ACTIVITY; REGION AB THE irritating, pungent compound, capsaicin (10-20 mu M), induces the formation of non-selective ion channels with a wide variety of conductances in protein-free lipid bilayers formed from a mixture of zwitterionic phospholipids. The channel-forming activity of capsaicin and four of its analogs followed the sequence: resiniferatoxin > capsaicin = pelargonic acid vanillylamide > methylcapsaicin >> veratrylamine. The ability to form channels correlated with the biological activity of these compounds observed in other studies that measured Ca-45 uptake into rat dorsal root ganglion cells. The correlation obtained suggests that an interaction with the lipid bilayer may be an important component of the biological activity of capsaicin. C1 UNIV PENN,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RP FEIGIN, AM (reprint author), MONELL CHEM SENSES CTR,3500 MARKET ST,PHILADELPHIA,PA 19104, USA. NR 14 TC 27 Z9 27 U1 1 U2 5 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 13 PY 1995 VL 6 IS 16 BP 2134 EP 2136 DI 10.1097/00001756-199511000-00009 PG 3 WC Neurosciences SC Neurosciences & Neurology GA TH461 UT WOS:A1995TH46100008 PM 8595187 ER PT J AU RAJAN, P STEWART, CL FINK, JS AF RAJAN, P STEWART, CL FINK, JS TI LIF-MEDIATED ACTIVATION OF STAT PROTEINS AFTER NEURONAL INJURY IN-VIVO SO NEUROREPORT LA English DT Article DE NEURONAL INJURY; CYTOKINE SIGNAL TRANSDUCTION; TRANSCRIPTION; PNS ID VASOACTIVE-INTESTINAL-PEPTIDE; LEUKEMIA INHIBITORY FACTOR; DIFFERENTIATION; EXPRESSION; BINDING; GROWTH AB LEUKEMIA inhibitory factor (LIF) is a member of a family of neuropoietic cytokines which influence neuronal survival, differentiation and response to injury. In cell lines LIF activates the Jak/Tyk tyrosine kinases and the STAT family of transcription factors. We have investigated whether the Jak-STAT intracellular signaling pathway is activated by LIF after neuronal injury in vivo. Axotomy of postganglionic sympathetic nerves resulted in sustained activation of members of the STAT transcription factor family, This activation is dependent on LIF as axotomy failed to activate STAT proteins in LIF-deficient mice. These data indicate that LIF-dependent activation of STAT proteins is one of the signal transduction pathways activated after neuronal injury. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HOFFMANN LA ROCHE INC,ROCHE RES CTR,ROCHE INST MOLEC BIOL,DEPT CELL & DEV BIOL,NUTLEY,NJ 07110. FU NINDS NIH HHS [NS-27514] NR 25 TC 41 Z9 44 U1 0 U2 1 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 13 PY 1995 VL 6 IS 16 BP 2240 EP 2244 DI 10.1097/00001756-199511000-00033 PG 5 WC Neurosciences SC Neurosciences & Neurology GA TH461 UT WOS:A1995TH46100032 PM 8595211 ER PT J AU SHAHID, NS STEINHOFF, MC HOQUE, SS BEGUM, T THOMPSON, C SIBER, GR AF SHAHID, NS STEINHOFF, MC HOQUE, SS BEGUM, T THOMPSON, C SIBER, GR TI SERUM, BREAST-MILK, AND INFANT ANTIBODY AFTER MATERNAL IMMUNIZATION WITH PNEUMOCOCCAL VACCINE SO LANCET LA English DT Article ID INFLUENZAE TYPE-B; HEMOPHILUS-INFLUENZAE; STREPTOCOCCUS-PNEUMONIAE; POLYSACCHARIDE VACCINE; PREGNANT-WOMEN; IMMUNIZATION; CHILDREN; NEWBORN AB Pneumococci are a leading cause of severe bacterial disease in infants and children world wide, A possible means of protecting infants in the first few months of life is immunisation of the mother during prospectively assessed pneumococcal pregnant women to determine the amount pneumococcal antibody transmitted to the infants in serum and milk and the half-life of the passively acquired antibody. Healthy pregnant women in Dhaka, Bangladesh, were randomised to receive pneumococcal or meningococcal vaccine with routine prenatal tetanus immunisation at 30-34 weeks of gestation. Serum and breast milk specimens from the mothers and sera from infants were collected up to 22 weeks of age and assayed for specific serum IgG, IgG1, and IgG2 and for milk IgA antibodies to pneumococcal serotypes 6B and 19F. 55 mothers and 56 infants were followed from birth to five months, Women who received pneumococcal vaccine had geometric mean antibody increases of 2.6 and 3.4 to types 6B and 19F, respectively, The mean infant/maternal antibody ratios were 0.56 and 0.59 (range 0.11-1.46) for these serotypes. Infant cord antibody titres correlated with maternal titres, Infant/maternal IgG ratios correlated with the interval between immunisation and birth and were higher for specific IgG1 than for IgG2. infants of pneumococcal vaccine recipients had geometric mean antibody concentrations of 6.8 and 7.5 mu g/mL to serotypes 6B and 19F in cord blood; in cord blood and in all subsequent serum specimens the concentrations were 2-3 fold higher than in control infants, The median half-life of passive antibody was about 35 days; at five months of age 63-71% of infants of pneumococcal Vaccine recipients had antibody concentrations greater than 0.15 mu g/mL. Breast milk IgA antibodies for pneumococcal serotype 19F, but. not for type 6B, were significantly higher in vaccine recipients up to five months after delivery. If maternal pneumococcal polysaccharide antibodies do not interfere with active immunisation of the infant with new glycoprotein conjugate pneumococcal vaccines, passive-active immunisation of infants can be a feasible strategy for developing regions. C1 INT CTR DIARRHOEAL DIS RES,DHAKA 1000,BANGLADESH. JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,BALTIMORE,MD 21205. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV INFECT DIS,BOSTON,MA 02111. NR 32 TC 121 Z9 123 U1 0 U2 1 PU LANCET LTD PI LONDON PA 42 BEDFORD SQUARE, LONDON, ENGLAND WC1B 3SL SN 0099-5355 J9 LANCET JI Lancet PD NOV 11 PY 1995 VL 346 IS 8985 BP 1252 EP 1257 DI 10.1016/S0140-6736(95)91861-2 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TE145 UT WOS:A1995TE14500009 PM 7475716 ER PT J AU DENOOIJ, JC HARIHARAN, IK AF DENOOIJ, JC HARIHARAN, IK TI UNCOUPLING CELL FATE DETERMINATION FROM PATTERNED CELL-DIVISION IN THE DROSOPHILA EYE SO SCIENCE LA English DT Article ID C-ELEGANS EMBRYOS; COMPOUND EYE; CYCLIN-A; EXPRESSION; PROTEIN; HOMOLOG; MELANOGASTER; INHIBITOR; MUTANTS; KINASES AB Cell proliferation and cell fate specification are under strict spatiotemporal control in the developing Drosophila eye. Cells excluded from five-cell preclusters synchronously enter a single additional cell cycle, the second mitotic wave, after which the remaining cells are sequentially recruited. When the second mitotic wave was blocked with the human cyclin-dependent kinase inhibitor p21(CIP1/WAF1), each cell type was still specified. Hence, cell fate determination is regulated independently of the division pattern of precursor cells. However, the second mitotic wave is needed to generate appropriate numbers of each cell type. Moreover, p21 can arrest precursor cell proliferation and allow appropriate fate choice in vivo. C1 MASSACHUSETTS GEN HOSP,CTR CANC,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. NR 28 TC 104 Z9 105 U1 0 U2 3 PU AMER ASSOC ADVAN SCIENCE PI WASHINGTON PA 1333 H ST NW, WASHINGTON, DC 20005 SN 0036-8075 J9 SCIENCE JI Science PD NOV 10 PY 1995 VL 270 IS 5238 BP 983 EP 985 DI 10.1126/science.270.5238.983 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD878 UT WOS:A1995TD87800047 PM 7481802 ER PT J AU SCULLY, RE MARK, EJ MCNEELY, WF MCNEELY, BU FERNANDEZDELCASTILLO, C MCDOWELL, RK KELSEY, PB AHMED, E AF SCULLY, RE MARK, EJ MCNEELY, WF MCNEELY, BU FERNANDEZDELCASTILLO, C MCDOWELL, RK KELSEY, PB AHMED, E TI CASE RECORDS OF THE MASSACHUSETTS GENERAL-HOSPITAL - ARTERIOVENOUS MALFORMATION OF THE SMALL-INTESTINE - SUBACUTE CHOLECYSTITIS WITH ULCERATION - CHRONIC CHOLECYSTITIS AND CHOLELITHIASIS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID SMALL-BOWEL; GASTROINTESTINAL-TRACT; TUMORS; ANGIODYSPLASIA C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 20 TC 4 Z9 4 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 NOV 9 PY 1995 VL 333 IS 19 BP 1273 EP 1279 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA TC715 UT WOS:A1995TC71500008 ER PT J AU HYMAN, BT TANZI, R AF HYMAN, BT TANZI, R TI MOLECULAR EPIDEMIOLOGY OF ALZHEIMERS-DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material ID APOLIPOPROTEIN-E; MUTATION; PROTEIN RP HYMAN, BT (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 TC 15 Z9 15 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 NOV 9 PY 1995 VL 333 IS 19 BP 1283 EP 1284 DI 10.1056/NEJM199511093331910 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA TC715 UT WOS:A1995TC71500010 PM 7566008 ER PT J AU NEWACHECK, PW HUGHES, DC ENGLISH, A FOX, HB PERRIN, J HALFON, N AF NEWACHECK, PW HUGHES, DC ENGLISH, A FOX, HB PERRIN, J HALFON, N TI THE EFFECT ON CHILDREN OF CURTAILING MEDICAID SPENDING SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Editorial Material ID LOW-INCOME CHILDREN; HEALTH-SERVICES; POOR; CARE; POVERTY C1 UNIV CALIF SAN FRANCISCO,SCH MED,DEPT PEDIAT,SAN FRANCISCO,CA 94109. NATL CTR YOUTH LAW,CHAPEL HILL,NC. FOX HLTH POLICY CONSULTANTS,WASHINGTON,DC. UNIV CALIF LOS ANGELES,DEPT PEDIAT,LOS ANGELES,CA 90024. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. RP NEWACHECK, PW (reprint author), UNIV CALIF SAN FRANCISCO,SCH MED,INST HLTH POLICY STUDIES,1388 SUTTER ST,SUITE 1100,SAN FRANCISCO,CA 94109, USA. NR 41 TC 14 Z9 14 U1 0 U2 1 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 NOV 8 PY 1995 VL 274 IS 18 BP 1468 EP 1471 DI 10.1001/jama.274.18.1468 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA TC477 UT WOS:A1995TC47700031 PM 7474195 ER PT J AU GARCIA, C SMITH, GA MCGIMPSEY, WG KOCHEVAR, IE REDMOND, RW AF GARCIA, C SMITH, GA MCGIMPSEY, WG KOCHEVAR, IE REDMOND, RW TI MECHANISM AND SOLVENT DEPENDENCE FOR PHOTOIONIZATION OF PROMAZINE AND CHLORPROMAZINE SO JOURNAL OF THE AMERICAN CHEMICAL SOCIETY LA English DT Article ID LASER FLASH-PHOTOLYSIS; QUANTUM YIELDS; ETHIDIUM IONS; FREE-RADICALS; PHOTOCHEMISTRY; PHENOTHIAZINE; BENZOPHENONE; ACTINOMETER; INTENSITY; STATES AB The mechanism for photoionization of the phenothiazine derivatives, promazine and chlorpromazine, has been studied as a function of solvent and excitation conditions. Sequential biphotonic absorption is responsible for photoionization induced by pulsed laser irradiation at 308 or 355 nm. In order to determine the excited states involved excitation was carried out under conditions where the second photon was exclusively absorbed by the lowest excited singlet state (using picosecond excitation pulses where the pulse duration is much less than singlet lifetime) or by the lowest triplet state using a two-color, two-pulse excitation protocol. Photoionization occurs upon two-photon excitation within the singlet manifold in aqueous solutions and methanol. In addition, photoionization is solvent dependent upon excitation of the triplet state at 355 nm or near its absorption maximum of 460 nm. In water the triplet absorption was bleached concomitant with the generation of absorption from the radical cation and hydrated electron. Quantum yields of photoionization of promazine were 0.02 and 0.03 in acetonitrile and water, respectively. In methanol or other alcohols, photoionization was not observed under the same excitation conditions. Triplet lifetimes, molar absorption coefficients, and quantum yields of intersystem crossing were determined in various solvents. The experimental results indicate that during single wavelength pulsed irradiation of these compounds, the second photon is absorbed predominantly by the lowest excited singlet state rather than the lowest excited triplet state. The energetics of the photoionization of promazine and chlorpromazine were estimated as a function of solvent. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. WORCESTER POLYTECH INST,DEPT CHEM,WORCESTER,MA 01609. UNIV PUERTO RICO,DEPT CHEM,HUMACAO,PR. NR 31 TC 34 Z9 34 U1 1 U2 3 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0002-7863 J9 J AM CHEM SOC JI J. Am. Chem. Soc. PD NOV 8 PY 1995 VL 117 IS 44 BP 10871 EP 10878 DI 10.1021/ja00149a010 PG 8 WC Chemistry, Multidisciplinary SC Chemistry GA TD410 UT WOS:A1995TD41000010 ER PT J AU KUDLICKI, W CHIRGWIN, J KRAMER, G HARDESTY, B AF KUDLICKI, W CHIRGWIN, J KRAMER, G HARDESTY, B TI FOLDING OF AN ENZYME INTO AN ACTIVE CONFORMATION WHILE BOUND AS PEPTIDYL-TRANSFER-RNA TO THE RIBOSOME SO BIOCHEMISTRY LA English DT Article ID TRANSLATION; PROTEINS AB Rhodanese bound to bacterial ribosomes as peptidyl-tRNA can be folded into an enzymatically active conformation by generating C-terminal extensions of the wild-type enzyme. Rhodanese was synthesized by coupled transcription/translation in a cell-free Escherichia coli system from plasmids containing the coding sequences for the wild-type enzyme or its C-terminally extended mutants. Two proteins with extensions of 23 amino acids or longer were enzymatically active while bound to the ribosomes whereas wild-type protein and a 13-amino acid extension were not. All forms of the enzyme were active after termination and release of the full-length protein from the ribosomes. All five of the bacterial chaperones were required to substantially increase the specific enzymatic activity of the extended rhodanese while the nascent protein was bound to ribosomes. The results provide direct support for the hypothesis that proteins acquire tertiary structure as they are formed in ribosomes. C1 UNIV TEXAS,DEPT CHEM & BIOCHEM,AUSTIN,TX 78712. AUDIE L MURPHY MEM VET ADM MED CTR,RES SERV,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT BIOCHEM,SAN ANTONIO,TX 78284. NR 18 TC 45 Z9 46 U1 0 U2 0 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0006-2960 J9 BIOCHEMISTRY-US JI Biochemistry PD NOV 7 PY 1995 VL 34 IS 44 BP 14284 EP 14287 DI 10.1021/bi00044a003 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TD845 UT WOS:A1995TD84500003 PM 7578030 ER PT J AU CHOI, SJ OH, DH SONG, CS ROY, AK CHATTERJEE, B AF CHOI, SJ OH, DH SONG, CS ROY, AK CHATTERJEE, B TI MOLECULAR-CLONING AND SEQUENCE-ANALYSIS OF THE RAT-LIVER CARNITINE OCTANOYLTRANSFERASE CDNA, ITS NATURAL GENE AND THE GENE PROMOTER SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE CARNITINE OCTANOYLTRANSFERASE; CDNA; PROMOTER; PEROXISOME; PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR ID ACYL-COA OXIDASE; PEROXISOMAL ENOYL-COA; BIFUNCTIONAL ENZYME; TRANSCRIPTIONAL REGULATION; NUCLEOTIDE-SEQUENCE; BETA-OXIDATION; MESSENGER-RNA; MALONYL-COA; DEHYDROGENASE; DNA AB The full-length cDNA and the natural gene for rat peroxisomal carnitine octanoyltransferase (COT) have been isolated and sequenced. The 2681 bp long cDNA contains an open reading frame for 613 amino acids, resulting in a protein with a deduced molecular weight of 70 301, and a C-terminal peroxisomal targeting sequence (Ala-His-Leu). The isolated COT cDNA has 51 bp of the 5' untranslated region (UTR), 791 bp of 3' UTR, two putative polyadenylation sites, and a poly(A(19-23)) tail. Screening of a rat genomic DNA library in the lambda phage with the COT cDNA probe resulted in the isolation of seven overlapping clones, together containing the complete COT gene with seventeen exons. All of the exon-intron boundary sequences conform to the GT-AG rule. The COT gene appears to spread over 40 to 60 kbp region of the rat genome. The transcription initiation site of the COT gene was determined through primer extension, and the promoter sequence up to the position -1140 was established. The promoter lacks the canonical TATA box and a promoter-reporter construct containing the sequence encompassing - 1140 to + 84 base positions and the firefly luciferase reporter cDNA yielded about 100-fold increase in promoter activity in transfected hepatoma cells. Some of the consensus sequences for putative cis elements present in the promoter sequence are: the two CCAAT motifs for CTF/NF1/CBP binding (at - 284 and - 93), two GC boxes for Sp1 binding (at - 160 and - 68), two AP2 sites (at - 359 and - 25), a half site (TGACCT) for the peroxisome proliferator activated receptor (PPAR) binding at - 737 within a partial palindromic sequence region. Potential regulatory elements, such as several palindromes and repeat motifs for five different sequence segments, are also identified. C1 UNIV TEXAS,HLTH SCI CTR,DEPT CELLULAR & STRUCT BIOL,SAN ANTONIO,TX 78284. YONSEI UNIV,BIOPROD RES CTR,SEOUL 120749,SOUTH KOREA. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. FU NIDDK NIH HHS [R37 DK-14744] NR 47 TC 24 Z9 25 U1 0 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD NOV 7 PY 1995 VL 1264 IS 2 BP 215 EP 222 DI 10.1016/0167-4781(95)00146-8 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TE679 UT WOS:A1995TE67900012 PM 7495866 ER PT J AU AIELLO, LP PIERCE, EA FOLEY, ED TAKAGI, H CHEN, H RIDDLE, L FERRARA, N KING, GL SMITH, LEH AF AIELLO, LP PIERCE, EA FOLEY, ED TAKAGI, H CHEN, H RIDDLE, L FERRARA, N KING, GL SMITH, LEH TI SUPPRESSION OF RETINAL NEOVASCULARIZATION IN-VIVO BY INHIBITION OF VASCULAR ENDOTHELIAL GROWTH-FACTOR (VEGF) USING SOLUBLE VEGF-RECEPTOR CHIMERIC PROTEINS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FACTOR FAMILY; CELLS; ANGIOGENESIS AB The majority of severe visual loss in the United States results from complications associated with retinal neovascularization in patients with ischemic ocular diseases such as diabetic retinopathy, retinal vein occlusion, and retinopathy of prematurity. Intraocular expression of the angiogenic protein vascular endothelial growth factor (VEGF) is closely correlated with neovascularization in these human disorders and with ischemia-induced retinal neovascularization in mice. In this study, we evaluated whether in vivo inhibition of VEGF action could suppress retinal neovascularization in a murine model of ischemic retinopathy. VEGF-neutralizing chimeric proteins were constructed by joining the extracellular domain of either human (Flt) or mouse (Flk) high-affinity VEGF receptors with IgG. Control chimeric proteins that did not bind VEGF were also used. VEGF-receptor chimeric proteins eliminated in vitro retinal endothelial cell growth stimulation by either VEGF (P < 0.006) or hypoxic conditioned medium (P < 0.005) without affecting growth under nonstimulated conditions. Control proteins had no effect. To assess in vivo response, animals with bilateral retinal ischemia received intravitreal injections of VEGF antagonist in one eye and control protein in the contralateral eye. Retinal neovascularization was quantitated histologically by a masked protocol. Retinal neovascularization in the eye injected with human Flt or murine Flk chimeric protein was reduced in 100% (25/25; P < 0.0001) and 95% (21/22; P < 0.0001) of animals, respectively, compared to the control treated eye. This response was evident after only a single intravitreal injection and was dose dependent with suppression of neovascularization noted after total delivery of 200 ng of protein (P < 0.002). Reduction of histologically evident neovascular nuclei per 6-mu m section averaged 47% +/- 4% (P < 0.001) and 37% +/- 2% (P < 0.001) for Flt and Flk chimeric proteins with maximal inhibitory effects of 77% and 66%, respectively. No retinal toxicity was observed by light microscopy. These data demonstrate VEGF's causal role in retinal angiogenesis and prove the potential of VEGF inhibition as a specific therapy for ischemic retinal disease. C1 JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. CHILDRENS HOSP, DEPT OPHTHALMOL, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT MED, BOSTON, MA 02115 USA. GENENTECH INC, S SAN FRANCISCO, CA 94080 USA. RP JOSLIN DIABET CTR, BEETHAM EYE INST, 1 JOSLIN PL, BOSTON, MA 02215 USA. NR 31 TC 891 Z9 921 U1 4 U2 18 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 NOV 7 PY 1995 VL 92 IS 23 BP 10457 EP 10461 DI 10.1073/pnas.92.23.10457 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD890 UT WOS:A1995TD89000003 PM 7479819 ER PT J AU ZERVOS, AS FACCIO, L GATTO, JP KYRIAKIS, JM BRENT, R AF ZERVOS, AS FACCIO, L GATTO, JP KYRIAKIS, JM BRENT, R TI MXI2, A MITOGEN-ACTIVATED PROTEIN-KINASE THAT RECOGNIZES AND PHOSPHORYLATES MAX PROTEIN SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DNA-BINDING ACTIVITY; C-MYC PROTEIN; TRANSCRIPTIONAL ACTIVATION; SEQUENCE; DOMAIN; COMPLEX; GROWTH; YEAST AB We describe Mxi2, a human protein that interacts with Max protein, the heterodimeric partner of the Myc oncoprotein. Mxi2 encodes a 297-residue protein whose sequence indicates that it is related to extracellular signal-regulated kinases (ERK protein kinases). Mxi2 in yeast interacts with Max and with the C terminus of c-Myc. Mxi2 phosphorylates Max both in vitro and in vivo. The Mxi2 putative substrate recognition region has sequence similarity to the helix-loop-helix region in Max and c-Myc, suggesting that substrate recognition might be mediated via this motif. Phosphorylation by Mxi2 may affect the ability of Max to oligomerize with itself and its partners, bind DNA, or regulate gene expression. C1 MASSACHUSETTS GEN HOSP, DIABET RES LAB, BOSTON, MA 02129 USA. MASSACHUSETTS GEN HOSP, DEPT MOLEC BIOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, DEPT GENET, BOSTON, MA 02115 USA. RP HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, CUTANEOUS BIOL RES CTR, 149 13TH ST, BOSTON, MA 02129 USA. NR 35 TC 128 Z9 131 U1 0 U2 6 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 NOV 7 PY 1995 VL 92 IS 23 BP 10531 EP 10534 DI 10.1073/pnas.92.23.10531 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD890 UT WOS:A1995TD89000018 PM 7479834 ER PT J AU BROCKERHOFF, SE HURLEY, JB JANSSENBIENHOLD, U NEUHAUSS, SCF DRIEVER, W DOWLING, JE AF BROCKERHOFF, SE HURLEY, JB JANSSENBIENHOLD, U NEUHAUSS, SCF DRIEVER, W DOWLING, JE TI A BEHAVIORAL SCREEN FOR ISOLATING ZEBRAFISH MUTANTS WITH VISUAL-SYSTEM DEFECTS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PHOTORECEPTORS AB Optokinetic and phototactic behaviors of zebrafish larvae were examined for their usefulness in screening for recessive defects in the visual system, The optokinetic response can be reliably and rapidly detected in 5-day larvae, whereas the phototactic response of larvae is variable and not robust enough to be useful for screening. We therefore measured optokinetic responses of mutagenized larvae as a genetic screen for visual system defects, Third-generation larvae, representing 266 mutagenized genomes, were examined for abnormal optokinetic responses, Eighteen optokinetic defective mutants were identified and two mutants that did not show obvious morphological defects, no optokinetic response a(noa) and partial optokinetic response a (pea), were studied further, We recorded the electroretinogram (ERG) to determine whether these two mutations affect the retina, The b-wave of noa larvae was grossly abnormal, being delayed in onset and significantly reduced in amplitude, In contrast, the ERG waveform of poa larvae was normal, although the b-wave was reduced in amplitude in bright light, Histologically, the retinas of noa and poa larvae appeared normal, We conclude that noa larvae have a functional defect in the outer retina, whereas the outer retina of poa larvae is likely to be normal. C1 UNIV WASHINGTON,HOWARD HUGHES MED INST,SEATTLE,WA 98195. UNIV OLDENBURG,DEPT NEUROBIOL,D-26111 OLDENBURG,GERMANY. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. RP BROCKERHOFF, SE (reprint author), HARVARD UNIV,DEPT MOLEC & CELLULAR BIOL,BIOL LABS,16 DIVIN AVE,CAMBRIDGE,MA 02138, USA. FU NEI NIH HHS [EY00811, EY00824]; NINDS NIH HHS [NS09611] NR 17 TC 254 Z9 257 U1 2 U2 15 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 1995 VL 92 IS 23 BP 10545 EP 10549 DI 10.1073/pnas.92.23.10545 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD890 UT WOS:A1995TD89000021 PM 7479837 ER PT J AU SCHAEFER, BC STROMINGER, JL SPECK, SH AF SCHAEFER, BC STROMINGER, JL SPECK, SH TI REDEFINING THE EPSTEIN-BARR VIRUS-ENCODED NUCLEAR ANTIGEN EBNA-1 GENE PROMOTER AND TRANSCRIPTION INITIATION SITE IN GROUP-I BURKITT-LYMPHOMA CELL-LINES SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE EPSTEIN-BARR VIRUS; VIRAL LATENCY; TATA-LESS PROMOTER ID LATENTLY INFECTED LYMPHOCYTES; NASOPHARYNGEAL CARCINOMA; PROTEIN EXPRESSION; MEMBRANE-PROTEIN; RNA; DISTINCT; PRODUCER AB The Epstein-Barr virus-encoded nuclear antigen EBNA-1 gene promoter for the restricted Epstein-Barr virus (EBV) latency program operating in group I Burkitt lymphoma (BL) cell lines was previously identified incorrectly. Here we present evidence from RACE (rapid amplification of cDNA ends) cloning, reverse transcription-PCR, and S1 nuclease analyses, which demonstrates that the EBNA-1 gene promoter in group I BL cell lines is located in the viral BamHI Q fragment, immediately upstream of two low-affinity EBNA-1 binding sites. Transcripts initiated from this promoter, referred to as Qp, have the previously reported Q/U/K exon splicing pattern. Qp is active in group I BL cell lines but not in group III BL cell lines or in EBV immortalized B-lymphoblastoid cell lines. In addition, transient transfection of Qp-driven reporter constructs into both an EBV-negative BL cell line and a group I BL cell line gave rise to correctly initiated transcripts. Inspection of Qp revealed that it is a TATA-less promoter whose architecture is similar to the promoters of housekeeping genes, suggesting that Qp may be a default promoter which ensures EBNA-1 expression in cells that cannot run the full viral latency program. Elucidation of the genetic mechanism responsible for the EBNA-1-restricted program of EBV latency is an essential step in understanding control of viral latency in EBV-associated tumors. C1 WASHINGTON UNIV,SCH MED,CTR IMMUNOL,DEPT PATHOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,CTR IMMUNOL,DEPT MOLEC MICROBIOL,ST LOUIS,MO 63110. WASHINGTON UNIV,SCH MED,DIV MOLEC ONCOL,ST LOUIS,MO 63110. RP SCHAEFER, BC (reprint author), DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115, USA. OI Schaefer, Brian C/0000-0001-8877-3507 FU NCI NIH HHS [CA47557, CA43143] NR 36 TC 120 Z9 124 U1 0 U2 0 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 1995 VL 92 IS 23 BP 10565 EP 10569 DI 10.1073/pnas.92.23.10565 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD890 UT WOS:A1995TD89000025 PM 7479841 ER PT J AU DETRICH, HW KIERAN, MW CHAN, FY BARONE, LM YEE, K RUNDSTADLER, JA PRATT, S RANSOM, D ZON, LI AF DETRICH, HW KIERAN, MW CHAN, FY BARONE, LM YEE, K RUNDSTADLER, JA PRATT, S RANSOM, D ZON, LI TI INTRAEMBRYONIC HEMATOPOIETIC-CELL MIGRATION DURING VERTEBRATE DEVELOPMENT SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DEVELOPING MOUSE; RAINBOW-TROUT; YOLK-SAC; ORIGIN; EMBRYO; EMBRYOGENESIS; MUTATION; ONTOGENY; IRIDEUS; LARVAL AB Vertebrate hematopoietic stem cells are derived from ventral mesoderm, which is postulated to migrate to both extra- and intraembryonic positions during gastrula and neurula stages. Extraembryonic migration has previously been documented, but the origin and migration of intraembryonic hematopoietic cells have not been visualized. The zebrafish and most other teleosts do not form yolk sac blood islands during early embryogenesis, but instead hematopoiesis occurs solely in a dorsal location known as the intermediate cell mass (IM) of Oellacher. In this report, we have isolated cDNAs encoding zebrafish homologs of the hematopoietic transcription factors GATA-1 and GATA-2 and have used these markers to determine that the IM is formed from mesodermal cells in a posterior-lateral position on the yolk syncytial layer of the gastrula yolk sac. Surprisingly, cells of the IM then migrate anteriorly through most of the body length prior to the onset of active circulation and exit onto the yolk sac. These findings support a hypothesis in which the hematopoietic program of vertebrates is established by variations in homologous migration pathways of extra- and intraembryonic progenitors. C1 CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. NORTHEASTERN UNIV,DEPT BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT,BOSTON,MA 02115. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. OI Kieran, Mark/0000-0003-2184-7692 FU NHLBI NIH HHS [HL09061, HL48801] NR 44 TC 404 Z9 408 U1 0 U2 23 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD NOV 7 PY 1995 VL 92 IS 23 BP 10713 EP 10717 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TD890 UT WOS:A1995TD89000055 PM 7479870 ER PT J AU RALL, CJN RIVERA, JA CENTENO, BA FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL RUSTGI, AK AF RALL, CJN RIVERA, JA CENTENO, BA FERNANDEZDELCASTILLO, C RATTNER, DW WARSHAW, AL RUSTGI, AK TI PERITONEAL EXFOLIATIVE CYTOLOGY AND KI-RAS MUTATIONAL ANALYSIS IN PATIENTS WITH PANCREATIC ADENOCARCINOMA SO CANCER LETTERS LA English DT Article DE PANCREATIC ADENOCARCINOMA; CYTOLOGY; PCR; KI-RAS; PERITONEAL LAVAGE ID ONCOGENE; DIAGNOSIS; CANCER; GENE; CARCINOMAS; TUMORS AB This is the first description of the detection of pancreatic adenocarcinoma peritoneal metastasis by established radiolabeled polymerase chain reaction (PCR) based Ki-ras mutational analysis. The present study evaluates both routine cytology and Ki-ras mutational analysis in the detection of peritoneal micrometastases in 24 subjects with pancreatic adenocarcinoma compared to seven control cases of chronic pancreatitis and seven control cases of cholecystitis. Locoregional extension, vascular invasion, and distal metastases were confirmed in 21/24 (88%) of the subjects with pancreatic adenocarcinoma by computed tomography, angiography, endosonography, or laparoscopy. The most common site of histologically confirmed extrapancreatic involvement was the vasculature (29%), followed by the liver (25%), duodenum (17%), peritoneum (17%), and lymph nodes (12%). Peritoneal lavage cytology was positive in 3/24 (12%) cases of pancreatic carcinoma while Ki-ras codon 12 mutational analysis was positive in 2/24 (8%). Two histologically confirmed cases of peritoneal metastases were not detected by either methodology, while peritoneal lavage cytology detected malignant cells in one case with histologically confirmed lymph node metastasis. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. FU NCI NIH HHS [K08 CA01586-04]; NIDDK NIH HHS [DK 07191-20]; PHS HHS [43351] NR 35 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3835 J9 CANCER LETT JI Cancer Lett. PD NOV 6 PY 1995 VL 97 IS 2 BP 203 EP 211 DI 10.1016/0304-3835(95)03978-6 PG 9 WC Oncology SC Oncology GA TJ018 UT WOS:A1995TJ01800011 PM 7497464 ER PT J AU MCBLANE, JF VANGENT, DC RAMSDEN, DA ROMEO, C CUOMO, CA GELLERT, M OETTINGER, MA AF MCBLANE, JF VANGENT, DC RAMSDEN, DA ROMEO, C CUOMO, CA GELLERT, M OETTINGER, MA TI CLEAVAGE AT A V(D)J RECOMBINATION SIGNAL REQUIRES ONLY RAG1 AND RAG2 PROTEINS AND OCCURS IN 2 STEPS SO CELL LA English DT Article ID SITE-SPECIFIC RECOMBINATION; BROKEN DNA-MOLECULES; MOUSE THYMOCYTES; STRAND TRANSFER; MECHANISM; REARRANGEMENT; EXPRESSION; GENES; MICE AB Formation of double-strand breaks at recombination signal sequences is an early step in V(D)J recombination. Here we show that purified RAG1 and RAGS proteins are sufficient to carry out this reaction. The cleavage reaction can be divided into two distinct steps. First, a nick is introduced at the 5' end of the signal sequence, The other strand is then broken, resulting in a hairpin structure at the coding end and a blunt, 5'-phosphorylated signal end. The hairpin is made as a direct consequence of the cleavage mechanism. Nicking and hairpin formation each require the presence of a signal sequence and both RAG proteins. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP MCBLANE, JF (reprint author), NIDDKD,MOLEC BIOL LAB,BETHESDA,MD 20892, USA. FU NIGMS NIH HHS [GM48026] NR 32 TC 513 Z9 519 U1 0 U2 10 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD NOV 3 PY 1995 VL 83 IS 3 BP 387 EP 395 DI 10.1016/0092-8674(95)90116-7 PG 9 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TC977 UT WOS:A1995TC97700008 PM 8521468 ER PT J AU DELEO, FR NAUSEEF, WM JESAITIS, AJ BURRITT, JB CLARK, RA QUINN, MT AF DELEO, FR NAUSEEF, WM JESAITIS, AJ BURRITT, JB CLARK, RA QUINN, MT TI A DOMAIN OF P47(PHOX) THAT INTERACTS WITH HUMAN NEUTROPHIL FLAVOCYTOCHROME B(558) SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CHRONIC GRANULOMATOUS-DISEASE; RESPIRATORY BURST OXIDASE; CELL-FREE SYSTEM; NADPH OXIDASE; MICROBICIDAL OXIDASE; PLASMA-MEMBRANE; SUPEROXIDE PRODUCTION; CYTOSOLIC COMPONENTS; CYTOCHROME-B; BINDING SITE AB The NADPH-dependent oxidase of human neutrophils is a multicomponent system including cytosolic and membrane proteins. Activation requires translocation of cytosolic proteins p47(phox), p67(phox) ,and Rac2 to the plasma membrane and association with the membrane flavocytochrome b to assemble a functioning oxidase. We report the location of a region in p47(phox) that mediates its interaction with flavocytochrome b. From a random peptide phage display Library, we used biopanning with purified flavocytochrome b to select phage peptides that mimicked potential p47(phox) binding residues. Using this approach, we identified a region of p47(phox) from residue 323 to 342 as a site of interaction with flavocytochrome b. Synthetic peptides (315)SRKRLSQD-AYRRNS(328), (323)AYRRNSVRFL(332) and (334)QRRRQARPG-PQSPG(347) inhibited superoxide (O-2(radical anion)) production in the broken cell system with IC, of 18, 57, and 15 mu M, respectively. (323)AYRRNSVRFL(332) and its derivative peptides inhibited phosphorylation of p47(phox). However, the functional importance of this peptide was independent of its effects on phosphorylation, since (323)AYRRNA-VRFL(332) inhibited O-2(radical anion) production, but had no effect on phosphorylation. None of the peptides blocked O-2(radical anion) production when added after enzyme activation, suggesting that they inhibited the assembly, rather than the activity, of the oxidase. Furthermore these peptides inhibited membrane association of p47(phox), the broken cell translocation assay and O-2(radical anion) production by electropermeabilized neutrophils, thereby supporting the interpretation that this region of p47(phox) interacts with flavocytochrome b. C1 MONTANA STATE UNIV,DEPT VET MOLEC BIOL,BOZEMAN,MT 59717. MONTANA STATE UNIV,DEPT MICROBIOL,BOZEMAN,MT 59717. UNIV IOWA,IOWA CITY,IA 52242. DEPT VET AFFAIRS MED CTR,DEPT MED,IOWA CITY,IA 52242. UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. OI DeLeo, Frank/0000-0003-3150-2516 FU BLRD VA [I01 BX000513]; NIAID NIH HHS [AI20866, R01 AI020866, R37 AI020866, AI28412]; NIAMS NIH HHS [AR40929] NR 49 TC 65 Z9 65 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 NOV 3 PY 1995 VL 270 IS 44 BP 26246 EP 26251 PG 6 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TC978 UT WOS:A1995TC97800038 PM 7592831 ER PT J AU KOH, TJ WANG, TC AF KOH, TJ WANG, TC TI MOLECULAR-CLONING AND SEQUENCING OF THE MURINE GASTRIN GENE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID CELLS; DNA; PRECURSOR; TRACT AB Gastrin is a peptide hormone important in acid regulation growth of enterochromaffin cells of the oxyntic mucosa, and smooth muscle contractility. We isolated a genomic clone of gastrin from a SV-129 murine genomic library. The murine gastrin gene contains an open reading frame of 101 amino acids. The deduced amino acid sequence has 91.1% homology with the rat and 67.3% homology with the human analogue. Southern blot analysis of the murine gastrin clone gave the same restriction pattern as that seen from mouse kidney genomic DNA, consistent with this being a single copy of the gastrin gene in the mouse genome. Transfection studies demonstrated that the murine gastrin gene expression is stimulated by epidermal growth factor to the same extent as the human gastrin gene. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,BOSTON,MA 02114. FU NIDDK NIH HHS [R01 DK48077, 5T3 DK7191 D21] NR 23 TC 14 Z9 15 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 2 PY 1995 VL 216 IS 1 BP 34 EP 41 DI 10.1006/bbrc.1995.2588 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TD653 UT WOS:A1995TD65300005 PM 7488110 ER PT J AU MORO, O TSOMIDES, TJ TAJIMA, M LERNER, EA AF MORO, O TSOMIDES, TJ TAJIMA, M LERNER, EA TI MAXADILAN BINDS TO MEMBRANE-FRACTIONS OF BRAIN-TISSUE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID GENE-RELATED PEPTIDE AB Maxadilan is a potent vasodilator peptide isolated from salivary glands extracts of the hematophagous sand fly. Besides effects on the cutaneous vasculature, it has also been shown to relax rabbit aortic rings while elevating levels of cAMP. As a result of the effects on the skin and aorta, it was elected to undertake an examination of the tissue distribution of binding sites for maxadilan. In addition to specific binding in rabbit aorta and spleen, binding was detected in brain from various species including human, bovine, rabbit, rat and mouse with a kD of between 85 and 201 pM. Competitive displacement of [I-125] maxadilan by a number of known vasoconstrictor peptides, vasodilator peptides and small molecule receptor ligands did not occur in the rabbit brain preparation. These results suggest the presence of specific binding sites in mammalian tissue for maxadilan whose endogenous ligand remains unknown. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. MIT,DEPT BIOL,CAMBRIDGE,MA 02139. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. SHISEIDO LIFE SCI LAB,YOKOHAMA,KANAGAWA 236,JAPAN. FU NCI NIH HHS [T32-CA09255]; NIAMS NIH HHS [R01 AR42005] NR 13 TC 14 Z9 15 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 2 PY 1995 VL 216 IS 1 BP 234 EP 241 DI 10.1006/bbrc.1995.2615 PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TD653 UT WOS:A1995TD65300032 PM 7488094 ER PT J AU FURUSAKA, A NISHIYAMA, M NISHIMAKI, H OGASAWARA, Y TAMEMOTO, H YAMAUCHI, T TOBE, K KADOWAKI, T TANAKA, T AF FURUSAKA, A NISHIYAMA, M NISHIMAKI, H OGASAWARA, Y TAMEMOTO, H YAMAUCHI, T TOBE, K KADOWAKI, T TANAKA, T TI ORNITHINE DECARBOXYLASE INDUCTION DURING LIVER-REGENERATION IN IRS-1-DEFICIENT MICE SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID INSULIN-RECEPTOR; EXPRESSION; PHOSPHORYLATION; POLYAMINES; INITIATION; GROWTH; GENE AB We investigated the induction of ornithine decarboxylase during liver regeneration after partial hepatectomy in IRS-1-deficient mice. There were no significant differences in ODC activity or the time course of changes in ODC activity between IRS-1-deficient mice and wild-type mice. PI 3'-kinase activity showed similar increases in both groups of mice. Furthermore, ODC induction in IRS-1 transfected CHO cells was studied after stimulation by addition of FCS. The maximal ODC activity was 2.5-fold greater in IRS-1-transfected CHO cells than in control CHO cells. Our results suggest that the IRS-1 pathway may be involved in ODC induction. The absence of a difference in ODC and PI 3'-kinase activity in the regenerating liver between IRS-1-deficient mice and wild-type mice may have been related to the compensatory effects of IRS-2/pp190 [Araki et al, Nature (1994) 372, 186-190; Tobe et al. J.Biol.Chem. (1995) 270, 5698-5701]. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. JIKEI UNIV,SCH MED,DEPT NUTR,TOKYO,JAPAN. JIKEI UNIV,SCH MED,DAISAN HOSP,DEPT INTERNAL MED,TOKYO,JAPAN. UNIV TOKYO,FAC MED,DEPT INTERNAL MED 3,TOKYO,JAPAN. RP FURUSAKA, A (reprint author), MASSACHUSETTS GEN HOSP,GASTROINTESTINAL UNIT,32 FRUIT ST,BOSTON,MA 02114, USA. NR 18 TC 2 Z9 2 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD NOV 2 PY 1995 VL 216 IS 1 BP 284 EP 290 DI 10.1006/bbrc.1995.2622 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TD653 UT WOS:A1995TD65300039 PM 7488102 ER PT J AU HART, AC SIMS, S KAPLAN, JM AF HART, AC SIMS, S KAPLAN, JM TI SYNAPTIC CODE FOR SENSORY MODALITIES REVEALED BY C-ELEGANS GLR-1 GLUTAMATE-RECEPTOR SO NATURE LA English DT Article ID NEMATODE CAENORHABDITIS-ELEGANS; EXPRESSION AB How does the nervous system encode environmental stimuli as sensory experiences? Both the type (visual, olfactory, gustatory, mechanical or auditory) and the quality of a stimulus (spatial position, intensity or frequency) are represented as a neural code. Here we undertake a genetic analysis of sensory modality coding in Caenorhabditis elegans. The ASH sensory neurons respond to two distinct sensory stimuli (nose touch and osmotic stimuli). A mutation in the glr-1 (glutamate receptor) gene eliminates the response to nose touch but not to osmotic repellents. The predicted GLR-1 protein is roughly 40% identical to mammalian AMPA-class glutamate receptor (GluR) subunits. Analysis of glr-1 expression and genetic mosaics indicates that GLR-1 receptors act in synaptic targets of the ASH neurons. We propose that discrimination between the ASH sensory modalities arises from differential release of ASH neurotransmitters in response to different stimuli. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. NR 18 TC 248 Z9 256 U1 1 U2 7 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 2 PY 1995 VL 378 IS 6552 BP 82 EP 85 DI 10.1038/378082a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TC469 UT WOS:A1995TC46900055 PM 7477294 ER PT J AU KIM, E NIETHAMMER, M ROTHSCHILD, A JAN, YN SHENG, M AF KIM, E NIETHAMMER, M ROTHSCHILD, A JAN, YN SHENG, M TI CLUSTERING OF SHAKER-TYPE K+ CHANNELS BY INTERACTION WITH A FAMILY OF MEMBRANE-ASSOCIATED GUANYLATE KINASES SO NATURE LA English DT Article ID TUMOR-SUPPRESSOR PROTEIN; SEPTATE JUNCTIONS; POTASSIUM CHANNEL; NMDA RECEPTOR; NEURONS; DIVERSITY; HOMOLOG; BRAIN; GENE AB ANCHORING Of ion channels at specific subcellular sites is critical for neuronal signalling, but the mechanisms underlying channel localization and clustering are largely unknown (reviewed in ref. 1). Voltage-gated K+ channels are concentrated in various neuronal domains, including presynaptic terminals, nodes of Ranvier and dendrites, where they regulate local membrane excitability. Here we present functional and biochemical evidence that cell-surface clustering of Shaker-subfamily K+ channels is mediated by the PSD-95 family of membrane-associated putative guanylate kinases, as a result of direct binding of the carboxy-terminal cytoplasmic tails of the K+ channel subunits to two PDZ (also known as GLGF or DHR) domains in the PSD-95 protein(2). The ability of PDZ domains to function as independent modules for protein-protein interaction, and their presence in other junction-associated molecules (such as ZO-1 (ref. 3) and syntrophin(4)), suggest that PDZ-domain-containing polypeptides may be widely involved in the organization of proteins at sites of membrane specialization. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,HOWARD HUGHES MED INST,DEPT NEUROBIOL,BOSTON,MA 02114. UNIV CALIF SAN FRANCISCO,HOWARD HUGHES MED INST,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL,SAN FRANCISCO,CA 94143. UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM,SAN FRANCISCO,CA 94143. RI Kim, Eunjoon/C-1566-2011 NR 29 TC 833 Z9 847 U1 2 U2 21 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD NOV 2 PY 1995 VL 378 IS 6552 BP 85 EP 88 DI 10.1038/378085a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TC469 UT WOS:A1995TC46900056 PM 7477295 ER PT J AU GUZE, PA AF GUZE, PA TI CULTIVATING CURRICULAR REFORM SO ACADEMIC MEDICINE LA English DT Article; Proceedings Paper CT AAMCs Consensus Conference on the Education of Medical Students about Family Violence and Abuse CY MAR 28-29, 1995 CL WASHINGTON, DC SP Assoc Amer Med Coll ID MEDICAL-EDUCATION AB Since the 1960s there has been pressure to reform medical education in a more humanistic direction. One reason this has been difficult is that most medical schools have been forced to maintain themselves on resources allocated to support research and the technology of specialized tertiary care. Nevertheless, many people,believe that medical-education can still change because of changes taking place outside the sciences, such as a redefinition-of the meaning of health and the need to provide better health care to the U.S. population at a lower cost. Taking this-optimistic view will help strengthen reformers' resolve for curricular change and the incorporation of important areas such as family violence into medical students' education. There are numerous barriers to curricular change. Yet there are useful principles that can guide reform efforts, such as having an explicit rationale for the desired change, focusing on educational goals rather than on resources for their implementation, recruiting support from the departmental and school leadership, anticipating negative reactions, and recognizing the need for negotiation. There are also principles to foster successful implementation, the most important of which is to have everyone involved agree an the goals of the new program and participate in the process. The way to increase an emphasis on family violence issues is to fmd areas in the curriculum where these issues can be integrated with current teaching. Finally, a medical school curriculum on family violence does not need to be all-inclusive, but instead should prepare a good foundation so that students tan expand their knowledge and skills during residency training and medical practice. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,AFFILIATED PROGRAMS,LOS ANGELES,CA. RP GUZE, PA (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. NR 3 TC 14 Z9 14 U1 0 U2 0 PU HANLEY & BELFUS INC PI PHILADELPHIA PA 210 S 13TH ST, PHILADELPHIA, PA 19107 SN 1040-2446 J9 ACAD MED JI Acad. Med. PD NOV PY 1995 VL 70 IS 11 BP 971 EP 973 DI 10.1097/00001888-199511000-00013 PG 3 WC Education, Scientific Disciplines; Health Care Sciences & Services SC Education & Educational Research; Health Care Sciences & Services GA TF412 UT WOS:A1995TF41200018 PM 7575951 ER PT J AU CHEW, FS LANIER, L AF CHEW, FS LANIER, L TI LEARNING RADIOLOGY FROM INTERACTIVE VIDEODISCS - BAR-CODE BOOK VERSUS COMPUTER-ASSISTED-INSTRUCTION SO ACADEMIC RADIOLOGY LA English DT Article DE INTERACTIVE VIDEODISC; COMPUTER-ASSISTED INSTRUCTION AB Rationale and Objectives. We compared an interactive videodisc with bar-code book with an interactive videodisc with computer-assisted instruction for learning radiology to determine whether there would be differences in instructional effectiveness, instruction time, or subjective preference. Methods. Two different videodisc modules were created. Each was presented in two formats with identical content: bar-code book and computer-assisted instruction. In a controlled crossover experimental design, 48 fourth-year medical students were assigned one barcode book module and one computer module. Pre- and posttests were administered. Results. Mean scores improved from pretest to posttest after students used the modules in either format (P <.01). There were no significant differences between students who used the bar-code book and chose who used the computer in pretest scores, posttest scores, gains in score from pretest to posttest, or instruction time for either module. Subjectively, 74% of the students preferred computer-assisted instruction, 20% preferred bar-code book, and 7% preferred neither. Conclusion. Although bar-code book and computer versions of an interactive videodisc can be educationally equivalent, most students preferred the computer. When videodisc is being integrated into the curriculum, the choice between bar-code book and computer-assisted instruction can be made on the basis of noneducational factors such as cost and availability. C1 HARVARD UNIV,SCH MED,BOSTON,MA. UNIV FLORIDA,SCH MED,DEPT RADIOL,GAINESVILLE,FL. RP CHEW, FS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. OI Chew, Felix/0000-0003-2711-2013 NR 9 TC 4 Z9 4 U1 0 U2 0 PU ASSOC UNIV RADIOLOGISTS PI RESTON PA 1891 PRESTON WHITE DR, RESTON, VA 22091 SN 1076-6332 J9 ACAD RADIOL JI Acad. Radiol. PD NOV PY 1995 VL 2 IS 11 BP 1016 EP 1020 DI 10.1016/S1076-6332(05)80707-X PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TB333 UT WOS:A1995TB33300013 PM 9419676 ER PT J AU PAYMAN, RN WALL, C ASHBERNAL, R AF PAYMAN, RN WALL, C ASHBERNAL, R TI OTOLITH FUNCTION-TESTS IN PATIENTS WITH UNILATERAL VESTIBULAR LESIONS SO ACTA OTO-LARYNGOLOGICA LA English DT Article DE UNILATERAL VESTIBULAR DEFICIT; VESTIBULOOCULAR REFLEX; VISUAL VESTIBULAR INTERACTIONS; OTOLITH ORGANS; DYNAMIC POSTUROGRAPHY; OPTOKINETIC NYSTAGMUS; ELECTRONYSTAGMOGRAPHY VERTICAL ROTATION ID AXIS ROTATIONAL RESPONSES; DYNAMIC POSTUROGRAPHY AB This study was designed to assess the utility of otolith-ocular reflex testing in patients with complete unilateral peripheral vestibular deficits. Ten subjects were given a clinical vestibular test battery (ENG & vertical rotation) and research oriented tests of otolith function including dynamic posturography with head tilt and earth-horizontal axis rotation with otolith,visual interactions. Clinical tests confirmed the presence of a vestibular deficit and the side of the lesion. The results suggested the following: posturography during head tilt is not a reliable means of detecting unilateral peripheral vestibular dysfunction, while earth-horizontal axis rotation is a reliable means of assessing asymmetric otolith function. The Bias response during earth-horizontal axis rotation was significantly less during rotation ipsilateral to the lesioned ear compared to contralateral rotation while the Mod response was normal. The optokinetic test results in these subjects were normal while otolith-visual interactions were symmetrically reduced in these patients. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. FU NIDCD NIH HHS [DC00290]; NINDS NIH HHS [NS07268] NR 25 TC 4 Z9 4 U1 0 U2 0 PU SCANDINAVIAN UNIVERSITY PRESS PI OSLO PA PO BOX 2959 TOYEN, JOURNAL DIVISION CUSTOMER SERVICE, N-0608 OSLO, NORWAY SN 0001-6489 J9 ACTA OTO-LARYNGOL JI Acta Oto-Laryngol. PD NOV PY 1995 VL 115 IS 6 BP 715 EP 724 DI 10.3109/00016489509139392 PG 10 WC Otorhinolaryngology SC Otorhinolaryngology GA TH979 UT WOS:A1995TH97900002 PM 8749190 ER PT J AU YU, YM RYAN, CM BURKE, JF TOMPKINS, RG YOUNG, VR AF YU, YM RYAN, CM BURKE, JF TOMPKINS, RG YOUNG, VR TI RELATIONS AMONG ARGININE, CITRULLINE, ORNITHINE, AND LEUCINE KINETICS IN ADULT BURN PATIENTS SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE CONDITIONALLY INDISPENSABLE AMINO ACIDS; PROTEIN TURNOVER; METABOLISM; PLASMA FLUXES; ALPHA-KETOISOCAPROATE ID WHOLE-BODY PROTEIN; INDISPENSABLE AMINO-ACIDS; CYCLE FUNCTION; METABOLISM; TURNOVER; TRACER; INJURY; ENRICHMENT; CHILDREN; TRAUMA AB Plasma fluxes of arginine, citrulline, and leucine, and the rate of conversion of labeled citrulline to arginine (Q(cit-->arg)) were determined in nine severely burned patients (($) over bar x: 56% body surface burn area, mean 10 d postinjury) while they received total parenteral nutrition (TPN)) including an L-amino acid mixture that supplied a generous amount of nitrogen (($) over bar x: 0.39 +/- 0.02 g . kg(-1). d(-1)). Plasma fluxes were also studied in these patients during a basal state (low-dose intravenous glucose) by using a primed, 4-h constant intravenous tracer-infusion protocol. Stable-nuclide labeled tracers were L-[N-15-N-15-guanidino,5,5,H-2(2)]arginine; L-[C-13-ureido]citrulline; L-[1-C-13]leucine; and (NaHCO3)-C-13 (prime only), with blood and expired air samples drawn at intervals to determine isotopic abundance of arginine, citrulline, ornithine, and alpha-ketoisocaproate (KIC; for leucine) in plasma and (CO2)-C-13 in breath. Leucine kinetics (flux and disappearance into protein synthesis) confirmed the anticipated higher protein turnover in these burn patients compared with healthy control subjects. The plasma arginine fluxes were correspondingly higher in burn patients than in healthy control subjects. However, the citrulline flux and rate of conversion of citrulline to arginine were not higher than values obtained in our laboratories in healthy adult subjects. We hypothesize that the higher rates of arginine loss from the body after burn injury would need to be balanced by an appropriate exogenous intake of preformed arginine to maintain protein homeostasis and promote recovery from this catabolic condition. C1 MASSACHUSETTS GEN HOSP,SHRINERS BURNS INST,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,TRAUMA SERV,BOSTON,MA 02114. MIT,HUMAN NUTR LAB,CAMBRIDGE,MA 02139. FU NCRR NIH HHS [RR88]; NIDDK NIH HHS [DK 15856]; NIGMS NIH HHS [GM 02700] NR 60 TC 37 Z9 37 U1 0 U2 1 PU AMER SOC CLIN NUTRITION INC 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 NOV PY 1995 VL 62 IS 5 BP 960 EP 968 PG 9 WC Nutrition & Dietetics SC Nutrition & Dietetics GA TC135 UT WOS:A1995TC13500011 PM 7572742 ER PT J AU FRAZAO, J COBURN, JW AF FRAZAO, J COBURN, JW TI SYMPTOMATIC HYPERCALCEMIA IN A DIABETIC PATIENT UNDERGOING CONTINUOUS AMBULATORY PERITONEAL-DIALYSIS - VALUE OF BONE-BIOPSY IN THE DIAGNOSIS AND MANAGEMENT SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE HYPERCALCEMIA; DIABETES MELLITUS; CONTINUOUS AMBULATORY PERITONEAL DIALYSIS; BONE BIOPSY; OSTEITIS FIBROSA ID PARATHYROID-GLAND RESPONSIVENESS; RENAL OSTEODYSTROPHY; HEMODIALYSIS-PATIENTS; HYPOCALCEMIA; OSTEOMALACIA; FAILURE; UREMIA AB An elderly man with diabetes mellitus and end-stage renal disease managed with continuous ambulatory peritoneal dialysis (CAPD) was hospitalized with peripheral vascular insufficiency; he developed hypercalcemia and became mentally obtunded, Lowering dialysate Ca from 3.5 mEq/L to 2.5 mEq/L, stopping calcium acetate, and ultimately hemodialysis with calcium-free dialysate did not lead to reversal of the hypercalcemia or improvement of his symptoms, The intact parathyroid hormone PTH level was 187 pg/mL, a value rarely associated with significant osteitis fibrosa, A search for other causes of hypercalcemia was unrevealing, and a iliac crest bone biopsy was done, The latter showed osteitis fibrosa, and the patient underwent parathyroidectomy, The hypercalcemia reversed quickly, and his mental symptoms slowly improved, The discussion reviews the probable causes of hypercalcemia in diabetic patient undergoing CAPD with 3.5 mEq/L dialysate calcium and using calcium-containing phosphate binders, with hyperparathyroidism certainly not the usual cause, The reason for the occurrence of significant hyperparathyroidism in the face of only modest elevation of PTH is considered, The value of bone biopsy in resolution of this problem is apparent. (C) 1995 by the National Kidney Foundation, Inc. C1 W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,MED SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,WADSWORTH DIV,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. RI Frazao, Joao/J-9811-2013 OI Frazao, Joao/0000-0002-8081-5474 NR 27 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 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD NOV PY 1995 VL 26 IS 5 BP 831 EP 835 DI 10.1016/0272-6386(95)90452-2 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA TC988 UT WOS:A1995TC98800021 PM 7485141 ER PT J AU WANG, M HERCZ, G SHERRARD, DJ MALONEY, NA SEGRE, GV PEI, Y AF WANG, M HERCZ, G SHERRARD, DJ MALONEY, NA SEGRE, GV PEI, Y TI RELATIONSHIP BETWEEN INTACT 1-84-PARATHYROID-HORMONE AND BONE HISTOMORPHOMETRIC PARAMETERS IN DIALYSIS PATIENTS WITHOUT ALUMINUM TOXICITY SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Article DE OSTEODYSTROPHY; BONE; PARATHYROID HORMONE; RENAL FAILURE ID GLA-PROTEIN; PERITONEAL-DIALYSIS; RENAL-FAILURE; HEMODIALYZED PATIENTS; DISEASE; SERUM; OSTEODYSTROPHY; OSTEOCALCIN; PLASMA; PREVALENCE AB With the markedly reduced usage of aluminum salts in renal failure, parathyroid hormone (PTH) has become the major determinant of currently seen bone disease. Clinicians now must consider what PTH level should be sought, Too low a level may lead to the aplastic bone lesion (low turnover bone), and too high a level may cause osteitis fibrosa, Furthermore, conventional normal PM levels may not be a suitable target because of the well-known resistance to PTH in uremic patients. In this report, we derive the PTH levels that best distinguish patients with low and high bone formation states from those with normal bone formation in a group of 175 dialysis patients without aluminum toxicity, Using bone histological parameters, we propose that ideally PTH levels should be maintained between 10 pmol/L (100 pg/mL) and 20 to 30 pmol/L (200 to 300 pg/mL) in chronic dialysis patients, levels two to four times the upper limit of values found in normal subjects. (C) 1995 by the National Kidney Foundation, Inc. C1 VET ADM MED CTR,DEPT MED,SEATTLE,WA. UNIV WASHINGTON,SEATTLE,WA 98195. UNIV TORONTO,DEPT MED,TORONTO,ON,CANADA. MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,BOSTON,MA 02114. NR 32 TC 182 Z9 191 U1 0 U2 2 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0272-6386 J9 AM J KIDNEY DIS JI Am. J. Kidney Dis. PD NOV PY 1995 VL 26 IS 5 BP 836 EP 844 DI 10.1016/0272-6386(95)90453-0 PG 9 WC Urology & Nephrology SC Urology & Nephrology GA TC988 UT WOS:A1995TC98800022 PM 7485142 ER PT J AU LAFFEL, LMB MCGILL, JB GANS, DJ AF LAFFEL, LMB MCGILL, JB GANS, DJ TI THE BENEFICIAL EFFECT OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION WITH CAPTOPRIL ON DIABETIC NEPHROPATHY IN NORMOTENSIVE IDDM PATIENTS WITH MICROALBUMINURIA SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID URINARY ALBUMIN EXCRETION; BLOOD-GLUCOSE CONTROL; ANTIHYPERTENSIVE THERAPY; INCIPIENT NEPHROPATHY; HYPERTENSION; PROGRESSION; MELLITUS; COMPLICATIONS; PREVENTION; PREDICTOR AB PURPOSE: To determine whether angiotens-inconverting enzyme (ACE) inhibition with captopril reduces the progression of microalbuminuria to overt proteinuria in normotensive patients with insulin-dependent diabetes mellitus (IDDM). PATIENTS AND METHODS: This study was a prospective randomized, double-blind, placebo-controlled trial involving 26 centers in the United States and Canada. One hundred forty-three subjects, 14 to 57 years of age, with IDDM for 4 to 33 years, blood pressure <140/90 mm Hg in the absence of antihypertensive therapy, and persistent albumin excretion 20 to 200 mu g/min were randomized to double-blind treatment with captopril 50 mg or placebo BID. Albumin excretion rate (AER), blood pressure, and glycohemoglobin were determined every 3 months, and creatinine clearance (CrCl) and urea excretion were measured every 6 months. RESULTS: Within 24 months, 6.0% (4/67) of captopril-treated subjects and 18.6% (13/70) of placebo-treated subjects progressed to clinical proteinuria, defined as AER >200 pg/min and at least 30% above baseline (risk reduction = 67.8%, P = 0.037). AER increased-at an annual rate of 11.8% (95% confidence interval [CI] -3.3% to 29.1%) in the placebo group, while it declined by 17.9% (CI -29.6% to -4.3%) in the captopril group (P = 0.004). CrCl decreased by 4.9 mL/min per 1.73 m(2) per year in the placebo group, while it remained stable in the captopril group (0.9 mL/min per 1.73 m(2) per year, P = 0.039 between groups). Ten subjects required treatment for hypertension; 8 in the placebo group and 2 in the captopril group. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV CLIN,YOUTH UNIT,BOSTON,MA 02215. WASHINGTON UNIV,DEPT MED,DIV ENDOCRINOL,ST LOUIS,MO. BRISTOL MYERS SQUIBB CO,PRINCETON,NJ. RP LAFFEL, LMB (reprint author), HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,EPIDEMIOL & GENET UNIT,1 JOSLIN PL,BOSTON,MA 02215, USA. NR 40 TC 210 Z9 218 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD NOV PY 1995 VL 99 IS 5 BP 497 EP 504 DI 10.1016/S0002-9343(99)80226-5 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA TD979 UT WOS:A1995TD97900010 PM 7485207 ER PT J AU HARARI, D GURWITZ, JH AVORN, J CHOODNOVSKIY, I MINAKER, KL AF HARARI, D GURWITZ, JH AVORN, J CHOODNOVSKIY, I MINAKER, KL TI CORRELATES OF REGULAR LAXATIVE USE BY FRAIL ELDERLY PERSONS SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID CALCIUM-CHANNEL BLOCKERS; PARKINSONS-DISEASE; DIABETES-MELLITUS; FECAL IMPACTION; BOWEL HABITS; HUMAN COLON; CONSTIPATION; MOTILITY; HOME; ENEMAS AB PURPOSE: TO examine the demographic, clinical, and pharmacological correlates of regular laxative use in elderly persons residing in a long-term care setting. METHODS: This was a cross-sectional study using retrospective record review undertaken in an academically affiliated long-term care facility in the United States. All individuals residing in the institution for at least 1 month (n = 694) were characterized regarding use of laxatives. Regular laxative use was defined as more than 30 doses of laxatives, stool softeners, or enemas taken over the most recent 1-month period. RESULTS: Residents with regular laxative use (n = 349) were compared with those who received no laxatives (n = 227). Factors significantly associated with regular laxative use at the P <0.05 significance level were simultaneously included in a multiple logistic regression model. Factors associated with regular laxative use were immobility, Parkinson's disease, diabetes mellitus, and use of iron supplements, calcium channel blockers, and antidepressants with moderate to strong anticholinergic properties. CONCLUSION: Regular laxative use is often associated with neurologic dysfunction that directly or indirectly affects the gut, or medications known to depress colonic motility. Identification of potentially modifiable correlates of regular laxative use in older individuals may suggest management strategies to avoid or reduce laxative, stool softener, and enema requirements, improve constipation symptoms, and enhance quality of life for the frail elderly population. C1 HARVARD UNIV,SCH MED,DIV AGING,BOSTON,MA. BROCKTON W ROXBURY VET AFFAIRS MED CTR,CTR GERIATR RES EDUC & CLIN,BROCKTON,MA. HEBREW REHABIL CTR AGED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BEACON HILL GERIATR MED UNIT,BOSTON,MA. MASSACHUSETTS GEN HOSP,GEN MED UNIT,BOSTON,MA. BRIGHAM & WOMENS HOSP,DIV GERONTOL,PROGRAM ANAL CLIN STRATEGIES,BOSTON,MA. FU NIA NIH HHS [KO8 AG00510] NR 57 TC 29 Z9 29 U1 2 U2 4 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD NOV PY 1995 VL 99 IS 5 BP 513 EP 518 DI 10.1016/S0002-9343(99)80228-9 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA TD979 UT WOS:A1995TD97900012 PM 7485209 ER PT J AU MEGERIAN, CA BUSABA, NY MCKENNA, MJ OJEMANN, RG AF MEGERIAN, CA BUSABA, NY MCKENNA, MJ OJEMANN, RG TI TEFLON GRANULOMA PRESENTING AS AN ENLARGING, GADOLINIUM ENHANCING, POSTERIOR-FOSSA MASS WITH PROGRESSIVE HEARING-LOSS FOLLOWING MICROVASCULAR DECOMPRESSION SO AMERICAN JOURNAL OF OTOLOGY LA English DT Article; Proceedings Paper CT Annual Meeting of the American-Neurotology-Society CY MAY 07-08, 1994 CL PALM BEACH, FL SP Amer Neurotol Soc ID NEUROGENIC HYPERTENSION; SURGICAL-TREATMENT; ETIOLOGY; IMPLANT AB Deleterious effects of Teflon strand placement during microvascular decompression (MVD) for hemifacial spasm are rare. In this report, a patient who had previously undergone suboccipital MVD for hemifacial spasm presented 3 years postoperatively with a progressive asymmetric sensorineural hearing loss and magnetic resonance imaging evidence of an enlarging ipsilateral gadolinium enhancing 1-cm cerebellopontine angle lesion. At surgery a granuloma was found displacing the structures of the internal auditory canal. Histologically, evidence of a Teflon fiber-induced giant cell granuloma was identified. This paper reviews the literature of Teflon-induced histopathology as it relates to posterior fossa MVD surgery, as well as its relation to this previously unreported complication. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOLARYNGOL,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROSURG,BOSTON,MA. NR 25 TC 21 Z9 22 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0192-9763 J9 AM J OTOL JI Am. J. Otol. PD NOV PY 1995 VL 16 IS 6 BP 783 EP 786 PG 4 WC Otorhinolaryngology SC Otorhinolaryngology GA TD815 UT WOS:A1995TD81500013 PM 8572142 ER PT J AU BARNES, JL TORRES, ES MITCHELL, RJ PETERS, JH AF BARNES, JL TORRES, ES MITCHELL, RJ PETERS, JH TI EXPRESSION OF ALTERNATIVELY SPLICED FIBRONECTIN VARIANTS DURING REMODELING IN PROLIFERATIVE GLOMERULONEPHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GROWTH-FACTOR-BETA; MESANGIAL CELL-MIGRATION; HABU SNAKE-VENOM; EXTRACELLULAR-MATRIX; MESSENGER-RNA; GENE-EXPRESSION; COLLAGEN; REGION; RAT; LOCALIZATION AB Fibronectin (Fn) plays an important role in tissue remodeling during embryogenesis, wound repair, and vascular disease, and is thought to regulate cellular processes such as cell adhesion, migration, proliferation, and differentiation through specialized domains within the molecule. In addition, Fn can be alternatively spliced at three regions extra domains EIIIA, EIIIB,and a variable segment V, potentially giving rise to functionally distinct variants of the molecule. We have previously shown a sequential expression of cellular Tn first by platelets, followed by macrophages, then mesangial cells in habu snake venom-induced proliferative glomerulonephritis (Am J Pathol 145: 585-597, 1994) These studies examined the cellular sources and glomerular localization of Fn in general but did not distinguish between the various alternatively spliced isoforms. In this study, we examine by in situ hybridization and immunohistochemistry the temporal expression and cellular sources of EIIIA, EIIIB, and V in a model of proliferative glomerulonephritis that has cell migration, proliferation, and extracellular matrix synthesis as features of tissue remodeling. Macrophages were the first cells to express Fn mRNA showing an EIIIA(+), EIIIB(-), and V95(+) pattern beginning at 8 hours after habu snake venom injection, Migrating mesangial cells at the margins of early lesions (8 and 24 hours) dirt not overexpress mRNA encoding these En variants, but immunofluorescence microscopy revealed V95 and EIIIA protein at the margins of lesions. EIIIB was absent in lesions at this time. At 48 hours and peaking at 72 hours after habu snake venom injection, mesangial cells in central aspects of glomerular lesions expressed abundant mRNA and protein for V95 and EIIIA. EIIIB mRNA and protein was slight in the mesangium at these times. Parietal epithelial cells, particularly adjacent to glomerular lesions, also expressed abundant mRNA and protein for all three variants throughout the course of the disease, beginning at 24 hours after habu snake venom injection. Expression of mRNA and protein for all three isoforms declined by 2 weeks after habu snake venom injection. These studies show that migrating mesangial cells do not require their own synthesis of Fn and suggest that they might rely on exogenous sources of Fn, particularly V95(+) and EIIIA(+) forms. Commencement of enhanced expression of EIIIA and EIIIB mRNA and protein by resident glomerular cells coincided with the temporal course of cell proliferation, acquisition of alpha-smooth muscle cell actin phenotype, and matrix synthesis, suggesting that Fn isoforms have specific functions during the course of glomerular remodeling. C1 AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. CEDARS SINAI MED CTR,DIV PULM MED,LOS ANGELES,CA 90048. RP BARNES, JL (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT MED,DIV NEPHROL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NIDDK NIH HHS [DK 38758] NR 47 TC 48 Z9 48 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 1995 VL 147 IS 5 BP 1361 EP 1371 PG 11 WC Pathology SC Pathology GA TD741 UT WOS:A1995TD74100020 PM 7485399 ER PT J AU JOSEPH, JT LISLE, DK JACOBY, LB PAULUS, W BARONE, R COHEN, ML ROGGENDORF, WH BRUNER, JM GUSELLA, JF LOUIS, DN AF JOSEPH, JT LISLE, DK JACOBY, LB PAULUS, W BARONE, R COHEN, ML ROGGENDORF, WH BRUNER, JM GUSELLA, JF LOUIS, DN TI NF2 GENE ANALYSIS DISTINGUISHES HEMANGIOPERICYTOMA FROM MENINGIOMA SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID BRAIN-TUMOR SPECIMENS; ANGIOBLASTIC MENINGIOMA; TISSUE; CULTURE AB The histogenesis of dural-based or ''central'' hemangiopericytomas (cHPCs) remains controversial. Some authors consider these tumors variants of meningiomas while others consider them akin to peripheral hemangiopericytomas (pHPCs). Meningiomas frequently have mutations in the neurofibromatosis 2 (NF2) gene, providing a molecular marker for meningiomas and other NF2-related tumors. We therefore analyzed the NF2-related tumors. We therefor analyzed the NF2 gene in cHPCs, pHPCs, and meningiomas to determine whether cHPCs are more similar at the molecular genetic level to meningiomas or hPHCs. Using paraffin-embedded archival material from 28 cHPCs (including three primary and recurrent tumors), 10 pHPCs, and 26 meningiomas, we scanned all 17 exons of the NF2 gene and flanking intronic sequences for mutations with single strand conformation polymorphism analysis and DNA sequencing. No NF2 mutations were found in either cHPCs or pHPCs, whereas 355 of meningiomas had NF2 gene alterations (P < 0.001). The NF2 gene mutations in meningiomas were all truncating mutations, consistent with previous studies. Our findings suggest that cHPCs are distinct from meningiomas at the molecular genetic level and support prior clinico-pathological data that distinguish these tumor-entities. C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. CASE WESTERN RESERVE UNIV,DEPT PATHOL,CLEVELAND,OH 44106. UNIV WURZBURG,SCH MED,DEPT NEUROPATHOL,WURZBURG,GERMANY. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT PATHOL,HOUSTON,TX 77030. FU NCI NIH HHS [CA51410, CA57683]; NINDS NIH HHS [NS24279] NR 33 TC 37 Z9 47 U1 0 U2 1 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD NOV PY 1995 VL 147 IS 5 BP 1450 EP 1455 PG 6 WC Pathology SC Pathology GA TD741 UT WOS:A1995TD74100028 PM 7485407 ER PT J AU BEAUMIER, L CASTILLO, L AJAMI, AM YOUNG, VR AF BEAUMIER, L CASTILLO, L AJAMI, AM YOUNG, VR TI UREA CYCLE INTERMEDIATE KINETICS AND NITRATE EXCRETION AT NORMAL AND THERAPEUTIC INTAKES OF ARGININE IN HUMANS SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE UREA PRODUCTION AND EXCRETION; NITRIC OXIDE; LEUCINE; LYSINE ID NITRIC-OXIDE; DIETARY ARGININE; METABOLISM; TRACER; FATE; CITRULLINE; ENRICHMENT; INFUSION; LEUCINE; BODY AB We investigated the effects of a high dietary supplement of arginine on plasma arginine, ornithine, and leucine kinetics and on urea production and excretion in five healthy young adult men. Subjects received either 56 or 561 mg arginine . kg(-1). day(-1) for 6 days via a complete L-amino acid diet, and on day 7 a tracer protocol (first 3 h fasted; next 5 h fed) was conducted, involving primed constant intragastric infusions of L-[N-15(2)-guanidino,5,5-H-2(2)]arginine, L-[5-C-13]ornithine, L-[5,5,5-H-2(3)]leucine, and [N-15(2)]urea, with a prime of (HCO3)-C-13. Plasma arginine and ornithine fluxes increased significantly (P < 0.05) with arginine supplementation, as did the rate of conversion of plasma labeled arginine to ornithine (P < 0.05) and rate of ornithine oxidation (P < 0.001). However, absolute changes in ornithine kinetics were less than those for arginine or those based on changes expected from the change in arginine intake, implying a complex compartmentation in both whole body arginine and ornithine metabolism. The plasma NO3 concentration, daily output of total NO3, and conversion of [N-15]arginine to NO3 did not differ between the diets. Urea production and excretion were reduced significantly with arginine supplementation, suggesting an anabolic effect on the whole body nitrogen economy, possibly via the raised plasma insulin levels (P = 0.013) during the prandial phase. C1 MIT, CLIN RES CTR, CAMBRIDGE, MA 02139 USA. SHRINERS BURNS INST & TRAUMA SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, BOSTON, MA 02114 USA. MASSTRACE INC, WOBURN, MA 01801 USA. RP BEAUMIER, L (reprint author), MIT, HUMAN NUTR LAB, 40 AMES ST, BLDG E17-434, CAMBRIDGE, MA 02139 USA. FU NCRR NIH HHS [RR-88]; NIDDK NIH HHS [DK-15896]; NIGMS NIH HHS [GM-02700] NR 54 TC 70 Z9 71 U1 1 U2 2 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD NOV PY 1995 VL 269 IS 5 BP E884 EP E896 PG 13 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TF099 UT WOS:A1995TF09900013 PM 7491940 ER PT J AU CROWLEY, ST RAY, CJ NAWAZ, DF MAJACK, RA HORWITZ, LD AF CROWLEY, ST RAY, CJ NAWAZ, DF MAJACK, RA HORWITZ, LD TI MULTIPLE GROWTH-FACTORS ARE RELEASED FROM MECHANICALLY INJURED VASCULAR SMOOTH-MUSCLE CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE ANGIOPLASTY; RESTENOSIS; PROLIFERATION ID ENDOTHELIAL-CELLS; GENE-EXPRESSION; ARTERIAL INJURY; WOUND REPAIR; ANTIBODY; COLLAGENASE; ANGIOPLASTY; RESTENOSIS; INDUCTION; RECEPTOR AB Local release of mitogenic and chemotactic signals during angioplasty-induced vascular injury may initiate restenosis. We investigated whether mechanical injury to vascular smooth muscle cells (VSMC) results in the release of biologically active peptide growth factors. Monolayers of bovine SMC cultures were mechanically injured by cell scraping. Conditioned medium (CM) from control and injured SMC cultures was collected, and the mitogenic activity was measured by [H-3]thymidine incorporation in recipient SMC cultures. Mitogenic activity from injured CM was detected within 15 min after injury. When the CM from injured cells was removed 15 min after injury and replaced with serum-free media, there was no detectabe mitogenic activity in the replacement CM assessed 1-6 days postinjury. Suramin, a nonspecific peptide growth factor antagonist, significantly inhibited the mitogenic activity of injured CM. Basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF A chain), and epidermal growth factor (EGF) were detected in CM from injured cells by immunoblot analysis. The mitogenic activity of injured CM was significantly inhibited with neutralizing antibodies to bFGF (34%), PDGF-AA (32%), PDGF-BB (25%), and EGF (25%). A neutralizing antibody to tranforming growth factor (TGF)-beta had no effect. In conclusion, bFGF, PDGF, and EGF are immediately released from mechanically injured VSMC. VSMC Likely contain preformed, biologically active growth factors that are efficiently released from the cell cytoplasm following mechanical injury. Conditioned medium from injured VSMC is highly mitogenic, and this activity is probably due to multiple growth factors interacting synergistically. C1 DENVER VET AFFAIRS MED CTR, DIV CARDIOL, DENVER, CO 80220 USA. UNIV COLORADO, SCH MED, DEPT PEDIAT, DENVER, CO 80262 USA. UNIV COLORADO, SCH MED, DIV CARDIOL, DENVER, CO 80262 USA. FU NHLBI NIH HHS [HL-48177] NR 33 TC 64 Z9 66 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 1995 VL 269 IS 5 BP H1641 EP H1647 PG 7 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA TF258 UT WOS:A1995TF25800019 PM 7503260 ER PT J AU KOSTYK, SK KOUREMBANAS, S WHEELER, EL MEDEIROS, D MCQUILLAN, LP DAMORE, PA BRAUNHUT, SJ AF KOSTYK, SK KOUREMBANAS, S WHEELER, EL MEDEIROS, D MCQUILLAN, LP DAMORE, PA BRAUNHUT, SJ TI BASIC FIBROBLAST GROWTH-FACTOR INCREASES NITRIC-OXIDE SYNTHASE PRODUCTION IN BOVINE ENDOTHELIAL-CELLS SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE DIAPHORASE; BLOOD VESSELS; RETINA; AORTA; RENAL ARTERY; VASCULAR TONE ID MOLECULAR-CLONING; NADPH-DIAPHORASE; FACTOR-BETA; PROLIFERATION; LOCALIZATION; CULTURE; TUMOR AB Basic fibroblast growth factor (bFGF) and nitric oxide (NO) are expressed by endothelial cells (EC) and are involved in regulation of endothelial functions. In vivo, bFGF has a hypotensive effect which is mediated, in part, through activation of nitric oxide synthase (NOS) and the subsequent generation of NO. Thus we hypothesized that regulation of NOS in EC might be modulated by bFGF. bFGF treatment of EC in vitro resulted in increased NADPH diaphorase staining, a histochemical marker associated with the presence of NOS. Using cGMP generation in a reporter cell as a bioassay for NO release, we demonstrated that bFGF treatment of EC leads to increased production of biologically active NO. Furthermore, bFGF treatment of EC resulted in an increase in cellular content of the endothelial form of NOS as shown by Western blot analysis. Finally, Northern blot analysis was used to demonstrate that message levels of the constitutive, calcium-dependent, endothelial form of NOS is increased in EC by treatment with bFGF in vitro. These results suggest that bFGF has potential to regulate vascular tone through the modulation of levels of endothelial NOS. C1 UNIV MASSACHUSETTS, DEPT BIOL SCI, LOWELL, MA 01854 USA. CHILDRENS HOSP, DEPT SURG RES, BOSTON, MA 02115 USA. CHILDRENS HOSP, JOINT PROGRAM NEONATOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, NEUROL SERV, BOSTON, MA 02114 USA. FU NEI NIH HHS [K11 EY-00311, EY-05985]; NHLBI NIH HHS [HL-02394] NR 31 TC 55 Z9 55 U1 0 U2 1 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 1995 VL 269 IS 5 BP H1583 EP H1589 PG 7 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA TF258 UT WOS:A1995TF25800011 PM 7503252 ER PT J AU SATO, N KIUCHI, K SHEN, YT VATNER, SF VATNER, DE AF SATO, N KIUCHI, K SHEN, YT VATNER, SF VATNER, DE TI ADRENERGIC RESPONSIVENESS IS REDUCED, WHILE BASE-LINE CARDIAC-FUNCTION IS PRESERVED IN OLD ADULT CONSCIOUS MONKEYS SO AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY LA English DT Article DE SYMPATHOMIMETIC AMINES; ALPHA- AND BETA-ADRENERGIC RECEPTORS; ADENYLYL CYCLASE; PERIPHERAL VASCULAR RESISTANCE ID VASCULAR ALPHA-ADRENOCEPTORS; RECEPTOR SUBTYPES; ADENYLATE-CYCLASE; RAT MYOCARDIUM; AGE; SENSITIVITY; EXERCISE; RESPONSES; REST; CATECHOLAMINES AB To examine the physiological deficit to adrenergic stimulation with aging, five younger adult (3 +/- 1 yr old) and nine older adult (17 +/- 1 yr old) healthy monkeys were studied after instrumentation with a left ventricular (LV) pressure gauge, aortic and left atrial catheters, and aortic flow probes to measure cardiac output directly. There were no significant changes in baseline hemodynamics in conscious older monkeys. For example, an index of contractility, the first derivative of LV pressure (LV dP/dt) was similar (3,191 +/- 240, young vs. 3,225 +/- 71 mmHg/s, old) as well as in isovolumic relaxation, tau (24.3 +/- 1.7 ms, young vs. 23.0 +/- 1.0 ms, old) was similar. However, inotropic, lusitropic, and chronotropic responses to isoproterenol (Iso; 0.1 mu g/kg), norepinephrine (NE; 0.4 mu g/kg), and forskolin (For; 75 nmol/kg) were significantly (P < 0.05) depressed in older monkeys. For example, Iso increased LV dP/dt by by 146 +/- 14% in younger monkeys and by only 70 +/- 5% in older monkeys. Iso also reduced tau more in younger monkeys (-28 +/- 7%) compared with older monkeys (-13 +/- 3%). Furthermore, peripheral vascular responsiveness to Iso, NE, For, and phenylephrine (PE; 5 mu g/kg) was significantly (P < 0.05) reduced in older monkeys. For example, phenylephrine (5 mu g/kg) increased total peripheral resistence by 69 +/- 4% in younger monkeys and by only 45 +/- 3% in older monkeys. Thus in older monkeys without associated cardiovascular disease, baseline hemodynamics are preserved, but adrenergic receptor responsiveness is reduced systemically, not just in the heart. C1 NEW ENGLAND REG PRIMATE RES CTR, SOUTHBOROUGH, MA 01772 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT MED, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, CHILDRENS SERV, BOSTON, MA 02114 USA. NR 45 TC 12 Z9 13 U1 0 U2 3 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6135 J9 AM J PHYSIOL-HEART C JI Am. J. Physiol.-Heart Circul. Physiol. PD NOV PY 1995 VL 269 IS 5 BP H1664 EP H1671 PG 8 WC Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular Disease SC Cardiovascular System & Cardiology; Physiology GA TF258 UT WOS:A1995TF25800022 ER PT J AU KURREK, MM ZAPOL, WM HOLZMANN, A FILIPPOV, G WINKLER, M BLOCH, KD AF KURREK, MM ZAPOL, WM HOLZMANN, A FILIPPOV, G WINKLER, M BLOCH, KD TI IN-VIVO LIPOPOLYSACCHARIDE PRETREATMENT INHIBITS CGMP RELEASE FROM THE ISOLATED-PERFUSED RAT LUNG SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE NITRIC OXIDE; GUANOSINE 3',5'-CYCLIC MONOPHOSPHATE ID NITRIC-OXIDE SYNTHASE; ESCHERICHIA-COLI ENDOTOXIN; ENDOTHELIAL-CELLS; PULMONARY VASOCONSTRICTION; PHOSPHODIESTERASE; HYPERTENSION; LOCALIZATION; VASODILATOR; INFUSION AB Administration of bacterial lipopolysaccharide (LPS) to rats stimulates synthesis of nitric oxide (NO), a free radical molecule that activates soluble guanylate cyclase, thereby increasing intracellular guanosine 3',5'-cyclic monophosphate (cGMP) concentration and inducing systemic vasodilatation. To investigate the effect of endotoxemia on the pulmonary NO/cGMP signal transduction system, we measured the release of cGMP by isolated-perfused lungs of rats that received an intraperitoneal injection of LPS (1 mg/kg) or saline 2 days earlier. Over 90 min, 1.4 +/- 0.78 and 0.079 +/- 0.016 nmol cGMP accumulated in pulmonary perfusates of saline- and LPS-treated rats, respectively (P < 0.05). Despite addition to the perfusate of Zaprinast, superoxide dismutase, or A23187, markedly less cGMP was released from the lungs of rats exposed to LPS than from the lungs of control rats. In contrast, after ventilation with 100 parts per million NO gas, cGMP accumulating in the perfusate of the lungs of both groups of rats was markedly increased, and the quantity of cGMP released from the lungs of LPS-treated rats was similar to that released by control rat lungs (2.8 +/- 0.57 vs. 3.3 +/- 0.88 nmol P = NS). With the use of immunoblot techniques, equal concentrations of constitutive endothelial NO synthase were detected in the lungs of rats treated with saline or LPS. These results demonstrate that the NO/cGMP signal transduction system is abnormal in the lungs of rats exposed to LPS, at least in part, at the level of endothelial NO synthase activation. C1 MASSACHUSETTS GEN HOSP, DEPT ANESTHESIA, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, CARDIOVASC RES CTR, GEN MED SERV, BOSTON, MA 02114 USA. BETH ISRAEL HOSP, DEPT ANESTHESIA, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. FU NHLBI NIH HHS [HL-45895, HL-42397] NR 30 TC 17 Z9 18 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD NOV PY 1995 VL 269 IS 5 BP L618 EP L624 PG 7 WC Physiology; Respiratory System SC Physiology; Respiratory System GA TE952 UT WOS:A1995TE95200008 PM 7491980 ER PT J AU SILVERMAN, ES THOMPSON, BT QUINN, DA KINANE, TB BONVENTRE, JV HALES, CA AF SILVERMAN, ES THOMPSON, BT QUINN, DA KINANE, TB BONVENTRE, JV HALES, CA TI NA+/H+ EXCHANGE IN PULMONARY-ARTERY SMOOTH-MUSCLE FROM SPONTANEOUSLY HYPERTENSIVE AND WISTAR-KYOTO RATS SO AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY LA English DT Article DE INTRACELLULAR PH; VASCULAR REMODELING ID INTRACELLULAR PH; H+ EXCHANGE; CELLS; GROWTH; ABSENCE AB Na+/H+ exchanger regulation of intracellular pH (pH(i)) may play a key permissive role in the mitogen-induced vascular smooth muscle cell growth that occurs in systemic and pulmonary vascular remodeling. Spontaneously hypertensive rats (SHR) have increased Na+/H+ exchange in systemic vessels as well as greater systemic vascular remodeling compared with normotensive Wistar-Kyoto rats (WKY). In contrast to WKY, SHR demonstrate only mild pulmonary hypertension and no increased remodeling to hypoxia compared with WKY. We therefore wondered whether Na+/H+ exchange in pulmonary artery smooth muscle (PASM) of SHR might not be elevated compared with WKY. Baseline PHi, V-max, pK(0.5), and Hill coefficient were compared in 12- to 14-wk-old SHR and WKY PASM and aortic smooth muscle (AoSM) segments by ratio fluorescence spectroscopy. The V-max, pK(0.5), and Hill coefficient were significantly increased in SHR AoSM segments compared with WKY AoSM segments (53, 0.55, and 53%, respectively; P < 0.05). There were no differences in these values between SHR and WKY PASM segments, unlike the AoSM segments. We conclude that the Na+/H+ exchanger activity in PASM in the SHR is the same as in the WKY, which is in contrast to systemic arteries where Na+/H+ exchange is greater in the SHR. C1 MASSACHUSETTS GEN HOSP, DEPT MED, PULM CRIT CARE UNIT, BOSTON, MA 02114 USA. SHRINERS HOSP CRIPPLED CHILDREN, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT MED, RENAL UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PEDIAT, PULM UNIT, BOSTON, MA 02114 USA. FU NHLBI NIH HHS [HL-39150] NR 33 TC 12 Z9 12 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1040-0605 J9 AM J PHYSIOL-LUNG C JI Am. J. Physiol.-Lung Cell. Mol. Physiol. PD NOV PY 1995 VL 269 IS 5 BP L673 EP L680 PG 8 WC Physiology; Respiratory System SC Physiology; Respiratory System GA TE952 UT WOS:A1995TE95200016 PM 7491988 ER PT J AU CANTIELLO, HF AF CANTIELLO, HF TI ACTIN-FILAMENTS STIMULATE THE NA+-K+-ATPASE SO AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY LA English DT Article DE ACTIN CYTOSKELETON; SODIUM- AND POTASSIUM-DEPENDENT ADENOSINE-TRIPHOSPHATASE; SODIUM ION PUMP ID AMINO-ACID-SEQUENCE; (NA+ + K+)ATPASE; MUSCLE-CONTRACTION; EPITHELIAL-CELLS; F-ACTIN; BINDING; ACTIVATION; MEMBRANE; MYOSIN; POLYMERIZATION AB In this report, the functional role of actin on Na+-K+-adenosinetriphosphatase (Na+-K+-ATPase) activity was explored. The Na+- and K+-dependent, ouabain-sensitive ATP hydrolysis mediated by rat kidney Na+-K+-ATPase increased by 74% in the presence of previously unpolymerized actin (24 mu M), whereas addition of polymerized actin was without effect. Addition of actin was associated instead with an increase in the affinity of the Na+-K+-ATPase for Na+ but not other enzymatic substrates. A maximal stimulatory effect (296%) was observed either at an Na+-K+-ATPase:actin ratio of 1:50,000 or at lower ratios (1:625) by shifting from the E(2) (K+ selective) to the E(1) (Na+ selective) conformation of the enzyme. Immunoblotting of actin to the purified Na+-K+-ATPase suggested that this interaction may be linked to binding of actin to the enzyme, which was further supported by sequence analysis indicating putative actin-binding domains in the alpha-subunit of the enzyme. The interaction between actin and the Na+-K+-ATPase may imply a novel functional role of the cytoskeleton in the control of ion transport. C1 HARVARD UNIV, SCH MED, DEPT MED, BOSTON, MA 02129 USA. RP CANTIELLO, HF (reprint author), MASSACHUSETTS GEN HOSP, RENAL UNIT, 149 13TH ST, BOSTON, MA 02129 USA. NR 37 TC 56 Z9 56 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0363-6127 J9 AM J PHYSIOL-RENAL JI Am. J. Physiol.-Renal Fluid Electrol. Physiol. PD NOV PY 1995 VL 269 IS 5 BP F637 EP F643 PG 7 WC Physiology; Urology & Nephrology SC Physiology; Urology & Nephrology GA TE649 UT WOS:A1995TE64900004 PM 7503229 ER PT J AU COHEN, LS SICHEL, DA ROBERTSON, LM HECKSCHER, E ROSENBAUM, JF AF COHEN, LS SICHEL, DA ROBERTSON, LM HECKSCHER, E ROSENBAUM, JF TI POSTPARTUM PROPHYLAXIS FOR WOMEN WITH BIPOLAR DISORDER SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 147th Annual Meeting of the American-Psychiatric-Association CY MAY 21-27, 1994 CL PHILADELPHIA, PA SP Amer Psychiat Assoc ID LITHIUM PROPHYLAXIS; AFFECTIVE PSYCHOSIS; PREGNANCY; DEPRESSION; PREVALENCE; CHILDREN; MOTHERS; MANIA AB Objective: The postpartum period has typically been considered a time of heightened vulnerability for development of affective disorders, and women with bipolar disorder have consistently demonstrated vulnerability to puerperal worsening of mood. This retrospective study examined the extent to which mood-stabilizing agents provide prophylactic benefit to bipolar women during the postpartum period. Method: The clinical course of 27 women meeting the DSM-III-R criteria for bipolar disorder was followed during pregnancy and the postpartum period. Information regarding severity of illness (as measured by number of episodes of mania, depression, or both) was obtained, in addition to data on pharmacotherapy (if any) received before, during, and after pregnancy. The extent to which the prophylactic use of antimanic agents minimized the risk of relapse was explored. Results: Only one of the 14 patients taking prophylactic agents during the acute puerperium relapsed within the first 3 months postpartum, while sight of the 13 who did not receive antimanic drugs showed evidence of recurrent affective instability during those 3 months. A survival analysis indicated that the women receiving prophylactic treatment with mood stabilizers maintained well-being significantly longer than the women who did not receive such treatment. Conclusions: Women with bipolar disorder appear to benefit from puerperal prophylaxis with mood stabilizers, Consistent with results of earlier studies, postpartum prophylaxis was associated with lower rates of relapse into affective disorders. The findings have implications for the early identification and treatment of subgroups of women at particular risk for puerperal illness. C1 MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. NR 33 TC 102 Z9 104 U1 1 U2 7 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 NOV PY 1995 VL 152 IS 11 BP 1641 EP 1645 PG 5 WC Psychiatry SC Psychiatry GA TC543 UT WOS:A1995TC54300013 PM 7485628 ER PT J AU BIEDERMAN, J WILENS, T MICK, E MILBERGER, S SPENCER, TJ FARAONE, SV AF BIEDERMAN, J WILENS, T MICK, E MILBERGER, S SPENCER, TJ FARAONE, SV TI PSYCHOACTIVE SUBSTANCE USE DISORDERS IN ADULTS WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER (ADHD) - EFFECTS OF ADHD AND PSYCHIATRIC COMORBIDITY SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SEEKING COCAINE ABUSERS; 15-YEAR FOLLOW-UP; FAMILIAL ASSOCIATION; OPIATE ADDICTS; CHILD SYNDROME; ALCOHOL-ABUSE; RISK-FACTORS; BOYS; ADOLESCENTS; PATTERNS AB Objective: The authors evaluated the association between attention deficit hyperactivity disorder (ADHD) and psychoactive substance use disorders in adults with ADHD, attending to comorbidity with mood, anxiety, and antisocial disorders. It was hypothesized that psychiatric comorbidity would be a risk factor for psychoactive substance use disorders. Method: Findings for 120 referred adults with a clinical diagnosis of childhood-onset ADHD were compared with those for non-ADHD adult comparison subjects (N=268). All childhood and adult diagnoses were obtained by structured psychiatric interviews for DSM-III-R. Results: There was a significantly higher lifetime risk for psychoactive substance use disorders in the ADHD adults than in the comparison subjects (52% versus 27%). Although the two groups did not differ in the rate of alcohol use disorders, the ADHD adults had significantly higher rates of drug and drug plus alcohol use disorders than the comparison subjects. ADHD significantly increased the risk for substance use disorders independently of psychiatric comorbidity. Antisocial disorders significantly increased the risk of substance use disorders independently of ADHD status. Mood and anxiety disorders increased the risk for substance use disorders in both the ADHD and comparison subjects, but more demonstrably in the comparison subjects. Conclusion: Although psychiatric comorbidity increased the risk for psychoactive substance use disorders in adults with ADHD, by itself ADHD was a significant risk factor for substance use disorders in persons with ADHD. C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,CAMBRIDGE,MA 02138. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT,ACC 725,BOSTON,MA 02114, USA. OI Mick, Eric/0000-0001-8505-8145; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [MH-01175, MH-41314] NR 59 TC 291 Z9 295 U1 0 U2 9 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 1995 VL 152 IS 11 BP 1652 EP 1658 PG 7 WC Psychiatry SC Psychiatry GA TC543 UT WOS:A1995TC54300015 PM 7485630 ER PT J AU HAUSER, R ELREEDY, S HOPPIN, JA CHRISTIANI, DC AF HAUSER, R ELREEDY, S HOPPIN, JA CHRISTIANI, DC TI AIRWAY-OBSTRUCTION IN BOILERMAKERS EXPOSED TO FUEL-OIL ASH - A PROSPECTIVE INVESTIGATION SO AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE LA English DT Article ID FLOW-VOLUME CURVE; BRONCHIAL REACTIVITY; LUNG-FUNCTION; PERFORMANCE; VARIABILITY; QUALITY; HEALTH; OZONE AB We prospectively investigated the lower airway response in boilermakers overhauling an oil-powered boiler. We studied 26 male boilermakers with a mean age (SD) of 43.3 (8.6) yr. Pre-exposure spirometry and methacholine challenge tests were performed before beginning the boiler overhaul; postex-posure tests were performed after approximately 4 wk of work on the boiler. Exposure to particulates with an aerodynamic diameter of 10 mu m and smaller (PM(10)) and respirable vanadium dust were estimated using daily work diaries and a personal sampling device for respirable particles. Using these estimates, we calculated average and peak exposure between pre- and postexposure tests for each subject. The average PM(10) concentration ranged from 1.44 to 6.69 mg/m(3), with a mean (SD) of 3.22 (1.42) mg/m(3); the average vanadium concentration ranged from 2.2 to 31.3, with a mean (SD) of 12.2 (9.1) mu g/m(3). The mean postexposure fall in FEV(1) was 140 +/- 160 ml (p < 0.01); 24 of 26 subjects had a drop in FEV(1). For each subject, the adjusted change in FEV(1) (Delta FEV1.adj) was calculated by dividing the change in FEV(1) by the average of the pre- and postexposure FEV(1) values. The Delta FEV1.adj was regressed, controlling age and current smoking status, on average and peak exposure to both PM(10) and vanadium. There was a dose-response relationship between average and peak PM(10) exposure and Delta FEV1.adj: beta = -0.91% per mg/m(3), p = 0.08 and beta = -1.03% per mg/m(3), p = 0.03, respectively. However, there was no relationship between Delta FEV1.adj and respirable vanadium dust concentration. Furthermore, there was no postexposure change in nonspecific airway responsiveness. In summary, we found a significant fall in FEV(1) and a dose-response relationship between Delta FEV1.adj and average and peak PM(10) exposure. This across-job drop in FEV(1) was not associated with a shift in bronchial responsiveness as measured by methacholine. C1 HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,OCCUPAT HLTH PROGRAM,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT ENVIRONM HLTH,ENVIRONM SCI & ENGN PROGRAM,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. FU NIEHS NIH HHS [ES00002, ES05947, ES07069] NR 34 TC 61 Z9 62 U1 1 U2 1 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1073-449X J9 AM J RESP CRIT CARE JI Am. J. Respir. Crit. Care Med. PD NOV PY 1995 VL 152 IS 5 BP 1478 EP 1484 PG 7 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA TC861 UT WOS:A1995TC86100008 PM 7582280 ER PT J AU WELLER, PF MARSHALL, WL LUCEY, DR RAND, TH DVORAK, AM FINBERG, RW AF WELLER, PF MARSHALL, WL LUCEY, DR RAND, TH DVORAK, AM FINBERG, RW TI INFECTION, APOPTOSIS, AND KILLING OF MATURE HUMAN EOSINOPHILS BY HUMAN IMMUNODEFICIENCY VIRUS-1 SO AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY LA English DT Article ID COLONY-STIMULATING FACTOR; PROGRAMMED CELL-DEATH; FACTOR GM-CSF; CD4+ T-CELLS; BLOOD EOSINOPHILS; HIV-1 INFECTION; HUMAN-MONOCYTES; HTLV-III/LAV; SERUM IGE; HLA-DR AB Although human eosinophils express low concentrations of CD4, the capacity of mature, non-replicating eosinophils to be infected with human immunodeficiency virus-1 (HIV-I) has not been established, Using peripheral blood eosinophils isolated free of contaminating lymphocytes and mononuclear leukocytes, we evaluated eosinophil infection with HIV-1. Eosinophils could be infected with strains of HIV-I as evidenced by HIV-induced cytolytic effects, progressive release of p24 antigen in cultures of infected eosinophils, recovery of HIV from infected eosinophils by co-cultivation, and detection of HIV-I gag viral DNA from infected eosinophils by polymerase chain reaction (PCR) amplification. Greater p24 antigen release from infected eosinophils was elicited by the phorbol ester, PMA; and eosinophil killing by HIV-1 was enhanced by the cytokine GM-CSF. By light and electron microscopy, HIV-infected eosinophils demonstrated apoptosis and necrosis, Apoptotic subdiploid nuclear staining was detected by flow cytometric analyses of propidium iodide-stained nuclei from HIV-infected eosinophils, and DNA isolated from HIV-infected eosinophils showed both nucleosomal fragmentation and diffuse degradation. Thus, mature eosinophils, non-replicating terminally differentiated leukocytes, can be infected with HIV-1. HIV-1 expression in eosinophils is promoted by increased granulocyte-macrophage colony-stimulating factor (GM-CSF) and can cause eosinophils to undergo death due to apoptosis and necrosis. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CHARLES A DANA RES INST,HARVARD THORNDIKE LABS,DEPT PATHOL,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. RP WELLER, PF (reprint author), HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,CHARLES A DANA RES INST,HARVARD THORNDIKE LABS,DEPT MED,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 FU NIAID NIH HHS [AI20241, AI22571, AI33372] NR 65 TC 20 Z9 20 U1 0 U2 0 PU AMER LUNG ASSOC PI NEW YORK PA 1740 BROADWAY, NEW YORK, NY 10019 SN 1044-1549 J9 AM J RESP CELL MOL JI Am. J. Respir. Cell Mol. Biol. PD NOV PY 1995 VL 13 IS 5 BP 610 EP 620 PG 11 WC Biochemistry & Molecular Biology; Cell Biology; Respiratory System SC Biochemistry & Molecular Biology; Cell Biology; Respiratory System GA TC813 UT WOS:A1995TC81300014 PM 7576698 ER PT J AU PETERSEIN, J SAINI, S AF PETERSEIN, J SAINI, S TI FAST MR-IMAGING - TECHNICAL STRATEGIES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Review ID GRASE GRADIENT-ECHO; PULSE SEQUENCES; MP-RAGE; LIVER; FLASH; CONTRAST; MOTION; ARTIFACTS; BREATH; RARE AB Since the introduction of MR imaging for medical use in the early 1980s, there has been a continuous trend toward reduction in scan times. Whereas it took over 24 hr to acquire and display the earliest MR images [1], scan times of well under a second are now feasible. The trend toward shorter scan times is based on a need to reduce motion-related artifacts, to provide more comprehensive studies in a reasonable examination time (such as those with multiple pulse sequences, multiple planes, or contrast media), or to increase patient throughput to reduce per-patient examination costs. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 47 TC 8 Z9 8 U1 1 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1995 VL 165 IS 5 BP 1105 EP 1109 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300015 PM 7572484 ER PT J AU REYNDERS, CS WHITMAN, GJ CHEW, FS AF REYNDERS, CS WHITMAN, GJ CHEW, FS TI POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER OF THE LUNG SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP REYNDERS, CS (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. 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 NOV PY 1995 VL 165 IS 5 BP 1118 EP 1118 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300018 PM 7572486 ER PT J AU PETERSEIN, J SAINI, S MITCHELL, DG DAVIS, PL JOHNSON, CD KUHLMAN, JE PARISKY, YR RUNGE, VM WEINREB, J BERNARDINO, ME DELANGE, EE GORCZYCA, D HERFKENS, RJ SCHNALL, M AF PETERSEIN, J SAINI, S MITCHELL, DG DAVIS, PL JOHNSON, CD KUHLMAN, JE PARISKY, YR RUNGE, VM WEINREB, J BERNARDINO, ME DELANGE, EE GORCZYCA, D HERFKENS, RJ SCHNALL, M TI GADOTERIDOL-ENHANCED MR-IMAGING OF MALIGNANT HEPATIC-TUMORS - EFFECTS OF TRIPLE VERSUS STANDARD DOSES ON LESION-LIVER CONTRAST SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID CT; METASTASES; DIFFERENTIATION; HEMANGIOMAS; EXPERIENCE; NEOPLASMS AB OBJECTIVE. The purpose of this study was to compare liver signal-to-noise ratio (SNR), lesion SNR, and lesion-liver contrast-to-noise-ratio (CNR) in patients with malignant liver lesions after the administration of a standard dose (0.1 mmol/kg of body weight) or a triple dose (0.3 mmol/kg) of a gadolinium chelate (gadoteridol). We hypothesized that the higher dose would produce a higher lesion-liver CNR and therefore increase the conspicuity of hepatic lesions. MATERIALS AND METHODS. A total of 85 patients with malignant hepatic masses (61 metastases, 22 hepatocellular carcinomas, and two lymphomas) proved by histologic or follow-up studies underwent MR imaging at 1.5 T. T1-weighted spin-echo imaging and gradient-echo imaging were done before and within 1 min after (gradient echo) as well as 5 (spin echo) and 15 (spin echo) min after the injection of 0.1 or 0.3 mmol of gadoteridol per kg, randomized before the start of the study (39 patients received the standard dose, and 46 received the triple dose). The signal intensities of the liver and lesions and the SD of background noise were measured by use of regions of interest to calculate the SNR of the liver and malignant lesions and the lesion-liver CNR. RESULTS. The lesion-liver CNR was increased significantly at 5 and 15 min after the administration of gadoteridol. No significant differences in the liver SNR, lesion SNR, and lesion-liver CNR (after 1 min: standard dose, -5 +/- 8, and triple dose, -4 +/- 14; after 5 min: standard dose, -1 +/- 5, and triple dose, 2 +/- 8; and after 15 min: standard dose, 1 +/- 5, and triple dose, 6 +/- 20) were found between the doses at all time points. CONCLUSION. Triple-dose gadoteridol does not improve the lesion-liver contrast of malignant hepatic lesions over that provided by the standard dose and is not warranted for liver MR imaging. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. THOMAS JEFFERSON UNIV HOSP,DEPT RADIOL,PHILADELPHIA,PA 19107. JEFFERSON MED COLL,PHILADELPHIA,PA 19107. PRESBYTERIAN UNIV HOSP,DEPT RADIOL,PITTSBURGH,PA 15213. MAYO CLIN,DEPT RADIOL,ROCHESTER,MN 55905. UNIV SO CALIF,MED CTR,DEPT RADIOL,LOS ANGELES,CA 90039. UNIV KENTUCKY,ALBERT B CHANDLER MED CTR,DEPT RADIOL,LEXINGTON,KY 40536. NYU,MED CTR,MRI,DEPT RADIOL,NEW YORK,NY 10016. EMORY UNIV HOSP,DEPT DIAGNOST RADIOL,ATLANTA,GA 30322. UNIV VIRGINIA HOSP,MED CTR,DEPT RADIOL,CHARLOTTESVILLE,VA 22908. UNIV CALIF LOS ANGELES,MED CTR,DEPT RADIOL,LOS ANGELES,CA 90024. STANFORD UNIV,MED CTR,DEPT RADIOL,STANFORD,CA 94305. HOSP UNIV PENN,DEPT RADIOL,PHILADELPHIA,PA 19104. RP PETERSEIN, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. RI Schnall, Mitchell/D-1149-2009 NR 21 TC 7 Z9 7 U1 0 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1995 VL 165 IS 5 BP 1157 EP 1161 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300027 PM 7572495 ER PT J AU SLATER, GJ SCHAPIRO, RH ONEILL, MJ SAINI, S AF SLATER, GJ SCHAPIRO, RH ONEILL, MJ SAINI, S TI ENDOSCOPIC RETROGRADE PANCREATOGRAPHY - IMAGING FINDINGS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article; Proceedings Paper CT 95th Annual Meeting of the American-Roentgen-Ray-Society CY APR 30-MAY 05, 1995 CL WASHINGTON, DC SP Amer Roentgen Ray Soc AB Endoscopic retrograde pancreatography (ERP) is commonly used in the diagnosis and management of pancreatic disorders. The aim of this pictorial essay is to provide an overview of the common appearances of normal anatomy, anatomic variants, and pancreatic diseases at ERP. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. RP SLATER, GJ (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 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 NOV PY 1995 VL 165 IS 5 BP 1181 EP 1186 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300031 PM 7572499 ER PT J AU BROMLEY, B BENACERRAF, B AF BROMLEY, B BENACERRAF, B TI ABNORMALITIES OF THE HANDS AND FEET IN THE FETUS - SONOGRAPHIC FINDINGS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article AB This pictorial essay illustrates abnormalities of the hands and feet that sonography depicts and describes their associations with chromosomal abnormalities, syndromes, and other pathology. Examination of the extremities, although not listed in the guidelines of the American Institute of Ultrasound in Medicine for standard obstetric sonography, is a critical adjunct to fetal imaging and is needed to diagnose many syndromes. Anomalies of the hands and feet may involve ail limbs or be focal, involving a single distal ray. Although this essay focuses on defects of the hands and feet, these defects are often part of more global defects that include the rest of the limb as well. For this reason, anomalies of the limbs that relate primarily to defects of the hands and feet will also be demonstrated. Evaluation of the hands and feet is an important part of the structural survey of the fetus at all gestational ages, as it provides an adjunct to the diagnosis of many syndromes, including chromosomal abnormalities. Even isolated limb anomalies may be important to diagnose antenatally so that proper care can be instituted postnatally for families and their newborns. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. RP BROMLEY, B (reprint author), DIAGNOST ULTRASOUND ASSOCIATES,333 LONGWOOD AVE,BOSTON,MA 02115, USA. NR 8 TC 22 Z9 22 U1 1 U2 1 PU AMER ROENTGEN RAY SOC PI RESTON PA 1891 PRESTON WHITE DR SUBSCRIPTION FULFILLMENT, RESTON, VA 22091 SN 0361-803X J9 AM J ROENTGENOL JI Am. J. Roentgenol. PD NOV PY 1995 VL 165 IS 5 BP 1239 EP 1243 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300043 PM 7572511 ER PT J AU HAHN, PF EISENBERG, PJ PITMAN, MB GAZELLE, GS MUELLER, PR AF HAHN, PF EISENBERG, PJ PITMAN, MB GAZELLE, GS MUELLER, PR TI CYTOPATHOLOGIC TOUCH PREPARATIONS (IMPRINTS) FROM CORE NEEDLE BIOPSIES - ACCURACY COMPARED WITH THAT OF FINE-NEEDLE ASPIRATES SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID GUNS AB OBJECTIVE. The aim of this study was to evaluate the touch preparation (imprint) cytology method for obtaining rapid interpretations from core material obtained during abdominal percutaneous biopsy. SUBJECTS AND METHODS. For 28 patients undergoing biopsy of abdominal masses, paired slides were prepared for rapid staining by use of smears of standard fine-needle aspirates and by use of a touch preparation of the core material obtained with a semiautomated biopsy gun. The slides were scored in comparison with the final cytopathologic and histopathologic diagnosis. RESULTS. Touch preparation slides were equivalent in diagnostic yield to fine needle aspirate smears, demonstrating similar cellular features. Touch preparation slides revealed features of tumor architecture not present on smears. CONCLUSION. Touch preparation cytology offers rapid diagnosis from a single core biopsy sample. Carefully performed, the touch preparation method preserves the core material for subsequent permanent fixation and sectioning. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02114. RP HAHN, PF (reprint author), HARVARD UNIV,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 13 TC 37 Z9 39 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 NOV PY 1995 VL 165 IS 5 BP 1277 EP 1279 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300050 PM 7572518 ER PT J AU KAUFMAN, JA GELLER, SC RIVITZ, SM WALTMAN, AC AF KAUFMAN, JA GELLER, SC RIVITZ, SM WALTMAN, AC TI OPERATOR ERRORS DURING PERCUTANEOUS PLACEMENT OF VENA-CAVA FILTERS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Article ID GREENFIELD AB Operator errors during percutaneous insertion of inferior vena cava (IVC) filters are procedural complications specific to filter placement that cannot be attributed to defects in the device itself. These errors can occur during preplacement imaging of the IVC, selection of the filter, or deployment of the filter. Although technical problems are reported to occur in 5-20% [1] of filter insertions, the precise frequency of operator errors is not known. This pictorial essay reviews the different types of operator errors that can occur during percutaneous insertion of IVC filters. RP KAUFMAN, JA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 9 TC 20 Z9 22 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 NOV PY 1995 VL 165 IS 5 BP 1281 EP 1287 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TA733 UT WOS:A1995TA73300051 PM 7572519 ER PT J AU MALUF, HM KOERNER, FC AF MALUF, HM KOERNER, FC TI SOLID PAPILLARY CARCINOMA OF THE BREAST - A FORM OF INTRADUCTAL CARCINOMA WITH ENDOCRINE DIFFERENTIATION FREQUENTLY ASSOCIATED WITH MUCINOUS CARCINOMA SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE PAPILLARY CARCINOMA; MUCINOUS CARCINOMA; INTRADUCTAL CARCINOMA; MUCOCELE; ENDOCRINE ID ATYPICAL DUCTAL HYPERPLASIA; MORPHOLOGIC FEATURES; MUCOID CARCINOMA; LESIONS; TUMORS; BENIGN; PURE AB We report 20 examples of a distinctive form of intraductal papillary carcinoma frequently associated with both mucinous carcinoma and infiltrating ductal carcinoma, not otherwise specified. All the patients were in the seventh decade of life or older. The clinical presentation and macroscopic appearance suggested a benign lesion in most cases, The tumors grew in a solid papillary pattern and displayed low-grade cytological features as well as intracellular and extracellular mucin. Endocrine differentiation was demonstrated by the Grimelius stain in 11 of 17 cases and by the chromogranin immunohistochemical technique in eight of 14 cases. Lymph node metastases were not observed, but pulmonary metastasis occurred in one case. All the tumors were positive for estrogen receptors. We postulate that these lesions are the preinvasive counterpart of mucinous carcinomas with endocrine differentiation. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. RP MALUF, HM (reprint author), VET ADM MED CTR,PATHOL & LAB MED SERV 113,DEPT PATHOL,1030 FEFFERSON AVE,MEMPHIS,TN 38104, USA. NR 28 TC 110 Z9 126 U1 0 U2 2 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 NOV PY 1995 VL 19 IS 11 BP 1237 EP 1244 DI 10.1097/00000478-199511000-00003 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA TA130 UT WOS:A1995TA13000003 PM 7573685 ER PT J AU NIELSEN, GP OCONNELL, JX DICKERSIN, GR ROSENBERG, AE AF NIELSEN, GP OCONNELL, JX DICKERSIN, GR ROSENBERG, AE TI CHONDROID LIPOMA, A TUMOR OF WHITE FAT-CELLS - A BRIEF REPORT OF 2 CASES WITH ULTRASTRUCTURAL ANALYSIS SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE CHONDROID LIPOMA; LIPOMA AB Chondroid lipoma is a recently described variant of lipoma with unusual morphologic features, Although classified as a fatty neoplasm, its phenotype is uncertain because it has not been determined whether cartilage is a real component or only simulated by light microscopy and whether the adipocytes demonstrate white or brown fat differentiation, issues that can be resolved only by electron microscopy. We present two cases of chondroid lipoma that ultrastructurally showed abundant intracytoplasmic lipid and glycogen and numerous pinocytotic vesicles, characteristic of white adipocytes. These findings support the conclusion that these tumors are composed solely of fat without true cartilage differentiation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. UNIV VANCOUVER HOSP,DEPT PATHOL,VANCOUVER,BC,CANADA. HLTH SCI CTR,VANCOUVER,BC,CANADA. NR 6 TC 18 Z9 20 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD NOV PY 1995 VL 19 IS 11 BP 1272 EP 1276 DI 10.1097/00000478-199511000-00007 PG 5 WC Pathology; Surgery SC Pathology; Surgery GA TA130 UT WOS:A1995TA13000007 PM 7573689 ER PT J AU BEUTLER, AM SCHUMACHER, HR WHITTUMHUDSON, JA SALAMEH, WA HUDSON, AP AF BEUTLER, AM SCHUMACHER, HR WHITTUMHUDSON, JA SALAMEH, WA HUDSON, AP TI IN-SITU HYBRIDIZATION FOR DETECTION OF INAPPARENT INFECTION WITH CHLAMYDIA-TRACHOMATIS IN SYNOVIAL TISSUE OF A PATIENT WITH REITERS-SYNDROME SO AMERICAN JOURNAL OF THE MEDICAL SCIENCES LA English DT Note DE CHLAMYDIAL INFECTION; REITERS SYNDROME; IN SITU HYBRIDIZATION; SYNOVIUM ID INSITU DNA HYBRIDIZATION; REACTIVE ARTHRITIS; CULTURE; DISEASE; WOMEN; INFERTILITY; CRITERIA; ANTIBODY; SMEARS; ACID AB The authors have shown that protein antigens, RNA, and DNA from Chlamydia trachomatis are present in synovial tissues of patients with Reiter's syndrome (RS). However, those studies gave no insight into the host cell type involved or the precise tissue location of the bacteria, To address such issues, the authors developed an in situ hybridization system to detect chlamydia, and they used that system to examine synovial biopsies from a patient with RS and a patient without RS. The in situ system uses a previously described digoxigenin-labeled DNA probe that hybridizes with chlamydial 16S rRNA sequences in paraformaldehyde-fixed samples. Control studies with chlamydia-infected and uninfected HeLa cells confirmed that the in situ system is as sensitive as is direct fluorescence cytology for detection of the organism. Morphology of host and chlamydia cells is preserved after hybridization. Studies using synovial tissue from an osteoarthritis patient produced no in hybridization signal, but similar hybridization to tissue from a culture-/direct fluorescence cytology- negative RS patient had a strong intracellar signal for chlamydia within a subsynovial cell layer. These in situ hybridization results confirm the extensive presence of chlamydia in synovia and extend the authors' earlier observation that chlamydial RNA is present in the synovia of patients with RS, The data also confirm their electron microscopy studies, indicating that chlamydia are intracellular in synovial tissue, and they further show that infected host cells are located beneath the synovial lining. C1 DEPT VET AFFAIRS MED CTR,MED RES SERV,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT MED,DIV RHEUMATOL,PHILADELPHIA,PA. DEPT VET AFFAIRS MED CTR,CTR ARTHRIT & IMMUNOL,PHILADELPHIA,PA 19104. TEMPLE UNIV,SCH MED,DEPT OBSTET & GYNECOL,DIV REPROD ENDOCRINOL,PHILADELPHIA,PA. MED COLL PENN,DEPT MICROBIOL & IMMUNOL,PHILADELPHIA,PA 19129. JOHNS HOPKINS UNIV,SCH MED,WILMER INST,BALTIMORE,MD 21205. FU NEI NIH HHS [EY-O3324]; NIAMS NIH HHS [AR-42541] NR 38 TC 39 Z9 39 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0002-9629 J9 AM J MED SCI JI Am. J. Med. Sci. PD NOV PY 1995 VL 310 IS 5 BP 206 EP 213 DI 10.1097/00000441-199511000-00006 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA TD448 UT WOS:A1995TD44800006 PM 7485225 ER PT J AU FARRER, LA CUPPLES, LA VANDUIJN, CM KURZ, A ZIMMER, R MULLER, U GREEN, RC CLARKE, V SHOFFNER, R WALLACE, DC CHUI, H FLANAGAN, SD DUARA, R STGEORGEHYSLOP, P AUERBACH, SA VOLICER, L WELLS, JM VAN BROECKHOVEN, C GROWDON, JH HAINES, JL AF FARRER, LA CUPPLES, LA VANDUIJN, CM KURZ, A ZIMMER, R MULLER, U GREEN, RC CLARKE, V SHOFFNER, R WALLACE, DC CHUI, H FLANAGAN, SD DUARA, R STGEORGEHYSLOP, P AUERBACH, SA VOLICER, L WELLS, JM VAN BROECKHOVEN, C GROWDON, JH HAINES, JL TI APOLIPOPROTEIN-E GENOTYPE IN PATIENTS WITH ALZHEIMERS-DISEASE - IMPLICATIONS FOR THE RISK OF DEMENTIA AMONG RELATIVES SO ANNALS OF NEUROLOGY LA English DT Article ID 1ST-DEGREE RELATIVES; E TYPE-4; ONSET; GENE; POPULATION; MUTATION; ALLELE; AGE; TRANSMISSION; SEGREGATION AB Numerous studies have shown that the risk of Alzheimer's disease (AD) is associated with the dose of the epsilon 4 allele of apolipoprotein E (ApoE). However, more than one third of AD patients lack epsilon 4 and many persons having epsilon 4 survive cognitively intact to old age. We evaluated the lifetime risk of disease in 3,999 first-degree relatives of 549 probands who met the criteria for probable or definite AD and whose ApoE genotypes were known. ApoE genotypes for relatives were not determined. After age 65 the risk among relatives was proportional, as much as 7 to 10% at age 85, to the number of epsilon 4 alleles present in the proband. Risks to relatives of ApoE 2/2 and 2/3 probands were nearly identical at all ages to risks for relatives of ApoE 3/3 probands. The expected proportion of relatives having at least one epsilon 4 allele was calculated for each genotype group based on the distribution of parents, sibs, and offspring in the sample. Among relatives ia the ApoE 3/3 group, the lifetime risk for AD by age 90 was three times greater than the expected proportion of epsilon 4 carriers, suggesting that factors other than ApoE contribute to AD susceptibility. Furthermore, the 44% risk of AD by age 93 among relatives of ApoE 4/4 probands indicates that as many as 50% of people having at least one epsilon 4 allele do not develop AD. We also found that among male relatives, risk of AD in the ApoE 3/4 group was similar to that for the ApoE 3/3 group but significantly less than the risk for the ApoE 4/4 group. In contrast, among female relatives the risk for the ApoE 3/4 group was nearly twice that for the ApoE 3/3 group and identical to the risk for the ApoE 4/4 group. These findings are consistent with a sex-modification effect of the E4 isoform on disease susceptibility. C1 BOSTON UNIV, SCH MED, DEPT BIOSTAT & EPIDEMIOL, BOSTON, MA 02118 USA. HARVARD UNIV, SCH MED, DEPT NEUROL, BOSTON, MA 02115 USA. ERASMUS UNIV ROTTERDAM, DEPT EPIDEMIOL & BIOSTAT, 3000 DR ROTTERDAM, NETHERLANDS. TECH UNIV MUNICH, PSYCHIAT KLIN, W-8000 MUNICH, GERMANY. UNIV GIESSEN, INST HUMANGENET, W-6300 GIESSEN, GERMANY. EMORY UNIV, DEPT NEUROL, ATLANTA, GA 30322 USA. EMORY UNIV, DEPT MOLEC BIOL & GENET, ATLANTA, GA 30322 USA. UNIV SO CALIF, LOS ANGELES, CA USA. BECKMAN RES INST CITY HOPE, DUARTE, CA USA. UNIV MIAMI, SCH MED, MIAMI, FL USA. UNIV TORONTO, DEPT NEUROL, TORONTO, ON, CANADA. EDITH NOURSE ROGERS MEM VET ADM HOSP, CTR GERIATR RES EDUC & CLIN, BEDFORD, MA 01730 USA. UNIV ANTWERP, BORN BUNGE LAB, NEUROGENET LAB, B-2020 ANTWERP, BELGIUM. MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET UNIT, BOSTON, MA 02114 USA. RP FARRER, LA (reprint author), BOSTON UNIV, SCH MED, DEPT NEUROL, BOSTON, MA 02118 USA. RI Haines, Jonathan/C-3374-2012; OI Farrer, Lindsay/0000-0001-5533-4225 FU NIA NIH HHS [R01-AG09029, P30-AG10130, R01-AG11503, U24 AG021886] NR 63 TC 75 Z9 77 U1 0 U2 3 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0364-5134 EI 1531-8249 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 1995 VL 38 IS 5 BP 797 EP 808 DI 10.1002/ana.410380515 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TE955 UT WOS:A1995TE95500014 PM 7486872 ER PT J AU HANSEN, M SCHOFIELD, DE BENACERAFF, BR MULLIKEN, JB AF HANSEN, M SCHOFIELD, DE BENACERAFF, BR MULLIKEN, JB TI LARGE NASAL TIP TERATOMA SO ANNALS OF PLASTIC SURGERY LA English DT Article ID CHILDHOOD AB Congenital teratoma rarely occurs in the craniofacial region. We present an infant with a nasal tip teratoma that was documented by ultrasonographic examination. The tumor was excised at 1 day of life, and the splayed upper and lower lateral cartilages were apposed primarily. The remaining redundant skin was excised in a second stage. To our knowledge, this is the first reported case of a nasal tip teratoma. C1 CHILDRENS HOSP,DIV PLAST SURG,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. NR 10 TC 6 Z9 6 U1 0 U2 0 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0148-7043 J9 ANN PLAS SURG JI Ann. Plast. Surg. PD NOV PY 1995 VL 35 IS 5 BP 522 EP 524 DI 10.1097/00000637-199511000-00014 PG 3 WC Surgery SC Surgery GA TF257 UT WOS:A1995TF25700017 PM 8579273 ER PT J AU PIERSON, RN MATHISEN, DJ AF PIERSON, RN MATHISEN, DJ TI PEDICLED PERICARDIAL PATCH REPAIR OF A CARINAL BRONCHOGENIC CYST SO ANNALS OF THORACIC SURGERY LA English DT Note AB Bronchogenic cysts should be completely removed. Small communications with the tracheobronchial tree occur, but extensive involvement is rare. A case of bronchogenic cyst replacing the carina and the medial wall of the right and left main bronchi is presented. Resection and reconstruction was accomplished by using a pedicled pericardial patch to close the defect created by removal of the bronchogenic cyst. Follow-up at 2 years shows an excellent result. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 3 TC 5 Z9 5 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0003-4975 J9 ANN THORAC SURG JI Ann. Thorac. Surg. PD NOV PY 1995 VL 60 IS 5 BP 1419 EP 1421 DI 10.1016/0003-4975(95)00621-Q PG 3 WC Cardiac & Cardiovascular Systems; Respiratory System; Surgery SC Cardiovascular System & Cardiology; Respiratory System; Surgery GA TE956 UT WOS:A1995TE95600053 PM 8526645 ER PT J AU LOCASCIO, JJ GROWDON, JH CORKIN, S AF LOCASCIO, JJ GROWDON, JH CORKIN, S TI COGNITIVE TEST-PERFORMANCE IN DETECTING, STAGING, AND TRACKING ALZHEIMERS-DISEASE SO ARCHIVES OF NEUROLOGY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; SENILE DEMENTIA; MEMORY IMPAIRMENT; NEUROPSYCHOLOGICAL MEASURES; NEUROFIBRILLARY TANGLES; HIPPOCAMPAL-FORMATION; SEMANTIC NETWORK; ENTORHINAL AREA; SYNAPSE LOSS; PLAQUES AB Objectives: To identify the specific cognitive deficits that characterize Alzheimer's disease (AD) and determine which cognitive tests, or combination of tests, are best for detecting AD (ie, distinguishing patients with AD from normal control subjects), staging AD (ie, distinguishing different severities of dementia), and tracking disease progression. Subjects: Patients with AD (n=123) and normal control subjects (n=60) of comparable age, education, and gender distribution. Setting: Outpatient care. Measures: Ten cognitive tests of memory, language, visuospatial abilities, and reasoning; the Information, Memory and Concentration subtest of the Blessed Dementia Scale,and the total score on an activities of daily living questionnaire. Design: Patients with AD were tested every 6 to 24 months over a span of up to 5.5 years. Results: Patients with AD were significantly inferior to normal control subjects on all cognitive tests. The scores of patients with AD worsened over time. Delayed recall of stories and figures showed sharp deterioration to an early floor, consistent with the finding that these tests discriminated patients with mild AD from normal control subjects well but were poor for staging. Confrontation naming, semantic fluency, and immediate recognition of geometric figures showed steady linear decline across time for patients with AD, consistent with these tests being found best for staging dementia severity. Conclusions: We postulate that the pathologic bases of impairment in delayed recall are atrophy of cholinergic ventral forebrain neurons and partial deafferentation of the hippocampus, both of which occur early in the course of AD. Worsening language and visuospatial abilities likely reflect progressive loss of neocortical neurons and their connections. C1 MIT,CLIN RES CTR,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. RP LOCASCIO, JJ (reprint author), MIT,DEPT BRAIN & COGNIT SCI,E10-003A,CAMBRIDGE,MA 02139, USA. FU NIA NIH HHS [5-R37-AG06605, AG06605, AG05134] NR 81 TC 166 Z9 167 U1 3 U2 7 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 NOV PY 1995 VL 52 IS 11 BP 1087 EP 1099 PG 13 WC Clinical Neurology SC Neurosciences & Neurology GA TD686 UT WOS:A1995TD68600011 PM 7487561 ER PT J AU PAVANLANGSTON, D YAMAMOTO, S DANKEL, EC AF PAVANLANGSTON, D YAMAMOTO, S DANKEL, EC TI DELAYED HERPES-ZOSTER PSEUDODENDRITES - POLYMERASE CHAIN-REACTION DETECTION OF VIRAL-DNA AND A ROLE FOR ANTIVIRAL THERAPY SO ARCHIVES OF OPHTHALMOLOGY LA English DT Article ID VIRUS-DNA; OPHTHALMICUS; KERATITIS; COMPLICATIONS AB Background: The late-onset pseudodendrites, delayed corneal mucous plaques, of herpes tester ophthalmicus are reported to be of mechanical or immune origin and to be worsened by antiviral therapy. Objective: To study pseudodendrites to ascertain a viral presence in the lesions and their response to antiviral therapy. Design: Prospective clinical study. Setting: Outpatient and inpatient hospital-based corneal specialty referral practice; molecular virology laboratory. Patients: Six patients, aged 33 to 89 years, four with delayed herpes tester ophthalmicus pseudodendrites and two with herpes tester ophthalmicus neurotrophic ulceration. One patient was immunosuppressed. Main Outcome Measures: Findings from clinicalevaluation; polymerase chain reaction assays of lesions and tear film of six patients; polymerase chain reaction and light and electron microscopy of the corneal button from one patient; and the clinical response of four patients to various antiviral drugs. Results: In contrast to reports in the current literature, Delayed pseudodendrites may also be infectious, as they are positive for tester DNA by polymerase chain reaction and appear responsive to certain antiviral therapy. The corneal button from an immunosuppressed patient had mature and immature viral particles in the basal cells within 2 weeks of transplantation. Conclusions: To our knowledge, this is the first report of viral DNA in delayed tester pseudodendrites. Recurrent viral infection may play a role in this form of tester keratopathy and warrant antiviral therapy. C1 HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. OSAKA UNIV,SCH MED,DEPT OPHTHALMOL,SUITA,OSAKA,JAPAN. SCHEPENS EYE RES INST,BOSTON,MA. RP PAVANLANGSTON, D (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,243 CHARLES ST,BOSTON,MA 02114, USA. FU NEI NIH HHS [R0-1-EY06584]; PHS HHS [N01-A1-15100] NR 18 TC 35 Z9 35 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 NOV PY 1995 VL 113 IS 11 BP 1381 EP 1385 PG 5 WC Ophthalmology SC Ophthalmology GA TD680 UT WOS:A1995TD68000019 PM 7487598 ER PT J AU GLIKLICH, RE LAURETANO, AM AF GLIKLICH, RE LAURETANO, AM TI THE RISK OF NASAL OSTEOTOMIES AFTER ETHMOID SINUS SURGERY SO ARCHIVES OF OTOLARYNGOLOGY-HEAD & NECK SURGERY LA English DT Article ID ENDOSCOPIC INTRANASAL ETHMOIDECTOMY; COMPLICATIONS SECONDARY; RHINOPLASTY AB Objective: To assess whether there is an increased risk of osteotomies causing fractures that extend into the orbit or cranial base in patients who undergo ethmoid sinus surgery. Design: Anatomic investigation in a cadave rmodel. Methods: Twenty-eight medial and lateral osteotomies were performed in 14 fresh-frozen cadaver heads after bilateral sphenoethmoidectomies (endoscopic technique, n=26; external technique, n=2). Anatomic examination performed by inspection after removal of dorsal nasal skin followed by rigid endoscopic intranasal examination. Results: Complete osteotomies were obtained in every case. There were no major comminutions along the osteotomies, but there was a 25% rate of minor comminutions. In no case did fractures extend into either the orbit or the base of the skull. In every case, the path of the osteotome was separated from the ethmoid surgical cavity by a relatively thick buttress of bone composed of the anterior lacrimal crest and the ascending process of the maxilla. The enlarged maxillary ostia created by the sinus surgery was not altered by the osteotomies or by dorsal narrowing. Conclusions: Nasal osteotomies can be performed with minimal risk of comminution or uncontrolled extension of the fracture lines following extensive ethmoid and sphenoid sinus surgery. These findings may not apply in patients with preexisting injuries or when osteotomies do not preserve the triangular nasal buttress. C1 BRIGHAM & WOMENS HOSP,DIV OTOLARYNGOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA. RP GLIKLICH, RE (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT OTOLARYNGOL,DIV FACIAL PLAST & RECONSTRUCT SURG,BOSTON,MA 02114, USA. NR 18 TC 2 Z9 2 U1 0 U2 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0886-4470 J9 ARCH OTOLARYNGOL JI Arch. Otolaryngol. Head Neck Surg. PD NOV PY 1995 VL 121 IS 11 BP 1315 EP 1318 PG 4 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TD683 UT WOS:A1995TD68300017 PM 7576482 ER PT J AU SCULLY, RE HENSON, DE NIELSEN, ML RUBY, SG AF SCULLY, RE HENSON, DE NIELSEN, ML RUBY, SG TI PRACTICE PROTOCOL FOR THE EXAMINATION OF SPECIMENS REMOVED FROM PATIENTS WITH OVARIAN-TUMORS - A BASIS FOR CHECKLISTS SO ARCHIVES OF PATHOLOGY & LABORATORY MEDICINE LA English DT Article ID PROGNOSTIC-SIGNIFICANCE; CELL TUMORS; CANCER; BORDERLINE; CARCINOMA C1 NCI,DIV CANC PREVENT & CONTROL,EARLY DETECT BRANCH,BETHESDA,MD 20892. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HINSDALE HOSP,DEPT PATHOL & LAB MED,HINSDALE,IL. NR 41 TC 11 Z9 11 U1 0 U2 2 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 NOV PY 1995 VL 119 IS 11 BP 1012 EP 1022 PG 11 WC Medical Laboratory Technology; Medicine, Research & Experimental; Pathology SC Medical Laboratory Technology; Research & Experimental Medicine; Pathology GA TF276 UT WOS:A1995TF27600011 PM 7487401 ER PT J AU CARROLL, JC NELSON, VS HURVITZ, EA PRIEBE, M AF CARROLL, JC NELSON, VS HURVITZ, EA PRIEBE, M TI HOME MECHANICAL VENTILATION IN MITOCHONDRIAL ENCEPHALOMYOPATHY SYNDROME SO ARCHIVES OF PHYSICAL MEDICINE AND REHABILITATION LA English DT Note ID STROKE-LIKE EPISODES; LACTIC-ACIDOSIS; MYOPATHY; ENCEPHALOPATHY; DNA AB Long-term home mechanical ventilation of children has only recently become more practically feasible and ethically acceptable by the medical community. It has been particularly controversial in cases of degenerative myopathies in which quality of life has been questioned. There are no reports in the literature of long-term home mechanical ventilation of a child with mitochondrial encephalomyopathy (MELAS) syndrome despite the many descriptions of possible etiologies of the concomitant respiratory failure. The patient reported here has used home mechanical ventilation for 6 years with few medical complications, no hospitalizations in the past 3 years, and increased function in activities of daily living. Despite the ill-defined nature of the disease and uncertain prognosis, we believe that long-term home mechanical ventilation of children with early onset MELAS syndrome is a viable option for both patients and their families and results in overall improvement in quality of life for the patient. (C) 1995 by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation. C1 UNIV MICHIGAN,MED CTR,DEPT PHYS MED & REHABIL,ANN ARBOR,MI 48109. UNIV MICHIGAN,MED CTR,DEPT PEDIAT & COMMUNICABLE DIS,ANN ARBOR,MI 48109. ANNA ARBOR MED CTR,DEPT VET AFFAIRS,ANN ARBOR,MI. DEPT VET AFFAIRS MED CTR,BAYLOR COLL MED,DEPT PHYS MED & REHABIL,HOUSTON,TX. NR 20 TC 1 Z9 1 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0003-9993 J9 ARCH PHYS MED REHAB JI Arch. Phys. Med. Rehabil. PD NOV PY 1995 VL 76 IS 11 BP 1014 EP 1016 DI 10.1016/S0003-9993(95)81040-4 PG 3 WC Rehabilitation; Sport Sciences SC Rehabilitation; Sport Sciences GA TB712 UT WOS:A1995TB71200008 PM 7487448 ER PT J AU MATSUSHITA, M EZEKOWITZ, RAB FUJITA, T AF MATSUSHITA, M EZEKOWITZ, RAB FUJITA, T TI THE GLY-54-]ASP ALLELIC FORM OF HUMAN MANNOSE-BINDING PROTEIN (MBP) FAILS TO BIND MBP-ASSOCIATED SERINE-PROTEASE SO BIOCHEMICAL JOURNAL LA English DT Article ID ALTERNATIVE COMPLEMENT PATHWAY; BACTERICIDAL ACTIVITY; CLASSICAL PATHWAY; ACTIVATION; DISTINCT; SALMONELLA; DEFECT; CLQ; C4B AB The human mannose-binding protein (MBP) is a pattern recognition molecule that appears to play a role in initial host defence. MBP activates the complement cascade and it may act as an opsonin both in the absence and in the presence of complement. A number of distinct MBP allelic forms exist in different population groups, An allele that occurs in 5-7 % of Caucasians was identified by an inability to activate the complement system. A homozygous mutation at base pair 230 of the MBP gene results in a Gly-to-Asp substitution at the fifth collagen repeat. It appears that the resultant protein, MBP(D), is able to form high-order multimers that bind bacteria but do not support complement activation. Recently a novel serine protease, the MBP-associated serine protease (MASP), has been described. MBP-MASP complexes circulate in serum and result in the direct activation of a novel complement pathway (lectin pathway) in the absence of the first complement components. In this study we demonstrate that MASP and its proenzyme proMASP are unable to bind to recombinant (r)MBP(D). This lack of a MASP-rMBP(D) association corresponds to a failure of the Gly-54 --> Asp form of MBP to activate complement. Our results provide a biochemical basis for the functional deficit in the Gly-54 --> Asp allelic form of MBP and suggest that the proMASP/MASP binding site maps to the fifth collagen repeat of MBP. C1 FUKUSHIMA MED COLL,DEPT BIOCHEM,FUKUSHIMA 96012,JAPAN. HARVARD UNIV,CHILDRENS HOSP,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115. DANA FABER CANC INST,BOSTON,MA 02115. NR 22 TC 58 Z9 59 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 NOV 1 PY 1995 VL 311 BP 1021 EP 1023 PN 3 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TC563 UT WOS:A1995TC56300045 PM 7487919 ER PT J AU SOLNICAKREZEL, L STEMPLE, DL DRIEVER, W AF SOLNICAKREZEL, L STEMPLE, DL DRIEVER, W TI TRANSPARENT THINGS - CELL FATES AND CELL MOVEMENTS DURING EARLY EMBRYOGENESIS SF ZEBRAFISH SO BIOESSAYS LA English DT Review ID XENOPUS-LAEVIS; PROSPECTIVE AREAS; ENVELOPING LAYER; SPERM ENTRY; FLOOR PLATE; EMBRYO; FUNDULUS; GASTRULATION; LINEAGE; MAP AB Development of an animal embryo involves the coordination of cell divisions, a variety of inductive interactions and extensive cellular rearrangements. One of the biggest challenges in developmental biology is to explain the relationships between these processes and the mechanisms that regulate them. Teleost embryos provide an ideal subject for the study of these issues. Their optical lucidity combined with modern techniques for the marking and observation of individual living cells allow high resolution investigations of specific morphogenetic movements and the construction of detailed fate maps. In this review we describe the patterns of cell divisions, cellular movements and other morphogenetic events during zebrafish early development and discuss how these events relate to the formation of restricted lineages. C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. FU NICHD NIH HHS [HD29761] NR 59 TC 47 Z9 47 U1 0 U2 4 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD NOV PY 1995 VL 17 IS 11 BP 931 EP 939 DI 10.1002/bies.950171106 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA TE884 UT WOS:A1995TE88400005 PM 8526887 ER PT J AU JEGGO, PA TACCIOLI, GE JACKSON, SP AF JEGGO, PA TACCIOLI, GE JACKSON, SP TI MENAGE-A-TROIS - DOUBLE-STRAND BREAK REPAIR, V(D)J RECOMBINATION AND DNA-PK SO BIOESSAYS LA English DT Review ID HUMAN AUTOANTIGEN KU; PROTEIN-KINASE; IONIZING-RADIATION; SCID MUTATION; CELL MUTANTS; GENE; SEQUENCE; ANTIGEN; RADIOSENSITIVITY; MECHANISM AB All organisms possess mechanisms to repair double strand breaks (dsbs) generated in their DNA by damaging agents. Site-specific dsbs are also introduced during V(D)J recombination; Four complementation groups of radiosensitive rodent mutants are defective in the repair of dsbs, and are unable to carry out V(D)J recombination effectively. The immune defect in Severe Combined Immunodeficient (scid) mice also results from an inability to undergo effective V(D)J recombination, and scid cell lines display a repair defect and belong to one of these complementation groups. These findings indicate a mechanistic overlap between the processes of DNA repair and V(D)J recombination. Recently, two of the genes defined by these complementation groups have been identified and shown to encode components of DNA-dependent protein kinase (DNA-PK). We review here the three fields which have become linked by these findings, and discuss the involvement of DNA-PK in dsb rejoining and in V(D)J recombination. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. UNIV CAMBRIDGE,DEPT ZOOL,CAMBRIDGE CB2 1QR,ENGLAND. WELLCOME CRC INST,CAMBRIDGE CB2 1QR,ENGLAND. RP JEGGO, PA (reprint author), UNIV SUSSEX,MRC,CELL MUTAT UNIT,BRIGHTON BN1 9RR,E SUSSEX,ENGLAND. RI Dry, Kate/I-2328-2014 FU NIAID NIH HHS [AI-35714, AI-20047]; Wellcome Trust NR 67 TC 230 Z9 232 U1 0 U2 1 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0265-9247 J9 BIOESSAYS JI Bioessays PD NOV PY 1995 VL 17 IS 11 BP 949 EP 957 DI 10.1002/bies.950171108 PG 9 WC Biochemistry & Molecular Biology; Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics GA TE884 UT WOS:A1995TE88400007 PM 8526889 ER PT J AU Yu, X White, LT Doumen, C Damico, LA LaNoue, KF Alpert, NM Lewandowski, ED AF Yu, X White, LT Doumen, C Damico, LA LaNoue, KF Alpert, NM Lewandowski, ED TI Kinetic analysis of dynamic C-13 NMR spectra: Metabolic flux, regulation, and compartmentation in hearts SO BIOPHYSICAL JOURNAL LA English DT Article ID CITRIC-ACID CYCLE; NUCLEAR-MAGNETIC-RESONANCE; PERFUSED RAT-HEART; INTACT HEARTS; ATP SYNTHESIS; CARBON FLUX; WORK LOAD; MITOCHONDRIA; MYOCARDIUM; SUBSTRATE AB Control of oxidative metabolism was studied using C-13 NMR spectroscopy to detect rate-limiting steps in C-13 labeling of glutamate. C-13 NMR spectra were acquired every 1 or 2 min from isolated rabbit hearts perfused with either 2.5 mM [2-C-13]acetate or 2.5 mM [2-C-13]butyrate with or without KCl arrest. Tricarboxylic acid cycle flux (V-TCA) and the exchange rate between alpha-ketoglutarate and glutamate (F-1) were determined by least-square fitting of a kinetic model to NMR data, Rates were compared to measured kinetics of the cardiac glutamate-oxaloacetate transaminase (GOT). Despite similar oxygen use, hearts oxidizing butyrate instead of acetate showed delayed incorporation of C-13 label into glutamate and lower V-TCA, because of the influence of beta-oxidation: butyrate = 7.1 +/- 0.2 mu mol/min/g dry wt; acetate = 10.1 +/- 0.2; butyrate + KCl = 1.8 +/- 0.1; acetate + KCl = 3.1 +/- 0.1 (mean +/- SD). F-1 ranged from a low of 4.4 +/- 1.0 mu mol/min/g (butyrate + KCl) to 9.3 +/- 0.6 (acetate), at least 20-fold slower than GOT flux, and proved to be rate limiting for isotope turnover in the glutamate pool. Therefore, dynamic C-13 NMR observations were sensitive not only to TCA cycle flux but also to the interconversion between TCA cycle intermediates and glutamate. C1 MASSACHUSETTS GEN HOSP,NMR CTR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT RADIOL,PET CTR,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. PENN STATE UNIV,MILTON S HERSHEY MED CTR,DEPT PHYSIOL,HERSHEY,PA 17033. FU NHLBI NIH HHS [R01HL49244] NR 52 TC 85 Z9 86 U1 0 U2 2 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1995 VL 69 IS 5 BP 2090 EP 2102 PG 13 WC Biophysics SC Biophysics GA TV017 UT WOS:A1995TV01700047 PM 8580353 ER PT J AU Melder, RJ Munn, LL Yamada, S Ohkubo, C Jain, RK AF Melder, RJ Munn, LL Yamada, S Ohkubo, C Jain, RK TI Selectin- and integrin-mediated T-lymphocyte rolling and arrest on TNF-alpha-activated endothelium: Augmentation by erythrocytes SO BIOPHYSICAL JOURNAL LA English DT Article ID CELL-ADHESION MOLECULE-1; NEUTROPHIL ADHESION; SMALL TUBES; BLOOD-FLOW; LEUKOCYTES; RECEPTOR; VENULES; RECIRCULATION; MIGRATION; KINETICS AB The adhesive and hemodynamic forces that lead to lymphocyte rolling and arrest on activated endothelium and the biophysical role of various adhesion molecules and blood elements in this process are poorly understood. By quantifying their behavior both in vivo and in vitro, we show here that erythrocytes facilitate selectin- and integrin-mediated rolling and binding of T-lymphocytes on tumor necrosis factor alpha-activated endothelium. The relative contribution of selectins and integrins to this process can be distinguished by using a simple mathematical expression of lymphocyte capture within the range of physiological shear stress. The need for selectin participation in lymphocyte capture increases with shear stress (>1 dyn/cm(2)), and both beta 1 and beta 2 integrins act in synergy to produce adhesive drag on captured cells. These findings are potentially useful in developing strategies for intervening with T-cells in a variety of normal and pathological responses as well as for the delivery of genetically modified T-cells to their targets in vivo. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP Melder, RJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB TUMOR BIOL,BOSTON,MA 02114, USA. RI Munn, Lance/L-3950-2016 OI Munn, Lance/0000-0003-0698-7232 NR 39 TC 74 Z9 74 U1 0 U2 0 PU BIOPHYSICAL SOCIETY PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 SN 0006-3495 J9 BIOPHYS J JI Biophys. J. PD NOV PY 1995 VL 69 IS 5 BP 2131 EP 2138 PG 8 WC Biophysics SC Biophysics GA TV017 UT WOS:A1995TV01700051 PM 8580357 ER PT J AU YAMADA, S MAYADAS, TN YUAN, F WAGNER, DD HYNES, RO MELDER, RJ JAIN, RK AF YAMADA, S MAYADAS, TN YUAN, F WAGNER, DD HYNES, RO MELDER, RJ JAIN, RK TI ROLLING IN P-SELECTIN DEFICIENT MICE IS REDUCED BUT NOT ELIMINATED IN THE DORSAL SKIN SO BLOOD LA English DT Article ID MONOCLONAL-ANTIBODY; MYOCARDIAL-ISCHEMIA; REPERFUSION INJURY; LEUKOCYTE ADHESION; LUNG INJURY; ADHERENCE; GMP-140; ENDOTHELIUM; MOLECULE-1; EXPRESSION AB P-selectin-mediated rolling is believed to be important in the recruitment of leukocytes to tissue after ischemia-reperfusion injury. The dorsal skin chamber was used to examine differences in the rolling and stable adhesion of circulating leukocytes in subcutaneous (SC) vessels of P-selectin-deficient and age-matched wild-type mice, both under basal conditions and after ischemia-reperfusion. Rolling in the postcapillary venules in SC tissue of P-selectin-deficient mice was significantly lower than that in wild-type mice under the basal conditions and post-ischemia-reperfusion (P < .05), but was not eliminated by the deletion of the P-selectin gene. No significant difference between P-selectin-deficient and wild-type mice in shear rate or leukocyte-endothelial adhesion was observed up to 24 hours after ischemia-reperfusion. These results show that P-selectin-mediated rolling is not a prerequisite for ischemia-reperfusion-induced leukocyte-endothelial adhesion in the skin. (C) 1995 by The American Society of Hematology. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. MIT,HOWARD HUGHES MED INST,DEPT BIOL,CAMBRIDGE,MA 02139. MIT,CTR CANC RES,CAMBRIDGE,MA 02139. RI Yuan, Fan/A-1287-2011 FU NCI NIH HHS [R35-CA-56591] NR 41 TC 47 Z9 47 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0006-4971 J9 BLOOD JI Blood PD NOV 1 PY 1995 VL 86 IS 9 BP 3487 EP 3492 PG 6 WC Hematology SC Hematology GA TB163 UT WOS:A1995TB16300027 PM 7579454 ER PT J AU NEER, RM AF NEER, RM TI SKELETAL SAFETY OF TILUDRONATE SO BONE LA English DT Article; Proceedings Paper CT Satellite Symposium on Tiludronate for Bone Diseases, at the XIIth International Conference on Calcium Regulating Hormones (XIIth ICCRH) CY FEB 14, 1995 CL MELBOURNE, AUSTRALIA DE TILUDRONATE; RESORPTION; TRABECULAR; CORTICAL; FRACTURES; MINERALIZATION; PAGETS DISEASE ID BONE-MINERAL DENSITY; BISPHOSPHONATE; DISEASE AB The medical uses of bisphosphonates derive from their exceptional ability to inhibit bone resorption, However, bone resorption is essential for the healing of fractures, the repair of microscopic fatigue cracks in bone, and the internal reorientation of trabecular and cortical bone in response to altered mechanical strains, In theory, overdose with bisphosphonates might interfere with the repair of fractures or weaken bone strength (by forcing bones to accumulate and propagate fatigue cracks or by abolishing the skeleton's adaptive powers), Regulatory agencies (particularly in the USA) have, therefore, set comprehensive and stringent safety criteria before the marketing of bisphosphonates can be approved, Some bisphosphonates can also inhibit bone mineralization, alter hepatic function, or cause gastritis/esophagitis, The safety profile of tiludronate will be described from this perspective, emphasizing the results of prolonged treatment in animals, and studies in humans. RP NEER, RM (reprint author), MASSACHUSETTS GEN HOSP,ENDOCRINE UNIT,55 FRUIT ST,BOSTON,MA 02114, USA. NR 26 TC 8 Z9 8 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 8756-3282 J9 BONE JI Bone PD NOV PY 1995 VL 17 IS 5 SU S BP S501 EP S503 DI 10.1016/8756-3282(95)00343-7 PG 3 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TG363 UT WOS:A1995TG36300008 PM 8573427 ER PT J AU Caviness, VS Kennedy, DN Makris, N Bates, J AF Caviness, VS Kennedy, DN Makris, N Bates, J TI Advanced application of magnetic resonance imaging in human brain science SO BRAIN & DEVELOPMENT LA English DT Article DE magnetic resonance imaging; volumetric morphometry; cortical mapping ID CENTRAL NERVOUS-SYSTEM; CEREBRAL-CORTEX; RAT; IMMUNOREACTIVITY; HYPOTHALAMUS; EXTRASTRIATE; ASYMMETRIES; ACTIVATION; NEURONS; STRIATE AB Magnetic resonance imaging (MRI) has revolutionized the practical demands of clinical neurology, This technology promises now to advance neurology in theoretical and applied realms of fundamental human brain science, We emphasize here two domains in which these advances will occur, The first is volumetric morphometry of the human brain, With MRI the multiple levels of processing of the brain may be characterized in terms of their absolute volumes and their relative sizes, perspectives indispensable for our understanding of the development and operation of neural systems, Volumetric morphometry also promises substantial increases in the specificity and sensitivity of neurological diagnosis, particularly where applied to disorders where structural abnormalities will be reflected only in volumetric abnormalities. The second direction of advance considered here is application of MRI in cortical mapping in support of cognitive neuroscience. In this application MRI provides means to map at high resolution the distribution of subcomponents of neural systems activated by behavioral paradigms, This line of investigation will carry forward rapidly our understanding of how the information processing algorithms of the brain are mapped upon the coordinates of the various gray matter structures of the brain, Among the practical consequences of this application will be a reasoned design of surgical field in tumor and epilepsy surgery. RP Caviness, VS (reprint author), HARVARD MED SCH,MASSACHUSETTS GEN HOSP,DEPT NEUROL,25 FRUIT ST,BOSTON,MA 02114, USA. RI Kennedy, David/H-3627-2012 FU NINDS NIH HHS [P01 NS27950] NR 61 TC 16 Z9 16 U1 1 U2 4 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 NOV-DEC PY 1995 VL 17 IS 6 BP 399 EP 408 DI 10.1016/0387-7604(95)00090-9 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA TM234 UT WOS:A1995TM23400001 PM 8747418 ER PT J AU KOOPMANN, J MAINTZ, D SCHILD, S SCHRAMM, J LOUIS, DN WIESTLER, OD VONDEIMLING, A AF KOOPMANN, J MAINTZ, D SCHILD, S SCHRAMM, J LOUIS, DN WIESTLER, OD VONDEIMLING, A TI MULTIPLE POLYMORPHISMS, BUT NO MUTATIONS, IN THE WAF1/CIP1 GENE IN HUMAN BRAIN-TUMORS SO BRITISH JOURNAL OF CANCER LA English DT Article DE WAF1; CZP1; P21; P53; CDKN1; BRAIN TUMORS ID P53 MUTATIONS; INHIBITOR; PROTEIN; KINASES; P21 AB The cyclin kinase inhibitor WAF1/CIP1, also termed CDKN1, mediates p53-induced cell cycle arrest in response to DNA damage. This property makes it an attractive tumour-suppressor candidate for a p53-associated tumour-suppressor gene. In order to investigate the role of WAF1/CIPI in the pathogenesis of primary human brain tumours we performed single-stranded conformation polymorphism (SSCP) analysis and direct sequencing of exon 2 of the gene in a representative series of 158 brain tumours and corresponding blood samples. In addition, all tumours were examined for mutations in exons 5-8 of the p53 gene. Analysis of WAF1/CIP1 revealed multiple polymorphisms, the most abundant being AGC-->AGA (Ser-->Arg) at codon 31 with an allele frequency of 8.5%. Less common polymorphisms included GTG-->GGG (Val-->Gly) at codon 25, GCC-->ACC (Ala-->Thr) at codon 64, CGC-->CTC (Arg-->Leu) at codon 32, GGC-->AGC (Gly-->Ser) at codon 14 and GCG-->GTG (Ala-->Val) at codon 39 each with an allele frequency of 0.3%. These polymorphisms were all located in a conserved region of exon 2. Two of the polymorphisms were also seen in a group of 157 healthy controls indicating that WAF1/CIP1 polymorphisms do not predispose to cancer. None of the tumours included in our series showed a somatic mutation in WAF1/CIP1. All samples were also analysed for loss of heterozygosity on the short arm of chromosome 6 in the region of the WAF1/CIP1 locus. Allelic loss was observed in only one patient with a glioblastoma. Mutations in the p53 gene were found in 22 of 158 tumours. No association was found between any polymorphism of the WAF1/CIP1 gene, p53 mutations and histopathological tumour type. Our data indicate that WAF1/CIP1 mutations are probably not involved in the formation of primary human brain tumours. C1 UNIV KLINIKEN BONN,INST NEUROPATHOL,D-53105 BONN,GERMANY. UNIV KLINIKEN BONN,NEUROCHIRURG KLIN,D-53105 BONN,GERMANY. MASSACHUSETTS GEN HOSP,NEUROSURG SERV,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL NEUROPATHOL,BOSTON,MA 02114. RI von Deimling, Andreas/F-7774-2013; OI von Deimling, Andreas/0000-0002-5863-540X; schild, steven/0000-0002-2850-4126 FU NCI NIH HHS [CA 57683] NR 21 TC 56 Z9 56 U1 0 U2 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0007-0920 J9 BRIT J CANCER JI Br. J. Cancer PD NOV PY 1995 VL 72 IS 5 BP 1230 EP 1233 DI 10.1038/bjc.1995.491 PG 4 WC Oncology SC Oncology GA TC820 UT WOS:A1995TC82000027 PM 7577473 ER PT J AU Daltroy, LH RobbNicholson, C Iversen, MD Wright, EA Liang, MH AF Daltroy, LH RobbNicholson, C Iversen, MD Wright, EA Liang, MH TI Effectiveness of minimally supervised home aerobic training in patients with systemic rheumatic disease SO BRITISH JOURNAL OF RHEUMATOLOGY LA English DT Article DE fatigue; rheumatoid arthritis; systemic lupus erythematosus; aerobic training; rehabilitation; health education; effectiveness outcomes ID CONTROLLED LONG-TERM; LUPUS-ERYTHEMATOSUS; REVISED CRITERIA; ARTHRITIS; CLASSIFICATION AB The effectiveness of an exercise prescription and unsupervised home exercise programme was tested on 37 subjects with rheumatoid arthritis and 34 with systemic lupus erythematosus. Subjects were randomly assigned to control or stationary bicycling at home, using loaned bicycles. Exercise subjects (with bicycles) did better than controls, but not significantly, on all outcomed measures (exercise tolerance test, fatigue, depression and helplessness) at 3 months. Bicycles were reclaimed at 3 months and all subjects in both groups given instructions for home exercise. Exercise in the second 3 months was predicted primarily by baseline exercise habits and fatigue. It is concluded that although safe, unsupervised home exercise programmes may benefit few patients. Future research should address methods of stimulating and maintaining unsupervised exercise programmes in patients with systemic rheumatic disease. C1 BRIGHAM & WOMENS HOSP,DIV RHEUMATOL IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT HLTH & SOCIAL BEHAV,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP Daltroy, LH (reprint author), BRIGHAM & WOMENS HOSP,RBB MULTIPURPOSE ARTHRITIS & MUSCULOSKELETAL DIS,PBB-B2,75 FRANCIS ST,BOSTON,MA 02115, USA. RI iversen, maura/O-5388-2015 OI iversen, maura/0000-0003-4708-9914 NR 14 TC 70 Z9 71 U1 1 U2 5 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0263-7103 J9 BRIT J RHEUMATOL JI Br. J. Rheumatol. PD NOV PY 1995 VL 34 IS 11 BP 1064 EP 1069 PG 6 WC Rheumatology SC Rheumatology GA TM084 UT WOS:A1995TM08400010 PM 8542209 ER PT J AU LOSTY, PD SUEN, HO MANGANARO, TF DONAHOE, PK SCHNITZER, JJ AF LOSTY, PD SUEN, HO MANGANARO, TF DONAHOE, PK SCHNITZER, JJ TI PRENATAL HORMONAL-THERAPY IMPROVES PULMONARY COMPLIANCE IN NITROFEN-INDUCED CONGENITAL DIAPHRAGMATIC-HERNIA IN THE RAT SO BRITISH JOURNAL OF SURGERY LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PEDIAT SURG RES LABS,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0007-1323 J9 BRIT J SURG JI Br. J. Surg. PD NOV PY 1995 VL 82 IS 11 BP 1565 EP 1565 PG 1 WC Surgery SC Surgery GA TE171 UT WOS:A1995TE17100096 ER PT J AU FRAZIER, AL WILLETT, WC COLDITZ, GA AF FRAZIER, AL WILLETT, WC COLDITZ, GA TI REPRODUCIBILITY OF RECALL OF ADOLESCENT DIET - NURSES HEALTH STUDY (UNITED-STATES) SO CANCER CAUSES & CONTROL LA English DT Article DE ADOLESCENCE; DIET; REPRODUCIBILITY; UNITED STATES; WOMEN ID SELF-ADMINISTERED QUESTIONNAIRE; BREAST-CANCER; ALCOHOL-CONSUMPTION; FREQUENCY; RISK; AGE; IRRADIATION; RELIABILITY; EXPOSURE AB Although diet and alcohol consumption at a young age have been hypothesized to play an etiologic role in adult malignancy, few studies have addressed these relations and few data exist on the ability to measure recalled diet during adolescence. We undertook a study to determine whether the recall of diet during high school 22 to 47 years later was reproducible within a prospective cohort of women. In 1986, participants in the Nurses' Health Study (United States), aged 40 to 65 years, reported their diet during high school using a 24-item food frequency questionnaire (FFQ). On the 1988 questionnaire, the participants recorded their alcohol consumption between the ages of 18 and 22. In 1994, a random sample of 275 women were asked to record again their high school diet and alcohol consumption. The average of Spearman correlations between the two recalls of high school diet was = 0.57 (range = 0.38 to 0.74). For alcohol intake, the correlation for the time period queried was 0.66. The correlation between the two recalls of high school diet was higher than the correlation between the first recall and current diet in 1986 (average r = 0.25). There was no effect of age on reproducibility of recall, These data suggest that recall of diet from the very distant past, during a distinct time period such as high school, is reasonably reproducible. Although further studies of validity are needed, such information may be sufficiently precise to assess the influence of remote diet in epidemiologic studies. C1 HARVARD UNIV,SCH MED,BOSTON,MA. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,CHANNING LAB,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT NUTR,BOSTON,MA 02115. RP FRAZIER, AL (reprint author), DANA FARBER CANC INST,DEPT PEDIAT ONCOL,44 BINNEY ST,BOSTON,MA 02115, USA. RI Colditz, Graham/A-3963-2009 OI Colditz, Graham/0000-0002-7307-0291 FU NCI NIH HHS [CA40356, KO7CA62252-01 A1] NR 29 TC 30 Z9 30 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0957-5243 J9 CANCER CAUSE CONTROL JI Cancer Causes Control PD NOV PY 1995 VL 6 IS 6 BP 499 EP 506 DI 10.1007/BF00054157 PG 8 WC Oncology; Public, Environmental & Occupational Health SC Oncology; Public, Environmental & Occupational Health GA TG147 UT WOS:A1995TG14700005 PM 8580297 ER PT J AU FUKUMURA, D SALEHI, HA WITWER, B TUMA, RF MELDER, RJ JAIN, RK AF FUKUMURA, D SALEHI, HA WITWER, B TUMA, RF MELDER, RJ JAIN, RK TI TUMOR-NECROSIS-FACTOR ALPHA-INDUCED LEUKOCYTE ADHESION IN NORMAL AND TUMOR VESSELS - EFFECT OF TUMOR TYPE, TRANSPLANTATION SITE, AND HOST STRAIN SO CANCER RESEARCH LA English DT Note ID ACTIVATED KILLER-CELLS; ENDOTHELIUM; MOLECULES; EXPRESSION; RADIATION; INVIVO; MICE AB Tumor necrosis factor alpha (TNF-alpha) can lead to tumor regression when injected locally or when used in an isolated limb perfusion, and it can enhance the tumoricidal effect of various therapies. TNF-alpha can also up-regulate adhesion molecules and, thus, facilitate the binding of leukocytes to normal vessels. The present study was designed to investigate the extent to which the host leukocytes roll and adhere to vessels of different tumors (MCaIV, a murine mammary adenocarcinoma; HGL21, a human malignant astrocytoma) at a given site or to the same tumor at different sites (dorsal skin and cranium), in different mouse strains [C3H and severe combined immunodeficient (SCID)], both with and without TNF-alpha-activation. There was no significant difference in hemodynamic parameters such as RBC velocity, diameter, or shear rate between PBS-treated control groups and corresponding TNF-alpha-treated groups. Under PBS control conditions, the leukocyte rolling count in MCaIV tumor vessels in the dorsal chamber in C3H and SCID mice and in the cranial window in C3H mice was significantly lower than that in normal vessels (P < 0.05), but stable cell adhesion was similar between normal and tumor vessels. TNF-alpha led to an increase (P < 0.05) in leukocyte-endothelial interaction in vessels in the following cases: normal tissue regardless of sites and strains, MCaIV tumor in the dorsal chamber in C3H and SCID mice, MCaIV tumor in the cranial window in C3H mice, and HGL21 tumor in the cranial window in SCID mice. However, the increase in rolling and adhesion in the MCaIV tumor in response to TNF-alpha was significantly lower than in the corresponding normal vessels (P < 0.05) in the dorsal chamber in C3H and SCID mice and in the cranial window in C3H mice. The HGL21 tumor in the cranial window in SCID mice showed leukocyte rolling and adhesion comparable to that in normal pial vessels. These findings suggest that (a) in general, basal leukocyte rolling is lower in tumor vessels than in normal vessels; (b) leukocyte rolling and adhesion in tumors can be enhanced by TNF-alpha-mediated activation; and (c) the TNF-alpha response is dependent on tumor type, transplantation site, and host strain. These results have significant implications in the gene therapy of cancer using TNF-alpha-gene-transfected cancer cells or lymphocytes. C1 TEMPLE UNIV,SCH MED,DEPT PHYSIOL,PHILADELPHIA,PA 19140. TEMPLE UNIV,SCH MED,DEPT NEUROSURG,PHILADELPHIA,PA 19140. RP FUKUMURA, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,EDWIN L STEELE LAB,BOSTON,MA 02114, USA. NR 28 TC 116 Z9 118 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 1 PY 1995 VL 55 IS 21 BP 4824 EP 4829 PG 6 WC Oncology SC Oncology GA TC468 UT WOS:A1995TC46800019 PM 7585514 ER PT J AU WIENCKE, JK KELSEY, KT VARKONYI, A SEMEY, K WAIN, JC EUGENE, M CHRISTIANI, DC AF WIENCKE, JK KELSEY, KT VARKONYI, A SEMEY, K WAIN, JC EUGENE, M CHRISTIANI, DC TI CORRELATION OF DNA-ADDUCTS IN BLOOD MONONCLEAR CELLS WITH TOBACCO CARCINOGEN-INDUCED DAMAGE IN HUMAN LUNG SO CANCER RESEARCH LA English DT Article ID P-32 POSTLABELING ANALYSIS; CIGARETTE-SMOKING; CANCER PATIENTS; ORAL-MUCOSA; LYMPHOCYTES; ASSAY; BENZOPYRENE; EPIDEMIOLOGY; PREVENTION; EXPOSURE AB The formation of carcinogen-DNA adducts within the respiratory epithelium is thought to be a critical factor in the induction of lung cancer from tobacco smoke. A reliable surrogate measure of carcinogen damage to the lung would be of great value in molecular epidemiological studies of cancer risk. The validity of measurements of DNA adducts formed from hydrophobic aromatic hydrocarbons in peripheral blood mononuclear cells (MNCs) was investigated by comparing the levels of aromatic DNA adducts detected in lung tissue from 31 lung cancer patients with those detected in MNCs from the same individuals using the P-32-postlabeling assay. The associations of smoking history and intake of dietary antioxidants with adduct levels also were assessed. Tissue-specific, as well as common DNA adducts were detected in lung and blood; total MNC adduct levels were highly correlated with total lung adducts. After smoking cessation, adduct levels appeared to decay in both tissues at similar rates. Multivariate analyses (Poisson regression modeling) indicated that dietary antioxidant intake (carotenoids, vitamin A, and retinol) modified the levels of aromatic DNA adducts in both the lungs and blood. Of all models tested, the optimal one for predicting lung adduct levels included the measure of blood MNC adduct levels only. Therefore, blood MNCs are a valid surrogate tissue for estimating the burden of DNA adducts in respiratory tissue in molecular epidemiological studies. C1 HARVARD UNIV,SCH PUBL HLTH,INST OCCUPAT HLTH,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PULM & CRIT CARE UNIT,BOSTON,MA 02114. RP WIENCKE, JK (reprint author), UNIV CALIF SAN FRANCISCO,SCH MED,DEPT EPIDEMIOL & BIOSTAT,MOLEC EPIDEMIOL LAB,SAN FRANCISCO,CA 94143, USA. RI Kelsey, Karl/I-1252-2014 FU NCI NIH HHS [CA06409]; NIEHS NIH HHS [P01-ES06409, P42-ES04705] NR 45 TC 103 Z9 104 U1 0 U2 0 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA 615 CHESTNUT ST, 17TH FLOOR, PHILADELPHIA, PA 19106-4404 USA SN 0008-5472 J9 CANCER RES JI Cancer Res. PD NOV 1 PY 1995 VL 55 IS 21 BP 4910 EP 4914 PG 5 WC Oncology SC Oncology GA TC468 UT WOS:A1995TC46800034 PM 7585529 ER PT J AU SIEGEL, AJ LEWANDROWSKI, KB STRAUSS, HW FISCHMAN, AJ YASUDA, T AF SIEGEL, AJ LEWANDROWSKI, KB STRAUSS, HW FISCHMAN, AJ YASUDA, T TI NORMAL POST-RACE ANTIMYOSIN MYOCARDIAL SCINTIGRAPHY IN ASYMPTOMATIC MARATHON RUNNERS WITH ELEVATED SERUM CREATINE-KINASE-MB-ISOENZYME AND TROPONIN-T LEVELS - EVIDENCE AGAINST SILENT MYOCARDIAL-CELL NECROSIS SO CARDIOLOGY LA English DT Article DE ANTIMYOSIN MYOCARDIAL SCINTIGRAPHY; MARATHON RUNNERS; CREATINE KINASE MB ISOENZYME; TROPONIN T ID NUCLEAR CARDIOLOGY; PHYSICAL EXERTION; MEDICAL PROGRESS; INFARCTION; ANTIBODY; INJURY; DIAGNOSIS; SPECIFICITY; DAMAGE; ANGINA AB Recent epidemiologic studies confirm that heavy physical exertion can trigger myocardial infarction. Diagnosis of acute myocardial injury in marathon runners is complicated by elevations of serum creatine kinase MB isoenzyme activity in asymptomatic finishers with normal post-race infarct-avid myocardial scintigraphy. Such isoenzyme elevations can arise from exertional rhabdomyolysis of skeletal muscle biochemically altered by training, from silent injury to the myocardium or from a combined tissue source, To assess silent myocardial cell necrosis in marathon runners, we performed quantitative antimyosin myocardial scintigraphy after competition with serum immunoassays for creatine kinase MB isoenzyme and troponin T. Therefore, 8 male marathon runners with a mean age of 52 years underwent quantitative antimyosin myocardial scintigraphy immediately following the 1988 and 1993 Boston Marathons. Serum immunoassays for creatine kinase MB isoenzyme by a chemiluminescent method (CLIA) and troponin T by an enzyme-linked immunosorbent assay were performed in 4 runners after the 1993 race, Quantitative antimyosin myocardial scintigraphy was normal in all runners including 3 who participated after both races 5 years apart. Post-race serum creatine kinase MB isoenzyme and/or troponin T levels were in a range otherwise diagnostic of acute myocardial infarction in 3 of 4 subjects. Normal quantitative antimyosin myocardial imaging in asymptomatic marathon runners excludes silent myocardial cell necrosis as the source of elevated serum protein markers. Such imaging may be the optimal diagnostic modality for detection of myocardial cell necrosis in symptomatic athletes when results of conventional testing are inconclusive. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,DEPT MED,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT CLIN PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DIV NUCL MED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. STANFORD UNIV,MED CTR,DIV NUCL MED,STANFORD,CA 94305. STANFORD UNIV,SCH MED,STANFORD,CA. RP SIEGEL, AJ (reprint author), MCLEAN HOSP,DEPT MED,115 MILL ST,BELMONT,MA 02178, USA. NR 43 TC 27 Z9 27 U1 0 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0008-6312 J9 CARDIOLOGY JI Cardiology PD NOV-DEC PY 1995 VL 86 IS 6 BP 451 EP 456 DI 10.1159/000176922 PG 6 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA RU295 UT WOS:A1995RU29500002 PM 7585754 ER PT J AU TARPY, R CENTER, DM AF TARPY, R CENTER, DM TI WHEN SHOULD INHALED CORTICOSTEROIDS BE STARTED FOR ASTHMA SO CHEST LA English DT Editorial Material ID BRONCHOALVEOLAR LAVAGE; ATOPIC ASTHMA; INFLAMMATION C1 BOSTON UNIV,MED CTR,CTR PULM,PULM & CRIT CARE MED SECT,BOSTON,MA 02118. NR 13 TC 2 Z9 2 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 NOV PY 1995 VL 108 IS 5 BP 1188 EP 1190 DI 10.1378/chest.108.5.1188 PG 3 WC Critical Care Medicine; Respiratory System SC General & Internal Medicine; Respiratory System GA TD708 UT WOS:A1995TD70800005 PM 7587410 ER PT J AU BURNS, SA NEWBURGER, JW XIAO, M MAYER, JE WALSH, AZ NEUFELD, EJ AF BURNS, SA NEWBURGER, JW XIAO, M MAYER, JE WALSH, AZ NEUFELD, EJ TI INDUCTION OF INTERLEUKIN-8 MESSENGER-RNA IN HEART AND SKELETAL-MUSCLE DURING PEDIATRIC CARDIOPULMONARY BYPASS SO CIRCULATION LA English DT Article DE INTERLEUKINS; MUSCLES; BYPASS ID NEUTROPHIL CHEMOTACTIC FACTOR; REPERFUSION INJURY; ACTIVATION; EXPRESSION; ELASTASE; SURGERY; RELEASE; ALPHA AB Background Interleukin-8 (IL-8), the major neutrophil chemoattractant factor, contributes to inflammatory tissue injury by activating neutrophils and promoting their migration into tissue. IL-8 levels increase in serum of patients undergoing cardiopulmonary bypass (CPB). The purpose of this study was to determine if IL-8 gene expression is activated in tissues subjected to CPB with or without hypothermic arrest. Methods and Results IL-8 transcript levels were measured by ribonuclease protection in samples of human atrium and skeletal muscle from children before and after CPB for repair of congenital heart defects. Results were quantified by PhosphorImager. Atrial IL-8 mRNA levels increased during CPB in 14 of 16 patients tested (median increase, 2.9-fold; P=.0029). In skeletal muscle, IL-S mRNA increased in 11 of 12 patients (median, 12-fold; P=.012). Degree of IL-8 induction in atrium and muscle was not directly associated with total support time or cross-clamp time. Transcript increase in skeletal muscle occurred with or without a period of circulatory arrest, suggesting that the stimulus of CPB alone was sufficient to induce message production. Baseline values for IL-8 mRNA varied widely among patients in atrium and skeletal muscle. In situ hybridization analysis revealed diffuse increase in IL-8 mRNA throughout the tissue after CPB, with striking increase in some small veins. Conclusions We conclude that production of IL-8 mRNA occurs in most patients during CPB in both myocardium and skeletal muscle. This may result in high local IL-S concentrations, contributing to the tissue injury after CPB. C1 CHILDRENS HOSP,DANA FARBER CANC INST,DEPT CARDIOL,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,DEPT CARDIAC SURG,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,DEPT ANESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP,DANA FARBER CANC INST,DIV HEMATOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CARDIOVASC SURG,BOSTON,MA 02115. RI Neufeld, Ellis/F-9331-2011 NR 30 TC 34 Z9 36 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 NOV 1 PY 1995 VL 92 IS 9 SU S BP 315 EP 321 PG 7 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TE559 UT WOS:A1995TE55900054 ER PT J AU PRABHU, SD FREEMAN, GL AF PRABHU, SD FREEMAN, GL TI POSTEXTRASYSTOLIC MECHANICAL RESTITUTION IN CLOSED-CHEST DOGS - EFFECT OF HEART-FAILURE SO CIRCULATION LA English DT Article DE TACHYCARDIA; HEART FAILURE; MECHANICS; CONTRACTILITY; SYSTOLE ID END-SYSTOLIC PRESSURE; CANINE VENTRICULAR MYOCARDIUM; MAMMALIAN MYOCARDIUM; VOLUME RELATIONSHIP; CONTRACTILE STATE; PAPILLARY-MUSCLE; CONSCIOUS DOGS; INTERVAL; FORCE; STIMULATION AB Background Postextrasystolic mechanical restitution (MR(PES)) is thought to be an expression of intracellular Ca2+ handling by cardiac sarcoplasmic reticulum (SR). Since congestive heart failure is characterized by abnormal intracellular Ca2+ homeostasis, we sought to delineate MR,, behavior before and after the production of heart failure to obtain insights into the relation between altered mechanical performance and Ca2+ handling. Methods and Results Ten dogs instrumented with left ventricular (LV) micromanometers and piezoeleetric dimension crystals were studied under control conditions; 6 dogs also were studied after tachycardia heart failure (THF) produced by rapid LV pacing for 4 weeks. After priming at a basic cycle length of 375 ms, test pulses were delivered at fixed extrasystolic intervals (ESIs; 300, 375, or 450 ms) and graded postextrasystolic intervals (PESIs). Postextrasystolic mechanical response was assessed using single-beat elastance. MR,, curves were constructed by expressing normalized mechanical response as a function of the PESI. Control MR(PES) was a monoexponential function whose time constant (TC) and PESI-(axis) intercept (PESI(0)) increased significantly (P<.01) with increases in the antecedent ESI. THF significantly slowed MR(PES) kinetics at each antecedent ESI (P<.025), increased normalized maximal contractile response (CR(max) P<.01), and shortened PESI(0) (P<.025). Increases in the TC and CR(max) were most pronounced with the smallest antecedent ESI (percent control postextrasystolic TC 363.7 +/- 60.5%, ESI of 300 ms versus 139.0 +/- 15.1%, ESI of 450 ms, P<.005; percent control CR(max), 128.6 +/- 4.9%, ESI of 300 ms versus 104.9 +/ -1.0%, ESI of 450 ms; P<.005). Conclusions MR(PES) is much less dynamic in THF: The failing heart operates at lower levels of contractile performance after higher stimulation frequencies and cannot increase its speed of contractile recovery to compensate for higher heart rate. Prolongation of M(PES) kinetics is consistent with depression of SR Ca2+ release mechanisms in THF and implicates this site in the loss of the capacity of the failing heart to maintain mechanical performance with tachycardia. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. RI Prabhu, Sumanth/D-5223-2009 NR 42 TC 18 Z9 18 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 NOV 1 PY 1995 VL 92 IS 9 BP 2652 EP 2659 PG 8 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TC796 UT WOS:A1995TC79600040 PM 7586369 ER PT J AU SAX, PE BOSWELL, SL WHITEGUTHRO, M HIRSCH, MS AF SAX, PE BOSWELL, SL WHITEGUTHRO, M HIRSCH, MS TI POTENTIAL CLINICAL IMPLICATIONS OF INTERLABORATORY VARIABILITY IN CD4(+) T-LYMPHOCYTE COUNTS OF PATIENTS INFECTED WITH HUMAN-IMMUNODEFICIENCY-VIRUS SO CLINICAL INFECTIOUS DISEASES LA English DT Article ID ANTIRETROVIRAL THERAPY; HIV INFECTION; SUBSETS; PROGRAM AB The CD4(+) T-lymphocyte count is an important factor in the management of patients infected with human immunodeficiency virus. Previous studies have found significant variability among the counts determined by different laboratories. We conducted a study of lymphocyte phenotyping in four laboratories to assess this variability and its possible clinical implications. One laboratory was situated at the study site; the other three were selected randomly from a total of 11 commercial and hospital laboratories available locally. Blood specimens were obtained from 24 patients and were sent to the four laboratories for a complete blood count and a lymphocyte subset analysis. Using the Kruskall-Wallis test, we found that the laboratories' ranks of four individual components of the CD4 cell count differed significantly: total white blood cell count (P < .0001), lymphocyte percentage (P = .003), lymphocyte count (P = .002), and CD4 percentage (P = .0004). Of the 24 patients in this survey, 14 (58.3%) had CD4-count results with enough variation to have led to conflicting treatment recommendations; three of the 24 patients fulfilled the revised Centers for Disease Control and Prevention case definition of AIDS on the basis of results from some but not all laboratories. In addition, the laboratories disagreed on whether CD4 cell counts of nine patients (37.5%) had increased or decreased since the previous determination. We conclude that when strict thresholds of CD4 cell counts are used as a basis for treatment recommendations or for diagnosis of AIDS, interlaboratory variability may be sufficient to alter the decisions made. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP SAX, PE (reprint author), BRIGHAM & WOMENS HOSP,DIV INFECT DIS,75 FRANCIS ST,BOSTON,MA 02115, USA. FU NCI NIH HHS [CA12464]; NIAID NIH HHS [AI07387] NR 18 TC 15 Z9 15 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 NOV PY 1995 VL 21 IS 5 BP 1121 EP 1125 DI 10.1093/clinids/21.5.1121 PG 5 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TC172 UT WOS:A1995TC17200007 PM 8589131 ER PT J AU MORENO, F GROTA, P CRISP, C MAGNON, K MELCHER, GP JORGENSEN, JH PATTERSON, JE AF MORENO, F GROTA, P CRISP, C MAGNON, K MELCHER, GP JORGENSEN, JH PATTERSON, JE TI CLINICAL AND MOLECULAR EPIDEMIOLOGY OF VANCOMYCIN-RESISTANT ENTEROCOCCUS-FAECIUM DURING ITS EMERGENCE IN A CITY IN SOUTHERN TEXAS SO CLINICAL INFECTIOUS DISEASES LA English DT Article AB During a 19-month period from April 1993 to October 1994, 41 isolates of vancomycin-resistant Enterococcus faecium (VREF) were detected in seven different hospitals in a city in southern Texas. A case-control study to determine the risk factors for acquisition was done in the hospital in which the majority of isolates were detected. Pulsed-field gel electrophoresis (PFGE) of whole-cell DNA was used to determine strain identity. Thirty-five (85%) of the 41 VREF isolates were of the vanB phenotype. Of these, 32 (91%) of 35 were the same strain by PFGE typing. The same vanB strain was documented in five different hospitals in the city. In contrast, 4 (67%) of 6 of the vanA phenotype VREF isolates were distinct strains by PFGE typing. Significant risk factors for colonization or infection with VREF were prior exposure to antibiotics (P=.04), the previous use of third-generation cephalosporins (P=.03), and the previous use of parenteral vancomycin (P=.002). Infection-control and antibiotic-utilization measures were implemented to control cross-transmission and selection of VREF isolates. During the emergence of VREF in our city, clonal dissemination of a single strain of vanB VREF among six hospitals was documented. Limited cross-transmission of vanA phenotype VREF isolates occurred, but most vanA VREF isolates were distinct strains selected in individual hospital environments. C1 UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,AUDIE L MURPHY MEM VET HOSP,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. BAPTIST MEM HOSP,SAN ANTONIO,TX. WILFORD HALL USAF MED CTR,SAN ANTONIO,TX 78236. NR 12 TC 100 Z9 100 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 NOV PY 1995 VL 21 IS 5 BP 1234 EP 1237 DI 10.1093/clinids/21.5.1234 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TC172 UT WOS:A1995TC17200025 PM 8589148 ER PT J AU KONTOYIANNIS, DP CALIA, KE BASGOZ, N CALDERWOOD, SB AF KONTOYIANNIS, DP CALIA, KE BASGOZ, N CALDERWOOD, SB TI PRIMARY SEPTICEMIA CAUSED BY VIBRIO-CHOLERAE NON-O1 ACQUIRED ON CAPE-COD, MASSACHUSETTS SO CLINICAL INFECTIOUS DISEASES LA English DT Note ID UNITED-STATES; INFECTIONS; VIRULENCE AB We describe a patient with non-O1, non-O139 Vibrio cholerae septicemia associated with hemorrhagic bullous skin lesions of the lower extremities. The patient had underlying liver disease, and he probably acquired the organism through ingestion of raw clams. Although his condition rapidly improved during appropriate therapy, the patient's cellulitis and skin lesions persisted and he developed a fluid collection of the lower extremity that required drainage. Molecular methods were used to examine the non-Ol V. cholerae isolate for several known virulence factors of V. cholerae O1. The isolate failed to express cholera toxin and toxin-coregulated pilus (Tcp) and was negative in Southern hybridizations for ctxB, tcpA, toxR, and toxT. The vast majority of vibrio infections in the United States are clustered in the Gulf Coast area. This patient acquired the infection on Cape God. To our knowledge, this is the first case of non-Ol V. cholerae septicemia reported to have occurred in Massachusetts. Given the high fatality rate of this infection, it is important for physicians to consider this diagnosis in patients who have underlying risk factors and appropriate epidemiologic exposures, even when they reside as far north as the New England states. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [AI-34968] NR 14 TC 19 Z9 19 U1 0 U2 2 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 NOV PY 1995 VL 21 IS 5 BP 1330 EP 1333 DI 10.1093/clinids/21.5.1330 PG 4 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TC172 UT WOS:A1995TC17200048 PM 8589171 ER PT J AU KANDULA, P SHIRAZI, P AF KANDULA, P SHIRAZI, P TI LOCALIZATION OF TC-99M SESTAMIBI AND TL-201 IN AN UNSUSPECTED CALCIFIED INTRATHORACIC MASS SO CLINICAL NUCLEAR MEDICINE LA English DT Article ID INCREASED ACCUMULATION; TUMOR; TECHNETIUM-99M-SESTAMIBI; LESIONS; MIBI AB Tc-99m MIBI and TI-201 uptake have been reported in benign and malignant lesions. However, concordant uptake of both radiotracers has been described infrequently. The authors report a patient with a case history of tuberculosis and breast cancer who underwent a TI-201 cardiac stress/planar study initially for complaints of angina pectoris, and 3 years later a follow-up Tc-99m MIBI cardiac study was completed for similar complaints. These studies incidentally revealed uptake of TI-201 and Tc-99m MIBI in a large left lung mass unchanged in size between the two studies. CT with intravenous contrast performed 2 months after the Tc-99m MIBI study revealed a 9 cm calcified soft-tissue mass in the left lung with adjacent pleural calcifications. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,DEPT NUCL MED,NUCL MED SERV 115,HINES,IL 60141. NR 13 TC 5 Z9 5 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0363-9762 J9 CLIN NUCL MED JI Clin. Nucl. Med. PD NOV PY 1995 VL 20 IS 11 BP 1000 EP 1002 DI 10.1097/00003072-199511000-00014 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TE189 UT WOS:A1995TE18900014 PM 8565352 ER PT J AU MAYOSMITH, WW WITTENBERG, J BENNETT, GL GERVAIS, DA GAZELLE, GS MUELLER, PR AF MAYOSMITH, WW WITTENBERG, J BENNETT, GL GERVAIS, DA GAZELLE, GS MUELLER, PR TI THE CT SMALL-BOWEL FECES SIGN - DESCRIPTION AND CLINICAL-SIGNIFICANCE SO CLINICAL RADIOLOGY LA English DT Article ID OBSTRUCTION AB Objective: To describe a new CT sign of the GI tract: the small bowel faeces sign, and discuss its significance. Methods: The small bowel faeces sign consists of gas bubbles mixed with particulate matter in dilated segments of small bowel. This was a retrospective study of 22 patients demonstrating this sign from 1989 to 1993. Final diagnosis was established by surgical, medical or laboratory findings. To determine the prevalence of the sign, the CT examination of 120 consecutive separate control patients were evaluated. Results: All 22 of the patients demonstrating this sign required hospitalization with surgical or medical intervention. Eighteen of 22 had mechanical small bowel obstruction. The remaining four patients had other abnormalities of small bowel to account for the Ending on CT. Twelve of the 22 patients were treated with surgery and the remaining 10 patients were treated with nasogastric tubes (n = 6) or other medical therapy (n = 4). None of the 120 control patients demonstrated the sign. Conclusion: The presence of gas and particulate material resembling faeces in a dilated segment of small bowel on CT is abnormal. Most (18/22; 82%) patients with this sign had small bowel obstruction. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP MAYOSMITH, WW (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,BOSTON,MA 02114, USA. NR 6 TC 45 Z9 49 U1 0 U2 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0009-9260 J9 CLIN RADIOL JI Clin. Radiol. PD NOV PY 1995 VL 50 IS 11 BP 765 EP 767 DI 10.1016/S0009-9260(05)83216-7 PG 3 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TE207 UT WOS:A1995TE20700006 PM 7489626 ER PT J AU Krosnick, A AF Krosnick, A TI Angiotensin II receptor antagonism: Losartan-sites and mechanisms of action - Editorial Comment SO CLINICAL THERAPEUTICS LA English DT Editorial Material RP Krosnick, A (reprint author), JOSLIN DIABET CTR,BOSTON,MA 02215, USA. 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 0149-2918 J9 CLIN THER JI Clin. Ther. PD NOV-DEC PY 1995 VL 17 IS 6 BP 1004 EP 1004 DI 10.1016/0149-2918(95)80079-4 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TN831 UT WOS:A1995TN83100001 ER PT J AU Krosnick, A AF Krosnick, A TI Activeness and safety of beclomethasone dipropionate, an intranasal corticosteroid, in the treatment of patients with allergic rhinitis - Editorial comment SO CLINICAL THERAPEUTICS LA English DT Editorial Material RP Krosnick, A (reprint author), JOSLIN DIABET CTR,BOSTON,MA 02215, USA. 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 0149-2918 J9 CLIN THER JI Clin. Ther. PD NOV-DEC PY 1995 VL 17 IS 6 BP 1031 EP 1031 DI 10.1016/0149-2918(95)80081-6 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TN831 UT WOS:A1995TN83100003 ER PT J AU Krosnick, A AF Krosnick, A TI Editorial comment SO CLINICAL THERAPEUTICS LA English DT Editorial Material RP Krosnick, A (reprint author), JOSLIN DIABET CTR,BOSTON,MA 02215, USA. 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 0149-2918 J9 CLIN THER JI Clin. Ther. PD NOV-DEC PY 1995 VL 17 IS 6 BP 1042 EP 1042 DI 10.1016/0149-2918(95)80083-2 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TN831 UT WOS:A1995TN83100005 ER PT J AU GHORAISHI, M AKOVA, YA TUGALTUTKUN, I FOSTER, CS AF GHORAISHI, M AKOVA, YA TUGALTUTKUN, I FOSTER, CS TI PENETRATING KERATOPLASTY IN ATOPIC KERATOCONJUNCTIVITIS SO CORNEA LA English DT Article DE PENETRATING KERATOPLASTY; ATOPIC KERATOCONJUNCTIVITIS AB Penetrating keratoplasty (PK) may be required for visual rehabilitation or tectonic purposes in patients with severe keratopathy due to atopic keratoconjunctivitis (AKC). The outcome of PK is often poor in such patients because of adnexal and ocular surface abnormalities. We studied nine AKC patients requiring PK and evaluated the visual outcome and prognostic factors in 11 eyes. The mean follow-up was 87.2 months (range, 30-180 months). Preoperatively all patients had visual acuity of hand motion to 20/200. Eighteen grafts were performed. Final visual acuity was 20/40 or better in 46% of the eyes. Ten eyes retained clear grafts and improved an average of 4.5 Snellen acuity lines. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,BOSTON,MA 02114. NR 0 TC 16 Z9 18 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 NOV PY 1995 VL 14 IS 6 BP 610 EP 613 PG 4 WC Ophthalmology SC Ophthalmology GA TE073 UT WOS:A1995TE07300015 PM 8575184 ER PT J AU RYAN, CM ATKINS, MB MIER, JW GELFAND, JA TOMPKINS, RG AF RYAN, CM ATKINS, MB MIER, JW GELFAND, JA TOMPKINS, RG TI EFFECTS OF MALIGNANCY AND INTERLEUKIN-2 INFUSION ON GUT MACROMOLECULAR PERMEABILITY SO CRITICAL CARE MEDICINE LA English DT Article DE PERMEABILITY, GUT; INTERLEUKIN-2; POLYETHYLENE GLYCOL; MELANOMA; INFLAMMATION; SHOCK; CYTOKINES; CARCINOMA, RENAL CELL; CRITICAL ILLNESS ID INTESTINAL PERMEABILITY; NITRIC-OXIDE; RECEPTOR LEVELS; IL-2 RECEPTOR; CANCER; INJURY; IMMUNOTHERAPY; ABSORPTION; INTEGRITY; THERAPY AB Objective: Enhanced gut permeability has been shown in patients with advanced malignancy, The dramatic inflammatory shock syndrome produced by high-dose interleukin-a immune therapy could further change gut barrier function, This study measured the effect of advanced renal cell carcinoma and malignant melanoma, and interleukin-2 treatment on gut permeability, Design: Nonrandomized, controlled study, Setting: University hospital, Patients: Adults with metastatic, unresectable renal cell carcinoma or metastatic, malignant melanoma, and normal volunteers, Interventions: Gut permeability was measured in patients with renal cell carcinoma or malignant melanoma before and during interleukin-a infusions, using polyethylene glycol 3350 and polyethylene glycol 400. The polyethylene glycols were administered orally within 48 hrs of interleukin-a therapy and the 24-hr urine excretions were measured. Measurements and Main Results: Increased permeability was seen in the baseline state of these patients (ratio of polyethylene glycol 3350 to polyethylene glycol 400 = 1.1 +/- 0.7 x 10(-2)) when compared with normal volunteers (ratio = 0.48 +/- 0.2 x 10(-2); p < .05), However, after interleukin-a treatment, no further increase in permeability was seem (ratio = 1.4 +/- 0.8 x 10(-2)). Conclusions: Gut permeability to polyethylene glycol 3350 is enhanced in advanced malignancy. High-dose interleukin-2 therapy does not further increase permeability of the gut. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. TUFTS UNIV NEW ENGLAND MED CTR,DEPT MED,BOSTON,MA 02111. TUFTS UNIV,SCH MED,BOSTON,MA 02111. FU NIGMS NIH HHS [T32 GM 07035, P50 GM 21700] NR 35 TC 3 Z9 4 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 NOV PY 1995 VL 23 IS 11 BP 1801 EP 1806 DI 10.1097/00003246-199511000-00003 PG 6 WC Critical Care Medicine SC General & Internal Medicine GA TE591 UT WOS:A1995TE59100003 PM 7587254 ER PT J AU SHEPHERD, KE LYNCH, KE WAIN, JC BROWN, EN WILSON, RS AF SHEPHERD, KE LYNCH, KE WAIN, JC BROWN, EN WILSON, RS TI ELASTIN FIBERS AND THE DIAGNOSIS OF BACTERIAL PNEUMONIA IN THE ADULT-RESPIRATORY-DISTRESS-SYNDROME SO CRITICAL CARE MEDICINE LA English DT Article DE ADULT RESPIRATORY DISTRESS SYNDROME; NECROSIS; LUNG; PNEUMONIA; CRITICAL ILLNESS; PATIENT OUTCOME ASSESSMENT; POTASSIUM HYDROXIDE; MECHANICAL VENTILATION; BIOPSY, LUNG ID VENTILATOR-ASSOCIATED PNEUMONIA; NOSOCOMIAL PNEUMONIA; INTUBATED PATIENTS; BRONCHOALVEOLAR LAVAGE; INFECTIONS; BRUSH; FAILURE AB Objective: It has been inferred from previous work that 40% potassium hydroxide preparations of lower respiratory tract secretions that demonstrate elastin fibers have a 100% specificity and positive predictive value in diagnosing bacterial pneumonia in intubated, mechanically ventilated patients without the adult respiratory distress syndrome (ARDS). Our aim was to assess the specificity of 40% potassium hydroxide preparations in diagnosing bacterial pneumonia in patients with ARDS and suspected pneumonia. Design: Prospective, case-referral clinical study, Setting: Referral hospital, Patients: Of 24 patients with ARDS who were intubated and mechanically ventilated with suspected bacterial pneumonia, 22 were assessable and evaluated for this report. Interventions: Tracheo-bronchial aspirates were obtained from all patients and analyzed for elastin fibers using 40%,potassium hydroxide. Measurements and Main Results: Of the 22 assessable patients, ten patients did not have a complicating bacterial pneumonia, Six of these ten patients had potassium hydroxide preparations that demonstrated elastin fibers (false positives), The other four patients had preparations that did not demonstrate elastin fibers (true negatives). Specificity was 40%. Conclusion: Elastin fiber preparations are not specific for diagnosing bacterial pneumonia in patients with ARDS. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA 02114. MEM SLOAN KETTERING CANC CTR,DEPT ANESTHESIOL & CRIT CARE MED,NEW YORK,NY 10021. CORNELL UNIV,COLL MED,NEW YORK,NY. RP SHEPHERD, KE (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANAESTHESIA,BOSTON,MA 02114, USA. NR 32 TC 9 Z9 9 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 NOV PY 1995 VL 23 IS 11 BP 1829 EP 1834 DI 10.1097/00003246-199511000-00008 PG 6 WC Critical Care Medicine SC General & Internal Medicine GA TE591 UT WOS:A1995TE59100008 PM 7587258 ER PT J AU WEINSTOCK, R LEONG, GB AF WEINSTOCK, R LEONG, GB TI ETHICAL ISSUES IN PSYCHIATRY SO CURRENT OPINION IN PSYCHIATRY LA English DT Article AB Ongoing ethical dilemmas in psychiatry continue in those areas in which legal and social interests compete with the profession's concern for patient welfare. This is especially highlighted by the psychiatric ethical problems raised by the recent renewed societal interest in euthanasia and physician-assisted suicide. C1 UNIV CALIF LOS ANGELES,PSYCHIAT SERV,W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA. HARRY S TRUMAN MEM VET HOSP,PSYCHIAT SERV,COLUMBIA,MO 65201. UNIV MISSOURI,DEPT NEUROL & PSYCHIAT,COLUMBIA,MO. NR 21 TC 0 Z9 0 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0951-7367 J9 CURR OPIN PSYCHIATR JI Curr. Opin. Psychiatr. PD NOV PY 1995 VL 8 IS 6 BP 383 EP 385 DI 10.1097/00001504-199511000-00008 PG 3 WC Psychiatry SC Psychiatry GA TG506 UT WOS:A1995TG50600008 ER PT J AU KELLEY, LC DEERING, KC KAYE, ET AF KELLEY, LC DEERING, KC KAYE, ET TI CUTANEOUS MYCOBACTERIUM-CHELONEI PRESENTING IN AN IMMUNOCOMPETENT HOST - CASE-REPORT AND REVIEW OF THE LITERATURE SO CUTIS LA English DT Article ID DISSEMINATED INFECTION; CLARITHROMYCIN AB Mycobacterium chelonei is in the family of fast-growing atypical mycobacteria. Clinical infection can have varying presentations. We present a case of a nonhealing thigh abscess that grew Mycobacterium chelonei on culture. The clinical presentations and causes of Mycobacterium chelonei infections are reviewed, along with current treatment options. RP KELLEY, LC (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,DEPT DERMATOL,ACC 489,BOSTON,MA 02114, USA. NR 10 TC 19 Z9 19 U1 0 U2 0 PU EXCERPTA MEDICA INC PI BELLE MEAD PA 105 RAIDER BLVD, BELLE MEAD, NJ 08502 SN 0011-4162 J9 CUTIS JI Cutis PD NOV PY 1995 VL 56 IS 5 BP 293 EP 295 PG 3 WC Dermatology SC Dermatology GA TF332 UT WOS:A1995TF33200012 PM 8565617 ER PT J AU MEYER, JS OBARA, K MURAMATSU, K MORTEL, KF SHIRAI, T AF MEYER, JS OBARA, K MURAMATSU, K MORTEL, KF SHIRAI, T TI COGNITIVE PERFORMANCE AFTER SMALL STROKES CORRELATES WITH ISCHEMIA, NOT ATROPHY OF THE BRAIN SO DEMENTIA LA English DT Article DE VASCULAR DEMENTIA; CEREBRAL ATROPHY; RECURRENT INFARCTION; CEREBRAL BLOOD FLOW ID MULTI-INFARCT DEMENTIA; CEREBRAL BLOOD-FLOW; RISK-FACTORS; MULTIINFARCT DEMENTIA; COMPUTED-TOMOGRAPHY; VASCULAR DEMENTIA; IMPAIRMENT; DEFICITS; LESIONS; COHORT AB Computerized tomographic measures of recurrent cerebral infarctions, atrophy and local perfusion were all prospectively correlated with cognitive testing during treatment of risk factors plus antiplatelet therapy among vascular dementia patients. Neurological and cognitive status were quantified among 22 demented patients with small strokes and compared with 22 age-matched normal volunteers. In vascular dementia, risk factor control plus antiplatelet therapy reduced cerebral infarctions, increased perfusion, and stabilized or improved cognitive test performance, despite age-related, progressive cerebral atrophy. C1 BAYLOR COLL MED,DEPT VET AFFAIRS MED CTR,CEREBROVASC RES LABS,HOUSTON,TX 77030. NR 51 TC 15 Z9 16 U1 1 U2 2 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1013-7424 J9 DEMENTIA JI Dementia PD NOV-DEC PY 1995 VL 6 IS 6 BP 312 EP 322 PG 11 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA TD390 UT WOS:A1995TD39000003 PM 8563784 ER PT J AU CHEN, Q JOHNSON, DM HAUDENSCHILD, DR GOETINCK, PF AF CHEN, Q JOHNSON, DM HAUDENSCHILD, DR GOETINCK, PF TI PROGRESSION AND RECAPITULATION OF THE CHONDROCYTE DIFFERENTIATION PROGRAM - CARTILAGE MATRIX PROTEIN IS A MARKER FOR CARTILAGE MATURATION SO DEVELOPMENTAL BIOLOGY LA English DT Article ID PROTEOGLYCAN CORE PROTEIN; COLLAGEN TYPE-I; VONWILLEBRAND-FACTOR; TRANSGENIC MICE; X COLLAGEN; CHICK-EMBRYO; IMMUNOHISTOCHEMICAL LOCALIZATION; MESSENGER-RNAS; GROWTH-FACTOR; LINK PROTEIN AB During endochondral bone formation, chondrocytes in the cartilaginous anlage of long bones progress through a spatially and temporally regulated differentiation program before being replaced by bone. To understand this process, we have characterized the differentiation program and analyzed the relationship between chondrocytes and their extracellular environment in the regulation of the program. Our results indicate that, within an epiphyseal growth plate, the zone of proliferating chondrocytes is not contiguous with the zone of hypertrophic chondrocytes identified by the transcription of the type X collagen gene. We find that the postproliferative chondrocytes which make up the zone between the zones of proliferation and hypertrophy specifically transcribe the gene for cartilage matrix protein (CMP). This zone has been termed the zone of maturation. The identification of this unique population of chondrocytes demonstrates that the chondrocyte differentiation program consists of at least three stages. CMP translation products are present in the matrix surrounding the nonproliferative chondrocytes of both the zones of maturation and hypertrophy. Thus, CMP is a marker for postmitotic chondrocytes. As a result of the changes in gene expression during the differentiation program, chondrocytes in each zone reside in an extracellular matrix with a unique macromolecular composition. Chondrocytes in primary cell culture can proceed through the same differentiation program as they do in the cartilaginous rudiments. In culture, a wave of differentiation begins in the center of a colony and spreads to its periphery. The cessation of proliferation coincides with the appearance of CMP and eventually the cells undergo hypertrophy and synthesize type X collagen. These results reveal distinct switches at the proliferative-maturation transition and at the maturation-hypertrophy transition during chondrocyte differentiation and indicate that chondrocytes synthesize new matrix molecules and thus modify their preexisting microenvironment as differentiation progresses. However, when ''terminally'' differentiated hypertrophic chondrocytes are released from their surrounding environment and incubated in pellet culture, they stop type X collagen synthesis, resume proliferation, and reinitiate aggrecan synthesis. Eventually they cease proliferation and reinitiate CMP synthesis and finally type X collagen. Thus they are capable of recapitulating all three stages of the differentiation program in vitro. The data suggest a high degree of plasticity in the chondrocyte differentiation program and demonstrate that the progression and maintenance of this program is regulated, at least in part, by the extracellular environment which surrounds a differentiating chondrocyte during endochondral bone formation. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP, CUTANEOUS BIOL RES CTR, BOSTON, MA 02129 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02129 USA. RI Haudenschild, Dominik/B-2381-2008; Chen, Qian/C-4354-2011 OI Haudenschild, Dominik/0000-0001-9947-9864; Chen, Qian/0000-0003-4406-5618 FU NICHD NIH HHS [HD 22016]; NIGMS NIH HHS [P20 GM104937] NR 59 TC 96 Z9 96 U1 0 U2 3 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0012-1606 EI 1095-564X J9 DEV BIOL JI Dev. Biol. PD NOV PY 1995 VL 172 IS 1 BP 293 EP 306 DI 10.1006/dbio.1995.0024 PG 14 WC Developmental Biology SC Developmental Biology GA TD804 UT WOS:A1995TD80400024 PM 7589809 ER PT J AU SCHLENSTEDT, G WONG, DH KOEPP, DM SILVER, PA AF SCHLENSTEDT, G WONG, DH KOEPP, DM SILVER, PA TI MUTANTS IN A YEAST RAN BINDING-PROTEIN ARE DEFECTIVE IN NUCLEAR TRANSPORT SO EMBO JOURNAL LA English DT Article DE NUCLEAR IMPORT; RAN; RNA EXPORT; YEAST; YRB1 ID MESSENGER-RNA TRANSPORT; SACCHAROMYCES-CEREVISIAE; GENE-PRODUCT; ESCHERICHIA-COLI; PORE COMPLEX; 2 STEPS; IMPORT; LOCALIZATION; TRANSLOCATION; PURIFICATION AB Ran, a Ras-like GTPase, has been implicated in controlling the movement of proteins and RNAs in and out of the nucleus, We have constructed strains of Saccharomyces cerevisiae which produce fusion proteins containing glutathione-S-transferase (GST) fused to Gsp1p, which encodes the essential yeast Ran homolog, and a mutant form of Gsp1p that mimics the GTP-bound state, A major protein with the apparent size of 34 kDa co-purifies with the GTP-bound form of Gsp1p, This protein was identified as Yrb1p (Yeast Ran Binding Protein) and stimulates GTP hydrolysis by Gsp1p in the presence of Rna1p, the Gsp1 GTPase activating protein. Yrb1p is located in the cytoplasm with some concentration at the nuclear periphery. Temperature-sensitive yrb1 mutants are defective in nuclear protein import and RNA export. A mutation in the highly conserved Ran binding region of Yrb1p reduces its ability to interact with Gsp1p. These data indicate that Yrb1p functions with Gsp1p and suggest that together they can control transport of macromolecules across the nuclear envelope. C1 HARVARD UNIV,SCH MED,DEPT BIOL CHEM & MOLEC PHARMACOL,BOSTON,MA 02115. DANA FARBER CANC INST,BOSTON,MA 02115. NR 63 TC 133 Z9 134 U1 1 U2 3 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 NOV 1 PY 1995 VL 14 IS 21 BP 5367 EP 5378 PG 12 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TF681 UT WOS:A1995TF68100023 PM 7489726 ER PT J AU INOMATA, N AKIYAMA, M KUBOTA, N JUPPNER, H AF INOMATA, N AKIYAMA, M KUBOTA, N JUPPNER, H TI CHARACTERIZATION OF A NOVEL PARATHYROID-HORMONE (PTH) RECEPTOR WITH SPECIFICITY FOR THE CARBOXYL-TERMINAL REGION OF PTH-(1-84) SO ENDOCRINOLOGY LA English DT Article ID PLASMA-MEMBRANE; PEPTIDE; CELLS; FRAGMENTS; BINDING; PROTEIN; EXPRESSION; CALCIUM; INVITRO; KIDNEY AB Carboxyl-terminal fragments of PTH (C-PTH) appear to have biological properties different from those mediated by the amino-terminal portions of PTH and PTH-related peptide (PTHrP). To characterize a C-PTH receptor that may be involved in mediating these functions, we performed RRAs and affinity cross-linking studies with several clonal cell lines. Radiolabeled recombinant [Leu(8,18),Tyr(34)]human PTH-(1-84) [mutPTH-(1-84)] and [Tyr(34)]human PTH-(19-84) [mutPTH-(19-84)] showed little or no specific binding to stably expressed recombinant PTH/PTHrP receptors. However, high affinity binding was observed using osteoblast-like osteosarcoma (ROS 17/2.8) and rat parathyroid (PT-r3) cells. The apparent K-d values were 20-30 nM for PTH-(1-84), mutPTH-(1-84), and mutPTH-(19-84), respectively; 400-800 nM for PTH-(39-84); and more than 5000 nM for PTH-(53-84). [Nle(8,18),Tyr(34)]bovine PTH-(1-34)amide [PTH-(1-34)], PTH-(44-68), PTHrP-(37-74), and PTHrP-(109-141) showed no displacement of either radioligand. C-PTH receptor number was increased up to a-fold by pretreating ROS 17/2.8 cells with increasing doses of PTH-(134), PTH-(1-84), or 8-bromo-cAMP, whereas no change was observed in response to dexamethasone or PTH-(39-84). Cross-linking studies using radiolabeled mutPTH-(1-84) or mutPTH-(19-84) revealed specific labeling of two proteins in ROS 17/2.8 cells that were approximately 40 and 90 kilodaltons in size (including the radioligand of approximately 10 kilodaltons). The intensity of affinity labeling of both proteins was dose dependently inhibited by increasing concentrations of unlabeled PTH-(1-84) and several carboxyl-terminal PTH-(1-84) fragments, but not by PTH-(1-34). Similar studies with PT-r3 cells revealed only a single protein band of about 90 kilodaltons. These data indicate that the carboxyl-terminal portion of PTH-(1-84) binds specifically to a unique receptor/binding protein distinct from the previously isolated PTH/PTHrP receptor. C1 MASSACHUSETTS GEN HOSP, DEPT MED, ENDOCRINE UNIT, BOSTON, MA 02114 USA. CHUGAI PHARMACEUT CO LTD, SHIZUOKA, JAPAN. HARVARD UNIV, SCH MED, BOSTON, MA USA. FU NIDDK NIH HHS [DK-11794] NR 29 TC 100 Z9 101 U1 0 U2 0 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1995 VL 136 IS 11 BP 4732 EP 4740 DI 10.1210/en.136.11.4732 PG 9 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TB983 UT WOS:A1995TB98300002 PM 7588200 ER PT J AU ZIEGLER, TR ALMAHFOUZ, A PEDRINI, MT SMITH, RJ AF ZIEGLER, TR ALMAHFOUZ, A PEDRINI, MT SMITH, RJ TI A COMPARISON OF RAT SMALL-INTESTINAL INSULIN AND INSULIN-LIKE GROWTH-FACTOR-I RECEPTORS DURING FASTING AND REFEEDING SO ENDOCRINOLOGY LA English DT Article ID IGF-I; BINDING-PROTEINS; SKELETAL-MUSCLE; GASTROINTESTINAL-TRACT; SMALL-BOWEL; EXPRESSION; GUT; COLON; IDENTIFICATION; RESECTION AB Insulin-like growth factor I (IGF-I) and insulin may be important regulators of intestinal growth. To investigate small intestinal IGF-I receptors (IGF-IR) and insulin receptors (IR) during intestinal cell atrophy and regeneration, we compared indexes of IGF-IR and IR expression in rat jejunum after 72 h of fasting and 24-72 h-of enteral refeeding. Fasting induced intestinal atrophy, reduced plasma insulin and IGF-I concentrations, and markedly decreased jejunal IGF-I messenger RNA (mRNA) levels; these changes were reversed by refeeding. Fasting significantly increased jejunal specific insulin binding, IR content (to 230% of the fed control value), and the 9.6- and 7.4-kilobase IR mRNA transcript levels (to 202% and 218% of control values, respectively). These IR indexes rapidly decreased to control levels with refeeding. Levels of IGF-IR (by Scatchard analysis) and IGF-I-R mRNA were not significantly altered with fasting. The 11-kilobase IGF-IR mRNA transcript increased significantly during the first 24 h of refeeding (to 166% of the control value), and IGF-IR number rose 3-fold. We conclude that rat jejunal IR and IGF-IR are differentially regulated by nutrient availability. Up-regulation of jejunal IGF-I and IGF-IR expression during refeeding suggests a role for the IGF action pathway in gut trophic responses to enteral nutrients. C1 HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, JOSLIN RES LAB, BOSTON, MA 02115 USA. HARVARD UNIV, BRIGHAM & WOMENS HOSP, SCH MED, DEPT MED, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK-43038, DK-48503]; NIGMS NIH HHS [GM 36428] NR 49 TC 39 Z9 39 U1 0 U2 2 PU ENDOCRINE SOC PI CHEVY CHASE PA 8401 CONNECTICUT AVE, SUITE 900, CHEVY CHASE, MD 20815-5817 USA SN 0013-7227 EI 1945-7170 J9 ENDOCRINOLOGY JI Endocrinology PD NOV PY 1995 VL 136 IS 11 BP 5148 EP 5154 DI 10.1210/en.136.11.5148 PG 7 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TB983 UT WOS:A1995TB98300055 PM 7588253 ER PT J AU Li, FR AF Li, FR TI Identification and management of inherited cancer susceptibility SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE germline mutations; inherited cancer susceptibility; tumor suppressor genes; cancer genetics; chemoprevention ID MOLECULAR EPIDEMIOLOGY; COLON-CANCER; GENE; RETINOBLASTOMA; PREVENTION; MUTATIONS; FAMILIES; HOMOLOG; BREAST AB Identification of inherited cancer-predisposing genes offers opportunities for cancer prevention. Inherited susceptibility genes have been identified, primarily through studies of unusual cancer cases and families but also through general population studies. Examples include the RB1 gene for retinoblastoma; the WT1 gene for Wilms' tumor; germline p53 mutations in families with the Li-Fraumeri syndrome; the NF1 and NF2 genes for neuroblastomatosis, types 1 and 2; the VHL gene for renal cancer and other tumors associated with Von Hippel-Lindau disease; the APC gene for aderomatous polyposis coli; the BRCA1 gene for hereditary breast and ovarian cancer; and the mismatch repair genes for colon and other common cancers. For some cancers, identification of gene carriers might be beneficial for targeting screening and chemopreventive interventions. On the other hand, predisposition testing for cancer has the potential for harm from loss of insurability and employability, psychological distress, social stigmatization and other adverse effects. Research is needed to identify predisposition testing procedures that maximize benefits while minimizing harm to subjects. Chemoprevention trials in genetically susceptible populations offer the prospect of finding effective methods of reducing future cancer risk. C1 Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, Boston, MA 02115 USA. RP Li, FR (reprint author), Harvard Univ, Sch Publ Hlth, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. EM frederick_li@dfci.harvard.edu NR 26 TC 15 Z9 15 U1 0 U2 2 PU US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE PI RES TRIANGLE PK PA NATL INST HEALTH, NATL INST ENVIRONMENTAL HEALTH SCIENCES, PO BOX 12233, RES TRIANGLE PK, NC 27709-2233 USA SN 0091-6765 J9 ENVIRON HEALTH PERSP JI Environ. Health Perspect. PD NOV PY 1995 VL 103 SU 8 BP 297 EP 300 DI 10.2307/3432329 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA V42AT UT WOS:000202841100032 PM 8741802 ER PT J AU Suit, HD Spiro, IJ Tanabe, K AF Suit, HD Spiro, IJ Tanabe, K TI Dermatofibrosarcoma protuberans: Control by radiation SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 1 Z9 1 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 218 EP 218 PG 2 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900223 ER PT J AU Fitzek, MM Aronen, H Efird, J Hochberg, F Fischman, A Pardo, FS AF Fitzek, MM Aronen, H Efird, J Hochberg, F Fischman, A Pardo, FS TI PET-FDG uptake as a prognostic indicator in gliomas SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 266 EP 266 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900272 ER PT J AU Nakfoor, BM Spiro, IJ Martins, P Effird, J Wang, CC AF Nakfoor, BM Spiro, IJ Martins, P Effird, J Wang, CC TI Locoregional control and disease specific survival after accelerated hyperfractionated radiotherapy in the treatment of supraglottic carcinoma SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 389 EP 389 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900390 ER PT J AU Posner, M Dreyfuss, A Norris, C Costello, R Rossi, R Poulin, M Clark, J Busse, P AF Posner, M Dreyfuss, A Norris, C Costello, R Rossi, R Poulin, M Clark, J Busse, P TI A phase II trial of docetaxel in squamous cell cancer of the head and neck SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 DANA FARBER CANC INST,HEAD & NECK ONCOL PROGRAM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 421 EP 421 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900422 ER PT J AU Zietman, AL Dallow, KC Shipley, WU AF Zietman, AL Dallow, KC Shipley, WU TI The treatment of localized prostate cancer by external beam irradiation: Long-term freedom from biochemical recurrence SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 459 EP 459 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900461 ER PT J AU Bodis, S Siziopikou, KP Harris, JR Schnitt, SJ Fisher, DE AF Bodis, S Siziopikou, KP Harris, JR Schnitt, SJ Fisher, DE TI Apoptosis accounts for the necrosis seen in DCIS SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 JOINT CTR RADIAT THERAPY,BOSTON,MA. BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,SCH MED,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA. UNIV ZURICH HOSP,ZURICH,SWITZERLAND. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 651 EP 651 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900648 ER PT J AU Spiro, IJ Suit, HD Fanberg, J Rosenberg, AE AF Spiro, IJ Suit, HD Fanberg, J Rosenberg, AE TI Combined radiation and surgery for malignant fibrous histiocytoma of subcutaneous tissue SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 864 EP 864 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91900862 ER PT J AU Shipley, UA AF Shipley, UA TI Chemotherapy and radiation therapy with selective organ-sparing treatment of invasive bladder cancer SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract ID PRESERVATION; CARCINOMA C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 4 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 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 1003 EP 1003 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91901000 ER PT J AU Anne, PR Triau, CM Coen, J Efird, JT Powell, SN AF Anne, PR Triau, CM Coen, J Efird, JT Powell, SN TI Lymphedema following conservative management of early stage breast cancer SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 1030 EP 1030 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91901027 ER PT J AU Shipley, WU Kaufman, DS Zietman, AL Griffin, PP Heney, NM Althausen, AF AF Shipley, WU Kaufman, DS Zietman, AL Griffin, PP Heney, NM Althausen, AF TI Selective bladder preservation by combined modality therapy for invasive bladder cancer SO EUROPEAN JOURNAL OF CANCER LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0959-8049 J9 EUR J CANCER JI Eur. J. Cancer PD NOV PY 1995 VL 31A SU 5 BP 1141 EP 1141 PG 1 WC Oncology SC Oncology GA TH919 UT WOS:A1995TH91901136 ER PT J AU HANDFORTH, A MAI, T TREIMAN, DM AF HANDFORTH, A MAI, T TREIMAN, DM TI RISING DOSE STUDY OF SAFETY AND TOLERANCE OF FLUNARIZINE SO EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY LA English DT Article DE FLUNARIZINE; SEIZURES ID PLACEBO-CONTROLLED TRIAL; REFRACTORY CHILDHOOD EPILEPSY; DOUBLE-BLIND CROSSOVER; ADD-ON THERAPY AB In a recent NIH-sponsored parallel-group placebo-controlled blinded study of flunarizine for the treatment of partial-onset seizures, the flunarizine serum concentration was controlled to a constant level among patients in order to reduce response variability. Flunarizine was found to exhibit modest anti-epileptic efficacy. A potential criticism of this study is that the chosen controlled concentration was too low to determine optimal efficacy. As a participating center in this study we investigated the effect of higher doses of open-label flunarizine on seizure frequency in 16 patients with refractory partial seizures. Following the completion of the blinded placebo/flunarizine phase, all patients were initiated at the flunarizine dose calculated to result in a serum concentration of 60 ng . ml(-1). The dose was subsequently increased each 8-12 weeks to a maximum of 2.7 times the initial dose. On the initial maintenance flunarizine dose, seizure control was improved, with an average seizure reduction of 47% compared to pre-blinded-phase baseline. When higher doses were administered, adverse reactions were more common yet improved seizure control did not occur in most patients. These findings complement those of the concentration-controlled NIH study and suggest that appropriate flunarizine doses were utilized in that study. C1 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT NEUROL,LOS ANGELES,CA 90024. RP HANDFORTH, A (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,NEUROL SERV,11301 WILSHIRE BLVD,LOS ANGELES,CA 90073, USA. FU NINDS NIH HHS [N01-NS-7-2328] NR 9 TC 6 Z9 7 U1 1 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0031-6970 J9 EUR J CLIN PHARMACOL JI Eur. J. Clin. Pharmacol. PD NOV PY 1995 VL 49 IS 1-2 BP 91 EP 94 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TE475 UT WOS:A1995TE47500016 PM 8751028 ER PT J AU MINETA, Y EISENBERG, E STRASSMAN, AM AF MINETA, Y EISENBERG, E STRASSMAN, AM TI DISTRIBUTION OF FOS-LIKE IMMUNOREACTIVITY IN THE CAUDAL MEDULLARY RETICULAR-FORMATION FOLLOWING NOXIOUS FACIAL STIMULATION IN THE RAT SO EXPERIMENTAL BRAIN RESEARCH LA English DT Article DE MEDULLARY RETICULAR FORMATION; C-FOS; NOCICEPTION; TRIGEMINAL NUCLEUS CAUDALIS; MEDULLARY DORSAL HORN ID TRIGEMINAL SUBNUCLEUS CAUDALIS; HETEROTOPIC NOCICEPTIVE INFORMATION; SUPERFICIAL DORSAL HORN; C-FOS; NEURONS; PROJECTIONS; RESPONSES; REPRESENTATION; EXPRESSION; NUCLEUS AB To investigate the topographic organization of nociceptive neurons in the caudal medullary reticular formation, the distribution of cells that exhibit c-fos expression was examined following a unilateral noxious facial stimulus: subcutaneous injection of formalin into the vibrissal pad of awake rats. Labelling for Fos-like immunoreactivity was present in a somatotopic distribution in a region of the lateral reticular formation adjacent to trigeminal nucleus caudalis, which corresponds approximately to lamina V of the medullary dorsal horn. Labelling in adjacent regions of the reticular formation showed no somatotopy but was predominantly ipsilateral. Contralateral labelling was concentrated ventrolaterally around the lateral reticular nucleus and dorsally near the nucleus of the solitary tract. C1 HARVARD UNIV,SCH MED,DEPT NEUROBIOL,BOSTON,MA 02115. SAGA MED SCH,DEPT ANESTHESIOL,SAGA,JAPAN. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. BETH ISRAEL HOSP,DEPT ANESTHESIA,BOSTON,MA 02215. FU NINDS NIH HHS [NS24594] NR 48 TC 13 Z9 14 U1 0 U2 1 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0014-4819 J9 EXP BRAIN RES JI Exp. Brain Res. PD NOV PY 1995 VL 107 IS 1 BP 34 EP 38 PG 5 WC Neurosciences SC Neurosciences & Neurology GA TH219 UT WOS:A1995TH21900005 PM 8751060 ER PT J AU ERICKSON, KA SCHROEDER, A NETLAND, PA AF ERICKSON, KA SCHROEDER, A NETLAND, PA TI VERAPAMIL INCREASES OUTFLOW FACILITY IN THE HUMAN EYE SO EXPERIMENTAL EYE RESEARCH LA English DT Article DE CALCIUM CHANNELS; VERAPAMIL; OUTFLOW FACILITY; HUMAN EYE; CALCIUM SIGNALING; CALCIUM CHANNEL BLOCKERS ID ETHACRYNIC-ACID; CELLS; CHANNEL AB Verapamil, a calcium channel antagonist, causes a reduction of intraocular pressure in humans. This study investigated whether verapamil's effect on intraocular pressure was related to increased outflow facility. Six pairs of human eyes were dissected and anterior segments were perfused under constant pressure with concentrations of verapamil HCl ranging from 10(-10)-10(-3) M. The maximal increase of outflow facility over baseline was 64% at 10(-9) M. These results indicate that verapamil causes a dose related increase in outflow facility in human eyes, which may account for the reduced intraocular pressure following topical administration of verapamil. (C) 1995 Academic Press Limited RP ERICKSON, KA (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OPHTHALMOL,HOWE LAB OPHTHALMOL,BOSTON,MA 02114, USA. FU NEI NIH HHS [EYO 7321] NR 15 TC 27 Z9 27 U1 0 U2 0 PU ACADEMIC PRESS (LONDON) LTD PI LONDON PA 24-28 OVAL RD, LONDON, ENGLAND NW1 7DX SN 0014-4835 J9 EXP EYE RES JI Exp. Eye Res. PD NOV PY 1995 VL 61 IS 5 BP 565 EP 567 DI 10.1016/S0014-4835(05)80050-8 PG 3 WC Ophthalmology SC Ophthalmology GA TC973 UT WOS:A1995TC97300005 PM 8654499 ER PT J AU CHUNG, DC RUSTGI, AK AF CHUNG, DC RUSTGI, AK TI DNA MISMATCH REPAIR AND CANCER SO GASTROENTEROLOGY LA English DT Review ID FAMILIAL ADENOMATOUS POLYPOSIS; NONPOLYPOSIS COLORECTAL-CANCER; TUMOR SUPPRESSOR GENES; MICROSATELLITE INSTABILITY; MOLECULAR-GENETICS; MUTATOR PHENOTYPE; COLON-CANCER; MUTATIONS; CARCINOGENESIS; ASSOCIATION AB The genetic basis of cancer involves certain classes of genes, particularly oncogenes, tumor-suppressor genes, and DNA mismatch repair genes. Originally identified in bacteria and yeast, the human homologues of DNA mismatch repair genes have been implicated in the pathogenesis of the hereditary nonpolyposis colorectal cancer syndromes, as well as a variety of different sporadic cancers. An appreciation of their role in cancer is predicated on an understanding of their function in the processes of DNA repair. This article reviews the recent developments and advances in the biology of the human DNA mismatch repair genes and their involvement in the pathogenesis of cancer. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,GASTROINTESTINAL UNIT,BOSTON,MA 02114. FU NCI NIH HHS [1 U01 CA68618-01]; NIDDK NIH HHS [DK01410] NR 109 TC 115 Z9 120 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD NOV PY 1995 VL 109 IS 5 BP 1685 EP 1699 DI 10.1016/0016-5085(95)90660-6 PG 15 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA TB816 UT WOS:A1995TB81600036 PM 7557155 ER PT J AU JOHNSON, EW IYER, LM RICH, SS ORR, HT GILNAGEL, A KURTH, JH ZABRAMSKI, JM MARCHUK, DA WEISSENBACH, J CLERICUZIO, CL DAVIS, LE HART, BL GUSELLA, JF KOSOFSKY, BE LOUIS, DN MORRISON, LA GREEN, ED WEBER, JL AF JOHNSON, EW IYER, LM RICH, SS ORR, HT GILNAGEL, A KURTH, JH ZABRAMSKI, JM MARCHUK, DA WEISSENBACH, J CLERICUZIO, CL DAVIS, LE HART, BL GUSELLA, JF KOSOFSKY, BE LOUIS, DN MORRISON, LA GREEN, ED WEBER, JL TI REFINED LOCALIZATION OF THE CEREBRAL CAVERNOUS MALFORMATION GENE (CCM1) TO A 4-CM INTERVAL OF CHROMOSOME 7Q CONTAINED IN A WELL-DEFINED YAC CONTIG SO GENOME RESEARCH LA English DT Article ID DINUCLEOTIDE REPEAT POLYMORPHISMS; NATURAL-HISTORY; HUMAN GENOME; LINKAGE MAP; YEAST; CONSTRUCTION; LIBRARIES; ANGIOMAS; VECTORS; LOCI AB Cerebral cavernous malformations (CCM) are vascular lesions present in some 20 million people worldwide that are responsible for seizures, migraine, hemorrhage, and other neurologic problems. Familial cases of CCM can be inherited as an autosomal dominant disorder with variable expression. A gene for CCM (CCM1) was recently mapped to a 33-cM segment of chromosome 7q in a large Hispanic family (Dubovsky et al. 1995). Here, the collection of several new short tandem repeat polymorphisms (STRPs) within the region of interest on 7q and the refinement of the marker order in this region using both linkage analysis in CEPH families and especially YAC-based STS content mapping are described. Affected members of three Hispanic families share allele haplotypes indicating a common ancestral mutation within these families. Using the shared haplotype information along with analysis of crossovers in affected individuals from both the Hispanic and Caucasian families, the region likely to contain the CCM1 gene has been reduced to a 4-cM segment of 7q between D7S2410 and D7S689. All markers within the refined chromosomal segment were located on a single YAC contig estimated to be -2 Mb in size. Four potential candidate genes have been mapped to this region. C1 NIH, NATL CTR HUMAN GENOME RES, BETHESDA, MD 20892 USA. WAKE FOREST UNIV, BOWMAN GRAY SCH MED, DEPT PUBL HLTH SCI & NEUROL, WINSTON SALEM, NC 27157 USA. UNIV MINNESOTA, MINCEP, MINNEAPOLIS, MN 55455 USA. UNIV MINNESOTA, INST HUMAN GENET, MINNEAPOLIS, MN 55455 USA. UNIV MINNESOTA, DEPT LAB MED & PATHOL, MINNEAPOLIS, MN 55455 USA. UNIV MINNESOTA, DEPT NEUROL, MINNEAPOLIS, MN 55455 USA. BARROW NEUROL INST, PHOENIX, AZ 85026 USA. DUKE UNIV, MED CTR, DEPT GENET, DURHAM, NC 27710 USA. GENETHON, F-91000 EVRY, FRANCE. UNIV NEW MEXICO, SCH MED, DEPT PEDIAT, ALBUQUERQUE, NM 87131 USA. UNIV NEW MEXICO, SCH MED, DEPT NEUROL, ALBUQUERQUE, NM 87131 USA. UNIV NEW MEXICO, SCH MED, DEPT RADIOL, ALBUQUERQUE, NM 87131 USA. MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET UNIT, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, NEUROL SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, DEPT PATHOL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. RP MARSHFIELD MED RES FDN, CTR MED GENET, MARSHFIELD, WI 54449 USA. OI Morrison, Leslie/0000-0002-0092-193X FU NINDS NIH HHS [NS16308] NR 45 TC 45 Z9 45 U1 0 U2 0 PU COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT PI COLD SPRING HARBOR PA 1 BUNGTOWN RD, COLD SPRING HARBOR, NY 11724 USA SN 1088-9051 EI 1549-5469 J9 GENOME RES JI Genome Res. PD NOV PY 1995 VL 5 IS 4 BP 368 EP 380 DI 10.1101/gr.5.4.368 PG 13 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA TK367 UT WOS:A1995TK36700005 PM 8750196 ER PT J AU VONDEIMLING, A LOUIS, DN WIESTLER, OD AF VONDEIMLING, A LOUIS, DN WIESTLER, OD TI MOLECULAR PATHWAYS IN THE FORMATION OF GLIOMAS SO GLIA LA English DT Article DE ASTROCYTOMA; OLIGODENDROGLIOMA; GLIOBLASTOMA MULTIFORME; MOLECULAR GENETICS; ONCOGENES; TUMOR SUPPRESSOR GENES; LOSS OF HETEROZYGOSITY; MOLECULAR CLASSIFICATION ID FACTOR RECEPTOR GENE; NEUROFIBROMATOSIS TYPE-1 GENE; HUMAN-MALIGNANT ASTROCYTOMA; GLIOBLASTOMA-MULTIFORME; P53 MUTATIONS; VONRECKLINGHAUSEN NEUROFIBROMATOSIS; DELETIONS; TUMORS; AMPLIFICATION; GROWTH AB The past few years have seen remarkable progress in understanding the molecular genetic basis of glioma formation. Affected oncogenes and tumor suppressor genes have been identified and putative tumor suppressor loci have been mapped. These studies have illustrated distinct molecular pathways for different glial neoplasms. We summarize the findings of an ongoing study initiated to characterize human gliomas on a molecular basis. The data are compiled from 150 astrocytic, oligodendroglial, and mixed gliomas that were assessed for genomic alterations characteristic of these neoplasms, i.e., loss of portions of chromosomes 1p, 9p, 10, 17p, 17q, and 19q, mutations of the p53 tumor suppressor gene, and amplification of the EGF receptor (EGFR) gene. Our findings support the hypothesis that distinct genetic pathways result in the formation of astrocytic and oligodendroglial neoplasms of different malignancy grades, and that glioblastoma multiforme may be subdivided into genetically distinct subsets, Such findings may not only lead to a better understanding of neoplastic transformation in glial cells, but may also have a major impact on clinical neuro-oncology. (C) 1995 Wiley-Liss, Inc. C1 UNIV BONN,MED CTR,DEPT NEUROPATHOL,D-53105 BONN,GERMANY. MASSACHUSETTS GEN HOSP,MOLEC NEUROONCOL LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RI von Deimling, Andreas/F-7774-2013 OI von Deimling, Andreas/0000-0002-5863-540X NR 58 TC 212 Z9 216 U1 0 U2 5 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0894-1491 J9 GLIA JI Glia PD NOV PY 1995 VL 15 IS 3 BP 328 EP 338 DI 10.1002/glia.440150312 PG 11 WC Neurosciences SC Neurosciences & Neurology GA TE716 UT WOS:A1995TE71600011 PM 8586467 ER PT J AU BIEDERMAN, J AF BIEDERMAN, J TI DEVELOPMENTAL SUBTYPES OF JUVENILE BIPOLAR DISORDER SO HARVARD REVIEW OF PSYCHIATRY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; ONSET; COMORBIDITY; PROBANDS; FAMILY; MANIA RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC725,FRUIT ST,BOSTON,MA 02114, USA. FU NIMH NIH HHS [R01 MH-41314-01A2] NR 23 TC 18 Z9 18 U1 1 U2 1 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1067-3229 J9 HARVARD REV PSYCHIAT JI Harv. Rev. Psychiatr. PD NOV-DEC PY 1995 VL 3 IS 4 BP 227 EP 230 DI 10.3109/10673229509017189 PG 4 WC Psychiatry SC Psychiatry GA TJ192 UT WOS:A1995TJ19200005 PM 9384951 ER PT J AU WEBSTER, EW AF WEBSTER, EW TI X-RAYS IN DIAGNOSTIC-RADIOLOGY SO HEALTH PHYSICS LA English DT Article DE X RAYS; DIAGNOSTIC RADIOLOGY; RADIATION, MEDICAL; HISTORICAL PROFILES ID UNITED-STATES; COMPUTED RADIOGRAPHY; PULMONARY NODULES; PERFORMANCE; VOLUME AB An overview of the technical developments in and growth of the diagnostic use of x rays over the century since their discovery is presented. The major developments described include the introduction of the hot cathode x-ray tube, the Potter-Bucky grid, the image intensifier, the computerized tomographic scanner, and the adoption of the digital computer for image processing, display, and storage. Other significant but smaller advances discussed include improved film/screen technology, the rotating anode tube, linear tomography, and some recent advances in image receptors. C1 HARVARD UNIV, SCH MED, DEPT RADIOL, BOSTON, MA 02114 USA. RP WEBSTER, EW (reprint author), MASSACHUSETTS GEN HOSP, FRUIT ST, BOSTON, MA 02114 USA. NR 78 TC 6 Z9 9 U1 0 U2 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0017-9078 EI 1538-5159 J9 HEALTH PHYS JI Health Phys. PD NOV PY 1995 VL 69 IS 5 BP 610 EP 635 DI 10.1097/00004032-199511000-00001 PG 26 WC Environmental Sciences; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Nuclear Science & Technology; Radiology, Nuclear Medicine & Medical Imaging GA TA722 UT WOS:A1995TA72200002 PM 7558857 ER PT J AU UBEL, PA LOEWENSTEIN, G AF UBEL, PA LOEWENSTEIN, G TI THE EFFICACY AND EQUITY OF RETRANSPLANTATION - AN EXPERIMENTAL SURVEY OF PUBLIC-ATTITUDES SO HEALTH POLICY LA English DT Article DE TRANSPLANTATION; EQUITY; PROGNOSIS; ETHICS; HEALTH POLICY ID HEALTH-CARE PRIORITIES; OREGON; TRANSPLANTATION; ORGANS AB Purpose: To measure the relative importance people place on prognosis and retransplantation status in allocating scarce transplantable livers. Methods: 138 subjects were asked to distribute scarce livers amongst transplant candidates with either a 70% chance or a 30% chance of surviving if transplanted, In one group of subjects, the prognostic difference was based on the presence or absence of a 'blood marker.' In the other group, the prognostic difference was based on whether candidates had been previously transplanted or not, with retransplant candidates having a 30% chance of surviving if transplanted. Results: Subjects answering the retransplantation survey gave a higher percentage of organs to the better prognostic group than subjects answering the blood marker survey, with a mean of 71.6% versus 65.0%, although this difference fell just short of statistical significance (P = 0.0581). Retransplantation survey respondents were significantly less likely to want to ignore prognostic information than were blood marker respondents (P = 0.026). Subjects in both survey groups were equally unwilling to abandon the poor prognostic group, with only 18% in each group choosing to give all the available organs to the better prognostic group. Conclusions: Respondents reacted more strongly to prognostic differences when they were due to retransplant status than to the results of a blood test, However, most people were not solely interested in the aggregate medical benefit brought by different allocation systems, but were also interested in the amount of benefit brought to the worst off. C1 CARNEGIE MELLON UNIV,DEPT SOCIAL & DECIS SCI,PHILADELPHIA,PA. RP UBEL, PA (reprint author), VET AFFAIRS MED CTR,UNIV & WOODLAND AVE,PHILADELPHIA,PA 19072, USA. NR 12 TC 32 Z9 32 U1 0 U2 2 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0168-8510 J9 HEALTH POLICY JI Health Policy PD NOV PY 1995 VL 34 IS 2 BP 145 EP 151 DI 10.1016/0168-8510(95)00714-4 PG 7 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA TE821 UT WOS:A1995TE82100005 PM 10153483 ER PT J AU MORADPOUR, D COMPAGNON, B WILSON, BE NICOLAU, C WANDS, JR AF MORADPOUR, D COMPAGNON, B WILSON, BE NICOLAU, C WANDS, JR TI SPECIFIC TARGETING OF HUMAN HEPATOCELLULAR-CARCINOMA CELLS BY IMMUNOLIPOSOMES IN-VITRO SO HEPATOLOGY LA English DT Article ID STERICALLY STABILIZED LIPOSOMES; MONOCLONAL-ANTIBODY; HIGHLY EFFICIENT; UNILAMELLAR LIPOSOMES; MALIGNANT PHENOTYPE; ENCAPSULATED DNA; SURFACE; LUNG; DELIVERY; GROWTH AB The monoclonal antibody AF-20 was raised against the human hepatocellular carcinoma (HCC) cell line FOCUS and binds with high affinity to a rapidly internalized 180-kd homodimeric glycoprotein that is abundantly expressed on the surface of human HCC and other human cancer cell lines. Immunoliposomes were produced by covalently coupling AF-20 to liposomes containing carboxyfluorescein. Interaction of immunoliposomes with various HCC cell lines in vitro was quantitatively assessed by now cytometry and qualitatively analyzed by fluorescence microscopy. Liposomes bearing an isotype-matched nonrelevant monoclonal antibody (MAb) and cell lines not expressing AF-20 antigen served as controls. AF-20-immunoliposomes specifically bound to HCC and other human cancer cell lines expressing the AF-20 antigen and were rapidly internalized at 37 degrees C. Interaction of AF-20-conjugated liposomes with these cell lines was between 5 and 200 times greater than that of unconjugated liposomes, whereas no difference was observed between control liposomes bearing a nonrelevant antibody and unconjugated liposomes. Specificity of liposome-target cell interaction was confirmed by competitive inhibition assays. Kinetic analysis showed rapid association of AF-20 immunoliposomes with target cells, with saturation conditions being reached after 60 minutes, We conclude that the MAb AF-20 directs highly efficient, specific, and rapid targeting of immunoliposomes to human HCC and other human cancer cell lines in vitro, This targeted liposomal delivery system represents a promising approach for the development of immunotargeted diagnosis and therapy strategies against HCC. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CTR CANC,SCH MED,MOLEC HEPATOL LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,CTR BLOOD RES LABS,BOSTON,MA. FU NCI NIH HHS [CA-35711]; NIAAA NIH HHS [AA-02666, AA-08169] NR 36 TC 23 Z9 23 U1 0 U2 2 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0270-9139 J9 HEPATOLOGY JI Hepatology PD NOV PY 1995 VL 22 IS 5 BP 1527 EP 1537 DI 10.1016/0270-9139(95)90161-2 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA TB997 UT WOS:A1995TB99700027 PM 7590672 ER PT J AU BORRESEN, AL LOTHE, RA MELING, GI LYSTAD, S MORRISON, P LIPFORD, J KANE, MF ROGNUM, TO KOLODNER, RD AF BORRESEN, AL LOTHE, RA MELING, GI LYSTAD, S MORRISON, P LIPFORD, J KANE, MF ROGNUM, TO KOLODNER, RD TI SOMATIC MUTATIONS IN THE HMSH2 GENE IN MICROSATELLITE UNSTABLE COLORECTAL CARCINOMAS SO HUMAN MOLECULAR GENETICS LA English DT Article ID DENATURANT GEL-ELECTROPHORESIS; CANCER; INSTABILITY; DNA; HOMOLOG; COLON AB Microsatellite instability is frequently seen in tumors from patients with hereditary nonpolyposis colorectal cancer (HNPCC). Germline mutations in the mismatch repair gene hMSH2 account for approximately 50% of these cases. Tumors from sporadic cases also exhibit this microsatellite instability phenotype, although at a lower frequency, and very few somatically derived mutations have so far been reported in such tumors. In this study DNA from 23 primary colorectal carcinomas (four familial and 19 sporadic cases) exhibiting microsatellite instability were screened for mutations in the hMSH2 gene using constant denaturant gel electrophoresis (CDGE). Among the sporadic cases, five (26%) were found to have somatically derived mutations. One tumor revealed two different mutations, possibly leading to a homozygous inactivation of the gene. One of the four familial cases was classified as having HNPCC, and a germline as well as a somatic mutation were found in this tumor. These results demonstrate that a considerable proportion of sporadic colorectal cancers with microsatellite instability, have somatic mutations in the hMSH2 gene. C1 DIAKONHJEMMET HOSP,DEPT SURG,N-0319 OSLO,NORWAY. UNIV OSLO,NATL HOSP,DEPT FORENS MED,N-0027 OSLO,NORWAY. DANA FARBER CANC INST,DIV CELL & MOLEC BIOL,BOSTON,MA 02115. DANA FARBER CANC INST,MOLEC BIOL CORE FACIL,BOSTON,MA 02115. RP BORRESEN, AL (reprint author), NORWEGIAN RADIUM HOSP,INST CANC RES,DEPT GENET,N-0310 OSLO,NORWAY. FU NCI NIH HHS [CA 06516]; NIAID NIH HHS [AI 28691]; NIGMS NIH HHS [GM 50006] NR 37 TC 143 Z9 146 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD NOV PY 1995 VL 4 IS 11 BP 2065 EP 2072 DI 10.1093/hmg/4.11.2065 PG 8 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA TD659 UT WOS:A1995TD65900008 PM 8589682 ER PT J AU SIEBERT, JD AMBINDER, RF NAPOLI, VM QUINTANILLAMARTINEZ, L BANKS, PM GULLEY, ML AF SIEBERT, JD AMBINDER, RF NAPOLI, VM QUINTANILLAMARTINEZ, L BANKS, PM GULLEY, ML TI HUMAN IMMUNODEFICIENCY VIRUS-ASSOCIATED HODGKINS-DISEASE CONTAINS LATENT, NOT REPLICATIVE, EPSTEIN-BARR-VIRUS SO HUMAN PATHOLOGY LA English DT Article DE IMMUNODEFICIENCY; HODGKINS DISEASE; HUMAN IMMUNODEFICIENCY VIRUS; EPSTEIN-BARR VIRUS; LYMPHOPROLIFERATIVE DISORDER ID REED-STERNBERG CELLS; RAJI CELLS; VIRAL-DNA; AIDS; EXPRESSION; INFECTION; TRANSACTIVATOR; LYMPHOMAS; GENE; DISORDERS AB Severe immunodeficiency is associated with reactivation of latent Epstein-Barr virus (EBV) that is manifested by virus replication. It is unknown whether EBV replication also occurs in the Hodgkin's disease (HD) tissue of patients infected with the human immunodeficiency virus (HIV). Therefore, we studied paraffin-embedded lymph nodes from 13 cases of HIV-associated HD to determine the latent or replicative state of EBV infection. All patients were seropositive HIV-infected men; additional clinical information was available for 12 patients. The risk factor(s) for HIV infection were homosexuality (n = 7), intravenous drug abuse (n = 2), homosexuality and intravenous drug abuse (n = 1), sexual promiscuity (n = 1), or hemophilia (n = 1). Advanced clinical stage and B symptoms were common at the time of initial diagnosis of HD. The histological subtype of Hodgkin's disease was universally mixed cellularity, except for a single case classified as nodular sclerosis. Seven cases exhibited foci of relative lymphoid depletion. Five cases contained foci of necrosis. Reed-Sternberg (RS) cells and RS cell variants were positive for CD30/BerH2 and negative for CD45/LCA CD45RO/UCHL1, and CD20/L26 in all cases. Tumor cells were positive for CD15/LeuM1 in seven cases. In all 13 cases, RS cells and RS cell variants were infected by latent EBV as shown by in situ hybridization to EBV-encoded ribonucleic acid (EBER1). In 12 of 13 cases neoplastic cells coexpressed EBV latent membrane protein 1 (LMP1). EBV replication was examined by two different methods: immunohistochemistry to identify EBV-encoded BZLF1 protein and in situ hybridization to detect EBV BHLF1 transcripts. No positivity in RS or RS cell variants was detected with either assay of EBV replication (95% confidence interval [Cl] = 0% to 23%). The findings confirm that EBV is detected more frequently in HIV-associated HD when compared with immunocompetent patients with HD. The findings also suggest that EBV is tightly latent within RS and RS cell variants of HN-associated HD. It appears that factors other than host immune status are important in maintaining EBV latency in HIV-associated HD. HUM PATHOL 26:1191-1195. This is a US government work. There are no restrictions on its use. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. JOHNS HOPKINS ONCOL CTR,DEPT PATHOL,BALTIMORE,MD. EMORY UNIV,SCH MED,DEPT PATHOL,ATLANTA,GA 30322. GRADY MEM HOSP,DEPT PATHOL,ATLANTA,GA 30335. INST NACL NUTR,DEPT PATHOL,TLALPAN,MEXICO. FU NCI NIH HHS [K08-CA01615, R01 CA 55529, R03 CA 62696] NR 34 TC 26 Z9 27 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 NOV PY 1995 VL 26 IS 11 BP 1191 EP 1195 DI 10.1016/0046-8177(95)90192-2 PG 5 WC Pathology SC Pathology GA TD654 UT WOS:A1995TD65400005 PM 7590691 ER PT J AU GULLEY, ML AMIN, MB NICHOLLS, JM BANKS, PM AYALA, AG SRIGLEY, JR EAGAN, PA RO, JY AF GULLEY, ML AMIN, MB NICHOLLS, JM BANKS, PM AYALA, AG SRIGLEY, JR EAGAN, PA RO, JY TI EPSTEIN-BARR-VIRUS IS DETECTED IN UNDIFFERENTIATED NASOPHARYNGEAL CARCINOMA BUT NOT IN LYMPHOEPITHELIOMA-LIKE CARCINOMA OF THE URINARY-BLADDER SO HUMAN PATHOLOGY LA English DT Article DE EPSTEIN-BARR VIRUS; NASOPHARYNGEAL CARCINOMA; BLADDER CARCINOMA; LYMPHOEPITHELIOMA-LIKE CARCINOMA ID LATENT MEMBRANE-PROTEIN; INSITU HYBRIDIZATION; DNA AMPLIFICATION; CHINESE PATIENTS; EXPRESSION; CELLS; ASSOCIATION; INFECTION; SPECIMENS; GENOMES AB The Epstein-Barr virus (EBV) is associated with nasopharyngeal carcinoma (NPC) and with lymphoepithelioma-like carcinomas developing-in certain anatomic sites. In this study, an in situ hybridization was used to identify EBV-encoded ribonucleic acid (RNA) (EBER1) transcripts in 32 of 45 cases of NPC but not in any of the 11 lymphoepithelioma-like carcinomas developing in the urinary bladder. EBER1 was most commonly detected in those NPCs having undifferentiated or nonkeratinizing squamous histology rather than the keratinizing squamous cell subtype of NPC. The EBV-encoded latent membrane protein I (LMP1) was expressed focally in only seven of 21 EBER1-positive NPCs by an immunohistochemical technique. These findings imply that EBER1 hybridization is more sensitive than LMP1 immunohistochemistry on paraffin sections in detecting carcinoma-associated virus. Previous in vitro studies have suggested that LMP1-expression might be a function of differentiation, but this study-of naturally infected NPCs showed no strong correlation between LMP1 positivity and degree of tumor differentiation, albeit a limited spectrum of differentiation that could be examined. In two cases in which frozen tissue was available, the NPCs were monoclonal with respect to viral DNA structure, implying that the virus was present before malignant transformation. Unlike NPCs, the lymphoepithelioma-like carcinomas of the bladder were uniformly EBV negative, lending further evidence to the growing body of literature linking EBV with lymphoepithelial carcinomas of foregut-derived tissues but not with similar-appearing tumors developing in other anatomic sites. HUM PATHOL 26:1207-1214. This is a US government work. There are no restrictions on its use. C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. HENRY FORD HOSP,DEPT PATHOL,DETROIT,MI 48202. UNIV HONG KONG,DEPT PATHOL,HONG KONG,HONG KONG. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT PATHOL,HOUSTON,TX 77030. SUNNYBROOK MED CTR,DEPT PATHOL,TORONTO,ON M4N 3M5,CANADA. RP GULLEY, ML (reprint author), UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,7703 FLOYD CURL DR,SAN ANTONIO,TX 78284, USA. FU NCI NIH HHS [K08-CA01615] NR 55 TC 63 Z9 65 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD NOV PY 1995 VL 26 IS 11 BP 1207 EP 1214 DI 10.1016/0046-8177(95)90195-7 PG 8 WC Pathology SC Pathology GA TD654 UT WOS:A1995TD65400008 PM 7590694 ER PT J AU GAFFEY, MJ IEZZONI, JC MEREDITH, SD BOYD, JC STOLER, MH WEISS, LM ZUKERBERG, LR LEVINE, PA ARNOLD, A WILLIAMS, ME AF GAFFEY, MJ IEZZONI, JC MEREDITH, SD BOYD, JC STOLER, MH WEISS, LM ZUKERBERG, LR LEVINE, PA ARNOLD, A WILLIAMS, ME TI CYCLIN D1 (PRAD1, CCND1) AND GLUTATHIONE-S-TRANSFERASE-PI GENE-EXPRESSION IN HEAD AND NECK SQUAMOUS-CELL CARCINOMA SO HUMAN PATHOLOGY LA English DT Article DE CHROMOSOME 11Q13; CYCLINS; CYCLIN D1; GLUTATHIONE-S-TRANSFERASE-PI ID CHROMOSOME 11Q13; FREQUENT AMPLIFICATION; CANDIDATE ONCOGENE; BCL-1 LOCUS; CANCER; REARRANGEMENT; CLONING; TUMORS AB Chromosome 11q13 amplification has been identified in a subset of head and neck squamous cell carcinomas (H&N SCCs). This: region contains several putative oncogenes, including cyclin D1 (PRAD1, CCND1), which encodes for an important cell cycle regulatory protein, and the locus encoding for the drug-detoxifying enzyme glutathione-S-transferase-pi (GST-pi). To determine the relationship of cyclin D1 and GST-pi gene amplification to expression of the encoded proteins, the authors examined 64 H&N SCCs by both Southern blot hybridization and immunohistochemistry using a recently described, affinity-purified, anticyclin D1 polyclonal antibody no. 19 as well as a polyclonal antibody against GST-pi. Anticyclin D1 antibody no. 19 labeled the tumor cell nuclei in 28 (44%) of the H&N SCCs, whereas cytoplasmic immunoreactivity for GST-pi was noted in 55 (86%) neoplasms. By Southern blot 24 tumors (37.5%) showed twofold to tenfold amplification of 11q13 loci; only two of these were coamplified for GST-pi. Immunopositivity with anticyclin D1 antibody no. 19 but not anti-GST-pi significantly correlated with 11q13 amplification (P <.0001). Of the 28 tumors positive with anticyclin D1 antibody no. 19, however, only 18 (64%) were amplified for 11q13, and six amplified tumors did not react with the no. 19 antibody. A strong trend was noted between anticyclin D1 antibody no. 19 reactivity and a hypopharyngeal primary site (P =.053), but no correlations were observed between immunoreactivity and cytological grade, architectural pattern, pathological stage, and disease-free or overall survival. The inconsistent association of cyclin D1 immunoreactivity with 11q13 amplification indicates that other mechanisms may exist for protein overexpression; Immunoreactivity for the GST-pi protein is prevalent in H&N SCC but is clearly unassociated with amplification. In this series, the presence or extent of cyclin D1 and GST-pi immunoreactivity was of no proven prognostic benefit in H&N SCC. Copyright (C) 1995 by W.B. Saunders Company C1 UNIV VIRGINIA,HLTH SCI CTR,DEPT PATHOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,HLTH SCI CTR,DEPT OTOLARYNGOL,CHARLOTTESVILLE,VA 22908. UNIV VIRGINIA,HLTH SCI CTR,DEPT INTERNAL MED,CHARLOTTESVILLE,VA 22908. CITY HOPE NATL MED CTR,DEPT PATHOL,DUARTE,CA 91010. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ENDOCRINE ONCOL,BOSTON,MA 02114. RP GAFFEY, MJ (reprint author), UNIV VIRGINIA,HLTH SCI CTR,DEPT SURG PATHOL,BOX 214,CHARLOTTESVILLE,VA 22908, USA. FU NCI NIH HHS [P30 CA 44579] NR 29 TC 46 Z9 47 U1 1 U2 3 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 NOV PY 1995 VL 26 IS 11 BP 1221 EP 1226 DI 10.1016/0046-8177(95)90197-3 PG 6 WC Pathology SC Pathology GA TD654 UT WOS:A1995TD65400010 PM 7590696 ER PT J AU DOSS, BJ GREENE, MF HILL, J HEFFNER, LJ BIEBER, FR GENEST, DR AF DOSS, BJ GREENE, MF HILL, J HEFFNER, LJ BIEBER, FR GENEST, DR TI MASSIVE CHRONIC INTERVILLOSITIS ASSOCIATED WITH RECURRENT ABORTIONS SO HUMAN PATHOLOGY LA English DT Article DE RECURRENT ABORTION; SPONTANEOUS ABORTION; INTERVILLOSITIS; CHRONIC VILLITIS; ALPHA-FETOPROTEIN; TH1-TYPE CYTOKINES ID MATERNAL FLOOR INFARCTION; SERUM ALPHA-FETOPROTEIN; UNKNOWN ETIOLOGY; PREGNANCY LOSS; VILLITIS; PLACENTA; WOMEN; CELLS; INFECTION; PRODUCTS AB Massive chronic intervillositis (MCI) is an unusual placental lesion associated with poor fetal growth and adverse pregnancy outcome; it has not previously been associated with spontaneous abortion or recurrent pregnancy loss. This article reports a patient who had 10 spontaneous abortions with repetitious massive chronic intervillositis documented in four of five gestations spanning all three trimesters. Characteristic placental histology included massive infiltration of the maternal intervillous space by chronic inflammatory cells and fibrin, without associated chronic villitis; the cellular infiltrate was composed predominantly of LCA and CD68 immunoreactive cells with scattered CD45RO positivity, consistent with a monocyte/macrophage population with occasional T lymphocytes. Elevated maternal serum alphafetoprotein was documented in two pregnancies, These findings support the concept that this unusual placental lesion may have an immunologic basis, and suggest that MCI may be a histopathologically recognizable cause of recurrent spontaneous abortion. Copyright (C) 1995 by W.B. Saunders Company C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,DIV WOMENS & PERINATAL PATHOL,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. HARVARD UNIV,CTR RECURRENT MISCARRIAGE,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. UNIV CHICAGO,DEPT PATHOL,CHICAGO,IL 60637. NR 40 TC 47 Z9 49 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 NOV PY 1995 VL 26 IS 11 BP 1245 EP 1251 DI 10.1016/0046-8177(95)90201-5 PG 7 WC Pathology SC Pathology GA TD654 UT WOS:A1995TD65400014 PM 7590700 ER PT J AU SMIR, BN RAMAIKA, CA CHO, CG GULLEY, ML AF SMIR, BN RAMAIKA, CA CHO, CG GULLEY, ML TI MOLECULAR EVIDENCE LINKS LYMPHOMATOUS POLYPOSIS OF THE GASTROINTESTINAL-TRACT WITH MANTLE CELL LYMPHOMA SO HUMAN PATHOLOGY LA English DT Note DE NON-HODGKINS LYMPHOMA; GASTROINTESTINAL POLYP; POLYPOSIS; BCL-1 ID LYMPHOCYTIC LYMPHOMA; CENTROCYTIC LYMPHOMA; ZONE LYMPHOMA; INTERMEDIATE DIFFERENTIATION; REARRANGEMENTS; DIAGNOSIS; GENE AB Lymphomatous polyposis (LP) is a subtype of non-Hodgkin's lymphoma manifested by numerous polyps affecting long segments of the gastrointestinal tract. The malignant cells of LP often share morphological and immunophenotypic similarity with cells of nodal-based mantle cell lymphoma. Recent genetic studies have shown that mantle cell lymphomas frequently possess a characteristic translocation of the JH/bcl-1 loci. In this study, polymerase chain reaction (PCR) and Southern blot analysis were used to show the presence of JH/bcl-1 translocation in a typical case of LP of the gastrointestinal tract, This provides strong molecular evidence for a biologic link between LP and mantle cell lymphoma. The findings also imply that detection of this translocation may be useful in the diagnosis of morphologically equivocal gastrointestinal biopsy specimens. HUM PATHOL 26:1282-1285. This is a US government work. There are no restrictions on its use. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 23 TC 12 Z9 12 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0046-8177 J9 HUM PATHOL JI Hum. Pathol. PD NOV PY 1995 VL 26 IS 11 BP 1282 EP 1285 DI 10.1016/0046-8177(95)90207-4 PG 4 WC Pathology SC Pathology GA TD654 UT WOS:A1995TD65400020 PM 7590706 ER PT J AU DAVDA, RK STEPNIAKOWSKI, KT LU, G ULLIAN, ME GOODFRIEND, TL EGAN, BM AF DAVDA, RK STEPNIAKOWSKI, KT LU, G ULLIAN, ME GOODFRIEND, TL EGAN, BM TI OLEIC-ACID INHIBITS ENDOTHELIAL NITRIC-OXIDE SYNTHASE BY A PROTEIN-KINASE C-INDEPENDENT MECHANISM SO HYPERTENSION LA English DT Article DE FATTY ACIDS, NONESTERIFIED; NITRIC OXIDE; ENDOTHELIUM, VASCULAR; ENDOTHELIUM-DERIVED RELAXING FACTOR; HYPERTENSION, OBESITY ID FATTY-ACIDS; VASCULAR-RESPONSE; NORMOTENSIVE MEN; ACTIVATION; INSULIN; ACETYLCHOLINE; METABOLISM; CELLS; RESISTANCE; RELAXATION AB Many obese hypertensive individuals have a cluster of cardiovascular risk factors. This cluster includes plasma nonesterified fatty acid concentrations and turnover rates that are higher and more resistant to suppression by insulin than in lean and obese normotensive individuals. The higher fatty acids may contribute to cardiovascular risk in these patients by inhibiting endothelial cell nitric oxide synthase activity. To test this hypothesis, we quantified the effects of oleic (18:1[cis]) and other 18-carbon fatty acids on nitric oxide synthase activity in cultured bovine pulmonary artery endothelial cells by measuring the conversion of [H-3]L-arginine to [H-3]L-citrulline. Oleic acid (from 10 to 100 mu mol/L) caused a concentration-dependent decrease in nitric oxide synthase activity at baseline and during ATP and ionomycin (Ca2+ ionophore) stimulation. At 100 mu mol/L, linoleic (18:2[cis]) and oleic acids caused similar reductions of nitric oxide synthase activity, whereas elaidic (18:1[trans]) and stearic (18:0) acids had no effect. Oleic acid also inhibited the endothelium-dependent vasodilator response to acetylcholine in rabbit femoral artery rings preconstricted with phenylephrine (P<.05) but had no effect on the response to nitroprusside. The pattern of 18-carbon fatty acid effects on nitric oxide synthase activity in endothelial cells is consistent with activation of protein kinase C. Although oleic acid increased protein kinase C activity in endothelial cells, neither depletion of protein kinase C by 24-hour pretreatment with phorbol 12-myristate 13-acetate nor its inhibition with staurosporine eliminated the inhibitory effect of oleic acid on nitric oxide synthase. The vascular ring studies further indicate that oleic acid reduces the response to acetylcholine by inhibiting nitric oxide synthase activity rather than reducing the activation of guanylate cyclase or the effects of cGMP. Thus, elevated oleic acid values in obese hypertensive individuals may contribute to impaired endothelium-dependent vasodilation by a protein kinase C-independent mechanism. C1 MED UNIV S CAROLINA,DEPT PHARMACOL,DIV CLIN PHARMACOL,CHARLESTON,SC 29425. MED UNIV S CAROLINA,DEPT MED,DIV NEPHROL,CHARLESTON,SC 29425. UNIV WISCONSIN,DEPT MED,MADISON,WI. UNIV WISCONSIN,DEPT PHARMACOL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. FU PHS HHS [R01-43164] NR 45 TC 159 Z9 169 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0194-911X J9 HYPERTENSION JI Hypertension PD NOV PY 1995 VL 26 IS 5 BP 764 EP 770 PG 7 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TD294 UT WOS:A1995TD29400008 PM 7591016 ER PT J AU ALPUCHEARANDA, CM BERTHIAUME, EP MOCK, B SWANSON, JA MILLER, SI AF ALPUCHEARANDA, CM BERTHIAUME, EP MOCK, B SWANSON, JA MILLER, SI TI SPACIOUS PHAGOSOME FORMATION WITHIN MOUSE MACROPHAGES CORRELATES WITH SALMONELLA SEROTYPE PATHOGENICITY AND HOST SUSCEPTIBILITY SO INFECTION AND IMMUNITY LA English DT Article ID HUMAN-IMMUNODEFICIENCY-VIRUS; INNATE RESISTANCE; TYPHIMURIUM INVASION; NATURAL-RESISTANCE; EPITHELIAL-CELLS; INFECTION; MICE; VIRULENCE; GENE; EXPRESSION AB Light microscopic studies indicated a correlation between the virulence for mice of different Salmonella serotypes and the ability to form or maintain spacious phagosomes (SP) within mouse macrophages. Although Salmonella typhimurium induced membrane ruffling, macropinocytosis, and SP formation in macrophages from BALB/c mice, serotypes which are nonpathogenic for mice produced markedly fewer SP. SP formation correlated with both serotype survival within mouse macrophages and reported lethality for mice. Time-lapse video microscopy demonstrated that the human pathogen S. typhi induced generalized macropinocytosis and SP formation in human monocyte-derived macrophages, indicating a similar morphology for the initial phases of this host-pathogen interaction. In contrast to bone marrow-derived macrophages from BALB/c mice, macrophages from S. typhimurium-resistant outbred (CD-1) and inbred (CBA/HN) mice did not initiate generalized macropinocytosis after bacterial infection and formed markedly fewer SP. These deficiencies were not due to the Ity resistance genotype of these mice, as macrophages from mice that were congenic except for the Ity locus demonstrated equal SP formation in response to S. typhimurium. The observation that S. typhimurium-resistant CD-1 and CBA/HN mice are deficient in the ability to form and/or maintain SP indicates that a variable host component is important for SP formation and suggests that the ability to induce or form SP affects susceptibility to S. typhimurium. When serotypes nonpathogenic for mice were used to infect BALB/c macrophages, or when CD-1 or CBA/HN mouse macrophages were infected by S. typhimurium, some of the SP that formed shrank within seconds. This rapid shrinkage suggests that SP maintenance is also important for S. typhimurium survival within macrophages. These studies indicate that both host and bacterial factors contribute to SP formation and maintenance, which correlate with Salmonella intracellular survival and the ability to cause lethal enteric (typhoid) fever. C1 MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NCI,GENET LAB,BETHESDA,MD 20892. RI Swanson, Joel/P-4362-2014 OI Swanson, Joel/0000-0003-0900-8212 FU NIAID NIH HHS [AI34504, AI 35950] NR 41 TC 65 Z9 65 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 NOV PY 1995 VL 63 IS 11 BP 4456 EP 4462 PG 7 WC Immunology; Infectious Diseases SC Immunology; Infectious Diseases GA TB400 UT WOS:A1995TB40000037 PM 7591085 ER PT J AU HESS, D FISHER, D PETERFREUND, RA KACMAREK, RM AF HESS, D FISHER, D PETERFREUND, RA KACMAREK, RM TI THE DELIVERY OF AEROSOLIZED STEROIDS FROM MDIS WITH NOZZLE EXTENSIONS - QUANTITATIVE LABORATORY EVALUATION OF A METHOD TO IMPROVE AEROSOL DELIVERY TO INTUBATED PATIENTS SO INTENSIVE CARE MEDICINE LA English DT Article ID METERED-DOSE INHALER; MECHANICALLY VENTILATED PATIENTS; BRONCHODILATOR DELIVERY; THERAPEUTIC AEROSOLS; RABBIT LUNG; EFFICIENCY; NEBULIZER; CATHETERS; CIRCUITS; LESIONS AB Objective. Pulmonary deposition of aerosolized drug from a metered dose inhaler (MDI) is low with intubated patients. In the laboratory, extension of the MDI nozzle to the endotracheal tube tip has been shown to increase the delivered dose of albuterol. The objectives of this study were to determine the dose of aerosolized steroid (beclomethasone and triamcinolone) delivered through a MDI nozzle extension, the effect of nozzle extension length and number of actuations on the delivered dose, and particle size delivered through the nozzle extension. Design: A 19-G catheter was used as the MDI nozzle extension. The nozzle extension was attached to a 60-ml syringe via the Luer-Lok connection, and the distal end was directed through a hole drilled into a 15-ml capped tube. The MDI was placed into the syringe and actuated by pressing the syringe plunger. Drug delivered through the nozzle extension into the tube was dissolved in methanol (beclomethasone) or ethanol (triamcinolone), Nozzle extension lengths of 10 cm, 20 cm and 30 cm were studied, For each nozzle extension length, delivery was assessed using one, two, three and five actuations of each drug. Drug remaining in the nozzle extension was recovered by rinsing with the appropriate solvent. Aerosol particle size leaving the nozzle extension was determined using a seven-stage cascade impactor. Beclomethasone and triamcinolone concentrations were determined by spectrophotometry at 239 nm. Setting: Respiratory care laboratory of a university teaching hospital. Results: For the pooled results, 70.2 +/- 14.1% of the dose was delivered through the nozzle extension, with no difference between beclomethasone and triamcinolone (p = 0.838). The proportion of drug delivered through the 10-cm extension (76.7 +/- 8.4%) was greater than that from the 20-cm (66.1 +/- 16.5%) and 30-cm (67.7 +/- 13.9%) extensions (p = 0.001). Less drug was delivered through the extension with one actuation (54.1 +/- 17.7%) than with two (71.2 +/- 7.7%), three (77.2 +/- 5.5%), or five actuations (78.2 +/- 4.3%) (p < 0.001). There was a decrease in MMAD with increasing nozzle extension length (3.14 +/- 0.61 mu m for 10 cm, 2.97 +/- 0.28 mu m for 20 cm, 2.37 +/- 0.27 mu m for 30 cm; p = 0.005). Conclusions: A high proportion of aerosolized steroid was delivered with a MDI actuated through a nozzle extension. The proportion delivered through the nozzle extension was significantly less with longer nozzle extensions and with fewer actuations, but this may not be clinically important. Although particle sizes were smaller from longer nozzle extensions, all were within the respirable range, These results suggest that steroids can be delivered efficiently using a MDI nozzle extension. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02114. RP HESS, D (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ELLISON 401,BOSTON,MA 02114, USA. NR 36 TC 3 Z9 3 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0342-4642 J9 INTENS CARE MED JI Intensive Care Med. PD NOV PY 1995 VL 21 IS 11 BP 945 EP 951 DI 10.1007/BF01712338 PG 7 WC Critical Care Medicine SC General & Internal Medicine GA TH092 UT WOS:A1995TH09200013 PM 8636529 ER PT J AU NADEL, AS BENACERRAF, BR AF NADEL, AS BENACERRAF, BR TI LATERAL VENTRICULAR ATRIUM - LARGER IN MALE THAN FEMALE FETUSES SO INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS LA English DT Article DE HYDROCEPHALUS; LATERAL VENTRICLES; FETUS; SONOGRAPHY ID SONOGRAPHIC EVALUATION; DILATATION INUTERO; FETAL AB Objective: To attempt to detect the presence of a gender difference in the size of the fetal lateral ventricular atrium. Methods: The width of the lateral ventricular atrium was measured sonographically on 543 consecutive fetuses scanned at 17-40 weeks, with a normal structural survey and documented gender assignment. Lateral ventricular measurements of male and female fetuses were compared. Results: The mean width (+/- S.D.) of the lateral ventricular atrium for the entire study population of 543 fetuses was 6.5 +/- 1.4 mm. The measurement was 6.7 +/- 1.3 in male and 6.3 +/- 1.4 in female fetuses (P < 0.001). The atrial measurements were greater than or equal to 8.5 mm in 10% of the male and 7% of the female fetuses (P > 0.05, NS). Conclusion: Male fetuses have slightly larger cerebral lateral ventricles than female fetuses. C1 MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL & RADIOL,BOSTON,MA 02114. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. NR 12 TC 21 Z9 21 U1 0 U2 0 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0020-7292 J9 INT J GYNECOL OBSTET JI Int. J. Gynecol. Obstet. PD NOV PY 1995 VL 51 IS 2 BP 123 EP 126 DI 10.1016/0020-7292(95)02523-F PG 4 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TJ562 UT WOS:A1995TJ56200004 PM 8635632 ER PT J AU GERBER, RL SMITH, AR OWEN, J HANLON, A WALLACE, M HANKS, G AF GERBER, RL SMITH, AR OWEN, J HANLON, A WALLACE, M HANKS, G TI PATTERNS OF CARE SURVEY RESULTS - TREATMENT PLANNING FOR CARCINOMA OF THE PROSTATE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE TREATMENT PLANNING; PROSTATE; PATTERNS OF CARE ID DEFINITIVE RADIOTHERAPY; COMPUTED-TOMOGRAPHY; CANCER; ANTIGEN; THERAPY; VOLUME AB Purpose: Treatment planning has been defined differently at various institutions to encompass tasks ranging from the initial evaluation of the patient to the delivery of the treatment as well as a more narrow view, focused primarily on isodose computation. To evaluate the impact of much of the new treatment-planning technology that has become available, it is necessary to define and develop recommended guidelines for the treatment-planning process. Methods and Materials: The 1989 Patterns of Care Study (PCS) included questionnaires to access treatment planning practices currently in use for the entire census of oncology facilities in the United States. These questionnaires were developed by a consensus committee consisting of both physicists and radiation oncologists whose charge was to formulate a description of current treatment-planning practices. The description was based on the committee's experience and knowledge of the treatment-planning process considered to be widely available and in general use, as well as a review of the literature. From the description of the treatment-planning process, a set of guidelines for treatment planning was developed for prostate as well as each of the other disease sites included in the PCS. Data from the study defined the general structure, methodology, process, and tools used by each institution involved in the Patterns of Care Survey Study. National averages for all of the variables were calculated with weighted averages, with the weights reflecting the sample design and number of patients in the different types of facilities. The data were stratified according to academic, hospital, or free-standing facility and were compared with the Consensus Guidelines for Treatment Planning of the Prostate. Discussion: Based on the consensus statement, the treatment-planning process was separated into the following categories: (a) Treatment-Planning Workup, (b) Treatment Plan Implementation, (c) Treatment Delivery, (d) Treatment Verification, and (e) Quality Assurance. The results from the survey were summarized for each category and compared with the consensus statement. Conclusions: Although there is an increasing trend toward using computed tomography (CT) information to acquire individualized patient data, volume definition and localization are often completed in the simulator without the direct use of CT information (47%). As more sophisticated beam arrangements and blocking are used, one needs to look at the full three-dimensional (3D) volume to ensure that there are no marginal misses due to blocking and beam arrangement. Improved and more widespread use of immobilization devices is also required with conformal treatments and reduced margins. The results of the survey helped to identify and establish the standard of practice for treatment planning of the prostate as well as to provide documentation for better defining a complete description of the treatment planning process. Well-documented guidelines will provide more consistent treatment of patients, which should have an impact on outcome. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. AMER COLL RADIOL,PHILADELPHIA,PA 19107. FOX CHASE CANC CTR,PHILADELPHIA,PA 19111. RP GERBER, RL (reprint author), WASHINGTON UNIV,SCH MED,EDWARD MALLINCKRODT INST RADIOL,CTR RADIAT ONCOL,510 S KINGSHIGHWAY BLVD,ST LOUIS,MO 63110, USA. FU NCI NIH HHS [N01-CM-87275] NR 17 TC 18 Z9 18 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD NOV 1 PY 1995 VL 33 IS 4 BP 803 EP 808 DI 10.1016/0360-3016(95)00278-1 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TE826 UT WOS:A1995TE82600003 PM 7591886 ER PT J AU BIEDERMAN, J FARAONE, SV AF BIEDERMAN, J FARAONE, SV TI CHILDHOOD MANIA REVISITED SO ISRAEL JOURNAL OF MEDICAL SCIENCES LA English DT Article DE BIPOLAR DISORDER; ATTENTION DEFICIT HYPERACTIVITY DISORDER; CHILDHOOD MANIA ID ATTENTION-DEFICIT DISORDER; BIPOLAR AFFECTIVE-DISORDER; DEPRESSIVE VARIANT SYNDROME; LA-TOURETTES SYNDROME; HYPERACTIVITY DISORDER; THERAPEUTIC CONSIDERATIONS; PREPUBERTAL CHILDREN; FAMILIAL ASSOCIATION; GENETIC-RELATIONSHIP; MULTIPLE THRESHOLDS C1 HARVARD UNIV,SCH MED,DEPT PSYCHIAT,BOSTON,MA 02115. MASSACHUSETTS MENTAL HLTH CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BROCKTON W ROXBURY VET AFFAIRS MED CTR,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BROCKTON W ROXBURY VET AFFAIRS MED CTR,DEPT PSYCHIAT,BOSTON,MA 02115. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PSYCHIAT SERV,PEDIAT PSYCHOPHARMACOL UNIT ACC 725,FRUIT ST,BOSTON,MA 02114, USA. OI Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 71 TC 2 Z9 2 U1 0 U2 0 PU ISRAEL JOURNAL MED SCIENCES PI JERUSALEM PA 2 ETZEL ST, FRENCH HILL, JERUSALEM 97853, ISRAEL SN 0021-2180 J9 ISRAEL J MED SCI JI Isr. J. Med. Sci. PD NOV PY 1995 VL 31 IS 11 BP 647 EP 651 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA TG276 UT WOS:A1995TG27600001 PM 7591696 ER PT J AU MUELLER, PR AF MUELLER, PR TI PERCUTANEOUS ETHANOL INJECTION THERAPY (PEIT) FOR HEPATOCELLULAR-CARCINOMA (HCC) SO JAPANESE JOURNAL OF CANCER RESEARCH LA English DT Note RP MUELLER, PR (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114, USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU JAPANESE CANCER ASSOCIATION PI TOKYO PA EDITORIAL OFFICE 7TH FLOOR, JOHKOH BLDG 2-23-11, KOISHIKAWA, TOKYO 112, JAPAN SN 0910-5050 J9 JPN J CANCER RES JI Jpn. J. Cancer Res. PD NOV PY 1995 VL 86 IS 11 BP COV2 EP COV2 PG 1 WC Oncology SC Oncology GA TG374 UT WOS:A1995TG37400001 ER PT J AU Reese, TG Davis, TL Weisskoff, RM AF Reese, TG Davis, TL Weisskoff, RM TI Automated shimming at 1.5 T using echo-planar image frequency maps SO JMRI-JOURNAL OF MAGNETIC RESONANCE IMAGING LA English DT Article DE MR imaging; image artifacts, MR; shimming; pulse sequences AB Using echo-planar imaging, we developed an automated image-based procedure to shim the static (B-o) field. Our method uses the rapid acquisition capability of echo-planar imaging to collect the required frequency data rapidly, rendering the shim data acquisition time negligible in comparison with the total study time. We address image distortion issues involved in echo-planar imaging acquisition of the data and formulate analytic methods for arriving at an optimal shim for the NMR imaging experiment in a single iteration, We investigated the use of cost functions other than least-squares (Chebychev, high-order numeric) and found that choice between the cost functions we tested was irrelevant to resultant image quality, at least when used in conjunction with low-order shims, With appropriate integration, the method has become routine practice for investigators at our laboratory. RP Reese, TG (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,DEPT RADIOL,BLDG 149 13TH ST,CHARLESTOWN NAVY YARD,BOSTON,MA 02129, USA. FU NCI NIH HHS [5P01CA48729] NR 0 TC 94 Z9 94 U1 0 U2 2 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 NOV-DEC PY 1995 VL 5 IS 6 BP 739 EP 745 DI 10.1002/jmri.1880050621 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TL103 UT WOS:A1995TL10300020 PM 8748496 ER PT J AU PETROF, BJ GOTTFRIED, SB EBY, J LAMANCA, J LEVINE, S AF PETROF, BJ GOTTFRIED, SB EBY, J LAMANCA, J LEVINE, S TI GROWTH-HORMONE DOES NOT PREVENT CORTICOSTEROID-INDUCED CHANGES IN RAT DIAPHRAGM STRUCTURE AND FUNCTION SO JOURNAL OF APPLIED PHYSIOLOGY LA English DT Article DE MYOSIN HEAVY CHAIN; FIBER TYPES; ATROPHY ID OBSTRUCTIVE PULMONARY-DISEASE; POSITIVE NITROGEN-BALANCE; MUSCLE-FIBER SIZE; FACTOR-I; CONTRACTILE PROPERTIES; MYOSIN PHENOTYPE; SDH ACTIVITY; MYOPATHY; HUMANS; BIOCHEMISTRY AB The present study tested the hypothesis that growth hormone (GH), an anabolic agent, could prevent the abnormalities of diaphragm structure and function associated with short-term administration of the corticosteroid triamcinolone (TR). During a 10-day period, male rats (n = 33) were assigned to control (CTL), TR (1 mg . kg(-1). day(-1) im), and TR-GH (2 mg . kg(-1). day(-1) im) groups. Diaphragm weight was significantly reduced in the TR and TR-GH animals compared with the CTL animals, but there was no difference in the diaphragm-to-body weight ratio. Fiber type (I, IIa, and IIx/b) proportions did not differ among the three groups. However, in TR rats there was a significant reduction in the contribution of type IIx/b fibers to total diaphragm cross-sectional area due to marked atrophy (similar to 42% decrease in mean fiber cross-sectional area). There was no significant reversal of TR-induced type IIx/b fiber atrophy by concomitant GH administration. TR and TR-GH groups both exhibited a leftward shift of the force-frequency relationship and enhanced in vitro fatigue resistance, whereas maximal specific force was unaltered. We conclude that GH does not prevent corticosteroid-induced effects on the diaphragm under these conditions, possibly as a result of reduced nutritional intake associated with TR administration. C1 MCGILL UNIV,MONTREAL GEN HOSP,MONTREAL,PQ H3A 1A1,CANADA. MED COLL PENN,VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. RP PETROF, BJ (reprint author), ROYAL VICTORIA HOSP,DIV RESP,MEAKINS CHRISTIE LABS,RM L408,687 PINE AVE W,MONTREAL,PQ H3A 1A1,CANADA. NR 39 TC 8 Z9 8 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 8750-7587 J9 J APPL PHYSIOL JI J. Appl. Physiol. PD NOV PY 1995 VL 79 IS 5 BP 1571 EP 1577 PG 7 WC Physiology; Sport Sciences SC Physiology; Sport Sciences GA TD929 UT WOS:A1995TD92900025 PM 8594016 ER PT J AU JIRANEK, W JASTY, M WANG, JT BRAGDON, C WOLFE, H GOLDBERG, M HARRIS, W AF JIRANEK, W JASTY, M WANG, JT BRAGDON, C WOLFE, H GOLDBERG, M HARRIS, W TI TISSUE-RESPONSE TO PARTICULATE POLYMETHYLMETHACRYLATE IN MICE WITH VARIOUS IMMUNE DEFICIENCIES SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Article ID FOREIGN-BODY REACTION; NUDE-MICE; EXPRESSION; TUMORS AB We examined the tissue response to subcutaneous injections of particulate polymethylmethacrylate powder in fully immunocompetent C3Hf/Sed mice as well as three strains of mice with different levels of lymphocyte dysfunction. Five weeks after the injection, we found clearly demarcated granulomas. Histological and immunohistochemical studies showed that these granulomas were similar among all strains, with either paucity or absence of lymphoid cells, In situ hybridization with use of complementary RNA probes indicated that macrophages were synthesizing interleukin-1 beta messenger RNA (mRNA), a marker of macrophage activation, and a cytokine implicated in pathological bone resorption. We concluded that, in mice, there is a lymphocyte-independent pathway of macrophage activation in response to particulate polymethylmethacrylate, This suggests that the foreign-body response to particulate orthopaedic biomaterials is macrophage-initiated and maintained and that lymphocytes are not essential to this response, although they may modulate it. CLINICAL RELEVANCE: The mammalian response to particulate biomaterials does not appear to fit a specific immune hypersensitivity response; rather, it seems to follow a non-specific pattern of macrophage phagocytosis, activation, and cellular response to monokine release, Differences in the response to debris among patients, manifested by differences in the rapidity and extent of osteolysis around joint prostheses, are more probably related to factors other than the hypersensitivity response, such as the amount of particles released, individual differences in macrophage activation, or intracellular damage created by the particles after phagocytosis. C1 TUFTS UNIV NEW ENGLAND MED CTR,BOSTON,MA 02111. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 34 TC 37 Z9 37 U1 0 U2 0 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. vol. PD NOV PY 1995 VL 77A IS 11 BP 1650 EP 1661 PG 12 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TG266 UT WOS:A1995TG26600003 PM 7593074 ER PT J AU TOMFORD, WW AF TOMFORD, WW TI TRANSMISSION OF DISEASE THROUGH TRANSPLANTATION OF MUSCULOSKELETAL ALLOGRAFTS SO JOURNAL OF BONE AND JOINT SURGERY-AMERICAN VOLUME LA English DT Review ID HUMAN-IMMUNODEFICIENCY-VIRUS; HEPATITIS-C VIRUS; POLYMERASE CHAIN-REACTION; NON-B-HEPATITIS; LYMPHADENOPATHY-ASSOCIATED VIRUS; TENDON-BONE ALLOGRAFTS; NON-A; GAMMA-IRRADIATION; POSTTRANSFUSION HEPATITIS; ORGAN-TRANSPLANTATION RP TOMFORD, WW (reprint author), MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED SURG,15 PARKMAN ST,ACC 508,BOSTON,MA 02114, USA. NR 164 TC 249 Z9 261 U1 1 U2 4 PU JOURNAL BONE JOINT SURGERY INC PI NEEDHAM PA 20 PICKERING ST, NEEDHAM, MA 02192 SN 0021-9355 J9 J BONE JOINT SURG AM JI J. Bone Joint Surg.-Am. vol. PD NOV PY 1995 VL 77A IS 11 BP 1742 EP 1754 PG 13 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TG266 UT WOS:A1995TG26600017 PM 7593087 ER PT J AU WEITZMAN, JB CHEN, A HEMLER, ME AF WEITZMAN, JB CHEN, A HEMLER, ME TI INVESTIGATION OF THE ROLE OF BETA-1 INTEGRINS IN CELL-CELL ADHESION SO JOURNAL OF CELL SCIENCE LA English DT Article DE BETA-1 INTEGRIN; CELL-CELL ADHESION; INTEGRIN TRANSFECTANT ID EPITHELIAL BASEMENT-MEMBRANES; MONOCLONAL-ANTIBODIES; T-CELLS; CYTOPLASMIC DOMAIN; INTERCELLULAR-ADHESION; HOMOTYPIC AGGREGATION; DEPENDENT ADHESION; COLLAGEN RECEPTOR; HUMAN-LYMPHOCYTES; LAMININ RECEPTOR AB Various beta 1 integrins (VLA-2, VLA-3, VLA-4) have been suggested to bind directly to themselves or to each other, thus mediating cell-cell adhesion. Here we expressed the human alpha 2 and alpha 3 subunits in three different cell lines (human erythroleukemia K562, human rhabdomyosarcoma RD and Chinese hamster ovary CHO cells). Although cell surface alpha 2 beta 1 and alpha 3 beta 1 in the transfectants mediated adhesion to matrix ligands (collagen or laminin 5, respectively), in no case did we observe enhanced cell-cell adhesion. In the presence of a range of different divalent cation concentrations, stimulatory anti-beta 1 antibodies or anti-alpha 3 antibodies, VLA-2 and VLA-3 still did not appear to interact directly, through either heterophilic (i.e. VLA-3/VLA-2) or hemophilic (i.e. VLA-3/VLA-3) mechanisms, to mediate cell-cell adhesion. Furthermore, in some but not all alpha 3 transfectants we observed an unexpected decrease in cell-cell adhesion, suggesting a novel anti-adhesive function. This inhibitory effect was not observed for alpha 2 transfection nor when the alpha 3 cytoplasmic tail was exchanged with that of another integrin a subunit. Finally, no evidence for VLA-4/VLA-4 mediated cell-cell adhesion was observed using alpha 4-transfected K562 and CHO cells. In conclusion, using many different combinations of cell lines, we found that cell-cell adhesion mediated by direct integrin/integrin interaction is not a widespread phenomenon, and is not observable in standard cell-cell adhesion assays. Furthermore, in some cell combinations, alpha 3 expression may actually cause diminished cell-cell adhesion. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. OI Weitzman, Jonathan/0000-0001-8445-0102 FU NIGMS NIH HHS [GM38903] NR 77 TC 37 Z9 37 U1 0 U2 0 PU COMPANY OF BIOLOGISTS LTD PI CAMBRIDGE PA BIDDER BUILDING CAMBRIDGE COMMERCIAL PARK COWLEY RD, CAMBRIDGE, CAMBS, ENGLAND CB4 4DL SN 0021-9533 J9 J CELL SCI JI J. Cell Sci. PD NOV PY 1995 VL 108 BP 3635 EP 3644 PN 11 PG 10 WC Cell Biology SC Cell Biology GA TD619 UT WOS:A1995TD61900028 PM 8586674 ER PT J AU DI, YP REPASKY, E LASZLO, A CALDERWOOD, S SUBJECK, J AF DI, YP REPASKY, E LASZLO, A CALDERWOOD, S SUBJECK, J TI HSP70 TRANSLOCATES INTO A CYTOPLASMIC AGGREGATE DURING LYMPHOCYTE-ACTIVATION SO JOURNAL OF CELLULAR PHYSIOLOGY LA English DT Article ID HEAT-SHOCK PROTEINS; STRESS PROTEINS; UNCOATING ATPASE; ESCHERICHIA-COLI; MAMMALIAN-CELLS; MEMBRANE; SPECTRIN; PURIFICATION; IDENTIFICATION; PHOSPHOLIPASE AB The percentage of T and B lymphocytes expressing a distinct cytoplasmic aggregate enriched in spectrin, ankyrin, and in several other proteins including protein kinase C greatly increases following various activation protocols. Members of the 70 kDa family of heat shock proteins (hsp70) temporarily bind to and stabilize unfolded segments of other proteins, a function apparently required for proper protein folding and assembly. Considering the multiprotein and dynamic nature of the lymphocyte aggregate, the possibility that hsp70 also might be associated with components of this structure is considered here. Double immunofluorescence analysis indicates that hsp70 is a component of the lymphocyte aggregate and is coincident with spectrin in a subpopulation of freshly isolated, untreated lymphocytes from various murine tissues and in a T-lymphocyte hybridoma. When cell lysates of lymph node T cells are immunoprecipitated using an antibody against hsp70 or spectrin and then analyzed by Western blot utilizing the alternate antibody, it was found that hsp70 and spectrin coprecipitated with one another. Moreover, this coprecipitation could be abolished by addition of ATP. This latter observation was extended to lymphoid cells using a transient permeabilization procedure, and it was shown that addition of exogenous ATP results in the dissipation of the aggregate structure itself. Finally, conditions that result in T-cell activation and aggregate formation, i.e., treatment with the phorbol ester PMA or T-cell receptor cross-linking, also lead to the repositioning of hsp70 into the aggregate from a membrane/cytosolic locale in congruence with spectrin. These data suggest that hsp70 is an active component of the aggregate and that it may function in the interactions believed to occur in this unique activation-associated organelle. (C) 1995 Wiley-Liss, Inc. C1 ROSWELL PK CANC INST,DEPT MOLEC & CELLULAR BIOL,BUFFALO,NY 14263. ROSWELL PK CANC INST,DEPT MOLEC IMMUNOL,BUFFALO,NY 14263. WASHINGTON UNIV,SCH MED,CTR RADIAT ONCOL,CANC BIOL SECT,ST LOUIS,MO 63108. DANA FARBER CANC INST,DEPT RADIAT ONCOL,BOSTON,MA 02115. RI Di, Yuanpu Peter/H-4191-2016 OI Di, Yuanpu Peter/0000-0003-2028-2087 FU NIGMS NIH HHS [GM45994] NR 32 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 0021-9541 J9 J CELL PHYSIOL JI J. Cell. Physiol. PD NOV PY 1995 VL 165 IS 2 BP 228 EP 238 DI 10.1002/jcp.1041650203 PG 11 WC Cell Biology; Physiology SC Cell Biology; Physiology GA TB806 UT WOS:A1995TB80600002 PM 7593200 ER PT J AU SCHULZ, JB MATTHEWS, RT JENKINS, BG BRAR, P BEAL, MF AF SCHULZ, JB MATTHEWS, RT JENKINS, BG BRAR, P BEAL, MF TI IMPROVED THERAPEUTIC WINDOW FOR TREATMENT OF HISTOTOXIC HYPOXIA WITH A FREE-RADICAL SPIN TRAP SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE EXCITOTOXICITY; FREE RADICALS; ISCHEMIA; N-METHYL-D-ASPARTATE; STROKE ID TERT-BUTYL-NITRONE; FOCAL ISCHEMIA; CEREBRAL-ISCHEMIA; RAT STRIATUM; INVIVO; INJURY; BRAIN; ANTAGONIST; MK-801; AMPA AB The therapeutic time window for N-methyl-D-aspartate (NMDA) antagonists, non-NMDA antagonists, and glutamate release inhibitors in focal models of ischemia appears to be about 1-2 h. In contrast, a free radical spin trap was found to have an improved therapeutic window. We compared the therapeutic time windows of the NMDA antagonist dizolcilpine maleate (MK-801), the glutamate release inhibitor lamotrigine, and the free radical spin trap n-tert-butyl-alpha-(2-sulfophenyl)-nitrone (S-PBN) against striatal lesions produced by the mitochondrial toxin malonate, which produces histotoxic hypoxia. Lamotrigine exerted neuroprotective effects when administered at 1 h before malonate injections, MK-801 protected at 1 h before and 1 h after malonate injections, whereas S-PBN showed efficacy when administered up to 6 h after malonate injections. Striatal injections of malonate produced a rapid increase in lactate production and early changes in diffusion-weighted imaging as assessed by magnetic resonance imaging. Therefore, the time course to evolve a lesion in our model of histotoxic hypoxia is comparable with that of other models of focal ischemia. These findings provide direct evidence that a free radical spin trap has an improved therapeutic window compared to an NMDA antagonist and a glutamate release inhibitor. This could be a therapeutic advantage in the treatment of clinical stroke patients. C1 MASSACHUSETTS GEN HOSP,SERV NEUROL,NEUROCHEM LAB,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,MGH NMR CTR,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RI Schulz, Jorg/D-9786-2012 OI Schulz, Jorg/0000-0002-8903-0593 FU NINDS NIH HHS [NS10828, NS31579, NS16367] NR 27 TC 52 Z9 52 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0271-678X J9 J CEREBR BLOOD F MET JI J. Cereb. Blood Flow Metab. PD NOV PY 1995 VL 15 IS 6 BP 948 EP 952 PG 5 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA TC486 UT WOS:A1995TC48600007 PM 7593355 ER PT J AU FISHER, M MEADOWS, ME DO, T WEISE, J TRUBETSKOY, V CHARETTE, M FINKLESTEIN, SP AF FISHER, M MEADOWS, ME DO, T WEISE, J TRUBETSKOY, V CHARETTE, M FINKLESTEIN, SP TI DELAYED TREATMENT WITH INTRAVENOUS BASIC FIBROBLAST GROWTH-FACTOR REDUCES INFARCT SIZE FOLLOWING PERMANENT FOCAL CEREBRAL-ISCHEMIA IN RATS SO JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM LA English DT Article DE BASIC FIBROBLAST GROWTH FACTOR; CEREBRAL INFARCTION; FOCAL CEREBRAL ISCHEMIA ID BRAIN; NEURONS AB Basic fibroblast growth factor (bFGF) is a polypeptide that supports the survival of brain cells (including neurons, glia, and endothelia) and protects neurons against a number of toxins and insults in vitro. This factor is also a potent dilator of cerebral pial arterioles in vivo. In previous studies, we found that intraventricularly administered bFGF reduced infarct volume in a model of focal cerebral ischemia in rats. In the current study, bFGF (45 mu g/kg/h) in vehicle, or vehicle alone, was infused intravenously for 3 h, beginning at 30 min after permanent middle cerebral artery occlusion by intraluminal suture in mature Sprague-Dawley rats. After 24 h, neurological deficit (as assessed by a 0- to 5-point scale, with 5 = most severe) was 2.6 +/- 1.0 in vehicle-treated and 1.5 +/- 1.3 in bFGF-treated rats (mean +/- SD; N = 12 vs. 11; p = 0.009). Infarct volume was 297 +/- 65 mm(3) in vehicle- and 143 +/- 135 mm(3) in bFGF-treated animals (p = 0.002). During infusion, there was a modest decrease in mean arterial blood pressure but no changes in arterial blood gases or core or brain temperature in bFGF-treated rats. Autoradiography following intravenous administration of In-111-labeled bFGF showed that labeled bFGF crossed the damaged blood-brain barrier to enter the ischemic (but not the nonischemic) hemisphere. Whether the infarct-reducing effects of bFGF depend on intraparenchymal or intravascular mechanisms requires further study. C1 UNIV MASSACHUSETTS,SCH MED,DEPT NEUROL,WORCESTER,MA. CNS GROWTH FACTOR RES LAB,DEPT NEUROL,BOSTON,MA. MASSACHUSETTS GEN HOSP,CTR IMAGING & PHARMACEUT RES,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. CREAT BIOMOLEC,HOPKINTON,MA. RP FISHER, M (reprint author), MED CTR CENT MASSACHUSETTS,DEPT NEUROL,119 BELMONT ST,WORCESTER,MA 01605, USA. FU NIA NIH HHS [AG 08207]; NINDS NIH HHS [NS 10828] NR 26 TC 158 Z9 169 U1 0 U2 3 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 NOV PY 1995 VL 15 IS 6 BP 953 EP 959 PG 7 WC Endocrinology & Metabolism; Hematology; Neurosciences SC Endocrinology & Metabolism; Hematology; Neurosciences & Neurology GA TC486 UT WOS:A1995TC48600008 PM 7593356 ER PT J AU Seidman, LJ Benedict, KB Biederman, J Bernstein, JH Seiverd, K Milberger, S Norman, D Mick, E Faraone, SV AF Seidman, LJ Benedict, KB Biederman, J Bernstein, JH Seiverd, K Milberger, S Norman, D Mick, E Faraone, SV TI Performance of children with ADHD on the Rey-Osterrieth complex figure: A pilot neuropsychological study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Rey-Osterrieth Complex Figure; ADHD; learning disability; comorbidity; organizational ability ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT; LEARNING-DISABILITIES; RISK-FACTORS; BOYS; FAMILY; COMORBIDITY; BEHAVIOR; PRODUCTIONS; SIBLINGS AB This study evaluates the performance of boys with Attention Deficit Hyperactivity Disorder (ADHD) on the Rey-Osterrieth Complex Figure (ROCF) taking into consideration familiality and comorbid psychiatric and learning disorders (LD). Sixty-five children with ADHD performed at developmentally lower levels of Copy Organization and Recall Style than did 45 controls. ADHD children with LD scored significantly lower on Copy Organization than did ADHD children without LD, whereas psychiatric comorbidity and familiality had no effect. These results suggest that a developmental analysis of the ROCF identifies organizational difficulties associated with ADHD and that these impairments cannot simply be attributed to comorbidities associated with ADHD. C1 MASSACHUSETTS GEN HOSP,PEDIAT PSYCHOPHARMACOL UNIT ACC725,BOSTON,MA 02114. OI Mick, Eric/0000-0001-8505-8145; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01MH-41314-01A2] NR 48 TC 55 Z9 59 U1 0 U2 3 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD NOV PY 1995 VL 36 IS 8 BP 1459 EP 1473 DI 10.1111/j.1469-7610.1995.tb01675.x PG 15 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA TM259 UT WOS:A1995TM25900012 PM 8988278 ER PT J AU HOSOKAWA, Y POLLAK, MR BROWN, EM ARNOLD, A AF HOSOKAWA, Y POLLAK, MR BROWN, EM ARNOLD, A TI MUTATIONAL ANALYSIS OF THE EXTRACELLULAR CA2+-SENSING RECEPTOR GENE IN HUMAN PARATHYROID TUMORS SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Editorial Material ID SEVERE PRIMARY HYPERPARATHYROIDISM; FAMILIAL HYPOCALCIURIC HYPERCALCEMIA; ENDOCRINE NEOPLASIA TYPE-1; CANDIDATE ONCOGENE; CHROMOSOME 11Q13; HORMONE RELEASE; ASSOCIATION; KINDREDS; CLONING; ADENOMA AB Despite recent progress, such as the identification of PRAD1/cyclin D1 as a parathyroid oncogene, it is likely that many genes involved in the molecular pathogenesis of parathyroid tumors remain unknown. Individuals heterozygous for inherited mutations in the extracellular Ca2+-sensing receptor gene that reduce its biological activity exhibit a disorder termed familial hypocalciuric hypercalcemia or familial benign hypercalcemia, which is characterized by reduced responsiveness of parathyroid and kidney to calcium and by PTH-dependent hypercalcemia. Those who are homozygous for such mutations present with neonatal severe hyperparathyroidism and have marked parathyroid hypercellularity. Thus, the Ca2+-sensing receptor gene is a candidate parathyroid tumor suppressor gene, with inactivating mutations plausibly explaining set-point abnormalities in the regulation of both parathyroid cellular proliferation and PTH secretion by extracellular Ca2+ similar to those seen in hyperparathyroidism. Using a ribonuclease A protection assay that has detected multiple mutations in the Ca2+-sensing receptor gene in familial hypocalciuric hypercalcemia and covers more than 90% of its coding region, we sought somatic mutations in this gene in a total of 44 human parathyroid tumors (23 adenomas, 4 carcinomas, 5 primary hyperplasias, and 12 secondary hyperplasias). No such mutations were detected in these 44 tumors. Thus, our studies suggest that somatic mutation of the Ca2+-sensing receptor gene does not commonly contribute to the pathogenesis of sporadic parathyroid tumors. As such, PTH set-point dysfunction in parathyroid tumors may well be secondary to other clonal proliferative defects and/or mutations in other components of the extracellular Ca2+-sensing pathway. C1 MASSACHUSETTS GEN HOSP, ENDOCRINE ONCOL LAB, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. BRIGHAM & WOMENS HOSP, DEPT MED, DIV RENAL, BOSTON, MA 02115 USA. BRIGHAM & WOMENS HOSP, DEPT MED, DIV ENDOCRINE HYPERTENS, BOSTON, MA 02115 USA. FU NIDDK NIH HHS [DK-02138, DK-41415, DK-44588] NR 29 TC 113 Z9 113 U1 0 U2 2 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 NOV PY 1995 VL 80 IS 11 BP 3107 EP 3110 DI 10.1210/jc.80.11.3107 PG 4 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TD909 UT WOS:A1995TD90900002 PM 7593409 ER PT J AU GOLDFINE, AB SIMONSON, DC FOLLI, F PATTI, ME KAHN, CR AF GOLDFINE, AB SIMONSON, DC FOLLI, F PATTI, ME KAHN, CR TI METABOLIC EFFECTS OF SODIUM METAVANADATE IN HUMANS WITH INSULIN-DEPENDENT AND NONINSULIN-DEPENDENT - DIABETES-MELLITUS IN-VIVO AND IN-VITRO STUDIES SO JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM LA English DT Article ID RAT ADIPOCYTES; GLUCOSE TRANSPORTER; VANADATE TREATMENT; SKELETAL-MUSCLE; ORAL VANADATE; FA/FA RATS; INDIRECT CALORIMETRY; PHOSPHATASE-ACTIVITY; GLYCOGEN-SYNTHASE; SWISS 3T3-CELLS AB To investigate the efficacy and mechanism of action of sodium metavanadate as an oral hypoglycemic agent, five insulin-dependent diabetes mellitus (IDDM) and five noninsulin-dependent diabetes mellitus (NIDDM) patients mere studied before and after 2 weeks of oral sodium metavanadate (NaVO3; 125 mg/day). Glucose metabolism measured during a two-step euglycemic insulin clamp was not significantly increased by vanadate therapy in patients with IDDM, but was improved by 29% during the low dose (0.5 mU/kg . min) insulin infusion and 39% during the high dose (1.0 mU/kg . min) in patients with NIDDM. The changes in glucose metabolism were largely accounted for by an increase in nonoxidative glucose disposal, as measured by indirect calorimetry. Basal hepatic glucose production and suppression of hepatic glucose production by insulin were unchanged by vanadate therapy. There was a significant decrease in insulin requirements in the patients with IDDM (39.1 +/- 6.6 to 33.8 +/- 4.7 U/day; P < 0.05). Cholesterol levels significantly decreased in both IDDM (4.53 +/- 0.16 vs. 4.27 +/- 0.22 mmol/L; P = 0.06) and NIDDM (6.92 +/- 0.75 vs. 5.28 +/- 0.46 mmol/L; P < 0.05). After NaVO3 therapy, there was a 1.7- to 3.9-fold increase in basal mitogen-activated protein and S6 kinase activities in mononuclear cells from patients with IDDM and NIDDM that mimicked the effect of insulin stimulation in controls. The most common adverse effect of oral NaVO3 was mild gastrointestinal intolerance. These data suggest that vanadate or related agents may have a potential role as adjunctive therapy in patients with diabetes mellitus. C1 BRIGHAM & WOMENS HOSP, DEPT MED, JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02215 USA. HARVARD UNIV, SCH MED, BOSTON, MA 02215 USA. OI folli, franco/0000-0001-9824-5222 FU NCRR NIH HHS [MO1-RR-02635]; NIDDK NIH HHS [DK-47462, DK-36836] NR 66 TC 169 Z9 170 U1 0 U2 3 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 NOV PY 1995 VL 80 IS 11 BP 3311 EP 3320 DI 10.1210/jc.80.11.3311 PG 10 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA TD909 UT WOS:A1995TD90900038 PM 7593444 ER PT J AU SCHWEITZER, M ASCH, DA AF SCHWEITZER, M ASCH, DA TI TIMING PAYMENTS TO SUBJECTS OF MAIL SURVEYS - COST-EFFECTIVENESS AND BIAS SO JOURNAL OF CLINICAL EPIDEMIOLOGY LA English DT Article DE COST-EFFECTIVENESS; DATA COLLECTION; EPIDEMIOLOGY; FINANCIAL INCENTIVES; HEALTH SERVICES RESEARCH; MAILED SURVEY; RESEARCH DESIGN; RESPONSE BIAS; SURVEY METHODS AB Although mailed surveys are an important component of epidemiological research, results from mailed surveys are often suspect because of poor response rates and the potential for nonresponse bias. Previous work has demonstrated that paying subjects to complete questionnaires increases response rates, but this work has not well addressed the impact of the timing of incentives on total cost, cost effectiveness, and response bias. We surveyed 400 university employees about health benefits. By random allocation, half received a check for $5 along with the mailed survey, and the other half received the promise of $5 on return of a completed survey. The response rates for both groups were about the same (64 and 59%, respectively), but prepayment was less expensive in aggregate and less expensive per response. In addition, we found that subjects with lower salaries were more likely to respond when paid in advance. We conclude that prepayment may actually be less expensive and more cost effective than payment on completion, but that the timing of payment may influence the profile of respondents. C1 UNIV PENN,SCH MED,DIV GEN INTERNAL MED,PHILADELPHIA,PA 19104. UNIV PENN,WHARTON SCH,DEPT OPERAT & INFORMAT MANAGEMENT,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,GEN INTERNAL MED SECT,PHILADELPHIA,PA. NR 9 TC 28 Z9 27 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0895-4356 J9 J CLIN EPIDEMIOL JI J. Clin. Epidemiol. PD NOV PY 1995 VL 48 IS 11 BP 1325 EP 1329 DI 10.1016/0895-4356(95)00040-2 PG 5 WC Health Care Sciences & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA TJ075 UT WOS:A1995TJ07500005 PM 7490595 ER PT J AU KOZIEL, MJ DUDLEY, D AFDHAL, N GRAKOUI, A RICE, CM CHOO, QL HOUGHTON, M WALKER, BD AF KOZIEL, MJ DUDLEY, D AFDHAL, N GRAKOUI, A RICE, CM CHOO, QL HOUGHTON, M WALKER, BD TI HLA CLASS I-RESTRICTED CYTOTOXIC T-LYMPHOCYTES SPECIFIC FOR HEPATITIS-C VIRUS - IDENTIFICATION OF MULTIPLE EPITOPES AND CHARACTERIZATION OF PATTERNS OF CYTOKINE RELEASE SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE HEPATITIS C VIRUS; EPITOPES; CYTOTOXIC T LYMPHOCYTES; CYTOKINES; CHRONIC HEPATITIS ID CELL CLONES; PEPTIDES; INFECTION; SEQUENCE; ANTIGEN; PATHOGENESIS; EXPRESSION; RECOGNIZE; DIVERSITY; MOLECULES AB Cytotoxic T lymphocytes (CTL) are important to the control of viral replication and their presence may be important to disease outcome, An understanding of the spectrum of proteins recognized by hepatitis C virus (HCV)-specific CTL and the functional properties of these cells is an important step in understanding the disease process and the mechanisms of persistent infection, which occurs in the majority of HCV-infected individuals, In this report we identify HCV-specific CTL responses restricted by the HLA class I molecules A2, A3, A11, A23, B7, B8, and B53, The epitopes recognized by these intrahepatic CTL conform to published motifs for binding to HLA class I molecules, although in some cases we have identified CTL epitopes for which no published motif exists, The use of vectors expressing two different strains of HCV, HCV-1 and HCV-H, revealed both strain-specific and cross-reactive CTL, These HCV-specific CTL were shown to produce cytokines including IFN-gamma, TNF-alpha, GM-CSF, IL-8, and IL-10 in an antigen- and HLA class I-specific manner, These studies indicate that the CTL response to HCV is broadly directed and that as many as five different epitopes may be targeted in a single individual, The identification of minimal epitopes may facilitate peptide-specific immunization strategies, In addition, the release of proinflammatory cytokines by these cells may contribute to the pathogenesis of HCV-induced liver damage. C1 HARVARD UNIV,SCH MED,BOSTON,MA 02114. BOSTON CITY HOSP,DIV GASTROENTEROL,BOSTON,MA 02118. BOSTON UNIV,SCH MED,BOSTON,MA 02118. WASHINGTON UNIV,DEPT MOLEC MICROBIOL,ST LOUIS,MO 63110. CHIRON CORP,EMERYVILLE,CA 94608. RP KOZIEL, MJ (reprint author), MASSACHUSETTS GEN HOSP,INFECT DIS UNIT,FRUIT ST,BOSTON,MA 02114, USA. RI Yang, Chen/G-1379-2010 FU NCI NIH HHS [CA57973]; NIAID NIH HHS [AI31563] NR 59 TC 278 Z9 285 U1 0 U2 2 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1995 VL 96 IS 5 BP 2311 EP 2321 DI 10.1172/JCI118287 PG 11 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA TC979 UT WOS:A1995TC97900029 PM 7593618 ER PT J AU SKARE, JT SHANG, ES FOLEY, DM BLANCO, DR CHAMPION, CI MIRZABEKOV, T SOKOLOV, Y KAGAN, BL MILLER, JN LOVETT, MA AF SKARE, JT SHANG, ES FOLEY, DM BLANCO, DR CHAMPION, CI MIRZABEKOV, T SOKOLOV, Y KAGAN, BL MILLER, JN LOVETT, MA TI VIRULENT-STRAIN ASSOCIATED OUTER-MEMBRANE PROTEINS OF BORRELIA-BURGDORFERI SO JOURNAL OF CLINICAL INVESTIGATION LA English DT Article DE LYME BORRELIOSIS; LYME DISEASE; OUTER MEMBRANE PROTEIN; PORIN; SPIROCHETE ID LYME-DISEASE; TREPONEMA-PALLIDUM; ESCHERICHIA-COLI; SURFACE PROTEIN; YERSINIA-ENTEROCOLITICA; MOLECULAR ANALYSIS; EPITHELIAL-CELLS; SALMONELLA-TYPHIMURIUM; NEISSERIA-GONORRHOEAE; NORTH-AMERICAN AB We have isolated and purified outer membrane vesicles (OMV) from Borrelia burgdorferi strain B31 based on methods developed for isolation of Treponema pallidum OMV. Purified OMV exhibited distinct porin activities with conductances of 0.6 and 12.6 nano-Siemen and had no detectable beta-NADH oxidase activity indicating their outer membrane origin and their lack of inner membrane contamination, respectively. Hydrophobic proteins were identified by phase partitioning with Triton X-114. Most of these hydrophobic membrane proteins were not acylated, suggesting that they are outer membrane-spanning proteins. Identification of pamitate-labeled lipoproteins revealed that several were enriched in the OMV, several were enriched in the protoplasmic cylinder inner membrane fraction, and others were found exclusively associated with the inner membrane. The protein composition of OMV changed significantly with successive in vitro cultivation of strain B31, Using antiserum with specificity for virulent strain B31, we identified OMV antigens on the surface of the spirochete and identified proteins whose presence in OMV could be correlated with virulence and protective immunity in the rabbit Lyme disease model. These virulent strain associated outer membrane-spanning proteins may provide new insight into the pathogenesis of Lyme disease. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,DIV INFECT DIS,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. RP SKARE, JT (reprint author), UNIV CALIF LOS ANGELES,SCH MED,DEPT MICROBIOL & IMMUNOL,10833 LE CONTE AVE,LOS ANGELES,CA 90024, USA. FU NIAID NIH HHS [AI-12601, AI-21352, AI-29733] NR 68 TC 71 Z9 71 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0021-9738 J9 J CLIN INVEST JI J. Clin. Invest. PD NOV PY 1995 VL 96 IS 5 BP 2380 EP 2392 DI 10.1172/JCI118295 PG 13 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA TC979 UT WOS:A1995TC97900037 PM 7593626 ER PT J AU SHAMES, B FOX, JG DEWHURST, F YAN, LL SHEN, ZL TAYLOR, NS AF SHAMES, B FOX, JG DEWHURST, F YAN, LL SHEN, ZL TAYLOR, NS TI IDENTIFICATION OF WIDESPREAD HELICOBACTER-HEPATICUS INFECTION IN FECES IN COMMERCIAL MOUSE COLONIES BY CULTURE AND PCR ASSAY SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID CAMPYLOBACTER-CINAEDI; DNA AB The identification of a new murine pathogen, Helicobacter hepaticus, and its association with chronic active hepatitis and liver tumors prompted an evaluation of the prevalence of H, hepaticus in commercially available mice. Of the 28 different strains or stocks, totaling 160 mice from four major commercial vendors, cultured for H. hepaticus, 100% of mice from two outbred strains from one vendor were infected with H. hepaticus, whereas of 13 inbred mouse strains from another vendor were infected, This high prevalence of H, hepaticus established a need for a rapid and reproducible, noninvasive assay for the screening of colony-maintained mice being used for biomedical research. The culturing of fecal material by using 0.45-mu m-pore-size filtration for H. hepaticus consistently yielded reproducible results but required extended periods of time (1 to 3 weeks) to obtain a definitive answer. Although it is rapid, the use of a direct PCR-based detection assay with fecal specimens is restricted by inhibitory agents. To circumvent these inhibitory agents and to augment our H. hepaticus culture technique, we have developed a novel PCR system in which the bacteria are isolated from fecal material in the presence of polyvinylpyropyrollidone and lysed by treatment with Chelex 100. The PCR is performed with Tth polymerase supplemented with a polymerase enhancer. By this PCR method, 24 H. hepaticus culture-positive and 30 H. hepaticus culture-negative fecal samples were correctly identified, Moreover, two samples which were PCR positive and culture negative initially were positive by both methods upon retesting of fresh material, Southern blot hybridizations and sequencing of PCR products showed them to be H, hepaticus specific. A comparison of results obtained under identical conditions indicated a 100-fold increase in sensitivity with Tth polymerase over Tag polymerase. This PCR method can be used as a noninvasive means of rapidly screening large numbers of colony mice for H. hepaticus. C1 MIT,DIV COMPARAT MED,CAMBRIDGE,MA 02139. FORSYTH DENT CTR,DEPT MOLEC GENET,BOSTON,MA 02115. FU NCRR NIH HHS [RR07036, RR01046]; OFP OPHS HHS [RFPS 94-69] NR 29 TC 148 Z9 157 U1 0 U2 2 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 NOV PY 1995 VL 33 IS 11 BP 2968 EP 2972 PG 5 WC Microbiology SC Microbiology GA TA461 UT WOS:A1995TA46100033 PM 8576355 ER PT J AU SWENSON, JM FERRARO, MJ SAHM, DF CLARK, NC CULVER, DH TENOVER, FC CHARACHE, P HOPKINS, J HARRELL, LJ RELLER, LB HARDY, D MOELLERING, RC WILSON, W HINDLER, J AF SWENSON, JM FERRARO, MJ SAHM, DF CLARK, NC CULVER, DH TENOVER, FC CHARACHE, P HOPKINS, J HARRELL, LJ RELLER, LB HARDY, D MOELLERING, RC WILSON, W HINDLER, J TI MULTILABORATORY EVALUATION OF SCREENING METHODS FOR DETECTION OF HIGH-LEVEL AMINOGLYCOSIDE RESISTANCE IN ENTEROCOCCI SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Article ID FREEZE-DRIED PANELS; MODIFYING ENZYMES; STREPTOMYCIN RESISTANCE; STREPTOCOCCUS-FAECALIS; ANTIBIOTIC-RESISTANCE; LABORATORY DETECTION; GPS-TA; IDENTIFICATION; GENTAMICIN; SYNERGISM AB Since the early 1970s, the synergistic activity of an aminoglycoside with a cell wall-active agent has been predicted by determining the ability of an enterococcus to grow in the presence of high levels of the aminoglycoside (usually greater than or equal to 2,000 mu g/ml). However, a variety of media and concentrations of aminoglycosides has been used for this screening procedure, In the present study, we sought to optimize the agar dilution, broth microdilution, and disk diffusion tests used to detect high-level gentamicin and streptomycin resistance in enterococci. For dilution tests, brain heart infusion agar or broth gave the best growth and performance, For agar dilution, 500 mu g of gentamicin per ml, 2,000 mu g of streptomycin per ml, and an inoculum of 1 x 10(6) CFU/ml were optimal, while for broth microdilution, 500 mu g of gentamicin per mi, 1,000 mu g of streptomycin per ml, and an inoculum of 5 x 10(5) CFU/ml were best, Growth of more than one colony in the agar dilution test was determined to be the best indicator of high-level resistance, For disk diffusion, Mueller-Hinton agar, 120-mu g gentamicin disks, and 300-mu g streptomycin disks with breakpoints of no zone for resistance and greater than or equal to 10 mm for susceptibility gave the best sensitivity and specificity if results for strains with zones of 7 to 9 mm are considered inconclusive, indicating that a broth or agar test should be performed to determine susceptibility or resistance. C1 MASSACHUSETTS GEN HOSP,CLIN MICROBIOL LAB,BOSTON,MA 02114. WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. RP SWENSON, JM (reprint author), CTR DIS CONTROL & PREVENT,NATL CTR INFECT DIS,HOSP INFECT PROGRAM,1-3361,MAILSTOP G08,ATLANTA,GA 30333, USA. NR 41 TC 43 Z9 45 U1 2 U2 2 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 NOV PY 1995 VL 33 IS 11 BP 3008 EP 3018 PG 11 WC Microbiology SC Microbiology GA TA461 UT WOS:A1995TA46100041 PM 8576363 ER PT J AU SWENSON, JM CLARK, NC SAHM, DF FERRARO, ML DOERN, G HINDLER, J JORGENSEN, JH PFALLER, MA RELLER, LB WEINSTEIN, MP ZABRANSKY, RJ TENOVER, FC AF SWENSON, JM CLARK, NC SAHM, DF FERRARO, ML DOERN, G HINDLER, J JORGENSEN, JH PFALLER, MA RELLER, LB WEINSTEIN, MP ZABRANSKY, RJ TENOVER, FC TI MOLECULAR CHARACTERIZATION AND MULTILABORATORY EVALUATION OF ENTEROCOCCUS-FAECALIS ATCC-51299 FOR QUALITY-CONTROL OF SCREENING-TESTS FOR VANCOMYCIN AND HIGH-LEVEL AMINOGLYCOSIDE RESISTANCE IN ENTEROCOCCI SO JOURNAL OF CLINICAL MICROBIOLOGY LA English DT Note AB Studies were conducted to validate the use of Enterococcus faecalis ATCC 51299 (which is vancomycin resistant and resistant to high levels of gentamicin and streptomycin) and E. faecalis ATCC 29212 (which is susceptible to vancomycin and against which gentamicin or streptomycin and cell wall-active agents have synergistic killing activity) as controls in an agar screening test for vancomycin resistance and high-level streptomycin and gentamicin resistance and a broth microdilution screening test for high-level streptomycin and gentamicin resistance. Both organisms performed as expected in these tests and will serve as appropriate controls. However, E. faecalis ATCC 29212 was occasionally noted to produce light growth on the vancomycin screening plate with certain lots of agar. Quality control ranges for disk diffusion tests with disks with large amounts of streptomycin (300 mu g) and gentamicin (120 mu g) were established for E. faecalis ATCC 29212; zone limits are 16 to 22 mm for gentamicin and 14 to 19 mm for streptomycin. No zones of inhibition were seen when E. faecalis ATCC 51299 was tested with these high-content disks. C1 WASHINGTON UNIV,SCH MED,DEPT PATHOL,ST LOUIS,MO 63110. MASSACHUSETTS GEN HOSP,MICROBIOL LAB,BOSTON,MA 02114. UNIV MASSACHUSETTS,MED CTR,DEPT CLIN MICROBIOL,WORCESTER,MA 01655. UNIV CALIF LOS ANGELES,MED CTR,CLIN MICROBIOL LAB,LOS ANGELES,CA 90024. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. OREGON HLTH SCI UNIV,DEPT PATHOL,PORTLAND,OR 97201. DUKE UNIV,MED CTR,CLIN MICROBIOL LAB,DURHAM,NC 27710. UNIV NEW BRUNSWICK,ROBERT WOOD JOHNSON HOSP,MICROBIOL LABS,NEW BRUNSWICK,NJ 08903. UNIV TEXAS,MED BRANCH,DEPT CLIN MICROBIOL,GALVESTON,TX 77550. RP SWENSON, JM (reprint author), CTR DIS CONTROL & PREVENT,HOSP INFECT PROGRAM,1-3361 MAILSTOP G08,1600 CLIFTON RD,ATLANTA,GA 30333, USA. NR 9 TC 25 Z9 25 U1 0 U2 3 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 NOV PY 1995 VL 33 IS 11 BP 3019 EP 3021 PG 3 WC Microbiology SC Microbiology GA TA461 UT WOS:A1995TA46100042 PM 8576364 ER PT J AU Blais, MA Benedict, KB Norman, DK AF Blais, MA Benedict, KB Norman, DK TI Concurrent validity of the MCMI-II modifier indices SO JOURNAL OF CLINICAL PSYCHOLOGY LA English DT Article ID SCALES AB The relationships between the three Modifier Indices (Disclosure X, Desirability Y, and Debasement Z) of the Millon Clinical Multiaxial Inventory-II (MCMI-II) and the validity and clinical scales of the Minnesota Multiphasic Personality Inventory-2 (MMPI-2) were explored. A sample of 125 psychiatric inpatients was administered both personality measures within 7 days of admission. The pattern of Pearson correlation coefficients and principal component factors was seen as generally supporting the validity of the three MCMI-II Modifier Indices. However, the Disclosure and Debasement Indices were highly intercorrelated and similar in their MMPI-2 associations. The Desirability Index functioned in a more unique manner and demonstrated both convergent and divergent relationships with MMPI-2 Validity and Clinical scales. C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP Blais, MA (reprint author), MASSACHUSETTS GEN HOSP,INPATIENT PSYCHIAT SERV,BLAKE-11,BOSTON,MA 02114, USA. NR 18 TC 5 Z9 5 U1 0 U2 0 PU CLINICAL PSYCHOLOGY PUBL CO PI BRANDON PA 4 CONANT SQUARE, BRANDON, VT 05733 SN 0021-9762 J9 J CLIN PSYCHOL JI J. Clin. Psychol. PD NOV PY 1995 VL 51 IS 6 BP 783 EP 789 DI 10.1002/1097-4679(199511)51:6<783::AID-JCLP2270510609>3.0.CO;2-8 PG 7 WC Psychology, Clinical SC Psychology GA TN399 UT WOS:A1995TN39900008 PM 8778126 ER PT J AU YAREMCHUK, MJ POSNICK, JC AF YAREMCHUK, MJ POSNICK, JC TI RESOLVING CONTROVERSIES RELATED TO PLATE AND SCREW FIXATION IN THE GROWING CRANIOFACIAL SKELETON SO JOURNAL OF CRANIOFACIAL SURGERY LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DEPT SURG,CAMBRIDGE,MA 02138. GEORGETOWN UNIV,DEPT SURG,WASHINGTON,DC 20007. RP YAREMCHUK, MJ (reprint author), MASSACHUSETTS GEN HOSP,DEPT CRANIOFACIAL SURG,WACC 453,BOSTON,MA 02114, USA. NR 0 TC 18 Z9 18 U1 1 U2 2 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 1049-2275 J9 J CRANIOFAC SURG JI J. Craniofac. Surg. PD NOV PY 1995 VL 6 IS 6 BP 525 EP 538 DI 10.1097/00001665-199511000-00023 PG 14 WC Surgery SC Surgery GA TE740 UT WOS:A1995TE74000023 PM 9020748 ER PT J AU MA, A DATTA, M MARGOSIAN, E CHEN, JZ HORAK, I AF MA, A DATTA, M MARGOSIAN, E CHEN, JZ HORAK, I TI T-CELLS, BUT NOT B-CELLS, ARE REQUIRED FOR BOWEL INFLAMMATION IN INTERLEUKIN 2-DEFICIENT MICE SO JOURNAL OF EXPERIMENTAL MEDICINE LA English DT Note ID CHRONIC INTESTINAL INFLAMMATION; RECEPTOR MUTANT MICE; GENE; REARRANGEMENT; LYMPHOCYTES; DEFICIENT; DISEASE AB Interleukin-2 (IL-2)-deficient (IL-2(-/-)) mice develop anemia and colonic inflammatory bowel disease. To elucidate the mechanism of this disease, we have bred IL-2(-/-) mice to two strains of immunodeficient mice, RAG-2-deficient (RAG-2(-/-), lacking B and T cells) and JH-deficient mice (JH(-/-), lacking B cells). IL-2(-/-), RAG-2(-/-) double-mutant mice are disease free, while IL-2(-/-), JH(-/-) double-mutant mice succumb to bowel disease at the same rate as IL-2(-/-) littermates. IL-2(-/-), JH(-/-) mice do not, however, succumb to anemia. Thus, spontaneous intestinal inflammation in IL-2(-/-) mice requires mature T cells, not B cells, while anemia is dependent on B cells. C1 CHILDRENS HOSP,BOSTON,MA 02115. BETH ISRAEL HOSP,BOSTON,MA 02115. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV WURZBURG,INST VIROL & IMMUNOBIOL,D-97078 WURZBURG,GERMANY. RP MA, A (reprint author), HARVARD UNIV,SCH MED,CTR BLOOD RES,ALPERT 156,200 LONGWOOD AVE,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [P30 DK43351-04] NR 14 TC 122 Z9 126 U1 0 U2 0 PU ROCKEFELLER UNIV PRESS PI NEW YORK PA 222 E 70TH STREET, NEW YORK, NY 10021 SN 0022-1007 J9 J EXP MED JI J. Exp. Med. PD NOV 1 PY 1995 VL 182 IS 5 BP 1567 EP 1572 DI 10.1084/jem.182.5.1567 PG 6 WC Immunology; Medicine, Research & Experimental SC Immunology; Research & Experimental Medicine GA TB894 UT WOS:A1995TB89400038 PM 7595226 ER PT J AU STOECKLE, JD AF STOECKLE, JD TI DO PATIENTS WANT TO BE INFORMED - DO THEY WANT TO DECIDE SO JOURNAL OF GENERAL INTERNAL MEDICINE LA English DT Editorial Material RP STOECKLE, JD (reprint author), MASSACHUSETTS GEN HOSP,PRIMARY CARE PROGRAM,BOSTON,MA 02114, USA. NR 0 TC 2 Z9 2 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0884-8734 J9 J GEN INTERN MED JI J. Gen. Intern. Med. PD NOV PY 1995 VL 10 IS 11 BP 643 EP 644 DI 10.1007/BF02602750 PG 2 WC Health Care Sciences & Services; Medicine, General & Internal SC Health Care Sciences & Services; General & Internal Medicine GA TG223 UT WOS:A1995TG22300008 PM 8583268 ER PT J AU WINTMAN, BI GELBERMAN, RH KATZ, JN AF WINTMAN, BI GELBERMAN, RH KATZ, JN TI DYNAMIC SCAPHOLUNATE INSTABILITY - RESULTS OF OPERATIVE TREATMENT WITH DORSAL CAPSULODESIS SO JOURNAL OF HAND SURGERY-AMERICAN VOLUME LA English DT Article AB Nineteen patients underwent 20 dorsal capsulodeses for dynamic scapholunate instability. Seventeen patients (18 wrists) were evaluated by a questionnaire and physical examination after a mean postoperative follow-up period of 34 months (range, 12-65). The diagnosis was based on a combination of characteristic symptoms of scapholunate instability and physical findings consisting of dorsal wrist tenderness at the scapholunate interval and a positive scaphoid shift test. Following surgery, a significant decrease was noted in symptoms of pain and dunking. Functional status was improved postoperatively; the most significant gains were seen in opening jars, sweeping, shoveling, and throwing. Fifteen of 17 patients returned to their original occupations, although 7 of those who returned to their original occupations did so with some restrictions. Objective evaluation by physical examination revealed a significant improvement in wrist stability as determined by the scaphoid shift test, and an average loss of 12 degrees of flexion. Fifteen of 17 patients (16 of 18 wrists) stated that they would undergo the surgery again if faced with the same choice. Our data demonstrate that dorsal radioscaphoid capsulodesis of the wrist in patients with dynamic scapholunate instability provides substantial improvement over preoperative status. C1 MASSACHUSETTS GEN HOSP,HARVARD COMBINED ORTHOPAED SURG PROGRAM,BOSTON,MA 02114. FU NIAMS NIH HHS [AR 36308] NR 0 TC 71 Z9 75 U1 0 U2 2 PU CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS PI NEW YORK PA 650 AVENUE OF THE AMERICAS, NEW YORK, NY 10011 SN 0363-5023 J9 J HAND SURG-AM JI J. Hand Surg.-Am. Vol. PD NOV PY 1995 VL 20A IS 6 BP 971 EP 979 DI 10.1016/S0363-5023(05)80145-5 PG 9 WC Orthopedics; Surgery SC Orthopedics; Surgery GA TH309 UT WOS:A1995TH30900012 PM 8583070 ER PT J AU LIN, T MATSUZAKI, G UMESUE, M OMOTO, K YOSHIDA, H HARADA, M SINGARAM, C HIROMATSU, K NOMOTO, K AF LIN, T MATSUZAKI, G UMESUE, M OMOTO, K YOSHIDA, H HARADA, M SINGARAM, C HIROMATSU, K NOMOTO, K TI DEVELOPMENT OF TCR-GAMMA-DELTA CD4(-)CD8(+)ALPHA-ALPHA BUT NOT TCR-ALPHA-BETA CD4(-)CD8(+)ALPHA-ALPHA I-IEL IS RESISTANT TO CYCLOSPORINE-A SO JOURNAL OF IMMUNOLOGY LA English DT Article ID T-CELL RECEPTOR; INTESTINAL INTRAEPITHELIAL LYMPHOCYTES; MONOCLONAL-ANTIBODY; MICE; DIFFERENTIATION; THYMUS; LYMPHOPOIESIS; EPITHELIUM; SELECTION; THYMOCYTES AB Present evidence suggests that cyclosporin A (CSA) inhibits the development of both alpha beta and gamma delta T cells in the thymus. However, whether CSA can inhibit the development of murine intestinal intraepithelial lymphocytes (i-IEL) is unknown as most i-IEL are clearly derived from a different lineage than the conventional thymus-derived T cells found in the periphery. Using the adult thymectomized, lethally irradiated bone-marrow reconstituted chimera (ATXBM mice) as a model for the development of extrathymically derived i-IEL and the fetal thymus-grafted (FTG) nude mice as a model for the development of thymically derived i-IEL, we demonstrate that CSA nearly completely inhibited the development of extrathymically, and possibly thymically, derived TCR-alpha beta i-IEL. Most of the TCR-alpha beta i-IEL whose development was inhibited by CSA belonged to the CD4(-)CD8(+) alpha alpha subset. In contrast, the development of extrathymically and thymically derived TCR-gamma delta i-IEL was completely resistant to CSA. The phenotype of CSA-resistant TCR-gamma delta i-IEL in these models was not different from those in control mice, and the TCR-gamma delta i-IEL in CSA-treated mice appear to be mature and activated as most were large, granular, and CD69(+). Lastly, we demonstrate that CSA does not affect the extrathymic positive selection of V delta 4 i-IEL in C3H hosts. These results suggest that despite their similarity, the intracellular activation cascade involved after TCR stimulation between TCR-alpha beta CD4(-)CD8(+) alpha alpha and TCR-gamma delta CD4(-)CD8(+)alpha alpha i-IEL are markedly different. C1 UNIV WISCONSIN HOSP,DEPT MED,GASTROENTEROL SECT,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. KYUSHU UNIV,MED INST BIOREGULAT,DEPT IMMUNOL,FUKUOKA 812,JAPAN. NAGOYA UNIV,SCH MED,DIS MECHANISM & CONTROL RES INST,GERMFREE LIFE LAB,NAGOYA,AICHI 466,JAPAN. NR 39 TC 15 Z9 15 U1 0 U2 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD NOV 1 PY 1995 VL 155 IS 9 BP 4224 EP 4230 PG 7 WC Immunology SC Immunology GA TB468 UT WOS:A1995TB46800013 PM 7594578 ER PT J AU YOUNT, NY WANG, MSC YUAN, J BANAIEE, N OUELLETTE, AJ SELSTED, ME AF YOUNT, NY WANG, MSC YUAN, J BANAIEE, N OUELLETTE, AJ SELSTED, ME TI RAT NEUTROPHIL DEFENSINS - PRECURSOR STRUCTURES AND EXPRESSION DURING NEUTROPHILIC MYELOPOIESIS SO JOURNAL OF IMMUNOLOGY LA English DT Article ID NATURAL PEPTIDE ANTIBIOTICS; ANTIMICROBIAL PEPTIDES; SMALL-INTESTINE; MESSENGER-RNA; HOST DEFENSE; BIOLOGICAL-ACTIVITY; MYOTONIC-DYSTROPHY; CATIONIC PEPTIDES; RICH PEPTIDES; PANETH CELLS AB Defensins constitute a family of 3- to 4-kDa antimicrobial peptides that are stored in the cytoplasmic granules of neutrophils, some macrophages, and intestinal Paneth cells, We have assessed defensin gene expression during myeloid differentiation by first characterizing cDNAs for each of the four known rat neutrophil defensins (RatNP 1-4). The cDNA sequences revealed that the peptides are synthesized as 87-94 amino acid precursors, each containing signal, pro-, and mature peptide segments, RatNP-3 and -4 mRNAs, but not those for RatNP-1 and -2 or other myeloid defensins, contained unique polypurine tracts located close to the termination codon in the 3' untranslated region. By using cDNA probes and/or riboprobes, we evaluated defensin transcript levels in a variety of tissues and in the full spectrum of neutrophil precursors, By in situ hybridization, defensin mRNAs were localized to neutrophil precursors in the bone marrow, with the highest mRNA levels occurring in promyelocytes and somewhat lower signals occurring in myeloblasts and myelocytes. Defensin mRNAs were not detectable in bands or mature neutrophils, nor at significant levels in tissues other than bone marrow, The accumulation of defensin protein in bone marrow cells was assessed by immunohistochemical staining with anti-RatNP-1 Ab. RatNP 1-4 mRNAs and protein levels were then correlated for each stage of neutrophilic differentiation to reveal the maturational profile of myeloid defensin gene expression in the rat. C1 UNIV CALIF IRVINE,COLL MED,DEPT PATHOL,IRVINE,CA 92717. UNIV CALIF IRVINE,COLL MED,DEPT MICROBIOL & MOLEC GENET,IRVINE,CA 92717. MASSACHUSETTS GEN HOSP,MED SERV,GASTROINTESTINAL UNIT,BOSTON,MA 02114. FU NIAID NIH HHS [AI22931, AI31696]; NIDDK NIH HHS [DK08851] NR 62 TC 49 Z9 54 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 NOV 1 PY 1995 VL 155 IS 9 BP 4476 EP 4484 PG 9 WC Immunology SC Immunology GA TB468 UT WOS:A1995TB46800045 PM 7594610 ER PT J AU HAUBRICH, RH FLEXNER, C LEDERMAN, MM HIRSCH, M PETTINELLI, CP GINSBERG, R LIETMAN, P HAMZEH, FM SPECTOR, SA RICHMAN, DD HAMMER, S COOLEY, T GULICK, R SULLIVAN, M SPINA, C FRASER, A LATHEY, J BASSIAKOS, Y CHANCE, M DROBNES, C CORUELL, E GRUE, L RAINES, C KUWAHARA, S MCPHERSON, J AF HAUBRICH, RH FLEXNER, C LEDERMAN, MM HIRSCH, M PETTINELLI, CP GINSBERG, R LIETMAN, P HAMZEH, FM SPECTOR, SA RICHMAN, DD HAMMER, S COOLEY, T GULICK, R SULLIVAN, M SPINA, C FRASER, A LATHEY, J BASSIAKOS, Y CHANCE, M DROBNES, C CORUELL, E GRUE, L RAINES, C KUWAHARA, S MCPHERSON, J TI A RANDOMIZED TRIAL OF THE ACTIVITY AND SAFETY OF RO-24-7429 (TAT ANTAGONIST) VERSUS NUCLEOSIDE FOR HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION SO JOURNAL OF INFECTIOUS DISEASES LA English DT Article ID PLACEBO-CONTROLLED TRIAL; TUMOR-NECROSIS-FACTOR; TRANS-ACTIVATOR GENE; DOUBLE-BLIND; REPLICATION; ZIDOVUDINE; TYPE-1; INHIBITION; EFFICACY; AZT AB Ro 24-7429, a Tat antagonist, dosed at 75, 150, or 300 mg/day, was compared with nucleoside analogue (zidovudine or didanosine) for 12 weeks in 96 human immunodeficiency virus (HIV)infected patients to assess safety and activity. The primary adverse effect of Ro 24-7429 was rash, which necessitated treatment discontinuation in 6 of 71 patients. Nucleoside analogue treatment produced an average increase in CD4 cell count of 28 cells/mm(3) at week 8 versus a decrease of 27 cells/mm(3) in recipients of Ro 24-7429 (P < .001). Serum HIV p24 antigen levels decreased by an average of 111 pg/mL in nucleoside recipients at week 8 compared with an increase of 41 pg/mL in recipients of Ro 24-7429 (P = .007). Nucleoside-treated patients had a mean 0.66 log(10) reduction in infectious peripheral blood mononuclear cells, while Ro 24-7429 recipients had a mean 0.02 log(10) reduction (P = .02). No dose-response relationships were observed in the Ro 24-7429 groups. In this study, Ro 24-7429 treatment showed no evidence of antiviral activity. C1 UNIV CALIF SAN DIEGO,DEPT PATHOL,SAN DIEGO,CA 92103. UNIV CALIF SAN DIEGO,DEPT PEDIAT,SAN DIEGO,CA 92103. JOHNS HOPKINS UNIV HOSP,BALTIMORE,MD 21205. CASE WESTERN RESERVE UNIV,SCH MED,DEPT MED,CLEVELAND,OH 44106. HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA. NIAID,DIV AIDS,BETHESDA,MD 20892. HOFFMANN LA ROCHE AG,NUTLEY,NJ. RP HAUBRICH, RH (reprint author), UNIV CALIF SAN DIEGO,CTR TREATMENT,DEPT MED,2760 5TH AVE,SUITE 300,SAN DIEGO,CA 92103, USA. FU NCRR NIH HHS [RR-00722, RR-00035]; NIAID NIH HHS [AI-27670] NR 22 TC 22 Z9 23 U1 0 U2 2 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 NOV PY 1995 VL 172 IS 5 BP 1246 EP 1252 PG 7 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA TA552 UT WOS:A1995TA55200010 PM 7594660 ER PT J AU Correa, AL Velez, G Albert, M Luther, M Rinaldi, MG Graybill, JR AF Correa, AL Velez, G Albert, M Luther, M Rinaldi, MG Graybill, JR TI Comparison of D0870 and fluconazole in the treatment of murine cryptococcal meningitis SO JOURNAL OF MEDICAL AND VETERINARY MYCOLOGY LA English DT Article ID ACQUIRED-IMMUNODEFICIENCY-SYNDROME; AMPHOTERICIN-B; SUSCEPTIBILITY; INFECTIONS; AIDS AB Cryptococcal meningitis is a common infection in patients with AIDS. Using a murine cryptococcosis model, we compared treatment with a new triazole, D0870, and fluconazole. Groups of ICR (Institute for Cancer Research) mice were infected intracerebrally with eight different isolates of Cryptococcus neoformans variety neoformans with different in vitro susceptibilities to fluconazole. For survival studies mice were challenged with two to four times LD(50) or six to nine times LD(50). Treatment was given for 10 days. Mice were observed through to day 30. To assess the effect of treatment on fungal tissue burden, mice received a three to five times LD(50) inoculum and treatment for 10 days. They were sacrificed on day 12 and serial dilutions of brain homogenates were cultured. Fluconazole prolonged survival primarily in isolates which were susceptible in vitro. D0870 prolonged survival in all isolates except one, which was also resistant in vitro to D0870 and fluconazole. Both drugs reduced colony counts of all isolates. D0870 warrants further development for use in cryptococcosis, and appears effective for isolates relatively resistant to fluconazole. There is a relative correlation of in vivo and in vitro susceptibility to D0870 as well as fluconazole. C1 UNIV TEXAS,HLTH SCI CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX 78284. RP Correa, AL (reprint author), AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,DIV INFECT DIS 111F,7400 MERTON MINTER BLVD,SAN ANTONIO,TX 78284, USA. NR 17 TC 6 Z9 6 U1 0 U2 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0268-1218 J9 J MED VET MYCOL JI J. Med. Vet. Mycol. PD NOV-DEC PY 1995 VL 33 IS 6 BP 367 EP 374 PG 8 WC Mycology SC Mycology GA TZ017 UT WOS:A1995TZ01700002 PM 8683404 ER PT J AU SYMES, AJ CORPUS, L FINK, JS AF SYMES, AJ CORPUS, L FINK, JS TI DIFFERENCES IN NUCLEAR SIGNALING BY LEUKEMIA INHIBITORY FACTOR AND INTERFERON-GAMMA - THE ROLE OF STAT PROTEINS IN REGULATING VASOACTIVE-INTESTINAL-PEPTIDE GENE-EXPRESSION SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE INTERFERON-GAMMA; VASOACTIVE INTESTINAL PEPTIDE; LEUKEMIA INHIBITORY FACTOR; STAT; CYTOKINE ID NEUROBLASTOMA CELL-LINE; TYROSINE PHOSPHORYLATION; TRANSCRIPTION FACTOR; RECEPTOR COMPONENT; MOLECULAR-CLONING; BINDING PROTEIN; NEURONAL CELLS; DNA ELEMENT; IFN-GAMMA; ACTIVATION AB To investigate the importance of STAT protein activation in leukemia inhibitory factor (LIF)-mediated induction of neuropeptide gene transcription, we compared signaling to the 180-bp cytokine response element (CyRE) in the vasoactive intestinal peptide (VIP) promoter by interferon-gamma (IFN-gamma) and LIF. We show that LIF and IFN-gamma activate STAT proteins but only LIF activates VIP gene transcription. Thus STAT activation is not sufficient for VIP transcriptional activation, In a CyRE reporter plasmid, in which the STAT site has been deleted, LIF, but not IFN-gamma, activates transcription, indicating that sequences within the CyRE distinct from the STAT site are important to LIF-mediated transcriptional activation. The CyRE does not mediate transcriptional activation to LIF in a non-VIPergic cell line, suggesting that cell-specific factors exist which are permissive for cytokine-dependent regulation of gene expression. Human and mouse sequences are highly conserved in the region of the CyRE, consistent with the functional importance of multiple regions of the CyRE. These findings show that regions within the CyRE distinct from the STAT site are important to the UF-dependent regulation of VIP gene expression and enable the CyRE to respond in a cell-specific and cytokine-specific manner. C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROBIOL LAB,BOSTON,MA 02114. RI Symes, Aviva/S-7471-2016 OI Symes, Aviva/0000-0003-2557-9939 FU NINDS NIH HHS [NS27514] NR 49 TC 21 Z9 21 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD NOV PY 1995 VL 65 IS 5 BP 1926 EP 1933 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA TA742 UT WOS:A1995TA74200003 PM 7595475 ER PT J AU GRIFFITHS, TD CONNOLLY, S NEWMAN, PK BATESON, MC AF GRIFFITHS, TD CONNOLLY, S NEWMAN, PK BATESON, MC TI NEUROMYOTONIA IN ASSOCIATION WITH MALIGNANT HYPERPYREXIA SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Note C1 MIDDLESBROUGH GEN HOSP,DEPT NEUROL,MIDDLESBROUGH TS5 5AZ,CLEVELAND,ENGLAND. MASSACHUSETTS GEN HOSP,DEPT CLIN NEUROPHYSIOL,BOSTON,MA 02114. BISHOP AUCKLAND GEN HOSP,BISHOP AUCKLAND BL14 6AD,DURHAM,ENGLAND. NR 3 TC 5 Z9 5 U1 0 U2 0 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON, ENGLAND WC1H 9JR SN 0022-3050 J9 J NEUROL NEUROSUR PS JI J. Neurol. Neurosurg. Psychiatry PD NOV PY 1995 VL 59 IS 5 BP 556 EP 557 DI 10.1136/jnnp.59.5.556 PG 2 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA TC963 UT WOS:A1995TC96300027 PM 8530950 ER PT J AU GEARING, M SCHNEIDER, JA ROBINS, RS HOLLISTER, RD MORI, H GAMES, D HYMAN, BT MIRRA, SS AF GEARING, M SCHNEIDER, JA ROBINS, RS HOLLISTER, RD MORI, H GAMES, D HYMAN, BT MIRRA, SS TI REGIONAL VARIATION IN THE DISTRIBUTION OF APOLIPOPROTEIN-E AND A-BETA IN ALZHEIMERS-DISEASE SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE AMYLOID; CEREBELLUM; DIFFUSE PLAQUE; STRIATUM ID AMYLOID PRECURSOR PROTEIN; TYPE-4 ALLELE; DEPOSITION; EPSILON-4; BINDING; PLAQUES; CORTEX AB While the epsilon 4 allele of apolipoprotein E (ApoE) has been identified as a risk factor in Alzheimer's disease (AD), the mechanism by which this risk is conveyed is not understood. Immunohistochemical studies demonstrating ApoE-A beta colocalization in senile plaques, neurofibrillary tangles, and blood vessels and in vitro studies of ApoE-A beta interactions suggest that ApoE plays a role in amyloid processing and/or fibrillogenesis. We examined the ApoE-A beta association in diffuse and neuritic plaques in the neocortex, striatum, and cerebellum, and determined the ApoE genotype in 100 brains derived from dementia patients with neuropathologically confirmed AD. As expected, the epsilon 4 allele was overrepresented in AD patients compared with patients without neurological disease (p < 0.001). ApoE-positive plaque counts in neocortex were higher in epsilon 4/4 individuals than in individuals with other genotypes (p < 0.0005). Overall, in the 100 cases, ApoE-positive plaques were less frequent than A beta-positive plaques in contiguous sections (p < 0.0001). In all cases, A beta-positive diffuse plaques in the striatum failed to label with ApoE antibody, whereas the majority of cerebellar diffuse plaques showed A beta-ApoE colocalization. Possible explanations for these discrepancies include regional variation in amyloid processing and fibrillogenesis, varying stages of plaque evolution, and technical considerations. C1 VET ADM MED CTR,ATLANTA,GA 30033. EMORY UNIV,SCH MED,DEPT PATHOL & LAB MED,ATLANTA,GA 30322. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. TOKYO INST PSYCHIAT,DEPT MOLEC BIOL,TOKYO,JAPAN. ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080. FU NIA NIH HHS [AG12406, AG06790, AG10130] NR 35 TC 61 Z9 61 U1 1 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 NOV PY 1995 VL 54 IS 6 BP 833 EP 841 DI 10.1097/00005072-199511000-00010 PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA TE949 UT WOS:A1995TE94900010 PM 7595656 ER PT J AU DYER, CA PHILIBOTTE, T AF DYER, CA PHILIBOTTE, T TI A CLONE OF THE MOCH-1 GLIAL TUMOR IN CULTURE - MULTIPLE PHENOTYPES EXPRESSED UNDER DIFFERENT ENVIRONMENTAL-CONDITIONS SO JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY LA English DT Article DE ASTROCYTE; MIXED GLIOMA; OLIGODENDROCYTE; PLASTICITY ID MYELIN BASIC-PROTEIN; 2',3'-CYCLIC NUCLEOTIDE 3'-PHOSPHOHYDROLASE; MONOCLONAL-ANTIBODIES O1; RAT-BRAIN; NERVOUS-SYSTEM; CELL-LINE; OLIGODENDROCYTES; MEMBRANE; INVITRO; GALACTOCEREBROSIDE AB The MOCH-1 glial cell line, which was derived from a glioblastoma taken from the brain of a MBP/c-neu transgenic mouse, was used as a model for studying the plastic nature of gliomas in culture. Fifteen MOCH-1 clones were derived and characterized under different growth conditions via Western blot analysis and immunocytochemical staining using a panel of antibodies specific for major myelin markers and glial fibrillary acidic protein. In low serum conditions, the clones resemble immature oligodendrocytes and express only immature oligodendrocyte markers. When placed in serum-free chemically defined medium (CDM), nine clones do not: change their phenotypes, while five variably express myelin markers. One clone, 4C8, differentiates into mature, membrane sheer-bearing oligodendrocyte-like cells and expresses major myelin markers in amounts and distributions similar to cultured primary oligodendrocytes. Our data show that 4C8 can reversibly switch from an oligodendrocyte-like phenotype to a reactive astrocyte-like phenotype, depending upon the presence of serum and other factors in different growth media. Our data indicate that serum ''pushes'' 4C8 into the astrocyte-like phenotype, while serum-free CDM ''pushes'' 4C8 into the oligodendrocyte-like phenotype. Furthermore, a population of mixed phenotypes results when the astrocyte-like 4C8 cells are placed in serum-free CDM. To our knowledge, this is the first report to show that by altering environment, a ''mixed glioma'' can arise from a homogeneous population of glial tumor cells, It is therefore possible that glial tumor cells in vivo may be induced to undergo similar phenotypic changes when they are exposed to different environmental signals in the central nervous system. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,SERV NEUROL,BOSTON,MA. RP DYER, CA (reprint author), EUNICE KENNEDY SHRIVER CTR MENTAL RETARDAT INC,200 TRAPELO RD,WALTHAM,MA 02254, USA. NR 45 TC 26 Z9 27 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 NOV PY 1995 VL 54 IS 6 BP 852 EP 863 DI 10.1097/00005072-199511000-00012 PG 12 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA TE949 UT WOS:A1995TE94900012 PM 7595658 ER PT J AU FARBER, SA NITSCH, RM SCHULZ, JG WURTMAN, RJ AF FARBER, SA NITSCH, RM SCHULZ, JG WURTMAN, RJ TI REGULATED SECRETION OF BETA-AMYLOID PRECURSOR PROTEIN IN RAT-BRAIN SO JOURNAL OF NEUROSCIENCE LA English DT Article DE BETA-AMYLOID PRECURSOR PROTEIN (APP); AMYLOID; BRAIN SLICES; PROTEIN SECRETION; ELECTRICAL STIMULATION; ACETYLCHOLINE; MUSCARINIC RECEPTORS; ALZHEIMERS DISEASE ID ALZHEIMERS-DISEASE; KINASE-C; HIPPOCAMPAL SLICES; NEURITE OUTGROWTH; PEPTIDE; IDENTIFICATION; ACTIVATION; RECEPTOR; RELEASE; PHOSPHORYLATION AB The beta-amyloid precursor protein (APP) is a ubiquitous, highly conserved secretory glycoprotein that is expressed at high levels in mammalian brain by neurons, astrocytes, and activated microglia. Secreted APP (APP(s)) is generated by the cleavage of APP within the beta-amyloid (AP) portion of its ectodomain. The formation and secretion of APP(s) can be increased by activation of particular neurotransmitter receptors and subsequent protein phosphorylation. We found that tissue slices from rat cortex, hippocampus, striatum,and cerebellum secrete APP(s) in vitro. APP(s) secretion was enhanced by electrical stimulation, but was not associated with a general increase in the release of total protein, lactate dehydrogenase (LDH) activity, or neuronal cell adhesion molecules. The pharmacological profile of stimulation-induced APP(s) secretion suggests complex interactions between muscarinic receptor subtypes in the tissue slices: in the unstimulated state, activation of Muscarinic Mi receptors increased APP(s) release while nonspecific activation of multiple muscarinic receptors had little effect on APP(s) release; in electrically stimulated slices, nonspecific inhibition of muscarinic receptors blunted the increase in APP secretion. The nonspecific muscarinic agonist carbachol increased APP(s) secretion only in the presence of an M2 receptor antagonist, suggesting that activation of M2 receptors suppresses APP(s) formation. These data indicate that secretory APP processing in brain includes depolarization-enhanced cleavage of the cell-associated holoprotein within its ectodomain, and that the net effect of depolarization involves several subtypes of acetylcholine receptors. C1 MIT,DEPT BRAIN & COGNIT SCI,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RI Schulz, Joachim/H-2430-2011; Farber, Steven/G-5851-2012 OI Farber, Steven/0000-0002-8037-7312 FU NIA NIH HHS [P-50-AG-05432]; NIMH NIH HHS [MH-28783] NR 50 TC 121 Z9 121 U1 0 U2 1 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 SN 0270-6474 J9 J NEUROSCI JI J. Neurosci. PD NOV PY 1995 VL 15 IS 11 BP 7442 EP 7451 PG 10 WC Neurosciences SC Neurosciences & Neurology GA TF264 UT WOS:A1995TF26400042 PM 7472496 ER PT J AU FRIM, DM PADWA, B BUCKLEY, D CROWELL, RM OGILVY, CS AF FRIM, DM PADWA, B BUCKLEY, D CROWELL, RM OGILVY, CS TI MANDIBULAR SUBLUXATION AS AN ADJUNCT TO EXPOSURE OF THE DISTAL INTERNAL CAROTID-ARTERY IN ENDARTERECTOMY SURGERY - TECHNICAL NOTE SO JOURNAL OF NEUROSURGERY LA English DT Note DE MANDIBULAR SUBLUXATION; CAROTID ARTERY; ENDARTERECTOMY; OPERATIVE TECHNIQUE ID PENETRATING INJURIES; SKULL; BASE AB The location of the carotid artery bifurcation and the distance atherosclerotic disease extends distally in the internal carotid artery (ICA) are two factors that contribute to the technical difficulty of carotid endarterectomy. When the bifurcation is high (above C-3) or the disease extends distally, standard approaches may not provide adequate exposure for dissection of plaque or for arteriotomy repair. A simple method of mandibular subluxation is described for added exposure of the distal carotid artery. The criteria for use of this method include: a carotid bifurcation at or above C-2; disease extending to within 2 cm of the skull base; and a small-caliber distal ICA lumen with the expectation of a patch graft extending close to the skull base. In dentulous patients, the mandible is subluxed by attaching an intradental wire from the ipsilater al mandibular bicuspid to an intradental wire around the contralateral maxillary bicuspid. In edentulous patients, a wire is placed around the ipsilateral mandible and secured to a wire placed through the anterior nasal spine. The entire preoperative subluxation requires 10 to 15 minutes under anesthesia and an additional 1 to 2 minutes postoperatively to remove the wires. A single skin suture and an absorbable intraoral suture were placed in some edentulous patients. This technique has been evaluated over a 15-month reference period during which 115 carotid endarterectomies were performed. The criteria stated above were met in seven cases (six patients, 6%) and jaw subluxation was performed pre operatively. An additional 1 to 2 cm of distal exposure was obtained by using this technique and endarterectomy proceeded without complication. A slight ''shift'' of the standard anatomical landmarks occurred due to the movement of the mandible, which was easily recognized. There were no significant postoperative complaints related to the subluxation; specifically, no temporomandibular joint pain, no other postoperative pain, and no tooth damage were encountered. It is concluded that this relatively simple approach to mandibular subluxation provided significant added exposure to the distal ICA without notably increasing operative time. In addition, there was no morbidity and little additional care was needed when compared with other more radical approaches to high carotid artery exposure. C1 MASSACHUSETTS GEN HOSP, NEUROSURG SERV, BOSTON, MA 02114 USA. MASSACHUSETTS GEN HOSP, ORAL & MAXILLOFACIAL SURG SERV, BOSTON, MA 02114 USA. NR 7 TC 22 Z9 23 U1 0 U2 0 PU AMER ASSOC NEUROLOGICAL SURGEONS PI ROLLING MEADOWS PA 5550 MEADOWBROOK DRIVE, ROLLING MEADOWS, IL 60008 USA SN 0022-3085 J9 J NEUROSURG JI J. Neurosurg. PD NOV PY 1995 VL 83 IS 5 BP 926 EP 928 DI 10.3171/jns.1995.83.5.0926 PG 3 WC Clinical Neurology; Surgery SC Neurosciences & Neurology; Surgery GA TA725 UT WOS:A1995TA72500028 PM 7472568 ER PT J AU NARULA, J SOUTHERN, JF DEC, GW PALACIOS, IF NEWELL, JB FALLON, JT STRAUSS, HW KHAW, BA YASUDA, T AF NARULA, J SOUTHERN, JF DEC, GW PALACIOS, IF NEWELL, JB FALLON, JT STRAUSS, HW KHAW, BA YASUDA, T TI ANTIMYOSIN UPTAKE AND MYOFIBRILLARLYSIS IN DILATED CARDIOMYOPATHY SO JOURNAL OF NUCLEAR CARDIOLOGY LA English DT Article DE MYOCARDITIS; MYOSIN; MONOCLONAL ANTIBODY; ENDOMYOCARDIAL BIOPSY; MYOCYTOLYSIS; RADIONUCLIDE IMAGING ID NONISCHEMIC CONGESTIVE CARDIOMYOPATHY; ENDOMYOCARDIAL BIOPSY; DOXORUBICIN CARDIOTOXICITY; ACUTE MYOCARDITIS; ANTIBODY; DEGENERATION; DIAGNOSIS; FAILURE AB Background. Although antimyosin scintigraphy detects myocyte necrosis associated with myocarditis, it has also been reported to yield positive results in a large number of patients with clinical dilated cardiomyopathy without histologic evidence of myocarditis. The question to be resolved is whether this discordance represents false-positive results of antimyosin scans or whether antimyosin scintigraphy more accurately identifies the presence of myocyte necrosis than does endomyocardial biopsy testing. Methods and Results. Forty patients with the acute onset of dilated cardiomyopathy (left ventricular ejection fraction < 45%; mean 27% +/- 11%) but no endomyocardial biopsy evidence of myocarditis, were identified from a consecutive series of 50 patients who had undergone indium 111 antimyosin antibody scintigraphy and endomyocardial biopsy for suspected myocarditis. The endomyocardial biopsy specimens were analyzed to identify features correlating with antimyosin uptake or improvement in left ventricular ejection fraction (LVEF) over time. Twenty-five patients showed left ventricular myocardial uptake of radiolabeled antimyosin antibody by both planar and tomographic imaging, The remaining 15 patients had no antimyosin uptake. Of the 25, 22 (88%) patients with positive findings on antimyosin scans had degenerated, myofibrillarlytic myocytes in their biopsy specimens. Of the 15 patients with negative findings on antimyosin scans, only 6 (40%) had similar myofibrillarlytic myocytes (X(2) = 8.13; p < 0.0047). No other histological feature correlated with the antimyosin positivity, Stepwise multiple regression analysis was performed for identification of predictors of short-term improvement in LVEF. Patients with positive findings on antimyosin scans showed a trend toward improvement with time (F = 3.97; p > 0.05). None of the histologic features predicted improvement in the LVEF. However, the combination of positive findings on an antimyosin scan and myofibrillarlysis did correlate significantly with spontaneous improvement in ejection fraction (F = 4.53; 0.01; < p < 0.05). Conclusions. This study identifies myofibrillarlysis as a common pathologic alteration in patients with recent onset of dilated cardiomyopathy and positive findings on antimyosin scan, who lack right ventricular biopsy evidence of myocarditis. Because myofibrillarlytic cell population may represent a histologic spectrum of viable to necrotic myocytes, it appears that antimyosin uptake detects necrotic myofibrillarlytic myocytes that are not identified by light microscopy. C1 MASSACHUSETTS GEN HOSP,DIV NUCL MED,CARDIAC UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 29 TC 19 Z9 19 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 1071-3581 J9 J NUCL CARDIOL JI J. Nucl. Cardiol. PD NOV-DEC PY 1995 VL 2 IS 6 BP 470 EP 477 DI 10.1016/S1071-3581(05)80038-8 PG 8 WC Cardiac & Cardiovascular Systems; Radiology, Nuclear Medicine & Medical Imaging SC Cardiovascular System & Cardiology; Radiology, Nuclear Medicine & Medical Imaging GA TJ888 UT WOS:A1995TJ88800002 PM 9420828 ER PT J AU ZAKNUN, J ELMALEH, DR GUAN, JH FISCHMAN, AJ AF ZAKNUN, J ELMALEH, DR GUAN, JH FISCHMAN, AJ TI EFFECT OF MONOUNSATURATION OF A BRANCHED FATTY-ACID ON ORGAN SELECTIVITY SO JOURNAL OF NUCLEAR MEDICINE LA English DT Article DE CARBON-11-BMHA; POSITRON EMISSION TOMOGRAPHY; FATTY ACID METABOLISM ID POSITRON EMISSION TOMOGRAPHY; BINDING PROTEIN; RAT-HEART; MYOCARDIAL-INFARCTION; EXTERNAL ASSESSMENT; CANINE MYOCARDIUM; METABOLISM; OXIDATION; DISEASE; TL-201 AB 1-[C-11]-3-R,S-methylheptadecanoic acid (BMHA) is a branched chain fatty acid analog that is transported into the myocardium. Due to incomplete metabolism, however, radiolabeled products are trapped within myocytes. Recently, we demonstrated that this compound is an excellent tracer to monitor fatty acid metabolism. Method: To evaluate the effect of mono-unsaturation on myocardial substrate utilization, we prepared 1-[C-11]-3-R,S-methyl-trans-heptadec-7-enoic acid (t-7-BMHA) and measured its biodistribution in rats. In addition, preliminary PET studies were performed on dogs. Results: Biodistribution studies demonstrated that myocardial-to-lung and myocardial-to-blood ratios for t-7-BMHA are higher than those for BMHA. Fifteen minutes after injection, heart-to-lung ratios were 5.23 compared to 2.92 and heart-to-liver ratios were 3.07 compared to 1.41 for t-7-BMHA and BMHA. By 30 min postinjection heart-to-lung ratios were 7.03 compared to 5.88 and heart-to-liver ratios were 4.43 compared to 1.09. The heart-to-blood ratio of t-7-BMHA was greater than 11:1. PET imaging with 1-[C-11]-t-7-BMHA demonstrated high myocardial extraction, prolonged retention of radioactivity and excellent image quality. Accumulation of radioactivity in the myocardium reached a plateau within 10 min postinjection, with heart-to-blood ratios exceeding 20:1 and heart-to-lung ratios exceeding 10:1. Blood clearance of radioactivity was biphasic with half-times of 1.46 and 14.7 min, respectively. Conclusion: These data suggest that introduction of a trans-double bond in BMHA improves myocardial selectivity and results in a potentially superior imaging agent. C1 MASSACHUSETTS GEN HOSP, DIV NUCL MED, BOSTON, MA 02114 USA. UNIV INNSBRUCK, NUCL MED CLIN, INNSBRUCK, AUSTRIA. NR 44 TC 1 Z9 1 U1 0 U2 1 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD NOV PY 1995 VL 36 IS 11 BP 2062 EP 2068 PG 7 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TC363 UT WOS:A1995TC36300032 PM 7472600 ER PT J AU KEARNS, GJ PERROTT, DH KABAN, LB AF KEARNS, GJ PERROTT, DH KABAN, LB TI A PROTOCOL FOR THE MANAGEMENT OF FAILED ALLOPLASTIC TEMPOROMANDIBULAR-JOINT DISC IMPLANTS SO JOURNAL OF ORAL AND MAXILLOFACIAL SURGERY LA English DT Article ID TEMPORARY SILICONE IMPLANT; PROPLAST-TEFLON IMPLANT; MUSCLE FLAP; TMJ DISK; RECONSTRUCTION; ARTHROPLASTY; REPLACEMENT; FASCIA; FOSSA AB Purpose. This is a retrospective evaluation of a protocol for management of failed alloplastic temporomandibular joint (TMJ) disc implants. Patients and Methods: The criteria for implant failure were defined as any one or combination of the following symptoms and signs: TMJ pain, jaw hypomobility, occlusal changes, and radiographic evidence of bone pathology related to the implant, The protocol consisted of removal of the implant, aggressive joint debridement, recontouring of the articulating surfaces, and placement of a pedicled temporalis muscle/fascia flap (TF) for joint lining. Arch bars and maxillomandibular guiding elastics were used if extensive condylar recontouring was necessary. No attempt was made to reconstruct the condyle or correct occlusal abnormalities at the time of implant removal. All 27 patients (42 joints) treated by this protocol during the study period were included for evaluation. There were 24 Proplast/Teflon (PTI) (Vitek, Inc, Houston, TX), 11 Silastic (SI) (Dow Coming, Midland, MI), and 7 Christensen Fossa implants (CFI) (TMJ Implants, Golden, CO) implants removed. Results: The mean follow-up period was 38.3 months (range, 3 to 65 months). Pain was well controlled in 24 of 27 patients (88.9%), Preoperative and postoperative mean maximal incisal opening (MIO) was 32.1 mm and 39.8 mm, respectively. Two patients (7.4%) required a second TMJ operation for persistent pain and limitation of opening. To date, 7 patients (25.9%) have required a secondary procedure (unilateral vertical ramus osteotomy, n = 1; Le Fort I osteotomy, n = 6) to correct occlusal prematurity on the operated side or bilateral open bite. The remaining patients have required no additional surgical treatment. Conclusions: The results of this study indicate that a proposed protocol is an effective means of controlling pain and improving jaw motion in patients with failed alloplastic TMJ disc implants. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH DENT MED,DEPT ORAL & MAXILLOFACIAL SURG,BOSTON,MA. RP KEARNS, GJ (reprint author), UNIV CALIF SAN FRANCISCO,DEPT ORAL & MAXILLOFACIAL SURG,521 PARNASSUS AVE,C-522,SAN FRANCISCO,CA 94143, USA. NR 58 TC 23 Z9 23 U1 1 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0278-2391 J9 J ORAL MAXIL SURG JI J. Oral Maxillofac. Surg. PD NOV PY 1995 VL 53 IS 11 BP 1240 EP 1247 DI 10.1016/0278-2391(95)90577-4 PG 8 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA TB801 UT WOS:A1995TB80100002 PM 7562188 ER PT J AU PAN, M WASA, M RYAN, U SOUBA, W AF PAN, M WASA, M RYAN, U SOUBA, W TI INHIBITION OF PULMONARY MICROVASCULAR ENDOTHELIAL GLUTAMINE TRANSPORT BY GLUCOCORTICOIDS AND ENDOTOXIN SO JOURNAL OF PARENTERAL AND ENTERAL NUTRITION LA English DT Article ID AMINO-ACIDS; CELLS; METABOLISM; LUNGS; RATS AB Background: During septic states, the lungs produce increased amounts of glutamine, an event that is mediated by both endotoxin and the glucocorticoid hormones and is presumed to be due to accelerated intracellular glutamine biosynthesis. Because enhanced net glutamine release in vivo could also be due to a decrease in cellular uptake, we assayed glutamine transport in cultured rat microvascular pulmonary endothelial cells. Methods: The effect of Escherichia coli endotoxin (LPS, 1 mu g/mL), various cytokines, and dexamethasone (DEX, 0.1 mu mol/L) on glutamine transport activity was studied in rat lung microvascular endothelial cells grown in varying glutamine concentrations (0, 0.1, 0.5, and 2 mmol/L). Experiments were also performed in cells treated with cycloheximide, actinomycin D, or chelerythrine chloride. Results: More than 90% of glutamine transport was mediated by the Na+-dependent transport system ASC. DEX and LPS inhibited endothelial glutamine uptake in a time- and dose-dependent manner, a response that was only observed when incubation medium contained the lower concentrations of glutamine. Neither DEX nor LPS altered transport activity in cells cultured in medium containing 2 mmol glutamine/L. There was no synergistic or additive effect when both compounds were added together. The cytokines tumor necrosis factor alpha, interleukin (IL) 1, IL-2, and IL-6 did not alter glutamine transport. Both DEX and LPS inhibited glutamine transport by decreasing transporter maximal transport velocity (V-max) without affecting transporter affinity (K-m) Cycloheximide and actinomycin D abrogated the inhibition of transport activity that was observed in DEX- or LPS-treated cells, whereas the protein kinase C inhibitor chelerythrine chloride had no effect on either control or stimulated glutamine transport. Conclusions: These data suggest that DEX and LPS ''downregulate'' glutamine uptake by lung microvascular endothelial cells by inducing the synthesis of an inhibitory protein that modulates the activity of the System ASC protein. This response in vitro appears to be influenced by the extracellular glutamine concentration. This decrease in microvascular endothelial glutamine transport may be one mechanism by which net lung glutamine release is enhanced during critical illness. C1 MASSACHUSETTS GEN HOSP,DIV SURG ONCOL,NUTR SUPPORT SERV,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. T CELL SCI,BOSTON,MA. FU NHLBI NIH HHS [HL 44986] NR 17 TC 9 Z9 11 U1 0 U2 0 PU AMER SOC PARENTERAL & ENTERAL NUTRITION PI SILVER SPRING PA 8630 FENTON STREET SUITE 412, SILVER SPRING, MD 20910 SN 0148-6071 J9 JPEN-PARENTER ENTER JI J. Parenter. Enter. Nutr. PD NOV-DEC PY 1995 VL 19 IS 6 BP 477 EP 481 DI 10.1177/0148607195019006477 PG 5 WC Nutrition & Dietetics SC Nutrition & Dietetics GA TH897 UT WOS:A1995TH89700007 PM 8748362 ER PT J AU CARDIN, S SOLL, AH TACHE, Y AF CARDIN, S SOLL, AH TACHE, Y TI DIFFERENT EFFECTS OF INDOMETHACIN AND NABUMETONE ON PROSTAGLANDIN-MEDIATED GASTRIC RESPONSES TO CENTRAL VAGAL ACTIVATION IN RATS SO JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS LA English DT Article ID THYROTROPIN-RELEASING-HORMONE; ACTIVE METABOLITE; 6-METHOXY-2-NAPHTHYLACETIC ACID; LESION FORMATION; PHARMACOLOGY; 6MNA AB Intracisternal injection of a stable thyrotropin-releasing hormone (TRH) analog increases gastric prostaglandins release and mucosal resistance to injury through central vagal pathways. The effects of two nonsteroidal anti-inflammatory drugs, indomethacin (INDO) and nabumetone on intracisternal injection of various doses of TRH-induced gastric acid secretion and changes in mucosal resistance were investigated in urethane-anesthetized rats. Doses of INDO (5 mg/kg) and nabumetone (13.75 mg/kg) producing similar acute anti-inflammatory response in the carrageenin-induced paw edema were injected i.p. in all studies. INDO potentiated the acid secretion induced by intracisternal injection of TRH at 25, 50 and 200 ng by 5.1-, 1.9- and 1.4-fold, respectively, whereas nabumetone did not modify the secretory response to TRH. Moderate erosions were observed in 100% of rats treated with the combination of INDO and TRH (200 ng) whereas no erosions were observed when TRH or INDO were given alone or TRH in combination with nabumetone. TRH at 7 ng reduced mucosal damage induced by intragastric administration of ethanol (60%, 1 ml/kg) by 63%. The mucosal protective action of TRH was abolished by INDO but not altered by nabumetone pretreatment. These data indicate that at comparable anti-inflammatory doses, nabumetone, unlike INDO, neither blocks the protection against ethanol injury induced by low doses of TRH injected intracisternally nor potentiates the gastric acid secretion or lesions induced by higher dose of TRH. We speculate that these differences reflect reduced inhibition of gastric prostaglandins by nabumetone. C1 W LOS ANGELES VET AFFAIRS MED CTR,CURE DIGEST DIS CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,BRAIN RES INST,LOS ANGELES,CA 90024. FU NIDDK NIH HHS [DK-30110]; NIMH NIH HHS [MH-00663] NR 26 TC 8 Z9 8 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0022-3565 J9 J PHARMACOL EXP THER JI J. Pharmacol. Exp. Ther. PD NOV PY 1995 VL 275 IS 2 BP 667 EP 673 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TE743 UT WOS:A1995TE74300019 PM 7473153 ER PT J AU CANTIELLO, HF AF CANTIELLO, HF TI CYCLIC AMP-INDEPENDENT REGULATION OF CYSTIC-FIBROSIS TRANSMEMBRANE CONDUCTANCE REGULATOR (CFTR) BY THE ACTIN CYTOSKELETON SO JOURNAL OF PHYSIOLOGY-LONDON LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP EAST,SCH MED,RENAL UNIT,BOSTON,MA. NR 3 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 0022-3751 J9 J PHYSIOL-LONDON JI J. Physiol.-London PD NOV PY 1995 VL 489P BP S6 EP S6 PG 1 WC Neurosciences; Physiology SC Neurosciences & Neurology; Physiology GA TH854 UT WOS:A1995TH85400293 ER PT J AU KORNMEHI, EW BREDVIK, BK KELMAN, CD RAIZMAN, MB DEVORE, DP AF KORNMEHI, EW BREDVIK, BK KELMAN, CD RAIZMAN, MB DEVORE, DP TI IN-VIVO EVALUATION OF A COLLAGEN CORNEAL ALLOGRAFT DERIVED FROM RABBIT DERMIS SO JOURNAL OF REFRACTIVE SURGERY LA English DT Article ID KERATOPROSTHESIS AB BACKGROUND: This study evaluates epithelialization, clarity, intraocular inflammation, and fibroblast ingrowth of a collagen corneal allograft derived from rabbit dermis. METHODS: Dermal collagen fibers were dispersed intact and chemically modified to make them soluble. The allografts consisted of a fibrous, opaque peripheral zone and a central clear area. Twelve New Zealand white rabbits underwent penetrating keratoplasty with implantation of an allograft. The grafts were evaluated daily for clarity, anterior segment inflammation, and extent of reepithelialization with a slit-lamp microscope. RESULTS: Epithelialization of the fibrous peripheral zone of the graft ranged from 0% to 90%. The central clear area did not epithelialize in any of the animals. Fibroblasts migrated into the peripheral zone in all eyes. Complications included ulceration of the central clear area in two eyes. There was no ulceration or leakage at the graft-host interface and no synechia, fibrous, or inflammatory retrocorneal membranes in any of the eyes. CONCLUSIONS: Our study is the first to describe the method of modifying dermal type I collagen into a clear corneal allograft. Survival of the corneal collagen allograft beyond 1 month may be limited by several factors including lack of epithelialization of the central clear area. C1 TUFTS UNIV,SCH MED,NEW ENGLAND EYE CTR,CORNEA & ANTERIOR SERGMENT SERV,BOSTON,MA 02111. HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,KERATOREFRACT SERV,BOSTON,MA. NEW YORK MED COLL,DEPT OPHTHALMOL,VALHALLA,NY 10595. COLLAGENESIS INC,ACTON,MA. NR 11 TC 10 Z9 10 U1 1 U2 3 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0883-0444 J9 J REFRACT SURG JI J. Refractive Surg. PD NOV-DEC PY 1995 VL 11 IS 6 BP 502 EP 506 PG 5 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA TJ891 UT WOS:A1995TJ89100014 PM 8624838 ER PT J AU Pinzur, MS Cox, W Kaiser, J Morris, T Patwardhan, A Vrbos, L AF Pinzur, MS Cox, W Kaiser, J Morris, T Patwardhan, A Vrbos, L TI The effect of prosthetic alignment on relative limb loading in persons with trans-tibial amputation: A preliminary report SO JOURNAL OF REHABILITATION RESEARCH AND DEVELOPMENT LA English DT Article DE below-knee amputation; gait analysis; ground reaction force; stance phase time ID AMPUTEES; GAIT AB The prosthetic sockets of 14 independent persons with unilateral trans-tibial (BK) amputation were mounted on an adjustable alignment pylon. Vertical ground reaction forces were recorded in neutral prosthetic alignment and in 10 degrees of prosthetic socket varus, valgus, flexion, and extension. Stance phase time, peak vertical ground reaction force, and impulse were all found to be increased on the sound limb when compared to the amputated residual limb. Significant differences were found in stance phase time and peak vertical ground reaction force when comparing malaligned with neutrally aligned prosthetic limbs. Significant differences were also seen in impulse between neutrally aligned and malaligned prosthetic limbs. The results suggest that prosthetic malalignment in persons with trans-tibial amputation leads to increased loading of the contralateral limb. C1 US DEPT VET AFFAIRS,VET AFFAIRS EDWARD HINES JR HOSP,REHABIL ENGN CTR,HINES,IL 60141. SCHECK & SIRESS ORTHOT & PROSTHET INC,OAK PK,IL 60302. RP Pinzur, MS (reprint author), LOYOLA UNIV,MED CTR,DEPT ORTHOPAED SURG,2160 S 1ST AVE,MAYWOOD,IL 60153, USA. NR 11 TC 24 Z9 28 U1 1 U2 5 PU JOURNAL REHAB RES & DEV PI BALTIMORE PA DEPT OF VETERANS AFFAIRS REHABIL RES & DEVELOP CTR 103 SOUTH GAY STREET, BALTIMORE, MD 21202-4051 SN 0007-506X J9 J REHABIL RES DEV JI J. Rehabil. Res. Dev. PD NOV PY 1995 VL 32 IS 4 BP 373 EP 377 PG 5 WC Rehabilitation SC Rehabilitation GA TN835 UT WOS:A1995TN83500009 PM 8770802 ER PT J AU LEE, WPA RANDOLPH, MA WEILAND, AJ YAREMCHUK, MJ AF LEE, WPA RANDOLPH, MA WEILAND, AJ YAREMCHUK, MJ TI PROLONGED SURVIVAL OF VASCULARIZED LIMB TISSUE ALLOGRAFTS BY DONOR IRRADIATION SO JOURNAL OF SURGICAL RESEARCH LA English DT Article ID PERIPHERAL-NERVE ALLOGRAFT; EXPERIMENTAL SKIN ALLOGRAFTS; CYCLOSPORIN-A; BONE ALLOGRAFTS; IMMUNOLOGICAL-UNRESPONSIVENESS; RECONSTRUCTIVE SURGERY; INDEFINITE SURVIVAL; TRANSPLANTATION; REJECTION; RAT AB The clinical feasibility of transplantation of a vascularized limb tissue allograft depends upon reducing immunosuppression and its associated toxicity for the graft recipient. Donor or allograft irradiation would eradicate allogeneic marrow and provide a possible alternative or beneficial addition to host immunosuppression. The effect of irradiation on survival of limb tissue allograft was investigated in this study. In a rat model, knee allografts consisting of bone, cartilage, and soft tissues were transplanted across a strong histocompatibility barrier by femoral vascular microanastomoses. The grafts were harvested 1 and 2 weeks postoperatively for histologic and immunologic assays. Gamma irradiation of the graft immediately before transplant decreased graft rejection slightly. However, total body irradiation of the donor followed by a ''waiting period'' of 2 or more days before transplant significantly delayed rejection. After such a 6-day and a 2-day pretreatment protocol, the host cellular immune responses were not observed 1 and 2 weeks after transplantation and eventual progression toward graft rejection coincided with emergence of host antibody production. Rejection of vascularized limb tissue allografts after donor irradiation thus appeared to be mediated primarily through the humoral pathway. We conclude that donor irradiation is a potentially useful adjunct in prolonging survival of vascularized limb tissue allografts. (C) 1995 Academic Press, Inc. C1 CORNELL UNIV,HOSP SPECIAL SURG,COLL MED,DEPT ORTHOPAED SURG,NEW YORK,NY 10021. RP LEE, WPA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,DIV PLAST SURG,BOSTON,MA 02114, USA. FU NIADDK NIH HHS [R01 AM25791] NR 45 TC 20 Z9 22 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0022-4804 J9 J SURG RES JI J. Surg. Res. PD NOV PY 1995 VL 59 IS 5 BP 578 EP 588 DI 10.1006/jsre.1995.1208 PG 11 WC Surgery SC Surgery GA TB544 UT WOS:A1995TB54400008 PM 7475004 ER PT J AU BIEDERMAN, J MILBERGER, S FARAONE, SV KIELY, K GUITE, J MICK, E ABLON, JS WARBURTON, R REED, E DAVIS, SG AF BIEDERMAN, J MILBERGER, S FARAONE, SV KIELY, K GUITE, J MICK, E ABLON, JS WARBURTON, R REED, E DAVIS, SG TI IMPACT OF ADVERSITY ON FUNCTIONING AND COMORBIDITY IN CHILDREN WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE RISK; ATTENTION-DEFICIT HYPERACTIVITY DISORDER; PSYCHOSOCIAL; ADVERSITY; COMORBIDITY ID MATERNAL PSYCHOPATHOLOGY; LEARNING-DISABILITIES; PSYCHIATRIC-DISORDER; ADHD CHILDREN; RISK-FACTORS; FAMILY; BEHAVIOR; ADOLESCENTS; ADJUSTMENT; RESILIENCE AB Objective: Prior research on risk factors for attention-deficit hyperactivity disorder (ADHD) has shown that familial risk factors play a role in the disorder's etiology. This study investigated whether features of the family environment were associated with ADHD. Method: One hundred forty children with ADHD and 120 normal control probands were studied. Subjects were Caucasian, non-Hispanic males between the ages of 6 and 17 years. Exposure to parental psychopathology and exposure to parental conflict were used as indicators of adversity, and their impact on ADHD and ADHD-related psychopathology and dysfunction in children was assessed. Results: Increased levels of environmental adversity were found among ADHD compared with control probands. The analyses showed significant associations between the index of parental conflict and several of the measures of psychopathology and psychosocial functioning in the children. In contrast, the index of exposure to parental psychopathology had a much narrower impact, affecting primarily the child's use of leisure time and externalizing symptoms. Conclusions: A relationship appears to exist between adversity indicators and the risk for ADHD as well as for its associated impairments in multiple domains. These findings confirm previous work and stress the importance of adverse family-environment variables as risk factors for children who have ADHD. C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP BIEDERMAN, J (reprint author), MASSACHUSETTS GEN HOSP,PEDIAT PHARMACOL PSYCHIAT UNIT ACC 725,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Mick, Eric/0000-0001-8505-8145; Faraone, Stephen/0000-0002-9217-3982 FU NIMH NIH HHS [R01 MH-41314-01A2] NR 55 TC 92 Z9 95 U1 1 U2 11 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 NOV PY 1995 VL 34 IS 11 BP 1495 EP 1503 DI 10.1097/00004583-199511000-00017 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA TB165 UT WOS:A1995TB16500017 PM 8543518 ER PT J AU MUCCINI, JA KOLLIAS, N PHILLIPS, SB ANDERSON, RR SOBER, AJ STILLER, MJ DRAKE, LA AF MUCCINI, JA KOLLIAS, N PHILLIPS, SB ANDERSON, RR SOBER, AJ STILLER, MJ DRAKE, LA TI POLARIZED-LIGHT PHOTOGRAPHY IN THE EVALUATION OF PHOTOAGING SO JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY LA English DT Article ID TOPICAL TRETINOIN; SKIN AB Background: The clinical characteristics of photodamaged skin, such as coarse and fine wrinkling, sallowness, hyperpigmentation, tactile roughness, laxity, and erythema, are not accurately evaluable from photographic records. Objective: The purpose of this study was to develop accurate and reproducible photographic techniques that generate an evaluable record of the characteristics of photodamaged skin. Methods: The method used involved illumination and photography through polarizing filters (polarized light photography). Results: Polarized light photography generates images that selectively enhance either the surface features or the subsurface features of the skin, providing an accurate and evaluable record for evaluation of photodamaged skin. Conclusion: Polarized light photography, when coupled with precise framing and mapping, yields an accurate and evaluable record of photodamaged skin. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,WELLMAN LABS PHOTOMED,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DERMATOL CLIN INVEST UNIT,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT DERMATOL,BOSTON,MA 02114. NR 15 TC 35 Z9 36 U1 0 U2 3 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 NOV PY 1995 VL 33 IS 5 BP 765 EP 769 DI 10.1016/0190-9622(95)91813-2 PN 1 PG 5 WC Dermatology SC Dermatology GA TD253 UT WOS:A1995TD25300010 PM 7593775 ER PT J AU MCDOWELL, KA CHEVALIER, RL THORNHILL, BA NORLING, LL AF MCDOWELL, KA CHEVALIER, RL THORNHILL, BA NORLING, LL TI UNILATERAL URETERAL OBSTRUCTION INCREASES GLOMERULAR SOLUBLE GUANYLYL CYCLASE ACTIVITY SO JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY LA English DT Article DE CGMP; LOSARTAN; PHOSPHODIESTERASE; ANGIOTENSIN II; VASODILATION ID RENIN-ANGIOTENSIN SYSTEM; NITRIC-OXIDE SYNTHESIS; RENAL HEMODYNAMICS; RAT; PRESSURE; EDRF; OCCLUSION; UROPATHY; KIDNEY; CELLS AB RBF and GFR are decreased in kidneys after ipsilateral unilateral ureteral obstruction (UUO) for 24 h. Despite net vasoconstriction, vasodilatory mechanisms respond to counterbalance the vasoconstriction: the inhibition of nitric oxide synthase activity is associated with a greater reduction in RBF with ipsilateral UUO. To determine whether the stimulation of soluble guanylyl cyclase differs between glomeruli from obstructed kidneys and normal kidneys, cGMP was measured after stimulation by 10(-3) M sodium nitroprusside (SNP) in glomeruli isolated from the kidneys of Sprague-Dawley rats after 24 h of UUO or sham operation. The generation of intracellular and extracellular (EC) cGMP (femtomoles of cGMP/100 glomeruli/per hour) was measured by RIA. After incubation with SNP, the EC accumulation of cGMP by UUO glomeruli was significantly greater than that by glomeruli from sham-operated rats (P < 0.05). When glomerular studies were repeated in the presence of the phosphodiesterase inhibitor isobutyl methylxanthine, there was no difference in the EC accumulation of cGMP, The direct measurement of cGMP hydrolysis by phosphodiesterase was significantly less in glomerular homogenate from UUO rats compared with sham-operated rats (P < 0.05). When 10(-5) M losartan, an angiotensin II receptor inhibitor, was included in glomerular incubations, there was a significant decrease in the EC glomerular cGMP response to SNP in UUO glomeruli (P < 0.05). This attenuated response was abolished by the addition of isobutyl methylxanthine. The addition of angiotensin II did not alter the accumulation of cGMP by UUO or sham glomeruli. These studies indicate that decreased phosphodiesterase activity in UUO glomeruli contributes to the enhanced accumulation of EC glomerular cGMP after the stimulation of soluble guanylyl cyclase by SNP. In addition, angiotensin II receptors modulate this response, suggesting a role for soluble guanylyl cyclase in countering angiotensin-mediated vasoconstriction due to UUO. C1 MASSACHUSETTS GEN HOSP,PEDIAT NEPHROL UNIT,BOSTON,MA 02114. UNIV VIRGINIA,SCH MED,DEPT PEDIAT,CHARLOTTESVILLE,VA 22908. FU NICHD NIH HHS [P30 HD28810]; NIDDK NIH HHS [5-P50 DK45179, T32DK07642] NR 33 TC 8 Z9 8 U1 0 U2 1 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1046-6673 J9 J AM SOC NEPHROL JI J. Am. Soc. Nephrol. PD NOV PY 1995 VL 6 IS 5 BP 1498 EP 1503 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA TF752 UT WOS:A1995TF75200025 PM 8589329 ER PT J AU SAYEGH, RA TAO, XJ ISAACSON, KB AF SAYEGH, RA TAO, XJ ISAACSON, KB TI IMMUNOHISTOCHEMICAL LOCALIZATION OF ALPHA-2-MACROGLOBULIN RECEPTOR LOW-DENSITY-LIPOPROTEIN RECEPTOR-RELATED PROTEIN, RECEPTOR-ASSOCIATED PROTEIN, AND GP330 IN THE HUMAN ENDOMETRIUM SO JOURNAL OF THE SOCIETY FOR GYNECOLOGIC INVESTIGATION LA English DT Article DE HUMAN ENDOMETRIUM; GP 330; ALPHA-2 MACROGLOBULIN RECEPTOR LOW-DENSITY LIPOPROTEIN RECEPTOR-RELATED PROTEIN; RECEPTOR-ASSOCIATED PROTEIN; IMMUNOHISTOCHEMISTRY ID ACTIVATOR INHIBITOR TYPE-1; ALPHA-2-MACROGLOBULIN RECEPTOR; HEYMANN NEPHRITIS; EMBRYO IMPLANTATION; COMPLEXES; BINDING; ANTIGEN; INTERNALIZES; CLEARANCE; LIGANDS AB OBJECTIVE: We investigated the expression of alpha-2 macroglobulin receptor/low-density lipoprotein receptor-related protein (LRP), an analogous receptor Gp330, and the 39-kd receptor-associated protein (RAP) in the human endometrium. METHODS: Specific polyclonal and monoclonal antibodies against LRP, Gp330, and RAP were used in standard immunohistochemical analyses of normal secretory and proliferative archival endometrial tissue. RESULTS: There was prominent and uniform stromal staining for LRP in secretory and proliferative endometrium. In both phases, 10-25% of glands stained positive for Gp330, with no appreciable stromal staining for Gp330. Also in both phases, 15-30% of glands stained positive for RAP, with apical staining in proliferative glands and uniform staining in secretory glands. Stromal staining for RAP was patchy, and appeared to be move incense in the secretory samples than in the proliferative ones. CONCLUSIONS: The human endometrium expresses LRP, RAP, and Gp330. These receptor proteins are known to be involved in endacytosis of multiple ligands. Some of these ligands, such as proteases, plasminogen activators, and cytokines, are produced by the endometrium and play a role in endometrial remodeling and receptivity to implantation. By virtue of their in vitro properties, it is conceivable that endometrial LRP, Gp330, and RAP ave involved in endometrial physiology. RP SAYEGH, RA (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV REPROD ENDOCRINOL & INFERTIL,BOSTON,MA 02114, USA. NR 26 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 1071-5576 J9 J SOC GYNECOL INVEST JI J. Soc. Gynecol. Invest. PD NOV-DEC PY 1995 VL 2 IS 6 BP 748 EP 753 DI 10.1016/1071-5576(95)94691-M PG 6 WC Obstetrics & Gynecology SC Obstetrics & Gynecology GA TC491 UT WOS:A1995TC49100005 PM 9420885 ER PT J AU SHERIDAN, RL KACMAREK, RM MCETTRICK, MM WEBER, JM RYAN, CM DOODY, DP RYAN, DP SCHNITZER, JJ TOMPKINS, RG AF SHERIDAN, RL KACMAREK, RM MCETTRICK, MM WEBER, JM RYAN, CM DOODY, DP RYAN, DP SCHNITZER, JJ TOMPKINS, RG TI PERMISSIVE HYPERCAPNIA AS A VENTILATORY STRATEGY IN BURNED CHILDREN - EFFECT ON BAROTRAUMA, PNEUMONIA, AND MORTALITY SO JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE LA English DT Article; Proceedings Paper CT 8th Scientific Assembly of the Eastern-Association-for-the-Surgery-of-Trauma CY JAN 11-14, 1995 CL SANIBEL, FL SP E Assoc Surg Trauma ID END-EXPIRATORY PRESSURE; RESPIRATORY-DISTRESS SYNDROME; EXTRACORPOREAL CO2 REMOVAL; HIGH AIRWAY PRESSURE; MECHANICAL VENTILATION; STATUS-ASTHMATICUS; INHALATION INJURY; PULMONARY-EDEMA; TIDAL VOLUME; FAILURE AB Objective: To document the incidence of barotrauma, pneumonia, and respiratory death associated with a mechanical ventilation protocol based on permissive hypercapnia in pediatric burn patients. Design: Retrospective review. Materials and Methods: Patients were managed using a mechanical ventilation protocol based on permissive hypercapnia, tolerating moderate (pH>7.20) respiratory acidosis to keep inflating pressures below 40 cm H2O. Main Results: Over a 2.5-year interval, 54 burned children (11% of 395 acute admissions) with an average age of 6.5 years (range 5 weeks to 17 years), average burn size of 44% (range 0 to 98%), and median burn size of 46% required mechanical ventilatory support for an average of 12.5 days (range 1 to 56 days). Inhalation injury was diagnosed in 34 (63%) of the children and 72% percent were admitted within 24 hours of injury. Overt barotrauma occurred in 5.6% of the patients, pneumonia in 32%, and respiratory death in 0%. Conclusions: A conventional ventilation protocol based on permissive hypercapnia is associated with acceptable rates of barotrauma and pneumonia. The low incidence of respiratory death associated with this strategy suggests that it also minimizes ventilator-induced lung injury. C1 MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ANESTHESIA,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. RP SHERIDAN, RL (reprint author), SHRINERS BURN INST,51 BLOSSOM ST,BOSTON,MA 02114, USA. FU NIGMS NIH HHS [P50 GM21700, T32 GM07035] NR 45 TC 41 Z9 43 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 Inf. Crit. Care PD NOV PY 1995 VL 39 IS 5 BP 854 EP 859 DI 10.1097/00005373-199511000-00008 PG 6 WC Critical Care Medicine; Surgery SC General & Internal Medicine; Surgery GA TG664 UT WOS:A1995TG66400008 PM 7474000 ER PT J AU BARRY, MJ WILLIFORD, WO CHANG, YC MACHI, M JONES, KM WALKERCORKERY, E LEPOR, H AF BARRY, MJ WILLIFORD, WO CHANG, YC MACHI, M JONES, KM WALKERCORKERY, E LEPOR, H TI BENIGN PROSTATIC HYPERPLASIA SPECIFIC HEALTH-STATUS MEASURES IN CLINICAL RESEARCH - HOW MUCH CHANGE IN THE AMERICAN-UROLOGICAL-ASSOCIATION SYMPTOM INDEX AND THE BENIGN PROSTATIC HYPERPLASIA IMPACT INDEX IS PERCEPTIBLE TO PATIENTS SO JOURNAL OF UROLOGY LA English DT Article DE PROSTATIC HYPERTROPHY; QUESTIONNAIRES; OUTCOME ASSESSMENT (HEALTH CARE) AB Purpose: We assessed the relationship between changes in scores for the American Urological Association (AUA) symptom index and benign prostatic hyperplasia (BPH) impact index with patient global ratings of improvement in a large Veterans Affairs trial comparing different pharmacological therapies for BPH. Materials and Methods: The primary analyses compared absolute score changes from baseline with global ratings of improvement-at 13 weeks for 1,218 men. Results: Subjects who rated themselves as being slightly improved had a mean decrease in AUA symptom index and BPH impact index scores of 3.1 and 0.4 points, respectively. However, the baseline scores strongly influenced this relationship. Conclusions: These data provide guidance for investigators using the AUA symptom index and BPH impact index as outcome measures. C1 VET AFFAIRS MED CTR,CTR COORDINATING,COOPERAT STUDIES PROGRAM,PERRY POINT,MD. MED COLL WISCONSIN,MILWAUKEE,WI 53226. NYU,MED CTR,DEPT UROL,NEW YORK,NY 10016. RP BARRY, MJ (reprint author), MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02114, USA. FU AHRQ HHS [HS 06336, HS 08397] NR 9 TC 246 Z9 248 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 NOV PY 1995 VL 154 IS 5 BP 1770 EP 1774 DI 10.1016/S0022-5347(01)66780-6 PG 5 WC Urology & Nephrology SC Urology & Nephrology GA RY817 UT WOS:A1995RY81700049 PM 7563343 ER PT J AU Grabowski, EF AF Grabowski, EF TI Thrombolysis, flow, and vessel wall interactions SO JOURNAL OF VASCULAR AND INTERVENTIONAL RADIOLOGY LA English DT Article; Proceedings Paper CT Summit Meeting on Thrombolytic Therapy in Peripheral Vascular Disease CY APR 07-09, 1995 CL SNOWBIRD, UT DE blood, flood dynamics; thrombolysis ID FLUID SHEAR-STRESS; ENDOTHELIAL-CELL MORPHOLOGY; FIBROBLAST GROWTH-FACTOR; PROTEIN-KINASE-C; TISSUE-FACTOR; VASCULAR ENDOTHELIUM; SUBENDOTHELIAL MATRIX; AGGREGATION; EXPRESSION; INCREASES AB Vascular endothelium remains a dynamic interface between blood, blood platelets, and the vessel wall, New developments make clear that many antithrombotic and prothrombotic responses of the endothelium depend on flow conditions in an adaptive manner: duration of a certain level of shear stress matters as well as level of shear, In general, over the course of several hours, endothelium appears to be more actively antithrombotic under moderate shear conditions (eg, 15 dyne/cm(2)) and more fibrinolytic under high shear conditions (eg, 30 dyne/cm(2)), Pulsatile flow and cyclic wall stress further modify these responses, Special consideration, moreover, must be given to branch points and regions of irregular geometry (ie, stenoses, aneurysms) in the circulation, In such locations-predilection sites for thrombosis, lipid uptake, and atherosclerosis-low levels of shear stress (eg, 0.5 dyne/cm(2)), large gradients in shear stress, and vessel wall bending stresses all become important, Preliminary work suggests that endothelial cells in such regions can become prothrombotic, leading to localized platelet adhesion/aggregation and fibrin formation on subendothelium and perhaps deeper structures following vessel injury, Flow effects on thrombolysis remain largely unstudied. RP Grabowski, EF (reprint author), HARVARD UNIV,SCH MED,MASSACHUSETTS GEN HOSP,55 FRUIT ST,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [HL33095] NR 37 TC 14 Z9 14 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 1051-0443 J9 J VASC INTERV RADIOL JI J. Vasc. Interv. Radiol. PD NOV-DEC PY 1995 VL 6 IS 6 SU S BP S25 EP S29 DI 10.1016/S1051-0443(95)71245-3 PN 2 PG 5 WC Radiology, Nuclear Medicine & Medical Imaging; Peripheral Vascular Disease SC Radiology, Nuclear Medicine & Medical Imaging; Cardiovascular System & Cardiology GA UQ610 UT WOS:A1995UQ61000006 PM 8770839 ER PT J AU YEAGER, RA MONETA, GL EDWARDS, JM TAYLOR, LM MCCONNELL, DB PORTER, JM AF YEAGER, RA MONETA, GL EDWARDS, JM TAYLOR, LM MCCONNELL, DB PORTER, JM TI DEEP-VEIN THROMBOSIS ASSOCIATED WITH LOWER-EXTREMITY AMPUTATION SO JOURNAL OF VASCULAR SURGERY LA English DT Article; Proceedings Paper CT 7th Annual Meeting of the American-Venous-Forum CY FEB 23-25, 1995 CL FT LAUDERDALE, FL SP Amer Venous Forum ID VENOUS THROMBOEMBOLISM; COAGULATION AB Purpose: Patients undergoing lower extremity amputation are perceived to be at high risk for deep vein thrombosis (DVT). Limited data are available, however, to confirm this impression. The purpose of this study is to prospectively document the incidence of DVT complicating lower extremity amputation. Methods: During a recent 28-month period, 72 patients (71 men, 1 woman; mean age 68 years) undergoing major lower extremity amputation (31 above-knee and 41 below-knee) were prospectively evaluated with perioperative duplex scanning for DVT. Results: DVT was documented in nine (12.5%) patients (one bilateral, four ipsilateral, and four contralateral to amputation). Patients with a history of venous disease were at significantly higher risk for development of DVT (p = 0.02). Thrombi were located at or proximal to the popliteal vein in eight patients and were isolated to the tibial veins in one patient; DVT was identified before operation in six patients and after operation in three. Patients with DVT were treated with heparin anticoagulation, with no patient experiencing clinical symptoms compatible with pulmonary embolism. Conclusions: In our recent experience, lower extremity amputation is associated with DVT at or proximal to the popliteal vein in 11% of patients. Documentation of DVT prevalence is essential to assist surgeons in planning a management strategy for prevention, diagnosis, and treatment of DVT associated with lower extremity amputation. C1 OREGON HLTH SCI UNIV,DEPT SURG,DIV VASC SURG,PORTLAND,OR 97201. RP YEAGER, RA (reprint author), PORTLAND VET AFFAIRS MED CTR,SURG SERV 112P,POB 1034,PORTLAND,OR 97207, USA. NR 17 TC 23 Z9 26 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0741-5214 J9 J VASC SURG JI J. Vasc. Surg. PD NOV PY 1995 VL 22 IS 5 BP 612 EP 615 DI 10.1016/S0741-5214(95)70048-X PG 4 WC Surgery; Peripheral Vascular Disease SC Surgery; Cardiovascular System & Cardiology GA TF306 UT WOS:A1995TF30600017 PM 7494364 ER PT J AU TYLER, KL SQUIER, MKT RODGERS, SE SCHNEIDER, BE OBERHAUS, SM GRDINA, TA COHEN, JJ DERMODY, TS AF TYLER, KL SQUIER, MKT RODGERS, SE SCHNEIDER, BE OBERHAUS, SM GRDINA, TA COHEN, JJ DERMODY, TS TI DIFFERENCES IN THE CAPACITY OF REOVIRUS STRAINS TO INDUCE APOPTOSIS ARE DETERMINED BY THE VIRAL ATTACHMENT PROTEIN SIGMA-1 SO JOURNAL OF VIROLOGY LA English DT Article ID PROGRAMMED CELL-DEATH; MOUSE L-CELLS; MAMMALIAN REOVIRUSES; SPECIFIED POLYPEPTIDES; MOLECULAR-BASIS; TRANSLATION PRODUCTS; SUBVIRION PARTICLES; DNA FRAGMENTATION; RNA SEGMENTS; E1A PROTEINS AB Reoviruses are important models for studies of viral pathogenesis; however, the mechanisms by which these viruses produce cytopathic effects in infected cells have not been defined, In this report, we show that murine L929 (L) cells infected with prototype reovirus strains type 1 Lang (T1L) and type 3 Dearing (T3D) undergo apoptosis and that T3D induces apoptosis to a substantially greater extent than T1L, Using T1L x T3D reassortant viruses, we found that differences in the capacity of T1L and T3D to induce apoptosis are determined by the viral S1 gene segment, which encodes the viral attachment protein al and the non-virion-associated protein sigma 1s. Apoptosis was induced by UV-inactivated, replication-incompetent reovirus virions, which do not contain sigma 1s and do not mediate its synthesis in infected cells, Additionally, T3D-induced apoptosis was inhibited by anti-reovirus monoclonal antibodies that inhibit no cell attachment and disassembly, These results indicate that sigma 1, rather than sigma 1s, is required for induction of apoptosis by the reovirus and suggest that interaction of virions with cell surface receptors is an essential step in this mechanism of cell killing. C1 UNIV COLORADO,HLTH SCI CTR,DEPT NEUROL,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DEPT MED,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DEPT MICROBIOL,DENVER,CO 80220. UNIV COLORADO,HLTH SCI CTR,DEPT IMMUNOL,DENVER,CO 80220. DENVER VET AFFAIRS MED CTR,NEUROL SERV,DENVER,CO 80220. VANDERBILT UNIV,SCH MED,DEPT PEDIAT,NASHVILLE,TN 37232. VANDERBILT UNIV,SCH MED,DEPT IMMUNOL & MICROBIOL,NASHVILLE,TN 37232. VANDERBILT UNIV,SCH MED,ELIZABETH B LAMB CTR PEDIAT RES,NASHVILLE,TN 37232. OI Tyler, Kenneth/0000-0003-3294-5888 FU NIAID NIH HHS [AI32539] NR 81 TC 146 Z9 152 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1995 VL 69 IS 11 BP 6972 EP 6979 PG 8 WC Virology SC Virology GA RZ100 UT WOS:A1995RZ10000048 PM 7474116 ER PT J AU MORGAN, JR LEDOUX, JM SNOW, RG TOMPKINS, RG YARMUSH, ML AF MORGAN, JR LEDOUX, JM SNOW, RG TOMPKINS, RG YARMUSH, ML TI RETROVIRUS INFECTION - EFFECT OF TIME AND TARGET-CELL NUMBER SO JOURNAL OF VIROLOGY LA English DT Article ID ECOTROPIC MURINE RETROVIRUSES; AMINO-ACID TRANSPORTER; MEDIATED GENE-TRANSFER; ENVELOPE GLYCOPROTEIN; MEMBRANE RECEPTORS; LEUKEMIA VIRUSES; HOST RANGE; BINDING; FIBROBLASTS; THERAPY AB Using a model amphotropic recombinant retrovirus encoding the Escherichia coli lacZ gene and quantitative assays to measure virus infection, we have determined the effects of time and target cell number on infectivity. Infection of various numbers of NIH 3T3 fibroblasts showed that the extent of lacZ virus infection was dependent on virus concentration and independent of target cell number. These results demonstrate that multiplicity of infection is not an accurate predictor of the efficiency of retroviral infection. Varying the time of viral infection revealed that maximal infection occurred after greater than 24 h of exposure of the cells to the lacZ virus. Half-maximal infection occurred after 5 h of exposure. After 2 h of adsorption at 37 degrees C, the majority of infectious virus was not adsorbed to cells but was unbound and able to infect other cells. These results are discussed in terms of both their relevance to the fundamental biology of retrovirus infection and the use of recombinant retroviruses for retrovirus-mediated gene transfer with purposes of gene therapy. C1 MASSACHUSETTS GEN HOSP,SURG SERV,BOSTON,MA 02114. RUTGERS STATE UNIV,DEPT CHEM & BIOCHEM ENGN,PISCATAWAY,NJ 08854. SHRINERS BURN INST,BOSTON,MA 02114. OI Morgan, Jeffrey/0000-0002-7546-3443 FU NIAMS NIH HHS [AR42012]; NICHD NIH HHS [HD28528] NR 50 TC 76 Z9 76 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1995 VL 69 IS 11 BP 6994 EP 7000 PG 7 WC Virology SC Virology GA RZ100 UT WOS:A1995RZ10000050 PM 7474118 ER PT J AU LI, JT HALLORAN, M LORD, CI WATSON, A RANCHALIS, J FUNG, M LETVIN, NL SODROSKI, JG AF LI, JT HALLORAN, M LORD, CI WATSON, A RANCHALIS, J FUNG, M LETVIN, NL SODROSKI, JG TI PERSISTENT INFECTION OF MACAQUES WITH SIMIAN-HUMAN IMMUNODEFICIENCY VIRUSES SO JOURNAL OF VIROLOGY LA English DT Article ID HUMAN MONOCLONAL-ANTIBODY; TYPE-1 VPU; ENVELOPE GLYCOPROTEIN; NEUTRALIZING ANTIBODIES; MACACA-NEMESTRINA; HUMAN RETROVIRUS; RHESUS-MONKEYS; CHIMERIC HUMAN; AIDS; CD4 AB Chimeric simian-human immunodeficiency viruses (SHIV) containing the human immunodeficiency virus type 1 (HIV-1) tat, rev, env, and, in some cases, vpu genes were inoculated into eight cynomolgus monkeys. Viruses could be consistently recovered from the CD8 depleted peripheral blood lymphocytes of all eight animals for at least 2 months, After this time, virus isolation varied among the animals, with viruses continuing to be isolated from some animals beyond 600 days after inoculation, The level of viral RNA in plasma during acute infection and the frequency of virus isolation after the initial 2-month period were higher for the Vpu-positive viruses, All of the animals remained clinically healthy, and the absolute numbers of CD4-positive lymphocytes were stable, Antibodies capable of neutralizing HIV-1 were generated at high titers in animals exhibiting the greatest consistency of virus isolation, Strain-specific HIV-1-neutralizing antibodies were initially elicited, and then more broadly neutralizing antibodies were elicited. env sequences from two viruses isolated more than a year after infection were analyzed. In the Vpu-negative SHIV, for which virus loads were lower, a small amount of env variation, which did not correspond to that found in natural HIV-1 variants, was observed, By contrast, in the Vpu-positive virus, which was consistently isolated from the host animal, extensive variation of the envelope glycoproteins in the defined variable gp120 regions was observed, Escape from neutralization by CD4 binding site monoclonal antibodies was observed for the viruses with the latter envelope glycoproteins, and the mechanism of escape appears to involve decreased binding of the antibody to the monomeric gp120 glycoproteins. The consistency with which SHIV infection of cynomolgus monkeys is initiated and the similarities in the neutralizing antibody response to SHIV and HIV-1 support the utility of this model system for the study of HIV-1 prophylaxis. C1 DANA FARBER CANC INST,DEPT PATHOL,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,DIV VIRAL PATHOGENESIS,BOSTON,MA. HARVARD UNIV,SCH PUBL HLTH,DEPT CANC BIOL,BOSTON,MA 02115. BRISTOL MYERS SQUIBB,PHARMACEUT RES INST,SEATTLE,WA. TANOX BIOSYST INC,HOUSTON,TX. FU NCI NIH HHS [CA06516]; NIAID NIH HHS [AI28691, AI33832] NR 48 TC 124 Z9 125 U1 1 U2 4 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1995 VL 69 IS 11 BP 7061 EP 7071 PG 11 WC Virology SC Virology GA RZ100 UT WOS:A1995RZ10000058 PM 7474126 ER PT J AU GONCALVES, J SHI, B YANG, XY GABUZDA, D AF GONCALVES, J SHI, B YANG, XY GABUZDA, D TI BIOLOGICAL-ACTIVITY OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 VIF REQUIRES MEMBRANE TARGETING BY C-TERMINAL BASIC DOMAINS SO JOURNAL OF VIROLOGY LA English DT Article ID ADP-RIBOSYLATION FACTOR; SOR GENE; PLASMA-MEMBRANE; GOLGI MEMBRANES; INFECTED-CELLS; DNA-SYNTHESIS; PROTEIN; HIV-1; SEQUENCE; TRANSCRIPTION AB Human immunodeficiency virus type 1 (HIV-1) encodes a Vif protein which is important for virus replication and infectivity. Vif is a cytoplasmic protein which exists in both membrane-associated and soluble forms. The membrane-associated form is an extrinsic membrane protein which is tightly associated with the cytoplasmic side of membranes. We have analyzed the mechanism of membrane targeting of Vif and its role in HIV-1 replication, Mutagenesis studies demonstrate that C-terminal basic domains are required for membrane association. Vif mutations which disrupt membrane association also inhibit HIV-1 replication, indicating that membrane localization of Vif is likely to be required for its biological activity in vivo. Membrane binding of Vif is almost completely abolished by trypsin treatment of membranes, These results demonstrate that membrane localization of Vif requires C-terminal basic domains and interaction with a membrane-associated protein(s), This interaction may serve to direct Vif to a specific cellular site, since immunofluorescence staining and plasma membrane fractionation studies show that Vif is localized predominantly to an internal cytoplasmic compartment rather than to the plasma membrane, The mechanism of membrane targeting of Vif is different in some respects from that of other extrinsic membrane proteins, such as Ras, Src, and MARCKS, which utilize a basic domain together with a lipid modification for membrane targeting. Membrane targeting of Vif is likely to play an important role in HIV-1 replication and thus may be a therapeutic target. C1 DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RI iMed.ULisboa, iMed.ULisboa/C-6292-2014; Goncalves, Joao/B-2013-2008; iMed.ULisboa, M2B /B-5277-2014 OI Goncalves, Joao/0000-0002-1245-3715; FU NIAID NIH HHS [AI36186, AI28691, AI33837] NR 44 TC 65 Z9 66 U1 0 U2 1 PU AMER SOC MICROBIOLOGY PI WASHINGTON PA 1325 MASSACHUSETTS AVENUE, NW, WASHINGTON, DC 20005-4171 SN 0022-538X J9 J VIROL JI J. Virol. PD NOV PY 1995 VL 69 IS 11 BP 7196 EP 7204 PG 9 WC Virology SC Virology GA RZ100 UT WOS:A1995RZ10000073 PM 7474141 ER PT J AU GOODMAN, WG BELIN, T GALES, B JUPPNER, H SEGRE, GV SALUSKY, IB AF GOODMAN, WG BELIN, T GALES, B JUPPNER, H SEGRE, GV SALUSKY, IB TI CALCIUM-REGULATED PARATHYROID-HORMONE RELEASE IN PATIENTS WITH MILD OR ADVANCED SECONDARY HYPERPARATHYROIDISM SO KIDNEY INTERNATIONAL LA English DT Article ID CHRONIC-RENAL-FAILURE; INTRAVENOUS CALCITRIOL; HEMODIALYSIS-PATIENTS; HYPERCALCEMIA; DIALYSIS; 1,25-DIHYDROXYVITAMIN-D; PROLIFERATION; SECRETION; TISSUE; INVIVO AB Differences in the regulation of parathyroid hormone (PTH) release by calcium are thought to account for excess PTH secretion in patients with secondary hyperparathyroidism (2 degrees HPTH). To determine whether calcium-regulated PTH release varies with the severity of 2 degrees HPTH in patients with end-stage renal disease, dynamic tests of parathyroid gland function were done using the four-parameter model in 26 patients with 2 degrees HPTH documented by bone biopsy. Estimates of the set point did not differ among patients categorized as mild (basal serum PTH < 400 pg/ml), moderate (basal PTH 400 to 600 pg/ml) or severe (basal PTH > 600 pg/ml) 2 degrees HPTH; values were 1.23 +/- 0.06 mmol/liter, 1.24 +/- 0.06 mmol/liter and 1.23 +/- 0.05 mmol/liter, respectively, and none of these set point estimates differed from results obtained in normal volunteers, 1.21 +/- 0.02 mmol/liter (NS). The slope of the sigmoidal ionized calcium-PTH curve also did not differ among groups. Set point values did not correspond to basal serum PTH levels, to the maximum serum PTH level observed during hypocalcemia or to the minimum serum PTH level seen during hypercalcemia in patients with 2 degrees HPTH. In contrast, basal serum PTH values were positively correlated with both the maximum serum PTH level observed during hypocalcemia (r = 0.76, P < 0.01), and the minimum serum PTH level attained during calcium infusions (r = 0.78, P < 0.01). Calcium-regulated PTH release does not differ with the degree of 2 degrees HPTH, and set point abnormalities do not account for excess PTH secretion in patients with chronic renal failure as judged by in vivo dynamic tests of parathyroid gland function. The results suggest that variations in parathyroid gland size are the major contributor to excessive PTH secretion in patients with chronic renal failure. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT PEDIAT,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,SCH MED,DEPT BIOMATH,LOS ANGELES,CA 90024. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,ENDOCRINE UNIT,BOSTON,MA. RP GOODMAN, WG (reprint author), UNIV CALIF LOS ANGELES,MED CTR,SCH MED,DEPT RADIOL SCI,BL-428,LOS ANGELES,CA 90024, USA. FU NCRR NIH HHS [RR-00865]; NIDDK NIH HHS [DK-35423] NR 36 TC 41 Z9 41 U1 0 U2 1 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD NOV PY 1995 VL 48 IS 5 BP 1553 EP 1558 DI 10.1038/ki.1995.446 PG 6 WC Urology & Nephrology SC Urology & Nephrology GA TA830 UT WOS:A1995TA83000021 PM 8544413 ER PT J AU WILLIAMS, ME HARRINGTON, JT MADIAS, NE LEVEY, AS SINGH, A AF WILLIAMS, ME HARRINGTON, JT MADIAS, NE LEVEY, AS SINGH, A TI MANAGEMENT OF THE DIABETIC TRANSPLANT RECIPIENT - DISCUSSION SO KIDNEY INTERNATIONAL LA English DT Discussion ID CORONARY-ARTERY DISEASE; STAGE RENAL-DISEASE; KIDNEY-TRANSPLANTATION; RISK-FACTORS; LONG-TERM; PANCREAS TRANSPLANTATION; CARDIOVASCULAR RISK; UROLOGIC COMPLICATIONS; ADVANCED GLYCOSYLATION; ALLOGRAFT RECIPIENTS C1 JOSLIN DIABET CTR,BOSTON,MA 02215. TUFTS UNIV,SCH MED,BOSTON,MA 02111. TUFTS UNIV NEW ENGLAND MED CTR,DIV NEPHROL,BOSTON,MA 02111. NR 171 TC 13 Z9 13 U1 0 U2 0 PU BLACKWELL SCIENCE PUBL INC CAMBRIDGE PI CAMBRIDGE PA 238 MAIN ST, CAMBRIDGE, MA 02142 SN 0085-2538 J9 KIDNEY INT JI Kidney Int. PD NOV PY 1995 VL 48 IS 5 BP 1660 EP 1674 DI 10.1038/ki.1995.461 PG 15 WC Urology & Nephrology SC Urology & Nephrology GA TA830 UT WOS:A1995TA83000036 PM 8544428 ER PT J AU CAO, J VESCIO, RA RETTIG, MB HONG, CH KIM, A LEE, JC LICHTENSTEIN, AK BERENSON, JR AF CAO, J VESCIO, RA RETTIG, MB HONG, CH KIM, A LEE, JC LICHTENSTEIN, AK BERENSON, JR TI A CD10-POSITIVE SUBSET OF MALIGNANT-CELLS IS IDENTIFIED IN MULTIPLE-MYELOMA USING PCR WITH PATIENT-SPECIFIC IMMUNOGLOBULIN GENE PRIMERS SO LEUKEMIA LA English DT Article DE CD10; PCR; MYELOMA; IMMUNOGLOBULIN; HEAVY-CHAIN VARIABLE REGION ID LYMPHOBLASTIC-LEUKEMIA ANTIGEN; PLASMA-CELLS; (CALLA)-POSITIVE MYELOMA; CIRCULATING LYMPHOCYTES; CLINICAL-FEATURES; PERIPHERAL-BLOOD; BONE-MARROW; CALLA; EXPRESSION; NEUTROPHILS AB Immunophenotypic studies show the presence of CD10-bearing malignant cells in a small subset of multiple myeloma (MM) patients. We used a sensitive PCR-based technique in order to determine the frequency that MM patients contain a malignant subpopulation which expresses this antigen. The immunoglobulin (Ig) heavy chain variable region (V-H) gene sequence expressed by the malignant clone in MM can be used as a tumor specific marker. After determining this sequence in six MM patients, patient specific V-H oligonucleotide primers from complementarity determining region (CDR) sequences were generated. Bone marrow mononuclear cells from these patients were incubated with two different anti-CD10 antibodies or isotype identical murine IgG controls. Cells were then sorted by flow cytometry into the 1% brightest cells containing >99.99% CD10-positive cells and two fractions including the 90 and 10% dimmest staining cells. PCR amplification was performed on DNA from approximately 10(4) cells (0.1 mu g) using patient specific CDR1 and CDR3 primers. Detectable PCR product was obtained in each sorted sample although the intensity of the band was much higher in cells lacking CD10 expression (the 90 and 10% dimmest fractions) than in the CD10-bearing (1% brightest) population. These results imply that there is a small population of CD10-bearing clonal cells in most, if not all patients with MM. C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,DIV HEMATOL ONCOL,LOS ANGELES,CA. JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90034. NR 43 TC 9 Z9 9 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0887-6924 J9 LEUKEMIA JI Leukemia PD NOV PY 1995 VL 9 IS 11 BP 1948 EP 1953 PG 6 WC Oncology; Hematology SC Oncology; Hematology GA TG562 UT WOS:A1995TG56200024 PM 7475288 ER PT J AU WENZEL, SL BAKHTIAR, L CASKEY, NH HARDIE, E REDFORD, C SADLER, N GELBERG, L AF WENZEL, SL BAKHTIAR, L CASKEY, NH HARDIE, E REDFORD, C SADLER, N GELBERG, L TI HOMELESS VETERANS UTILIZATION OF MEDICAL, PSYCHIATRIC, AND SUBSTANCE-ABUSE SERVICES SO MEDICAL CARE LA English DT Article DE HOMELESS VETERANS; SERVICE UTILIZATION ID MENTAL-HEALTH; CARE; ADJUSTMENT; ALCOHOL; PROGRAM; ADULTS; WOMEN AB This study focuses on the association between homeless veterans' prior utilization of medical, psychiatric, and substance abuse services and biopsychosocial characteristics reported at admission into a domiciliary care program. Given the large number of veterans in the US homeless population and their health care needs, understanding factors associated with health service use among homeless veterans is significant. Research participants were 429 homeless male veterans who had been admitted to the Domiciliary Care for Homeless Veterans Program site at the West Los Angeles Veterans Affairs Medical Center between February 1988 and July 1992 for treatment of medical, psychiatric, or substance disorders. Results of logistic regression analyses indicated that self-reported need (chronic medical problems, serious psychiatric symptoms, combat stress, alcohol use) and evaluated need for care (evidence of liver dysfunction) were important to veterans' use of health services in the 6 months before program admission. Predisposing social structure factors (education, residential stability, and usual sleeping place) were also significant predictors of service utilization. Overall, need factors were more strongly related to service use. Supplementary logistic regression analyses indicated that comorbidity of need factors deserves attention in understanding homeless veterans' use of services. In conclusion, it is important to attend to predisposing social structure factors as potential barriers to care for homeless veterans. C1 RAND CORP,SANTA MONICA,CA. W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT PSYCHIAT & BIOBEHAV SCI,LOS ANGELES,CA 90024. RP WENZEL, SL (reprint author), UNIV CALIF LOS ANGELES,DIV FAMILY MED,50-071 CHS,BOX 951683,LOS ANGELES,CA 90095, USA. NR 47 TC 46 Z9 46 U1 1 U2 5 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0025-7079 J9 MED CARE JI Med. Care PD NOV PY 1995 VL 33 IS 11 BP 1132 EP 1144 DI 10.1097/00005650-199511000-00006 PG 13 WC Health Care Sciences & Services; Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA TE669 UT WOS:A1995TE66900006 PM 7475422 ER PT J AU THADHANI, RI CAMARGO, CA XAVIER, RJ FANG, LST BAZARI, H AF THADHANI, RI CAMARGO, CA XAVIER, RJ FANG, LST BAZARI, H TI ATHEROEMBOLIC RENAL-FAILURE AFTER INVASIVE PROCEDURES - NATURAL-HISTORY BASED ON 52 HISTOLOGICALLY PROVEN CASES SO MEDICINE LA English DT Article ID CHOLESTEROL CRYSTAL EMBOLIZATION; CONTRAST MATERIAL; DISEASE; CATHETERIZATION; COMPLICATION; EMBOLISM C1 MASSACHUSETTS GEN HOSP,DEPT MED,RENAL UNIT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT EMERGENCY MED,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH PUBL HLTH,DEPT EPIDEMIOL,BOSTON,MA 02115. FU NHLBI NIH HHS [HL-07575] NR 48 TC 133 Z9 138 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0025-7974 J9 MEDICINE JI Medicine (Baltimore) PD NOV PY 1995 VL 74 IS 6 BP 350 EP 358 DI 10.1097/00005792-199511000-00005 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA TJ110 UT WOS:A1995TJ11000005 PM 7500898 ER PT J AU ZLOTECKI, RA BAXTER, LT BOUCHER, Y JAIN, RK AF ZLOTECKI, RA BAXTER, LT BOUCHER, Y JAIN, RK TI PHARMACOLOGICAL MODIFICATION OF TUMOR BLOOD-FLOW AND INTERSTITIAL FLUID PRESSURE IN A HUMAN TUMOR XENOGRAFT - NETWORK ANALYSIS AND MECHANISTIC INTERPRETATION SO MICROVASCULAR RESEARCH LA English DT Article ID HUMAN ADENOCARCINOMA LS174T; ANGIOTENSIN-II; SOLID TUMORS; MURINE TUMOR; SCID MICE; RAT; HYPERTENSION; NICOTINAMIDE; OXYGENATION; HYDRALAZINE AB Various vasoactive agents have been used to modify tumor blood Row with the ultimate goal of improving cancer detection and treatment, with widely disparate results. Furthermore, the lack of mechanistic interpretations has hindered understanding of how these agents affect the different physiological parameters involved in perfusion. Thus, there is a need to develop a unified framework for understanding the interrelated physiological effects of pharmacological and physical agents. The goals of this study were (1) to develop a mathematical model which helps determine the location and magnitude of changes in the vascular resistance of tumor and normal tissues and (2) to test the model with our own experimental studies and by comparison with results from the literature. The systemic and interstitial pressures and relative tumor blood Row were measured before and after administration of angiotensin II, epinephrine, norepinephrine, nitroglycerin, and hydralazine in SCID mice bearing LS174T human colon adenocarcinoma xenografts. A mathematical model was developed in analogy to electrical circuits which examined the pressure, flow, and resistance relationships for arterial and venous segments of the vasculature of a tumor and surrounding normal tissue. Vasoconstrictor-induced increases in the mean arterial blood pressure led to increases in tumor blood flow and interstitial pressure with the magnitude of change dependent on the agent (percentage change in blood flow: angiotensin > epinephrine > norepinephrine). The vasodilating agents induced decreases in tumor blood flow in parallel to the induced decreases in the systemic pressure, but only the long-acting arterial vasodilator hydralazine was capable of effecting a decrease in tumor interstitial pressure. The model was also found to be consistent with other data available in the literature on norepinephrine, pentoxifylline, nicotinamide, and hemodilution, and was useful in providing input as to the location and degree of the physiological effects of these agents. The results of the data and model show that the steal phenomenon is the dominant mechanism for redistribution of host blood flow to the tumor. However, some degree of arterial control was found to be present in the tumors. Moreover, the parallel increases in tumor interstitial pressure and blood flow contradict any hypothesis suggesting that elevated interstitial fluid pressure precipitates chronic vascular collapse, thus decreasing blood flow. (C) 1995 Academic Press, Inc. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT ONCOL,STEELE LAB,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NCI NIH HHS [R35-CA-56591] NR 38 TC 63 Z9 65 U1 0 U2 2 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0026-2862 J9 MICROVASC RES JI Microvasc. Res. PD NOV PY 1995 VL 50 IS 3 BP 429 EP 443 DI 10.1006/mvre.1995.1069 PG 15 WC Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TE681 UT WOS:A1995TE68100010 PM 8583955 ER PT J AU LU, FM LUX, SE AF LU, FM LUX, SE TI AN ACTIVE FORM OF HUMAN NOTCH-1 BINDS TO TRANSCRIPTION FACTOR CBF1 AND STIMULATES TRANSCRIPTION THROUGH A CBF1 RESPONSIVE PROMOTER ELEMENT SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 537 EP 537 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300538 ER PT J AU BOPPART, SA BREZINSKI, ME BOUMA, B TEARNEY, GJ SWANSON, EA FUJIMOTO, JG AF BOPPART, SA BREZINSKI, ME BOUMA, B TEARNEY, GJ SWANSON, EA FUJIMOTO, JG TI IN-VIVO IMAGING OF DEVELOPING MORPHOLOGY USING OPTICAL COHERENCE TOMOGRAPHY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MIT,LINCOLN LAB,LEXINGTON,MA 02173. MASSACHUSETTS GEN HOSP,CARDIAC UNIT,BOSTON,MA 02114. MIT,DEPT ELECT ENGN,CAMBRIDGE,MA 02139. RI Boppart, Stephen/C-7338-2009 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 662 EP 662 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300663 ER PT J AU DUNNE, PW MA, L WALCH, ET LUO, Z AVRUCH, J EPSTEIN, HF AF DUNNE, PW MA, L WALCH, ET LUO, Z AVRUCH, J EPSTEIN, HF TI IDENTIFICATION OF SIGNAL-TRANSDUCTION PROTEINS THAT INTERACT WITH MYOTONIC-DYSTROPHY PROTEIN-KINASE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 BAYLOR COLL MED,DEPT NEUROL,HOUSTON,TX 77030. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 747 EP 747 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300746 ER PT J AU HASSON, T HEINTZELMAN, MB SANTOS-SACCHI, J COREY, DP MOOSEKER, MS AF HASSON, T HEINTZELMAN, MB SANTOS-SACCHI, J COREY, DP MOOSEKER, MS TI MYOSIN-VIIA, THE GENE-PRODUCT DEFECTIVE IN THE DEAF BLINDNESS DISEASE USHER SYNDROME TYPE 1B, EXHIBITS A UNIQUE EXPRESSION PROFILE IN COCHLEA AND RETINA SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 YALE UNIV, DEPT BIOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT CELL BIOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT PATHOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT SURG OTOLARYNGOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT NEUROBIOL, NEW HAVEN, CT 06520 USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, HHMI, BOSTON, MA 02114 USA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 836 EP 836 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300837 ER PT J AU YANG, B YANG, BL GOETINCK, PF AF YANG, B YANG, BL GOETINCK, PF TI ROLE OF THE G3 DOMAIN OF AGGRECAN IN GLYCOSAMINOGLYCAN CHAIN ATTACHMENT AND IN SECRETION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 936 EP 936 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300933 ER PT J AU BACIU, PC GOETINCK, PF AF BACIU, PC GOETINCK, PF TI SYNDECAN-4 RECRUITMENT INTO FOCAL CONTACTS IS REGULATED BY PKC DURING SERUM INDUCTION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 941 EP 941 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51300941 ER PT J AU NOSEK, MT MARTYN, JAJ AF NOSEK, MT MARTYN, JAJ TI BURN INJURY-INDUCED UP-REGULATION OF THE RAT SKELETAL-MUSCLE ACETYLCHOLINE-RECEPTOR INCLUDES INCREASED GAMMA-SUBUNIT EXPRESSION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 SHRINERS BURN INST,DEPT ANESTHESIA,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1032 EP 1032 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301032 ER PT J AU STANKEWICH, MC VU, QU SCHNEEBERGER, EE LYNCH, RD AF STANKEWICH, MC VU, QU SCHNEEBERGER, EE LYNCH, RD TI THE TIME-COURSE FOR CA2+-INDUCED TIGHT JUNCTION (TJ) ASSEMBLY IS MODULATED BY CHANGES IN CELL CHOLESTEROL (CH) CONTENT SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 UNIV LOWELL,DEPT BIOL SCI,LOWELL,MA 01854. MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1124 EP 1124 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301124 ER PT J AU SPIEGELMAN, B BRUN, R TONTONOZ, P HU, E ALTIOK, S AF SPIEGELMAN, B BRUN, R TONTONOZ, P HU, E ALTIOK, S TI PPAR-GAMMA - A MASTER REGULATOR OF ADIPOGENESIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NR 0 TC 1 Z9 1 U1 1 U2 2 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1343 EP 1343 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301343 ER PT J AU BACIU, PC GOETINCK, PF AF BACIU, PC GOETINCK, PF TI PROTEIN-KINASE-C REGULATES THE RECRUITMENT OF SYNDECAN-4 INTO FOCAL CONTACTS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Article ID HEPARAN-SULFATE PROTEOGLYCANS; CELL-SUBSTRATUM ADHESION; BINDING DOMAIN; EXTRACELLULAR-MATRIX; CULTURED FIBROBLASTS; FIBRONECTIN; LOCALIZATION; ASSOCIATION; SEQUENCES; ACTIN AB Cell surface heparan sulfate proteoglycans have been implicated as co-receptors facilitating cell adhesion and growth factor binding. Recent studies on the role of a family of transmembrane heparan sulfate proteoglycans, syndecans, in cell adhesion has identified one member, syndecan-4, to be present within focal contacts. The current study investigates the mechanisms regulating the association of syndecan-4 with focal contacts based upon its immunolocalization with vinculin in quiescent, serum-stimulated, and 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced cultures. In quiescent cells, syndecan-4 did not localize to focal contacts. However, activation of protein kinase C by TPA or serum induces the active recruitment of syndecan-4 into focal contacts. This induction preferentially localizes syndecan-4 to focal contacts behind the leading lamella, the subnuclear region, and along the trailing edge of migratory cells. Focal contacts in either freshly adhered cells or in the leading lamellae of migrating cells did not stain for syndecan-4. In addition to the observed subcellular distribution and recruitment, syndecan-4 was observed to co-localize with endogenously synthesized fibronectin fibrils within focal contacts as well as with fibrils present in the matrix. These findings suggest that protein kinase C activation results in syndecan-4 recruitment to focal contacts and its association with sites of matrix deposition. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. FU NICHD NIH HHS [HD-22016, HD-22050] NR 40 TC 114 Z9 114 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 IS 11 BP 1503 EP 1513 PG 11 WC Cell Biology SC Cell Biology GA TF512 UT WOS:A1995TF51200007 PM 8589452 ER PT J AU AMANO, S HIBINO, T NISHIYAMA, T BURGESON, RE AF AMANO, S HIBINO, T NISHIYAMA, T BURGESON, RE TI LAMININ-5 SYNTHESIS AND EXTRACELLULAR PROCESSING BY HUMAN KERATINOCYTES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. RI Nishiyama, Toshio/C-5434-2013 NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1601 EP 1601 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301600 ER PT J AU MOGHE, PV PARASHURAMA, N EZZELL, RM TONER, M TOMPKINS, RG YARMUSH, ML AF MOGHE, PV PARASHURAMA, N EZZELL, RM TONER, M TOMPKINS, RG YARMUSH, ML TI EFFECT OF COLLAGEN GEL CONFIGURATION ON INTEGRIN LOCALIZATION IN CULTURED RAT HEPATOCYTES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT SURG,BOSTON,MA. SHRINERS BURNS INST,BOSTON,MA. NR 3 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1648 EP 1648 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301647 ER PT J AU FRANK, SR HANSEN, SH CASANOVA, JE AF FRANK, SR HANSEN, SH CASANOVA, JE TI CHARACTERIZATION OF A NOVEL HUMAN PROTEIN WITH HOMOLOGY TO YEAST SEC7 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP EAST,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1682 EP 1682 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301679 ER PT J AU FAROKHZAD, OC SHELLEY, CS ARNAOUT, MA AF FAROKHZAD, OC SHELLEY, CS ARNAOUT, MA TI EXPRESSION OF THE CD11B GENE DURING MYELOID DIFFERENTIATION REQUIRES THE NOVEL TRANSCRIPTION FACTOR MS-2 SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DEPT MED,LEUKOCYTE BIOL & INFLAMMAT PROGRAM,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 1 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1784 EP 1784 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301783 ER PT J AU KOUNNAS, MZ MOIR, RD REBECK, GW BUSH, AI ARGRAVES, WS TANZI, RE HYMAN, BT STRICKLAND, DK AF KOUNNAS, MZ MOIR, RD REBECK, GW BUSH, AI ARGRAVES, WS TANZI, RE HYMAN, BT STRICKLAND, DK TI LDL RECEPTOR-RELATED PROTEIN (LRP) BINDS SECRETED BETA-AMYLOID PRECURSOR PROTEIN AND MEDIATES ITS DEGRADATION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 AMER RED CROSS,HOLLAND LABS,DEPT BIOCHEM,ROCKVILLE,MD 20855. MASSACHUSETTS GEN HOSP,GENET & AGING LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP,NEUROL SERV,BOSTON,MA 02114. RI Bush, Ashley/A-1186-2007 OI Bush, Ashley/0000-0001-8259-9069 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1901 EP 1901 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301901 ER PT J AU CORBETT, AH KOEPP, DM SCHLENSTEDT, G LEE, MS WONG, DH HOPPER, AK SILVER, PA AF CORBETT, AH KOEPP, DM SCHLENSTEDT, G LEE, MS WONG, DH HOPPER, AK SILVER, PA TI PROTEINS INVOLVED IN MACROMOLECULAR TRANSPORT ACROSS THE NUCLEAR-ENVELOPE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. PENN STATE UNIV,HERSHEY,PA 17033. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1991 EP 1991 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301991 ER PT J AU NEVILLE, C GONZALES, D ROSENTHAL, N AF NEVILLE, C GONZALES, D ROSENTHAL, N TI FIBER-SPECIFIC REGULATION OF MUSCLE GENE-EXPRESSION SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. RI Rosenthal, Nadia/O-7009-2015 NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 1997 EP 1997 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51301997 ER PT J AU HIBINO, T TAKAHASHI, T TAKEDA, A LEUTHARDT, D BACIU, P GOETINCK, PF AF HIBINO, T TAKAHASHI, T TAKEDA, A LEUTHARDT, D BACIU, P GOETINCK, PF TI CLONING OF PSORIASTATIN, A CATHEPSIN L-SPECIFIC INHIBITOR, FROM PSORIATIC EPIDERMIS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,CUTANEOUS BIOL RES CTR,CAMBRIDGE,MA 02138. SHISEIDO RES CTR,YOKOHAMA,KANAGAWA,JAPAN. SHOWA UNIV,DEPT CLIN PATHOL,TOKYO,JAPAN. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2007 EP 2007 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302005 ER PT J AU VALENTE, AJ ABRAMOVA, MA PEARSON, DW CLARK, JR CLARK, RA AF VALENTE, AJ ABRAMOVA, MA PEARSON, DW CLARK, JR CLARK, RA TI TRANSCRIPTIONAL REGULATION OF THE CALRETICULIN GENE IN THE HL-60 MYELOID CELL-LINE SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 AUDIE L MURPHY MEM VET ADM MED CTR,DEPT MED,SAN ANTONIO,TX 78284. UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2028 EP 2028 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302025 ER PT J AU GOLDMANN, WH LEHMANN, H LUDWIG, M RIEF, M TEMPEL, M HOFMANN, UG ISENBERG, G WANG, N INGBER, DE EZZELL, RM AF GOLDMANN, WH LEHMANN, H LUDWIG, M RIEF, M TEMPEL, M HOFMANN, UG ISENBERG, G WANG, N INGBER, DE EZZELL, RM TI DIFFERENCES IN VISCOELASTICITY IN VINCULIN-DEFICIENT MOUSE F9 (5.51)CELLS DETERMINED BY ATOMIC-FORCE MICROSCOPY, RHEOLOGY AND MAGNETOMETRY SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. TECH UNIV MUNICH,DEPT BIOPHYS,W-8000 MUNICH,GERMANY. HARVARD UNIV,CHILDRENS HOSP,SCH PUBL HLTH,DEPT SURG,BOSTON,MA 02115. RI Goldmann, Wolfgang/H-5572-2013 NR 1 TC 0 Z9 0 U1 0 U2 3 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2165 EP 2165 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302163 ER PT J AU CHEN, Q JOHNSON, D GOETINCK, PF AF CHEN, Q JOHNSON, D GOETINCK, PF TI ASSEMBLY OF CARTILAGE MATRIX PROTEIN FILAMENTOUS NETWORKS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CBRC,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. RI Chen, Qian/C-4354-2011 OI Chen, Qian/0000-0003-4406-5618 NR 0 TC 1 Z9 1 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2221 EP 2221 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302220 ER PT J AU HANSEN, SH OLSSON, A CASANOVA, JE AF HANSEN, SH OLSSON, A CASANOVA, JE TI WORTMANNIN, AN INHIBITOR OF PHOSPHOINOSITIDE 3-KINASE - INHIBITS TRANSCYTOSIS IN POLARIZED EPITHELIAL-CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP EAST,DEPT PEDIAT,BOSTON,MA 02129. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2327 EP 2327 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302323 ER PT J AU KANDIKONDA, S ODA, D NIEDERMAN, R SORKIN, BC AF KANDIKONDA, S ODA, D NIEDERMAN, R SORKIN, BC TI E-CADHERIN-MEDIATED ADHESION IS REQUIRED FOR NORMAL GROWTH-REGULATION OF HUMAN GINGIVAL EPITHELIAL-CELLS SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 FORSYTH DENT CTR,RES INST,DEPT CELL BIOL,BOSTON,MA 02115. UNIV WASHINGTON,DEPT ORAL BIOL,SEATTLE,WA 98195. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2380 EP 2380 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302376 ER PT J AU KRAEFT, SK TRAINCART, F VERON, M CHEN, LB AF KRAEFT, SK TRAINCART, F VERON, M CHEN, LB TI SUBNUCLEAR LOCALIZATION OF NUCLEOSIDE DIPHOSPHATE KINASE NM23 PROTEIN IN NORMAL AND TUMOR-CELL LINES SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. INST PASTEUR,UNITE BIOCHIM CELLULAIRE,CNRS,URA 1129,F-75724 PARIS,FRANCE. NR 0 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2445 EP 2445 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302443 ER PT J AU ANDERSON, E LEE, GY CROOP, JM AF ANDERSON, E LEE, GY CROOP, JM TI POLYCYSTIC OVARIAN CONDITION (PCO) - HYPERANDROGENISM, APOPTOSIS AND EPITHELIALIZATION IN A RAT MODEL SO MOLECULAR BIOLOGY OF THE CELL LA English DT Meeting Abstract ID DEHYDROEPIANDROSTERONE C1 HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 3 TC 0 Z9 0 U1 0 U2 0 PU AMER SOC CELL BIOL PI BETHESDA PA PUBL OFFICE 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 1059-1524 J9 MOL BIOL CELL JI Mol. Biol. Cell PD NOV PY 1995 VL 6 SU S BP 2473 EP 2473 PG 1 WC Cell Biology SC Cell Biology GA TF513 UT WOS:A1995TF51302472 ER PT J AU CHENG, TJ CHRISTIANI, DC LIBER, HL WAIN, JC XU, XP WIENCKE, JK KELSEY, KT AF CHENG, TJ CHRISTIANI, DC LIBER, HL WAIN, JC XU, XP WIENCKE, JK KELSEY, KT TI MUTANT FREQUENCY AT THE HPRT LOCUS IN HUMAN-LYMPHOCYTES IN A CASE-CONTROL STUDY OF LUNG-CANCER SO MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS LA English DT Article DE HPRT; MUTANT FREQUENCY; LUNG CANCER; CIGARETTE SMOKE; FOLATE; VITAMIN-A; LYMPHOCYTE ID FACTORS INFLUENCING MUTATION; CIGARETTE SMOKERS; BETA-CAROTENE; VITAMIN-A; 6-THIOGUANINE RESISTANCE; CIRCULATING LYMPHOCYTES; BREAST-CANCER; RISK; SUSCEPTIBILITY; EPIDEMIOLOGY AB A clonal assay to determine the mutant frequency (MF); at the hypoxanthine-guanine phosphoribosyl transferase (hprt) locus in human lymphocytes has been used by a number of investigators to study exposure to mutagens and carcinogens in a variety of populations, We have studied hprt MF in 106 subjects (40 controls and 66 cases) enrolled in a case-control investigation of lung cancer. Epidemiological data collected included smoking history, intake of dietary micronutrients, and occupational and environmental exposures as well as medical history, all obtained from an interviewer-administered questionnaire. All subjects were also genotyped for the known polymorphism in glutathione S-transferase class mu (GST-mu). In analysis of cases and controls, hprt MF was not associated with age, smoking, the polymorphism in GST mu, dietary intake, occupational exposures, family history of cancer or usage of medications. Since MF and cloning efficiency (CE) are not independent when CE is low, further analysis in cases and controls with a CE greater than or equal to 30% (27 cases and 22 controls) was also conducted. In analysis of controls, hprt MF increased with age and was inversely associated with intake of folate and vitamins A and C. The presence of lung cancer was not associated with hprt MF. Thus, our study supports the previous observation that dietary components may affect the MF at the hprt locus, C1 HARVARD UNIV, SCH PUBL HLTH, DEPT CANC BIOL, BOSTON, MA 02115 USA. HARVARD UNIV, SCH PUBL HLTH, DEPT ENVIRONM HLTH, OCCUPAT HLTH PROGRAM, BOSTON, MA 02115 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, PULM & CRIT CARE UNIT, BOSTON, MA 02114 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, THORAC SURG UNIT, BOSTON, MA 02114 USA. UNIV CALIF SAN FRANCISCO, DEPT EPIDEMIOL & BIOSTAT, MOLEC EPIDEMIOL LAB, SAN FRANCISCO, CA 94143 USA. RI Cheng, Tsun-Jen /D-3495-2012; Kelsey, Karl/I-1252-2014; OI CHENG, TSUN-JEN/0000-0002-2613-8230 FU NCI NIH HHS [CA 06409]; NIEHS NIH HHS [ES 00002, ES 06409] NR 40 TC 15 Z9 16 U1 1 U2 1 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0027-5107 EI 1873-135X J9 MUTAT RES-FUND MOL M JI Mutat. Res.-Fundam. Mol. Mech. Mutagen. PD NOV PY 1995 VL 332 IS 1-2 BP 109 EP 118 DI 10.1016/0027-5107(95)00161-8 PG 10 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA TK344 UT WOS:A1995TK34400014 PM 7500985 ER PT J AU BONNEMANN, CG MODI, R NOGUCHI, S MIZUNO, Y YOSHIDA, M GUSSONI, E MCNALLY, EM DUGGAN, DJ ANGELINI, C HOFFMAN, EP OZAWA, E KUNKEL, LM AF BONNEMANN, CG MODI, R NOGUCHI, S MIZUNO, Y YOSHIDA, M GUSSONI, E MCNALLY, EM DUGGAN, DJ ANGELINI, C HOFFMAN, EP OZAWA, E KUNKEL, LM TI BETA-SARCOGLYCAN (A3B) MUTATIONS CAUSE AUTOSOMAL RECESSIVE MUSCULAR-DYSTROPHY WITH LOSS OF THE SARCOGLYCAN COMPLEX SO NATURE GENETICS LA English DT Article ID GLYCOPROTEIN COMPLEX; DEFICIENCY; PROTEINS; MUSCLE; HETEROGENEITY; SARCOLEMMA; LINKAGE; ADHALIN AB The dystrophin associated proteins (DAPs) are good candidates for harboring primary mutations in the genetically heterogeneous autosomal recessive muscular dystrophies (ARMD). The transmembrane components of the DAPs cab be separated into the dystroglycan and the sarcoglycan complexes. Here we report the isolation of cDNAs encoding the 43 kD sarcoglycan protein beta-sarcoglycan (A3b) and the localization of the human gene to chromosome 4q12. We describe a young girl with ARMD with truncating mutations on both alleles. Immunostaining of her muscle biopsy shows specific loss of the components of the sarcoglycan complex (beta-sarcoglycan, alpha-sarcoglycan (adhalin), and 35 kD sarcoglycan). Thus secondary destabilization of the sarcoglycan complex may be an important pathophysiological event in ARMD. C1 CHILDRENS HOSP,HOWARD HUGHES MED INST,DIV GENET,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA 02115. UNIV PITTSBURGH,SCH MED,DEPT MOLEC GENET & BIOCHEM,PITTSBURGH,PA 15261. UNIV PITTSBURGH,SCH MED,DEPT PEDIAT,PITTSBURGH,PA 15261. UNIV PITTSBURGH,SCH MED,DEPT HUMAN GENET,PITTSBURGH,PA 15261. NATL CTR NEUROL & PSYCHIAT,NATL INST NEUROSCI,DEPT CELL BIOL,KODAIRA,TOKYO 187,JAPAN. UNIV PADUA,NEUROL CLIN 1,I-35128 PADUA,ITALY. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BOSTON,MA 02114. UNIV PITTSBURGH,MED CTR,DEPT CARDIOL,PITTSBURGH,PA 15261. GUNMA UNIV,DEPT NEUROL,MAEBASHI,GUMMA 371,JAPAN. FU NINDS NIH HHS [5 RO1 NS 23740-09]; Telethon [552] NR 51 TC 375 Z9 379 U1 0 U2 1 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1061-4036 J9 NAT GENET JI Nature Genet. PD NOV PY 1995 VL 11 IS 3 BP 266 EP 273 DI 10.1038/ng1195-266 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA TC639 UT WOS:A1995TC63900014 PM 7581449 ER PT J AU STROMINGER, JL AF STROMINGER, JL TI PEPTIDE VACCINATION AGAINST CANCER SO NATURE MEDICINE LA English DT Editorial Material C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. RP STROMINGER, JL (reprint author), HARVARD UNIV,DEPT MOLEC & CELLULAR BIOL,CAMBRIDGE,MA 02138, USA. NR 14 TC 3 Z9 3 U1 0 U2 0 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1995 VL 1 IS 11 BP 1140 EP 1140 DI 10.1038/nm1195-1140 PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700035 PM 7584983 ER PT J AU WEINSTEIN, BM STEMPLE, DL DRIEVER, W FISHMAN, MC AF WEINSTEIN, BM STEMPLE, DL DRIEVER, W FISHMAN, MC TI GRIDLOCK, A LOCALIZED HERITABLE VASCULAR PATTERNING DEFECT IN THE ZEBRAFISH SO NATURE MEDICINE LA English DT Article ID HEART AB We are using the zebrafish, Danio rerio, to identify genes that generate and pattern the vertebrate vasculature. We have isolated a recessive mutation, gridlock(m145) (grl(m145)) in which blood flow to the tail is impeded by a localized vascular defect. Using a novel microangiographic method, we show that the blockade is in the anterior trunk, where the paired lateral dorsal aortae normally merge to form the single midline aorta. Arterial-venous shunts and collateral vessels develop in most mutant embryos, bypassing the lesion and reconstituting caudal blood flow. The grl defect resembles coarctation of the aorta, a human congenital cardiovascular malformation of unknown aetiology, in the location of the lesion and its consequences and in the mutants' dependence on collateral vessels for survival. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP WEINSTEIN, BM (reprint author), MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,149 13TH ST,BOSTON,MA 02129, USA. FU NHLBI NIH HHS [R01-HL49579, T32-HL07208]; NICHD NIH HHS [R01-HD29761] NR 15 TC 213 Z9 219 U1 3 U2 19 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1995 VL 1 IS 11 BP 1143 EP 1147 DI 10.1038/nm1195-1143 PG 5 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700037 PM 7584985 ER PT J AU ISACSON, O DEACON, TW PAKZABAN, P GALPERN, WR DINSMORE, J BURNS, LH AF ISACSON, O DEACON, TW PAKZABAN, P GALPERN, WR DINSMORE, J BURNS, LH TI TRANSPLANTED XENOGENEIC NEURAL CELLS IN NEURODEGENERATIVE DISEASE-MODELS EXHIBIT REMARKABLE AXONAL TARGET SPECIFICITY AND DISTINCT GROWTH-PATTERNS OF GLIAL AND AXONAL FIBERS SO NATURE MEDICINE LA English DT Article ID CD44 EXPRESSION; NERVOUS-SYSTEM; NEUROBLASTS; ASTROCYTES; NEURONS; OLIGODENDROCYTES; GLYCOPROTEIN; SURVIVAL; PATHWAYS; SUBSETS AB Clinical trials are under way using fetal cells to repair damaged neuronal circuitry. However, little is known about how transplanted immature neurons can grow anatomically correct connections in the adult central nervous system (CNS). We transplanted embryonic porcine neural cells in vivo into adult rat brains with neuronal and axonal loss typical of Parkinson's or Huntington's disease. Using complementary species-specific cellular markers, we found donor axons and CD44(+) astroglial fibres in host white matter tracts up to 8 mm from CNS transplant sites, although only donor axons were capable of reaching correct gray matter target regions. This work demonstrates that adult host brain can orient growth of transplanted neurons and that there are differences in transplant donor glial and axonal growth patterns in cellular repair of the mature CNS. C1 MCLEAN HOSP,NEUROGENERAT LAB,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,DEPT NEUROL,BELMONT,MA 02178. MASSACHUSETTS GEN HOSP,DEPT NEUROSURG,BELMONT,MA 02178. DIACRIN INC,BOSTON,MA 02129. RP ISACSON, O (reprint author), HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,BOSTON,MA 02115, USA. FU NINDS NIH HHS [NS29178, 5T32 NS07340, NS30064] NR 37 TC 163 Z9 167 U1 0 U2 5 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1995 VL 1 IS 11 BP 1189 EP 1194 DI 10.1038/nm1195-1189 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700045 PM 7584993 ER PT J AU KHAW, BA TORCHILIN, VP VURAL, I NARULA, J AF KHAW, BA TORCHILIN, VP VURAL, I NARULA, J TI PLUG AND SEAL - PREVENTION OF HYPOXIC CARDIOCYTE DEATH BY SEALING MEMBRANE LESIONS WITH ANTIMYOSIN-LIPOSOMES SO NATURE MEDICINE LA English DT Article ID MYOSIN-SPECIFIC ANTIBODY; MYOCARDIAL-INFARCTION; REPERFUSION; SIZE; LOCALIZATION AB The hallmark of cell death is the development of cell membrane lesions. Such lesions in the myocardium are usually associated with acute myocardial infarction. Minimizing myocardial necrosis by thrombolytic reperfusion therapy constitutes the only major treatment to date. We envisioned a method to seal these membrane lesions using immunoliposomes as a novel adjunctive approach. An antigen to intracellular cytoskeletal myosin in hypoxic embryonic cardiocytes is used as an anchoring site, and a specific antibody on immunoliposomes as the anchor to plug and to seal the membrane lesions. H9C2 cells were used because they are cardiocytes and are propagated in tissue culture and their viability may be assessed by various methods. Viability assessed by [H-3]thymidine uptake in hypoxic cardiocyte cultures (n = 6 each) treated with antimyosin-immunoliposomes (3.26 +/- 0.483 x 10(6) c.p.m.) was similar to that of normoxic cells (3.68 +/- 0.328 x 10(6) c.p.m.), but was greater than those of untreated hypoxic cells (0.115 +/- 0.155 x 10(6) c.p.m.) or hypoxic cells treated with plain liposomes (1.140 +/- 0.577 x 10(6) c.p.m.). These results were reconfirmed by trypan blue exclusion and by fluorescent, confocal and transmission electron microscopy. They indicated that cell death in hypoxic cardiocytes can be prevented by targeted cell membrane sealing. This concept of cell salvage should be applicable in the prevention of cell death in different biological systems. C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02115. RP KHAW, BA (reprint author), NORTHWESTERN UNIV,CTR DRUG TARGETING & ANAL,205 MUGAR BLDG,BOSTON,MA 02115, USA. NR 21 TC 63 Z9 65 U1 0 U2 3 PU NATURE PUBLISHING CO PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 1995 VL 1 IS 11 BP 1195 EP 1198 DI 10.1038/nm1195-1195 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA TC537 UT WOS:A1995TC53700046 PM 7584994 ER PT J AU SHRIEVE, DC LOEFFLER, JS AF SHRIEVE, DC LOEFFLER, JS TI ADVANCES IN RADIATION-THERAPY FOR BRAIN-TUMORS SO NEUROLOGIC CLINICS LA English DT Article ID BIS-CHLORETHYL NITROSOUREA; RAT SPINAL-CORD; MALIGNANT GLIOMA; GLIOBLASTOMA-MULTIFORME; STEREOTAXIC RADIOSURGERY; RANDOMIZED TRIAL; CLINICAL-TRIAL; ONCOLOGY GROUP; INTERSTITIAL BRACHYTHERAPY; FINAL REPORT AB Despite important advances in surgery and chemotherapy, much of the recent progress that has been achieved in the treatment of brain tumors has resulted from developments in radiation therapy. This article reviews some of the recent advances in radiotherapeutic strategies being used in the treatment of brain tumors in adults. The overall management of each specific tumor type is discussed. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. RP SHRIEVE, DC (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BRAIN TUMOR,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115, USA. NR 89 TC 17 Z9 17 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD NOV PY 1995 VL 13 IS 4 BP 773 EP & PG 0 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TE014 UT WOS:A1995TE01400005 PM 8583996 ER PT J AU FINE, HA AF FINE, HA TI NOVEL BIOLOGIC THERAPIES FOR MALIGNANT GLIOMAS - ANTIANGIOGENESIS, IMMUNOTHERAPY, AND GENE-THERAPY SO NEUROLOGIC CLINICS LA English DT Review ID ENDOTHELIAL GROWTH-FACTOR; PRIMARY HUMAN ASTROCYTOMAS; ACTIVATED KILLER CELLS; TUMOR NECROSIS FACTOR; HERPES-SIMPLEX VIRUS; PLATELET FACTOR-IV; BRAIN-TUMORS; GAMMA-INTERFERON; RECOMBINANT INTERLEUKIN-2; EXTRACELLULAR-MATRIX AB Despite recent advances in neurosurgical techniques and radiotherapy prognosis remains poor for most patients.;It is becoming increasingly clear that novel treatment strategies are needed. This article explores some of the promising new therapies for malignant gliomas in terms of their biologic principles and preclinical data. Antiangiogenesis, immunotherapy, and gene therapy are discussed. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BRAIN TUMOR,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. RP FINE, HA (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 128 TC 26 Z9 26 U1 0 U2 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD NOV PY 1995 VL 13 IS 4 BP 827 EP & PG 0 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TE014 UT WOS:A1995TE01400008 PM 8583999 ER PT J AU WEN, PY FINE, HA BLACK, PM SHRIEVE, DC ALEXANDER, E LOEFFLER, JS AF WEN, PY FINE, HA BLACK, PM SHRIEVE, DC ALEXANDER, E LOEFFLER, JS TI HIGH-GRADE ASTROCYTOMAS SO NEUROLOGIC CLINICS LA English DT Review ID RECURRENT MALIGNANT GLIOMAS; ENDOTHELIAL GROWTH-FACTOR; THERAPY-ONCOLOGY-GROUP; HYPERFRACTIONATED RADIATION-THERAPY; POSITRON EMISSION TOMOGRAPHY; ACTIVITY I-125 SOURCES; I PHASE-II; BRAIN-TUMORS; GLIOBLASTOMA-MULTIFORME; ANAPLASTIC ASTROCYTOMA AB High-grade astrocytomas are the most common primary brain tumors in adults. Until recently, there has been Little progress in the treatment of these tumors. Promising new therapies, however, are emerging based on technologic advances in surgery and radiotherapy; improved understanding of the molecular, cellular, and immunobiologic aspects of these tumors; and advances in gene therapy. This article reviews some of the advances that have been made in the diagnosis and treatment of high-grade astrocytomas. C1 HARVARD UNIV,CHILDRENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,JOINT CTR RADIAT THERAPY,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT NEUROSURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02115. RP WEN, PY (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,CTR BRAIN TUMOR,DIV NEUROL,NEUROONCOL SECT,BOSTON,MA 02115, USA. FU NCI NIH HHS [K11CA01467, K11CA01496]; NINDS NIH HHS [P20 NS31110] NR 167 TC 24 Z9 24 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0733-8619 J9 NEUROL CLIN JI Neurol. Clin. PD NOV PY 1995 VL 13 IS 4 BP 875 EP & PG 0 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA TE014 UT WOS:A1995TE01400011 PM 8584002 ER PT J AU Lipton, SA AF Lipton, SA TI Nitric oxide and related molecules in neuronal death and survival SO NEUROLOGIST LA English DT Editorial Material C1 CHILDRENS HOSP,DEPT NEUROL,LAB CELLULAR & MOLEC NEUROSCI,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,DEPT NEUROL,NEUROSCI PROGRAM,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 1074-7931 J9 NEUROLOGIST JI Neurologist PD NOV PY 1995 VL 1 IS 6 BP 309 EP 310 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA UM376 UT WOS:A1995UM37600001 ER PT J AU GEARING, M SCHNEIDER, JA REBECK, GW HYMAN, BT MIRRA, SS AF GEARING, M SCHNEIDER, JA REBECK, GW HYMAN, BT MIRRA, SS TI ALZHEIMERS-DISEASE WITH AND WITHOUT COEXISTING PARKINSONS-DISEASE CHANGES - APOLIPOPROTEIN-E GENOTYPE AND NEUROPATHOLOGIC CORRELATES SO NEUROLOGY LA English DT Article ID LEWY BODY DISEASE; ELECTRON-MICROSCOPIC IMMUNOCYTOCHEMISTRY; TYPE-4 ALLELE; DIAGNOSIS; EPSILON-4; DEMENTIA; VARIANT; LIGHT AB The frequency of the apolipoprotein E (ApoE) epsilon 4 allele and its relationship with coexistent Parkinson's disease (PD) neuropathology in Alzheimer's disease (AD) have not been extensively explored. We determined ApoE genotype in 100 dementia patients with neuropathologically confirmed AD with and without concomitant Parkinson's disease (PD) changes (nigral degeneration and Lewy bodies at various sites). Fifty ''AD+PD'' patients were matched closely with 50 ''pure AD'' patients for age, sex, and duration of dementia. We found identical overrepresentation of the epsilon 4 allele in the two groups: 72% of the patients in each group had at least one ApoE epsilon 4 allele, compared with approximately 25% in the general population (p < 0.005) and in our institutional autopsy population (p < 0.001). Age at onset varied inversely with epsilon 4 allele dosage in men but not in women in both the AD and the AD+PD groups. As with amyloid deposition and plaque frequency in AD, we observed an association between epsilon 4 dosage and PD-related changes. Specifically, the severity of ubiquitin-positive neuritic change in CA2/3 of the hippocampus, but not the frequency of cortical Lewy bodies, varied significantly with epsilon 4 dosage in the AD+PD cases. C1 VET AFFAIRS MED CTR,ATLANTA,GA 30033. EMORY UNIV,SCH MED,DEPT PATHOL & LAB MED,ATLANTA,GA 30322. HARVARD UNIV,SCH MED,DEPT NEUROL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. FU NIA NIH HHS [AG05134, AG10130, AG06790] NR 46 TC 63 Z9 64 U1 0 U2 1 PU LITTLE BROWN CO PI BOSTON PA 34 BEACON STREET, BOSTON, MA 02108-1493 SN 0028-3878 J9 NEUROLOGY JI Neurology PD NOV PY 1995 VL 45 IS 11 BP 1985 EP 1990 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA TG312 UT WOS:A1995TG31200008 PM 7501146 ER PT J AU REPPERT, SM SAUMAN, I AF REPPERT, SM SAUMAN, I TI PERIOD AND TIMELESS TANGO - A DANCE OF 2 CLOCK GENES SO NEURON LA English DT Review ID DROSOPHILA RP REPPERT, SM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEV CHRONOBIOL LAB,BOSTON,MA 02114, USA. RI Sauman, Ivo/H-2071-2014 NR 23 TC 34 Z9 34 U1 0 U2 3 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD NOV PY 1995 VL 15 IS 5 BP 983 EP 986 DI 10.1016/0896-6273(95)90086-1 PG 4 WC Neurosciences SC Neurosciences & Neurology GA TF887 UT WOS:A1995TF88700003 PM 7576665 ER PT J AU REPPERT, SM WEAVER, DR CASSONE, VM GODSON, C KOLAKOWSKI, LF AF REPPERT, SM WEAVER, DR CASSONE, VM GODSON, C KOLAKOWSKI, LF TI MELATONIN RECEPTORS ARE FOR THE BIRDS - MOLECULAR ANALYSIS OF 2 RECEPTOR SUBTYPES DIFFERENTIALLY EXPRESSED IN CHICK BRAIN SO NEURON LA English DT Article ID PASSER-DOMESTICUS; HOUSE SPARROW; SUPRACHIASMATIC NUCLEUS; BINDING-SITES; LOCALIZATION AB Two receptors (CKA and CKB) of the G protein-coupled melatonin receptor family were cloned from chick brain. CKA encodes a protein that is 80% identical at the amino acid level to the human Mel(1a) melatonin receptor and is thus designated the chick Mel(1a) melatonin receptor. CKB encodes a protein that is 80% identical to the Xenopus melatonin receptor and defines a new receptor subtype, the Moll, melatonin receptor, which is distinct from the Mel(1a) and Mel(1b) melatonin receptor subtypes. A melatonin receptor family consisting of three subtypes is supported by PCR cloning of distinct melatonin receptor fragments from Xenopus and zebrafish. Expression of CKA and CKB results in similar ligand binding and functional characteristics. The widespread distribution of CKB and CKB mRNA in brain provides a molecular substrate for the profound actions of melatonin in birds. C1 TEXAS A&M UNIV,DEPT BIOL,COLLEGE STN,TX 77843. HARVARD UNIV,CHILDRENS HOSP,SCH MED,INA SUE PERLMUTTER LAB,BOSTON,MA 02115. RP REPPERT, SM (reprint author), HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEV CHRONOBIOL LAB,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK42125] NR 28 TC 269 Z9 284 U1 0 U2 9 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD NOV PY 1995 VL 15 IS 5 BP 1003 EP 1015 DI 10.1016/0896-6273(95)90090-X PG 13 WC Neurosciences SC Neurosciences & Neurology GA TF887 UT WOS:A1995TF88700007 PM 7576645 ER PT J AU ARONIN, N CHASE, K YOUNG, C SAPP, E SCHWARZ, C MATTA, N KORNREICH, R LANDWEHRMEYER, B BIRD, E BEAL, MF VONSATTEL, JP SMITH, T CARRAWAY, R BOYCE, FM YOUNG, AB PENNEY, JB DIFIGLIA, M AF ARONIN, N CHASE, K YOUNG, C SAPP, E SCHWARZ, C MATTA, N KORNREICH, R LANDWEHRMEYER, B BIRD, E BEAL, MF VONSATTEL, JP SMITH, T CARRAWAY, R BOYCE, FM YOUNG, AB PENNEY, JB DIFIGLIA, M TI CAG EXPANSION AFFECTS THE EXPRESSION OF MUTANT HUNTINGTIN IN THE HUNTINGTONS-DISEASE BRAIN SO NEURON LA English DT Article ID TRINUCLEOTIDE REPEAT EXPANSION; LENGTH; UBIQUITIN; INSTABILITY; ONSET; AGE AB A trinucleotide repeat (GAG) expansion in the huntingtin gene causes Huntington's disease (HD). In brain tissue from HD heterozygotes with adult onset and more clinically severe juvenile onset, where the largest expansions occur, a mutant protein of equivalent intensity to wild-type huntingtin was detected in cortical synaptosomes, indicating that a mutant species is synthesized and transported with the normal protein to nerve endings. The increased size of mutant huntingtin relative to the wild type was highly correlated with CAG repeat expansion, thereby linking an altered electrophoretic mobility of the mutant protein to its abnormal function. Mutant huntingtin appeared in gray and white matter with no difference in expression in affected regions. The mutant protein was broader than the wild type and in 6 of 11 juvenile cases resolved as a complex of bands, consistent with evidence at the DNA level for somatic mosaicism. Thus, HD pathogenesis results from a gain of function by an aberrant protein that is widely expressed in brain and is harmful only to some neurons. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02114. UNIV MASSACHUSETTS,MED CTR,DEPT PHYSIOL,WORCESTER,MA 01655. UNIV MASSACHUSETTS,MED CTR,DEPT PATHOL,WORCESTER,MA 01655. UNIV MASSACHUSETTS,MED CTR,DEPT MED,WORCESTER,MA 01655. UNIV MASSACHUSETTS,MED CTR,DEPT CELL BIOL,WORCESTER,MA 01655. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. DIANON SYST INC,STAMFORD,CT 06497. FU NIA NIH HHS [AG08671]; NINDS NIH HHS [NS15655, NS16367] NR 33 TC 119 Z9 120 U1 1 U2 5 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0896-6273 J9 NEURON JI Neuron PD NOV PY 1995 VL 15 IS 5 BP 1193 EP 1201 DI 10.1016/0896-6273(95)90106-X PG 9 WC Neurosciences SC Neurosciences & Neurology GA TF887 UT WOS:A1995TF88700023 PM 7576661 ER PT J AU ARAVAGIRI, M MARDER, SR YUWILER, A MIDHA, KK KULA, NS BALDESSARINI, RJ AF ARAVAGIRI, M MARDER, SR YUWILER, A MIDHA, KK KULA, NS BALDESSARINI, RJ TI DISTRIBUTION OF FLUPHENAZINE AND ITS METABOLITES IN BRAIN-REGIONS AND OTHER TISSUES OF THE RAT SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE DOPAMINE RECEPTORS; FLUPHENAZINE; FLUPHENAZINE GLUCURONIDE; FLUPHENAZINE-N-OXIDE; FLUPHENAZINE SULFOXIDE; 7-HYDROXY-FLUPHENAZINE; METABOLISM; RAT; RADIOIMMUNOASSAY ID SCHIZOPHRENIC-PATIENTS; REDUCED HALOPERIDOL; ACTIVE METABOLITES; STRIATAL TISSUE; PLASMA-LEVELS; RADIOIMMUNOASSAY; TRIFLUOPERAZINE; DOG; PROCHLORPERAZINE; PERPHENAZINE AB Rats were given 5, 10, or 20 mg/kg oral doses of fluphenazine (FLU;) dihydrochloride daily for 15 days. FLU and its sulfoxide (FL-SO), 7-hydroxy (7-OH-FLU) and N-4'-oxide (FLU-NO) metabolites were assayed in plasma, liver, kidney, fat, whole brain, and brain regions by specific and sensitive radioimmunoassays (RIA). All metabolites were detected in tissues at higher levels than in plasma, and the levels increased with dose. FLU was 10- to 27-foId higher in brain regions than in plasma. Brain vs plasma levels of FLU correlated more closely than levels of its metabolites. Liver contained the highest levels of all analytes at all doses. FLU-SO was the major metabolite in brain regions (24% to 96% of FLU) and accumulated in fat 43 to 75 times more than FLU. Levels of 7-OH-FLU and FLU-NO were very low in brain (1% to 20% of FLU). FLU-SO and FLU-NO had only 1% to 3% the affinity for D-1 and D-2 receptors, but 7-OH-FLU had 20% the D-2 and 5% the D-1 affinity of FLU. The low affinity for dopamine receptors and low brain-levels of metabolites of FLU indicate that they ave not likely to contribute importantly to pharmacologic responses of FLU. Also, the estimated relative ''activity factor'' for these compounds in the brain indicated that the contribution to neuropharmacologic activity by metabolites is less than 1% of FLU. Consequently, clinical monitoring of plasma FLU alone may be sufficient. C1 UNIV CALIF LOS ANGELES, MENTAL HLTH CLIN RES CTR, PSYCHOPHARMACOL UNIT, LOS ANGELES, CA USA. UNIV CALIF LOS ANGELES, DEPT PSYCHIAT, NEUROBIOCHEM LAB, LOS ANGELES, CA USA. UNIV SASKATCHEWAN, COLL PHARM & NUTR, SASKATOON, SK, CANADA. HARVARD UNIV, SCH MED, DEPT PSYCHIAT, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, NEUROSCI PROGRAM, BOSTON, MA 02115 USA. MASSACHUSETTS GEN HOSP, MCLEAN DIV, MAILMAN RES CTR, BIPOLAR & PSYCHIAT DISORDERS PROGRAM, BELMONT, MA USA. MASSACHUSETTS GEN HOSP, MCLEAN DIV, MAILMAN RES CTR, PSYCHIAT RES LABS, BELMONT, MA USA. RP ARAVAGIRI, M (reprint author), W LOS ANGELES VET AFFAIRS MED CTR, PSYCHOPHARMACOL UNIT, BLDG 210 RM 4, 11301 WILSHIRE BLDG, LOS ANGELES, CA 90073 USA. FU NIMH NIH HHS [MH-30911, MH-41573, MH-31154] NR 50 TC 26 Z9 26 U1 0 U2 1 PU ELSEVIER SCIENCE PUBL CO INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD NOV PY 1995 VL 13 IS 3 BP 235 EP 247 PG 13 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA TG529 UT WOS:A1995TG52900004 PM 8602896 ER PT J AU Latina, MA AF Latina, MA TI A technique to evaluate fluid flow in glaucoma shunts SO OPHTHALMIC SURGERY AND LASERS LA English DT Article C1 TUFTS UNIV,DEPT OPHTHALMOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,WELLMAN LABS PHOTOMED,BOSTON,MA. NR 2 TC 5 Z9 5 U1 0 U2 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 SN 0022-023X J9 OPHTHALMIC SURG LAS JI Ophthalmic Surg. Lasers PD NOV-DEC PY 1995 VL 26 IS 6 BP 576 EP 578 PG 3 WC Ophthalmology; Surgery SC Ophthalmology; Surgery GA TT478 UT WOS:A1995TT47800013 PM 8746582 ER PT J AU TUGALTUTKUN, I URGANCIOGLU, M FOSTER, CS AF TUGALTUTKUN, I URGANCIOGLU, M FOSTER, CS TI IMMUNOPATHOLOGIC STUDY OF THE CONJUNCTIVA IN PATIENTS WITH BEHCET-DISEASE SO OPHTHALMOLOGY LA English DT Article ID CELL-ADHESION MOLECULE-1; ENDOTHELIAL-CELLS; ASSOCIATION; ANTIGENS; VCAM-1; HYPERSENSITIVITY; INFLAMMATION; INVOLVEMENT; ANTIBODIES; EXPRESSION AB Purpose: Even though conjunctiva is not primarily involved in patients with uveitis due to Behcet disease, it may reflect the immunopathologic process when inflammation is induced by biopsy of conjunctiva, a phenomenon similar to the induced inflammation at skin pathergy sites. Methods: Conjunctival biopsy specimens obtained 48 hours after a 2-mm biopsy of the epibulbar conjunctiva in 26 Turkish patients with inactive ocular Behcet disease and 9 Turkish patients with inactive idiopathic uveitis were studied by immunoperoxidase using a panel of monoclonal antibodies: anti-CD1, -CD3, -CD4, -CD5, -CD14, -CD22, -CD25, and -CD67, HLA-DR, E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1). Results: Immunopathology of the conjunctival specimens obtained at the time of first biopsy was not significantly different between the Behcet disease and the idiopathic uveitis groups. The second-biopsy specimens of the patients with Behcet disease showed significantly greater numbers of T cells (CD3+, CD4+) and granulocytes (CD67+) as well as HLA-DRS and ICAM-1 + cells in the substantia propria. Vascular endothelium of the conjunctiva in a patient with Behcet disease had significantly more pronounced expression of the adhesion molecules, E-selectin, and ICAM-1. None of the conjunctival specimens in either group showed VCAM-1 positivity. Conclusions: These results show that a more intense antigen-independent inflammation develops with recruitment of both neutrophils and T lymphocytes of helper/inducer phenotype in the conjunctiva of patients with Behcet disease in response to surgical trauma. Increased expression of E-selectin and ICAM-1 in the conjunctiva of patients with Behcet disease may suggest a critical role for these adhesion molecules in the initial events of inflammation. C1 HARVARD UNIV, MASSACHUSETTS EYE & EAR INFIRM, SCH MED, DEPT OPHTHALMOL, BOSTON, MA 02114 USA. UNIV ISTANBUL, ISTANBUL FAC MED, DEPT OPHTHALMOL, OCULAR IMMUNOL & UVEITIS SERV, ISTANBUL, TURKEY. NR 55 TC 22 Z9 22 U1 0 U2 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1995 VL 102 IS 11 BP 1660 EP 1668 PG 9 WC Ophthalmology SC Ophthalmology GA TD883 UT WOS:A1995TD88300022 PM 9098259 ER PT J AU POWER, WJ GHORAISHI, M MERAYOLLOVES, J NEVES, RA FOSTER, CS AF POWER, WJ GHORAISHI, M MERAYOLLOVES, J NEVES, RA FOSTER, CS TI ANALYSIS OF THE ACUTE OPHTHALMIC MANIFESTATIONS OF THE ERYTHEMA MULTIFORME STEVENS-JOHNSON SYNDROME TOXIC EPIDERMAL NECROLYSIS DISEASE SPECTRUM SO OPHTHALMOLOGY LA English DT Article ID STEVENS; MANAGEMENT AB Purpose: To evaluate the epidemiology, possible etiologic factors, complications encountered, and treatment administered to a group of patients with ocular involvement in the erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis disease spectrum who were seen at two large tertiary referral centers over a 34-year period. Methods: Hospital records from 1960 to 1994 at the Massachusetts General Hospital and Shriners Hospital for Crippled Children were reviewed for patients with erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis. Only patients fulfilling specific clinical diagnostic criteria and those who received a diagnosis by a dermatologist were included in the review. Results: A total of 366 patients with erythema multiforme, Stevens-Johnson syndrome, or toxic epidermal necrolysis were identified. Drugs were the most commonly identified etiologic factor in all three conditions; sulfonamides were the most frequently identified agents. Eighty-nine patients (24%) had ocular manifestations at the time of their acute hospital stay. Ocular involvement was seen in 9% of patients with erythema multiforme, in 69% with Stevens-Johnson syndrome, and in 50% with toxic epidermal necrolysis. The ocular problems were more severe in patients with both Stevens-Johnson syndrome and toxic epidermal necrolysis. There was no significant difference between the number of patients who were treated with systemic steroids and those who were not (P = 0.42). Conclusion: The erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis disease spectrum remains an important cause of severe visual loss in a significant number of patients. Systemic steroids used during the acute phase of the disease appear to have no effect on the development of ocular manifestations. Studies on the acute immunopathogenic mechanisms occurring in these diseases are warranted if more effective therapies are to be found. C1 MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,SERV IMMUNOL,BOSTON,MA 02114. MASSACHUSETTS EYE & EAR INFIRM,DEPT OPHTHALMOL,UVEITIS SERV,BOSTON,MA 02114. NR 23 TC 133 Z9 140 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0161-6420 J9 OPHTHALMOLOGY JI Ophthalmology PD NOV PY 1995 VL 102 IS 11 BP 1669 EP 1676 PG 8 WC Ophthalmology SC Ophthalmology GA TD883 UT WOS:A1995TD88300023 PM 9098260 ER PT J AU TEARNEY, GJ BREZINSKI, ME SOUTHERN, JF BOUMA, BE HEE, MR FUJIMOTO, JG AF TEARNEY, GJ BREZINSKI, ME SOUTHERN, JF BOUMA, BE HEE, MR FUJIMOTO, JG TI DETERMINATION OF THE REFRACTIVE-INDEX OF HIGHLY SCATTERING HUMAN TISSUE BY OPTICAL COHERENCE TOMOGRAPHY SO OPTICS LETTERS LA English DT Article ID SKIN AB We describe two new techniques, based on optical coherence tomography (OCT), for determining the refractive index of highly scattering human tissue. Sire obtained refractive indices of in vitro human tissue, using OCT to measure the physical and optical path lengths of the sample. We obtained measurements of the refractive index of in vitro and in vivo human tissue, using OCT to track the focal length shift that results from translating the focus along the optic axis within the tissue. The refractive indices of human skin, adipose, and muscle were measured and compared with previously published estimates. (C) 1995 Optical Society of America C1 MIT,ELECTR RES LAB,CAMBRIDGE,MA 02139. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RP TEARNEY, GJ (reprint author), MIT,DEPT ELECT ENGN & COMP SCI,CAMBRIDGE,MA 02139, USA. NR 8 TC 369 Z9 381 U1 6 U2 41 PU OPTICAL SOC AMER PI WASHINGTON PA 2010 MASSACHUSETTS AVE NW, WASHINGTON, DC 20036 SN 0146-9592 J9 OPT LETT JI Opt. Lett. PD NOV 1 PY 1995 VL 20 IS 21 BP 2258 EP 2260 DI 10.1364/OL.20.002258 PG 3 WC Optics SC Optics GA TB355 UT WOS:A1995TB35500036 PM 19862316 ER PT J AU GORDON, BR AF GORDON, BR TI IMMUNOTHERAPY BASICS SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Review ID ALLERGY; HYPOSENSITIZATION; GENERATION; IGE AB Immunotherapy is the use of controlled exposure to allergens to produce durable antiinflammatory effects, thus reducing the severity of allergic disorders. Immunotherapy is useful when other methods of allergy therapy are not fully satisfactory and can be effectively combined with rhinologic surgical treatment. Immunotherapy should always be considered as a treatment option for allergy patients and can often be of benefit, provided that appropriate indications and contraindications are observed. Physicians caring-for patients with allergies should therefore become familiar with methods of allergy and diagnosis and with the therapeutic potential of immunotherapy. The history of immunotherapy, possible mechanisms, indications, contraindications, testing methods, and initiation of treatment are reviewed. C1 CAPE COD HOSP,MASSACHUSETTS EYE & EAR INFIRM,DIV OTOLARYNGOL HEAD & NECK SURG,HYANNIS,MA. HARVARD UNIV,CAMBRIDGE,MA 02138. NR 49 TC 3 Z9 3 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1995 VL 113 IS 5 BP 597 EP 602 DI 10.1177/019459989511300511 PG 6 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TE969 UT WOS:A1995TE96900010 PM 7478650 ER PT J AU GORDON, BR AF GORDON, BR TI FUTURE IMMUNOTHERAPY - WHAT LIES AHEAD SO OTOLARYNGOLOGY-HEAD AND NECK SURGERY LA English DT Review AB There is currently great interest in developing improved methods of immunotherapy and new techniques of immune system manipulation to ameliorate allergic diseases. This article reviews current research trends in the immunologic treatment of allergy, including the use of chemically modified allergens, nonparenteral allergen exposure, sustained-release allergen delivery, anti-immunoglobulin E antibodies, gamma-globulin, immune complexes, cytokines, and T-cell-tolerogenic peptides. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. CAPE COD HOSP,DIV OTOLARYNGOL HEAD & NECK SURG,HYANNIS,MA. HARVARD UNIV,CAMBRIDGE,MA 02138. NR 25 TC 0 Z9 0 U1 0 U2 0 PU MOSBY-YEAR BOOK INC PI ST LOUIS PA 11830 WESTLINE INDUSTRIAL DR, ST LOUIS, MO 63146-3318 SN 0194-5998 J9 OTOLARYNG HEAD NECK JI Otolaryngol. Head Neck Surg. PD NOV PY 1995 VL 113 IS 5 BP 603 EP 605 DI 10.1016/S0194-5998(95)70052-8 PG 3 WC Otorhinolaryngology; Surgery SC Otorhinolaryngology; Surgery GA TE969 UT WOS:A1995TE96900011 PM 7478651 ER PT J AU COLLINS, JJ BERDE, CB GRIER, HE NACHMANOFF, DB KINNEY, HC AF COLLINS, JJ BERDE, CB GRIER, HE NACHMANOFF, DB KINNEY, HC TI MASSIVE OPIOID RESISTANCE IN AN INFANT WITH A LOCALIZED METASTASIS TO THE MIDBRAIN PERIAQUEDUCTAL GRAY SO PAIN LA English DT Note DE CANCER; CONGENITAL RHABDOID TUMOR; PEDIATRIC AB We report the case of a 4-month-old infant with terminal malignancy who had systemic metastases and a localized metastasis to the dorsal midbrain periaqueductal gray (PAG). Extraordinary doses of opioids (dose equivalent of 2680 mg morphine sulfate/h, i.v.) were required to achieve adequate analgesia. The behavior of the infant, interpreted as being representative of a response to pain, may have been an aversive reaction due to the location of the lesion in the dorsal PAG. We propose that the lesion in the PAG impaired the responsiveness of this infant to the effect of opioids. This report is to alert clinicians to the possible role of the PAG in impaired opioid responsiveness in patients with terminal malignancy, as well as the possibility that pain-like signs (e.g., tachycardia,tachypnea, vocalization, facial grimacing) may indicate an aversive reaction rather than pain in non-verbal patients. C1 CHILDRENS HOSP,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL & ONCOL,PAIN TREATMENT SERV,BOSTON,MA 02115. CHILDRENS HOSP,DEPT ANESTHESIA,BOSTON,MA 02115. CHILDRENS HOSP,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT ANESTHESIA,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 12 TC 10 Z9 10 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0304-3959 J9 PAIN JI Pain PD NOV PY 1995 VL 63 IS 2 BP 271 EP 275 DI 10.1016/0304-3959(95)00094-9 PG 5 WC Anesthesiology; Clinical Neurology; Neurosciences SC Anesthesiology; Neurosciences & Neurology GA TG134 UT WOS:A1995TG13400017 PM 8628594 ER PT J AU Blickman, JG Boland, GWL Cleveland, RH Bramson, RT Lee, MJ AF Blickman, JG Boland, GWL Cleveland, RH Bramson, RT Lee, MJ TI Pseudomembranous colitis: CT findings in children SO PEDIATRIC RADIOLOGY LA English DT Article AB A spectrum of nodular haustral thickening and an ''accordion'' pattern have been reported as specific features of pseudomembranous colitis (PMC) in adults. A retrospective review of nine patients with PMC was performed to assess whether this spectrum of CT findings also occurred in children. In four girls and five boys, CT scans were performed within 3 days of a positive stool toxin assay for Clostridium difficile. Documented CT abnormalities included nodular haustral thickening, the ''accordion'' pattern, colonic wall thickening, ascites, and pericolonic edema. These results were then correlated as to their impact on the clinical outcome. Circumferential colon wall thickening was identified in 7/9 (78%) patients (mean thickening 14.5 mm). Nodular haustral thickening was identified in 4/9 (44%) and the ''accordion'' pattern in 2/9 (22%). Other findings included pericolonic edema in 3/9 (33%) and ascites in 1/9 (11%). Wall thickening was confined to the left colon and rectum in 2/9 (22%), to the right colon in 219 (22%), and involved the whole colon in 3/9 (33%). Although CT findings associated with PMC in children may be suggestive for this diagnosis, CT is less specific than laboratory and clinical findings. C1 CHILDRENS HOSP,BOSTON,MA 02115. RP Blickman, JG (reprint author), MASSACHUSETTS GEN HOSP,DIV PEDIAT IMAGING,BOSTON,MA 02114, USA. NR 7 TC 5 Z9 5 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0301-0449 J9 PEDIATR RADIOL JI Pediatr. Radiol. PD NOV PY 1995 VL 25 SU 1 BP S157 EP S159 PG 3 WC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging SC Pediatrics; Radiology, Nuclear Medicine & Medical Imaging GA TM948 UT WOS:A1995TM94800046 PM 8577512 ER PT J AU BROOKS, MJ MELNIK, G AF BROOKS, MJ MELNIK, G TI THE REFEEDING SYNDROME - AN APPROACH TO UNDERSTANDING ITS COMPLICATIONS AND PREVENTING ITS OCCURRENCE SO PHARMACOTHERAPY LA English DT Review ID TOTAL PARENTERAL-NUTRITION; RECEIVING INTRAVENOUS HYPERALIMENTATION; ACUTE-RENAL-FAILURE; SEVERE HYPOPHOSPHATEMIA; ANOREXIA-NERVOSA; HEMOLYTIC-ANEMIA; WERNICKES ENCEPHALOPATHY; METABOLIC ABNORMALITIES; PHOSPHATE-DEPLETION; PATIENT AB The refeeding syndrome (RS) is a complication of nutritional support that potentially causes considerable morbidity and mortality. Compensatory metabolic alterations secondary to chronic starvation predispose malnourished patients to RS. Providing nutritional support initiates an intracellular shift of potassium, magnesium, and phosphate that results in many adverse effects. The literature addressing RS focuses on only one electrolyte abnormality, hypophosphatemia; however, often all three electrolyte levels are perturbed. Thus RS should be characterized as a syndrome of generalized fluid and electrolyte imbalance. Recommended electrolyte supplementation and laboratory monitoring can help prevent the disorder in susceptible patients. C1 UNIV TEXAS,HLTH SCI CTR,DEPT PHARMACOL,SAN ANTONIO,TX 78284. AUDIE L MURPHY MEM VET ADM MED CTR,DEPT PHARM,SAN ANTONIO,TX 78284. RP BROOKS, MJ (reprint author), APPL CLIN COMMUN INC,4 CENTURY DR,PARSIPPANY,NJ 07054, USA. NR 76 TC 63 Z9 70 U1 2 U2 8 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD NOV-DEC PY 1995 VL 15 IS 6 BP 713 EP 726 PG 14 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG174 UT WOS:A1995TG17400005 PM 8602378 ER PT J AU MOORE, JG COBURN, JW SANDERS, MC MCSORLEY, DJ SIRGO, MA AF MOORE, JG COBURN, JW SANDERS, MC MCSORLEY, DJ SIRGO, MA TI EFFECTS OF SUCRALFATE AND RANITIDINE ON ALUMINUM CONCENTRATIONS IN ELDERLY VOLUNTEERS SO PHARMACOTHERAPY LA English DT Article ID GASTROINTESTINAL ABSORPTION; RENAL-FAILURE; TOXICITY; DEFEROXAMINE; DISEASE; PATIENT AB Elevated aluminum concentrations have been implicated in several disease states in the elderly. We examined the effects of sucralfate, a basic aluminum salt of sucrose sulfate, and ranitidine, administered individually and in combination, on plasma and urine aluminum concentrations in the elderly in a prospective, randomized, three-arm crossover study. Subjects were 20 healthy volunteers over age 65 years, with no clinically significant comorbidities or recent use of aluminum-containing drugs or histamine (H)(2)-antagonists. The three regimens were ranitidine 300 mg at bedtime, sucralfate 1 g 4 times/day, and ranitidine 300 mg at bedtime plus sucralfate 1 g 4 times/day, administered for 4 weeks, with a washout period of at least 1 week between regimens. Plasma and urine aluminum concentrations were measured on days 0, 1, 7, 14, and 28 of each regimen. After 28 days, mean plasma aluminum concentrations were significantly higher in subjects receiving sucralfate alone (8.5 +/- 1.8 mu g/L) and sucralfate plus ranitidine (5.1 +/- 1.3 mu g/L) compared with those receiving ranitidine alone (2.4 +/- 0.7 mu g/L). Urine aluminum concentrations were significantly higher in subjects receiving sucralfate alone (133.2 +/- 32.8 mu g/g creatinine) and sucralfate plus ranitidine (148.1 +/- 51.9 mu g/g creatinine) compared with those receiving ranitidine alone (11.0 +/- 3.7 mu g/g creatinine). There was no significant difference in plasma or urine aluminum concentrations between subjects who received sucralfate alone versus those who received sucralfate plus ranitidine. Sucralfate 4 g/day in elderly subjects produces a significant increase in both plasma and urine aluminum concentrations, compared with ranitidine 300 mg/day. This increase most likely is secondary to gastrointestinal absorption of aluminum in the sucralfate formulation. The clinical relevance of this increase requires further evaluation. C1 GLAXO INC,RES TRIANGLE PK,NC 27709. VET AFFAIRS MED CTR,SALT LAKE CITY,UT 84148. UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. W LOS ANGELES VET AFFAIRS MED CTR,MED SERV,LOS ANGELES,CA 90073. W LOS ANGELES VET AFFAIRS MED CTR,RES SERV,LOS ANGELES,CA 90073. NR 17 TC 6 Z9 8 U1 0 U2 0 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER BOX 806 171 HARRISON AVE, BOSTON, MA 02111 SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD NOV-DEC PY 1995 VL 15 IS 6 BP 742 EP 746 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG174 UT WOS:A1995TG17400009 PM 8602382 ER PT J AU SHIRLEY, BW KUBASEK, WL STORZ, G BRUGGEMANN, E KOORNNEEF, M AUSUBEL, FM GOODMAN, HM AF SHIRLEY, BW KUBASEK, WL STORZ, G BRUGGEMANN, E KOORNNEEF, M AUSUBEL, FM GOODMAN, HM TI ANALYSIS OF ARABIDOPSIS MUTANTS DEFICIENT IN FLAVONOID BIOSYNTHESIS SO PLANT JOURNAL LA English DT Article ID ANTHOCYANIN BIOSYNTHESIS; TRANSCRIPTIONAL ACTIVATORS; LINKAGE MAP; THALIANA; GENE; PLANT; HOMOLOGY; PETUNIA; MYB; CONSTRUCTION AB Eleven loci that play a role in the synthesis of flavonoids in Arabidopsis are described. Mutations at these loci, collectively named transparent testa (tt), disrupt the synthesis of brown pigments in the seed coat (testa). Several of these loci (tt3, tt4, tt5 and ttg) are also required for the accumulation of purple anthocyanins in leaves and stems and one locus (ttg) plays additional roles in trichome and root hair development. Specific functions were previously assigned to tt1-7 and ttg. Here, the results of additional genetic, biochemical and molecular analyses of these mutants are described. Genetic map positions were determined for tt8, tt9 and tt10. Thin layer chromatography identified tissue- and locus-specific differences in the flavonols and anthocyanidins synthesized by mutant and wild-type plants. It was found that UV light reveals distinct differences in the floral tissues of tt3, tt4, tt5, tt6 and ttg, even though these tissues are indistinguishable under visible light. Evidence was also uncovered that tt8 and ttg specifically affect dihydroflavonol reductase gene expression. A summary of these and previously published results are incorporated into an overview of the genetics of flavonoid biosynthesis in Arabidopsis. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. NICHHD,CELL BIOL & METAB BRANCH,BETHESDA,MD 20892. WAGENINGEN UNIV AGR,DEPT GENET,6703 HA WAGENINGEN,NETHERLANDS. RP SHIRLEY, BW (reprint author), VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOL,BLACKSBURG,VA 24061, USA. RI Winkel, Brenda/A-6602-2008; OI Winkel, Brenda/0000-0003-3481-024X; Storz, Gisela/0000-0001-6698-1241; Koornneef, Maarten/0000-0002-7759-4869 NR 53 TC 314 Z9 331 U1 7 U2 49 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7412 J9 PLANT J JI Plant J. PD NOV PY 1995 VL 8 IS 5 BP 659 EP 671 DI 10.1046/j.1365-313X.1995.08050659.x PG 13 WC Plant Sciences SC Plant Sciences GA TF908 UT WOS:A1995TF90800004 PM 8528278 ER PT J AU SHEEN, J HWANG, SB NIWA, Y KOBAYASHI, H GALBRAITH, DW AF SHEEN, J HWANG, SB NIWA, Y KOBAYASHI, H GALBRAITH, DW TI GREEN-FLUORESCENT PROTEIN AS A NEW VITAL MARKER IN PLANT-CELLS SO PLANT JOURNAL LA English DT Article ID GENE FUSION; EXPRESSION; MAIZE; TRANSFORMATION; TRANSIENT AB The green-fluorescent protein (GFP) from jellyfish Aequorea victoria has been used as a convenient new vital marker in various heterologous systems. However, it has been problematic to express GFP in higher eukaryotes, especially in higher plants. This paper reports that either a strong constitutive or a heat-shock promoter can direct the expression of GFP which is easily detectable in maize mesophyll protoplasts. In this single-cell system, bright green fluorescence emitted from GFP is visible when excited with UV or blue light even in the presence of blue fluorescence from the vacuole or the red chlorophyll autofluorescence from chloroplasts using a fluorescence microscope. No exogenous substrate, co-factor, or other gene product is required. GFP is very stable in plant cells and shows little photobleaching. Viable cells can be obtained after fluorescence-activated cell sorting based on GFP. The paper further reports that GFP can be detected in intact tissues after delivering the constructs into Arabidopsis leaf and root by microprojectile bombardment. The successful detection of GFP in plant cells relies on the use of a universal transcription enhancer from maize or the translation enhancer from tobacco mosaic virus (TMV) to boost the expression. This new reporter could be used to monitor gene expression, signal transduction, co-transfection, transformation, protein trafficking and localization, protein-protein interaction, cell separation and purification, and cell lineage in higher plants. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. UNIV SHIZUOKA,SCH FOOD & NUTR SCI,YADA,SHIZUOKA 422,JAPAN. UNIV ARIZONA,DEPT PLANT SCI,TUCSON,AZ 85721. RP SHEEN, J (reprint author), MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114, USA. RI Kobayashi, Hirokazu/E-7903-2010 OI Kobayashi, Hirokazu/0000-0002-8040-0826 NR 30 TC 274 Z9 292 U1 4 U2 35 PU BLACKWELL SCIENCE LTD PI OXFORD PA OSNEY MEAD, OXFORD, OXON, ENGLAND OX2 0EL SN 0960-7412 J9 PLANT J JI Plant J. PD NOV PY 1995 VL 8 IS 5 BP 777 EP 784 DI 10.1046/j.1365-313X.1995.08050777.x PG 8 WC Plant Sciences SC Plant Sciences GA TF908 UT WOS:A1995TF90800016 PM 8528289 ER PT J AU ZIENOWICZ, RJ MAY, JW AF ZIENOWICZ, RJ MAY, JW TI HERNIA PREVENTION AND AESTHETIC CONTOURING OF THE ABDOMEN FOLLOWING TRAM FLAP BREAST RECONSTRUCTION BY THE USE OF POLYPROPYLENE MESH SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID ABDOMINIS MYOCUTANEOUS FLAP; WALL WEAKNESS; STRATEGIES AB The value of synthetic mesh use in the treatment of recurrent abdominal hernias is well recognized and has led to its advocacy by some authors as an adjunct in primary hernia repair. Mesh use in the donor-site closure associated with TRAM flap reconstruction is typically restricted to situations where undue tension or questionable tissue integrity may be predisposing factors to herniation. Although more liberal use of mesh has been advocated for these circumstances, fear of mesh complications may continue to restrict its use. We present a series of 65 consecutive patients who had routine mesh application to fascial closures following TRAM flap breast reconstruction. The use of mesh provides an added margin of strength to fascial reconstruction and was found to have additional benefit as a technical adjunct to the aesthetic aspects of the abdominoplasty. Mean patient follow-up was 56.4 months. The resulting rates of hernia (1.5 percent) and mesh-related infection (1.5 percent) demonstrate its considerable safety. We recommend consideration of polypropylene mesh use for improved strength and aesthetic quality of the donor-site closure following TRAM flap breast reconstruction. C1 MASSACHUSETTS GEN HOSP,DIV PLAST SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RHODE ISL HOSP,DEPT PLAST SURG,PROVIDENCE,RI 02902. BROWN UNIV,PROVIDENCE,RI 02912. NR 16 TC 55 Z9 55 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 NOV PY 1995 VL 96 IS 6 BP 1346 EP 1350 DI 10.1097/00006534-199511000-00017 PG 5 WC Surgery SC Surgery GA TC736 UT WOS:A1995TC73600017 PM 7480232 ER PT J AU PAIGE, KT CIMA, LG YAREMCHUK, MJ VACANTI, JP VACANTI, CA AF PAIGE, KT CIMA, LG YAREMCHUK, MJ VACANTI, JP VACANTI, CA TI INJECTABLE CARTILAGE SO PLASTIC AND RECONSTRUCTIVE SURGERY LA English DT Article ID CHONDROCYTES; POLYMERS AB Slowly polymerizing calcium alginate gels were investigated as a means of delivering large numbers of isolated chondrocytes by means of injection to determine if these gels would promote engraftment and could provide three-dimensional templates for new cartilage growth. Chondrocytes isolated from the articular surface of calf forelimbs were added to a 1% sodium alginate dissolved in a 0.1 M potassium phosphate buffer solution (pH 7.4) to generate a final cellular density of 10 X 10(6)/ml (representing approximately 10 percent of the cellular density of human juvenile articular cartilage). The calcium alginate-chondrocyte mixture was injected through a 22-gauge needle in 100-mu l aliquots under the panniculus carnosus on the dorsum of nude mice and incubated for 6 (n = 4), 8 (n = 11), and 12 (n = 12) weeks in vivo. Time-zero specimens (n = 10) consisting of 100-mu l aliquots of the calcium alginate-chondrocyte mixture it ere used to calculate initial weight. At harvest, all. calcium alginate-chondrocyte specimens exhibited a pearly opalescence and were firm to palpation as early as 6 weeks after injection. By 12 weeks of in vivo incubation, the specimens weighed 0.15 +/- 0.04 gm, significantly more than the initial weight of 0.11 +/- 0.01 gm (p < 0.05). Specimens stained with hematoxylin and eosin demonstrated lacunae within a basophilic ground-glass substance. Control specimens of calcium alginate without chondrocytes (n = 4) had a doughy consistency 12 weeks after injection and had no histologic evidence of cartilage formation. This study demonstrates that an injectable calcium alginate matrix can provide a three-dimensional scaffold for the successful transplantation and engraftment of chondrocytes. This technique holds the promise of a minimally invasive means of delivering autogenous cartilage to correct or reconstruct facial contour deficiencies. C1 CHILDRENS HOSP,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,CAMBRIDGE,MA 02139. NR 13 TC 138 Z9 163 U1 0 U2 9 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 NOV PY 1995 VL 96 IS 6 BP 1390 EP 1398 DI 10.1097/00006534-199511000-00024 PG 9 WC Surgery SC Surgery GA TC736 UT WOS:A1995TC73600024 PM 7480239 ER PT J AU HUNT, N STERN, TA AF HUNT, N STERN, TA TI THE ASSOCIATION BETWEEN INTRAVENOUS HALOPERIDOL AND TORSADES-DE-POINTES - 3 CASES AND A LITERATURE-REVIEW SO PSYCHOSOMATICS LA English DT Review ID Q-T PROLONGATION; ACUTE MYOCARDIAL-INFARCTION; DE-POINTES; VENTRICULAR-TACHYCARDIA; CARDIAC-ARRHYTHMIA; TERFENADINE USE; THERAPY; TACHYARRHYTHMIA; MANAGEMENT; MECHANISM AB Torsades de Pointes (TDP) is a potentially malignant ventricular arrhythmia that often has a drug-induced origin. Oral, but not intravenous, haloperidol has been generally associated with this arrhythmia. The authors detail three patient cases of TDP that occurred while the patients were receiving intravenous haloperidol. The authors discuss the known risk factors for the development of TDP and review the literature on ventricular arrhythmias associated with haloperidol use. C1 MED UNIV S CAROLINA,DEPT PSYCHIAT & BEHAV SCI,CHARLESTON,SC 29425. MASSACHUSETTS GEN HOSP,PSYCHIAT CONSULTAT SERV,BOSTON,MA 02114. RP HUNT, N (reprint author), MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,FRUIT ST,WARREN BLDG,ROOM 605,BOSTON,MA 02114, USA. NR 55 TC 81 Z9 84 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 NOV-DEC PY 1995 VL 36 IS 6 BP 541 EP 549 PG 9 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900004 PM 7501784 ER PT J AU LABBATE, LA FAVA, M OLESHANSKY, M ZOLTEC, J LITTMAN, A HARIG, P AF LABBATE, LA FAVA, M OLESHANSKY, M ZOLTEC, J LITTMAN, A HARIG, P TI PHYSICAL-FITNESS AND PERCEIVED STRESS - RELATIONSHIPS WITH CORONARY-ARTERY DISEASE RISK-FACTORS SO PSYCHOSOMATICS LA English DT Article ID ISCHEMIC HEART-DISEASE; PSYCHOLOGICAL STRESS; FOLLOW-UP; AMERICAN; MEN; MORTALITY; REDUCTION; OFFICERS AB This study evaluated the relationship between two biochemical risk factors for coronary artery disease, serum lipids and dehydroepiandrosterone-sulfate (DHEA-S), and both fitness and perceived stress among a cohort of senior male Army officers (N = 331). The participants under went a number of assessments gauging their fitness [exercise tolerance as measured by maximum ventilatory oxygen uptake (MVO(2))], psychological well-being, and biochemical cardiovascular risk factors. Perceived stress was significantly and inversely related to DHEA-S levels, even after. adjusting for age, though no relationship was found between perceived stress and serum lipids. Significant correlations were found between MVO(2) and high-density lipoprotein cholesterol and inversely between MVO(2) and triglycerides. Overall, the study's findings are generally consistent with the view that psychological stress and physical activity have opposite effects on parameters that affect cardiovascular status. C1 MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,BOSTON,MA 02114. USA,OFF SURGEON GEN,FALLS CHURCH,VA. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. USA,COLL WAR,CARLISLE,PA. RP LABBATE, LA (reprint author), WALTER REED ARMY MED CTR,DEPT PSYCHIAT,WASHINGTON,DC 20307, USA. NR 17 TC 24 Z9 24 U1 1 U2 2 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1995 VL 36 IS 6 BP 555 EP 560 PG 6 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900006 PM 7501786 ER PT J AU HIBBERD, PL SURMAN, OS BASS, M TOLKOFFRUBIN, NE COSIMI, AB SCHOOLEY, RT DORAN, M DELVECCHIO, A ROSAL, M RUBIN, R AF HIBBERD, PL SURMAN, OS BASS, M TOLKOFFRUBIN, NE COSIMI, AB SCHOOLEY, RT DORAN, M DELVECCHIO, A ROSAL, M RUBIN, R TI PSYCHIATRIC DISEASE AND CYTOMEGALOVIRUS VIREMIA IN RENAL-TRANSPLANT RECIPIENTS SO PSYCHOSOMATICS LA English DT Article; Proceedings Paper CT Conference on Psychiatric, Psychosocial, and Ethical Issues in Organ Transplantation CY MAY 28, 1992 CL UNIV PITTSBURGH, PITTSBURGH, PA HO UNIV PITTSBURGH AB Although cytomegalovirus (CMV) is rarely cultured from peripheral-blood leukocytes of immunocompetent patients, it may be cultured from up to 60% of renal transplant recipients, 1 to 4 months after transplantation. During this same period, renal transplant recipients are often referred for psychiatric evaluation. Since CMV may infect the central nervous system, the relationship between isolation of CMV from peripheral-blood leukocytes (viremia) and psychiatric evaluation was investigated in 80 renal allograft recipients at the Massachusetts General Hospital. Five of 16 (31%) patients with viremia and 7 of 64 (11%) patients without viremia required psychiatric consultation (P = 0.04, two-tailed Fisher exact test). CMV viremia may be an important but treatable contributor. to psychiatric symptoms in the transplant recipient. C1 MASSACHUSETTS GEN HOSP,DEPT MED,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT PSYCHIAT,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT SURG,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 7 TC 2 Z9 3 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 NOV-DEC PY 1995 VL 36 IS 6 BP 561 EP 563 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900007 PM 7501787 ER PT J AU FALK, WE AF FALK, WE TI DEMENTIA AND NORMAL AGING - HUPPERT,FA, BRAYNE,C, OCONNOR,DW SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP FALK, WE (reprint author), MASSACHUSETTS GEN HOSP,GERIATR NEUROBEHAV CLIN,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1995 VL 36 IS 6 BP 581 EP 583 PG 3 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900012 ER PT J AU MURRAY, GB AF MURRAY, GB TI AKATHISIA AND RESTLESS LEGS - SACHDEV,P SO PSYCHOSOMATICS LA English DT Book Review C1 HARVARD UNIV,SCH MED,BOSTON,MA. RP MURRAY, GB (reprint author), MASSACHUSETTS GEN HOSP,CONSULTAT SERV,FELLOWSHIP PROGRAM,BOSTON,MA 02114, USA. NR 1 TC 1 Z9 1 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 NOV-DEC PY 1995 VL 36 IS 6 BP 581 EP 581 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900011 ER PT J AU VIGUERA, AC AF VIGUERA, AC TI CHILD-ABUSE - MEDICAL DIAGNOSIS AND MANAGEMENT - REECE,RM SO PSYCHOSOMATICS LA English DT Book Review RP VIGUERA, AC (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 1 TC 0 Z9 0 U1 0 U2 1 PU AMER PSYCHIATRIC ASSOCIATION PI WASHINGTON PA 1400 K ST NW, WASHINGTON, DC 20005 SN 0033-3182 J9 PSYCHOSOMATICS JI Psychosomatics PD NOV-DEC PY 1995 VL 36 IS 6 BP 583 EP 583 PG 1 WC Psychiatry; Psychology SC Psychiatry; Psychology GA TC559 UT WOS:A1995TC55900013 ER PT J AU GRAHAM, LS AF GRAHAM, LS TI THE AAPM/RSNA PHYSICS TUTORIAL FOR RESIDENTS - QUALITY-CONTROL FOR SPECT SYSTEMS SO RADIOGRAPHICS LA English DT Article; Proceedings Paper CT 1994 Radiological-Society-of-North-America Scientific Assembly CY NOV 27-DEC 02, 1994 CL CHICAGO, IL SP Radiol Soc N Amer DE EMISSION CT ECT; EMISSION CT ECT, QUALITY ASSURANCE; PHYSICS; QUALITY ASSURANCE ID TOMOGRAPHY AB A comprehensive set of acceptance tests is the basis for an effective quality control program. Acceptance tests indicate whether the scintillation camera meets published specifications but should also include evaluation of certain parameters not specified by the vendor but that can seriously affect image quality. Once a camera is ''accepted,'' initial quality control tests serve as a benchmark for future measurements, Tomographic systems must be subjected to the same basic quality control program as planar cameras. Flood field images must be acquired and evaluated daily; spatial resolution must be tested once each week, Less frequently, parameters such as multiple-window spatial registration, collimator uniformity, system sensitivity, and camera ''dead time'' should be evaluated, Single photon emission computed tomographic systems require additional tests to ensure optimum performance, Center-of-rotation calibration and verification of detector registration are needed to avoid losses of spatial resolution, Flood corrections based on high-count images eliminate residual detector nonuniformities and correct for subtle collimator defects. Pixel size must be calibrated to avoid errors in attenuation correction and distortion when cardiac and brain reorientation software is used. Completed clinical studies must be checked for unacceptable patient movement and incomplete views, A quality control Program may be time-consuming, but, from the standpoint of maximum benefit to patients and confidence in clinical interpretations; there is no alternative. C1 UNIV CALIF LOS ANGELES,SCH MED,DIV BIOMED PHYS,LOS ANGELES,CA. RP GRAHAM, LS (reprint author), W LOS ANGELES VET AFFAIRS MED CTR,11301 WILSHIRE BLVD,NEUTRON THERAPY BLDG 345,LOS ANGELES,CA 90073, USA. NR 35 TC 4 Z9 5 U1 0 U2 0 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0271-5333 J9 RADIOGRAPHICS JI Radiographics PD NOV PY 1995 VL 15 IS 6 BP 1471 EP 1481 PG 11 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TF402 UT WOS:A1995TF40200021 PM 8577970 ER PT J AU KOPANS, DB AF KOPANS, DB TI MAMMOGRAPHY SCREENING AND THE CONTROVERSY CONCERNING WOMEN AGED 40 TO 49 SO RADIOLOGIC CLINICS OF NORTH AMERICA LA English DT Article ID BREAST-CANCER; DIFFERENT PERSPECTIVE; TUMOR SIZE; TRIAL; DIAGNOSIS; SURVIVAL AB The screening controversy arose from inappropriate and scientifically insupportable data analysis of the early results from the randomized, controlled trials of screening. Data were used that were inadequate for making medical recommendations by using subgroup analyses from trials that were not designed to permit subgroup analysis by age. Contrary to suggestions made by some opposed to screening women younger than the age of 50, there are no parameters such as breast density, cancer detection rate, or positive predictive value that change abruptly at age 50 or any other age. The most recent meta-analysis provides statistically significant ''proof'' that screening can reduce the death rate from breast cancer by at least 24% for women aged 40 to 49. C1 HARVARD UNIV,SCH MED,DEPT RADIOL,BOSTON,MA 02115. RP KOPANS, DB (reprint author), MASSACHUSETTS GEN HOSP,15 PARKMAN ST,SUITE 219,BOSTON,MA 02114, USA. NR 53 TC 23 Z9 23 U1 0 U2 1 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 SN 0033-8389 J9 RADIOL CLIN N AM JI Radiol. Clin. N. Am. PD NOV PY 1995 VL 33 IS 6 BP 1273 EP & PG 0 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TH661 UT WOS:A1995TH66100019 PM 7480670 ER PT J AU ROSENTHAL, DI SPRINGFIELD, DS GEBHARDT, MC ROSENBERG, AE MANKIN, HJ AF ROSENTHAL, DI SPRINGFIELD, DS GEBHARDT, MC ROSENBERG, AE MANKIN, HJ TI OSTEOID OSTEOMA - PERCUTANEOUS RADIOFREQUENCY ABLATION SO RADIOLOGY LA English DT Article DE BONE NEOPLASMS, THERAPY; INTERVENTIONAL PROCEDURES; OSTEOMA; RADIOFREQUENCY (RF) ABLATION; THERAPEUTIC RADIOLOGY ID CT GUIDANCE; RESECTION; ELECTRODE; DRILL; BONE AB PURPOSE: To evaluate a percutaneous technique for in situ destruction of osteoid osteoma. MATERIALS AND METHODS: Radiofrequency ablation was performed in 18 patients with osteoid osteoma (17 male, one female; age range, 8-42 years). Diagnosis was established by means of clinical and radiographic features and confirmed by means of needle biopsy findings. No attempt was made to remove the lesion. A small radio-frequency electrode introduced into the lesion through the biopsy track was used to produce thermal necrosis of a I-cm sphere of tissue. RESULTS: Symptoms were completely relieved in 16 (89%) of 18 patients. In one patient, a second procedure was required for pain relief. All but two patients underwent treatment as outpatients: These two were hospitalized for 1 night only. All patients resumed normal daily activities immediately. No casts or external supports were required; there were no complications. Twelve patients were followed up for more than 1 year. There were no recurrences. CONCLUSION: Radio-frequency ablation of osteoid osteoma is a promising alternative to surgery in selected patients. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT ORTHOPAED,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. RP ROSENTHAL, DI (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,32 FRUIT ST,WHITE BLDG,RM 289,BOSTON,MA 02114, USA. NR 33 TC 192 Z9 200 U1 0 U2 2 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1995 VL 197 IS 2 BP 451 EP 454 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TB336 UT WOS:A1995TB33600023 PM 7480692 ER PT J AU STEIN, B BROMLEY, B MICHLEWITZ, H MILLER, WA BENACERRAF, BR AF STEIN, B BROMLEY, B MICHLEWITZ, H MILLER, WA BENACERRAF, BR TI FETAL LIVER CALCIFICATIONS - SONOGRAPHIC APPEARANCE AND POSTNATAL OUTCOME SO RADIOLOGY LA English DT Article DE FETUS, GASTROINTESTINAL TRACT; FETUS, US; LIVER, CALCIFICATION; LIVER, INFECTION ID INFECTION AB PURPOSE: To determine the importance of intrahepatic calcifications seen sonographically in the fetus. MATERIALS AND METHODS: The authors retrospectively reviewed sonograms obtained in fetuses scanned between 16 and 40 gestational weeks in whom intrahepatic calcifications were seen. The number and character of these calcifications were determined Follow-up scans obtained in utero and after birth were also reviewed. Outcome was determined after birth. RESULTS: Thirty-three fetuses had intrahepatic calcifications at 16-38 weeks gestation. Four of the 33 fetuses died, one of which had liver calcifications as the only sonographic finding. This fetus had cytomegalovirus and was the only fetus with increasing numbers of calcifications on follow-up scans. All fetuses with isolated liver calcifications had a normal postnatal outcome (96% survival rate for fetuses with isolated intrahepatic calcifications). Of eight fetuses with additional anomalies, five lived; only two were healthy newborns. CONCLUSION: The outcome in fetuses with isolated intrahepatic calcifications is usually excellent, although viral causes must be excluded if additional findings appear. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,DEPT OBSTET & GYNECOL,BOSTON,MA 02114. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET & GYNECOL,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. NR 8 TC 18 Z9 19 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 NOV PY 1995 VL 197 IS 2 BP 489 EP 492 PG 4 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TB336 UT WOS:A1995TB33600030 PM 7480699 ER PT J AU ZIMMER, C WEISSLEDER, R POSS, K BOGDANOVA, A WRIGHT, SC ENOCHS, WS AF ZIMMER, C WEISSLEDER, R POSS, K BOGDANOVA, A WRIGHT, SC ENOCHS, WS TI MR-IMAGING OF PHAGOCYTOSIS IN EXPERIMENTAL GLIOMAS SO RADIOLOGY LA English DT Article DE BRAIN, MR; BRAIN NEOPLASMS; IRON ID GLIAL-CELLS; CULTURE AB PURPOSE: To determine whether phagocytosis can be observed in vivo in glioma cells. MATERIALS AND METHODS: Rat C6 glioma cells were studied in culture and after intracerebral implantation into 13 rats. Monocrystalline iron oxide nanoparticles (MION), a model marker of phagocytosis, was administered intravenously to tumor-bearing rats at 2-20 mg of iron per kilogram. Magnetic resonance (MR) imaging was performed at multiple time points. RESULTS: Glioma cells in culture showed uptake of MION in amounts of up to 10 ng of iron per 10(6) cells, corresponding to approximately 50,000 particles per cell. Fluorescently labeled MION was found to be located primarily in tubular lysosomes. Intracerebral gliomas showed characteristic changes in signal intensity at MR imaging that peaked 12 hours after administration of MION and lasted up to 5 days; these changes corresponded to uptake and subsequent biodegradation of MION by tumor cells. CONCLUSION: Phagocytosis of glioma cells can be detected in vivo with iron oxide-enhanced MR imaging, and this may permit accurate delineation of tumor margins. C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,MR PHARMACEUT PROGRAM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NCI NIH HHS [R01 CA 59649-02] NR 15 TC 87 Z9 88 U1 1 U2 6 PU RADIOLOGICAL SOC NORTH AMER PI EASTON PA 20TH AND NORTHAMPTON STS, EASTON, PA 18042 SN 0033-8419 J9 RADIOLOGY JI Radiology PD NOV PY 1995 VL 197 IS 2 BP 533 EP 538 PG 6 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA TB336 UT WOS:A1995TB33600038 PM 7480707 ER PT J AU HYTIROGLOU, P THUNG, SN GERBER, MA AF HYTIROGLOU, P THUNG, SN GERBER, MA TI HISTOLOGICAL CLASSIFICATION AND QUANTITATION OF THE SEVERITY OF CHRONIC HEPATITIS - KEEP IT SIMPLE SO SEMINARS IN LIVER DISEASE LA English DT Review ID CHRONIC ACTIVE HEPATITIS; CHRONIC LIVER-DISEASE; VIRAL-HEPATITIS; NOMENCLATURE C1 CUNY,MT SINAI SCH MED,LILLIAN & HENRY M STRATTON HANS POPPER DEPT PATHO,NEW YORK,NY 10021. TULANE UNIV,SCH MED,DEPT PATHOL & LAB MED,NEW ORLEANS,LA 70112. RP HYTIROGLOU, P (reprint author), BRONX VET AFFAIRS MED CTR,DEPT PATHOL & LAB MED 113,130 W KINGSBRIDGE RD,BRONX,NY 10468, USA. NR 27 TC 47 Z9 47 U1 0 U2 0 PU THIEME MEDICAL PUBL INC PI NEW YORK PA 381 PARK AVE SOUTH, NEW YORK, NY 10016 SN 0272-8087 J9 SEMIN LIVER DIS JI Semin. Liver Dis. PD NOV PY 1995 VL 15 IS 4 BP 414 EP 421 DI 10.1055/s-2007-1007291 PG 8 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA TD831 UT WOS:A1995TD83100009 PM 8578324 ER PT J AU JANICEK, MJ SHAFFER, K AF JANICEK, MJ SHAFFER, K TI SCINTIGRAPHIC AND RADIOGRAPHIC PATTERNS OF SKELETAL METASTASES IN BREAST-CANCER - VALUE OF SEQUENTIAL IMAGING IN PREDICTING OUTCOME SO SKELETAL RADIOLOGY LA English DT Article DE BREAST CANCER; SKELETAL METASTASES; BONE SCINTIGRAPHY; RADIOGRAPHY; PROGNOSIS ID LOCAL-REGIONAL RECURRENCE; BONE METASTASES; THERAPY; MASTECTOMY; FLARE AB Objective. To determine whether temporal changes in scintigraphic and bone radiographic findings have prognostic significance in patients with skeletal metastases from breast cancer. Design. Clinical information and films were retrospecitvely reviewed in 101 randomly selected patients with skeletal metastases. Images from sequential bone scans and bone radiographs were correlated with survival after detection of the metastases. Results. Time to detection of skeletal metastases and the length of time for which patients were classified as radiologically stable after development of skeletal metastases correlated with survival (r=0.843; r=0.821, respectively). Failure to develop a radiographically and scintigraphically stable pattern after treatment was associated with significantly decreased survival compared with the rest of the patients (mean survival 2.1+/-1.3 years vs 4.3+/-2.3 years; p<0.001). Scintigraphic regression of metastases was associated with significant survival benefit and longer stabilization of disease compared to all other patterns (mean survival 5.0+/-2.7 years for regressive disease vs 3.7+/-1.9 years for stable disease and 2.2+/-1.3 years for progressive disease; p<0.001). Conclusions. Sequential scintigraphic and radiographic imaging is useful in breast cancer patients not only for detection of metastases and monitoring of treatment effect, but also because these studies provide valuable prognostic information. RP JANICEK, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT RADIOL,44 BINNEY ST,BOSTON,MA 02115, USA. NR 21 TC 6 Z9 7 U1 0 U2 0 PU SPRINGER VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 SN 0364-2348 J9 SKELETAL RADIOL JI Skeletal Radiol. PD NOV PY 1995 VL 24 IS 8 BP 597 EP 600 PG 4 WC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging SC Orthopedics; Radiology, Nuclear Medicine & Medical Imaging GA TH113 UT WOS:A1995TH11300006 PM 8614859 ER PT J AU VAICKUS, L BREITMEYER, JB SCHLOSSMAN, RL ANDERSON, KC AF VAICKUS, L BREITMEYER, JB SCHLOSSMAN, RL ANDERSON, KC TI PLATELET TRANSFUSION AND ALTERNATIVES TO TRANSFUSION IN PATIENTS WITH MALIGNANCY SO STEM CELLS LA English DT Review DE PLATELETS; CYTOKINES; INTERLEUKIN 6; THROMBOCYTOPENIA; THROMBOPOIETIN ID CYTOMEGALO-VIRUS INFECTION; RECOMBINANT HUMAN INTERLEUKIN-11; BONE-MARROW TRANSPLANTATION; VERSUS-HOST DISEASE; NON-B-HEPATITIS; POSTTRANSFUSION HEPATITIS; BLOOD-DONORS; THROMBOCYTOPENIC PATIENTS; DELAYED ALLOIMMUNIZATION; HLA-ALLOIMMUNIZATION AB Platelet transfusions have long had an important role in the treatment of patients with thrombocytopenia due to disease or myelotoxic treatment or in patients with reduced platelet function, However, platelet transfusions are associated with numerous risks, both immunologic (e,g., transfusion reactions, alloimmunization, immunosuppression) and infectious (e,g,, viral, bacterial), In addition, several laboratory and clinical factors can influence post-transfusion platelet recovery, Recent technological advances have introduced the potential for using alternatives to platelet transfusions, such as cytokines or platelet substitutes, which may avoid the risks of transfusion, Platelet development from megakaryocytes is a process that is highly regulated by cytokines and animal research suggests that selected cytokines involved in this process may be useful in the treatment of thrombocytopenia, Newer developments, including the utilization of recombinant cytokines with relatively selective stimulation of platelet production (e,g., interleukin 6 [IL-6]) and the recent discovery of a megakaryocyte colony stimulating factor (thrombopoietin), represent major therapeutic opportunities in the treatment of thrombocytopenia, Platelet substitutes, e,g,, thromboerythrocytes, also show promise in the management of platelet deficiencies. C1 DANA FARBER CANC INST,BOSTON,MA 02115. RP VAICKUS, L (reprint author), SERONO LABS INC,IMMUNOL ONCOL,100 LONGWATER CIRCLE,NORWELL,MA 02061, USA. NR 86 TC 1 Z9 1 U1 0 U2 0 PU ALPHAMED PRESS PI DAYTON PA 4100 S KETTERING BLVD, DAYTON, OH 45439-2092 SN 1066-5099 J9 STEM CELLS JI Stem Cells PD NOV PY 1995 VL 13 IS 6 BP 588 EP 596 PG 9 WC Cell & Tissue Engineering; Biotechnology & Applied Microbiology; Oncology; Cell Biology; Hematology SC Cell Biology; Biotechnology & Applied Microbiology; Oncology; Hematology GA TG399 UT WOS:A1995TG39900002 PM 8590860 ER PT J AU FINKLESTEIN, SP AF FINKLESTEIN, SP TI BASIC FIBROBLAST GROWTH-FACTOR INCREASES REGIONAL CEREBRAL BLOOD-FLOW AND REDUCES INFARCT SIZE AFTER EXPERIMENTAL-ISCHEMIA IN A RAT MODEL - EDITORIAL COMMENT SO STROKE LA English DT Note RP FINKLESTEIN, SP (reprint author), MASSACHUSETTS GEN HOSP,CNS,GROWTH FACTOR RES LAB,BOSTON,MA, USA. NR 7 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0039-2499 J9 STROKE JI Stroke PD NOV PY 1995 VL 26 IS 11 BP 2158 EP 2159 PG 2 WC Clinical Neurology; Peripheral Vascular Disease SC Neurosciences & Neurology; Cardiovascular System & Cardiology GA TB623 UT WOS:A1995TB62300044 ER PT J AU CIULLA, TA TOLENTINO, F MORROW, JF DRYJA, TP AF CIULLA, TA TOLENTINO, F MORROW, JF DRYJA, TP TI VITREOUS AMYLOIDOSIS IN FAMILIAL AMYLOIDOTIC POLYNEUROPATHY - REPORT OF A CASE WITH THE VAL30MET TRANSTHYRETIN MUTATION SO SURVEY OF OPHTHALMOLOGY LA English DT Review DE AMYLOID; FAMILIAL AMYLOIDOTIC POLYNEUROPATHY; MUTATION; PREALBUMIN; TRANSTHYRETIN; VITREOUS AMYLOIDOSIS ID FINNISH HEREDITARY AMYLOIDOSIS; AMINO-ACID-SEQUENCE; CORNEAL LATTICE DYSTROPHY; PARS-PLANA VITRECTOMY; APOLIPOPROTEIN-A-I; PRE-ALBUMIN; FIBRIL PROTEIN; NONFAMILIAL AMYLOIDOSIS; CEREBRAL-HEMORRHAGE; ORBITAL AMYLOIDOSIS AB We present a clinical pathological review of vitreous amyloidosis in a case of familial amyloidotic polyneuropathy, type I. Vitreous opacification was the first manifestation of disease in the proband, who was successfully treated with vitrectomy. The eyes were obtained at autopsy after the patient died from an unrelated cause, and the histopathology is presented here. Analysis of DNA from the pathology specimen revealed the most commonly reported transthyretin mutation, Val30Met. The classification of systemic and ocular amyloidosis as well as the genetics of familial amyloidotic polyneuropathy are briefly reviewed. C1 MASSACHUSETTS EYE & EAR INFIRM,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT OPHTHALMOL,BOSTON,MA. NR 124 TC 15 Z9 17 U1 0 U2 1 PU SURVEY OPHTHALMOLOGY INC PI BROOKLINE PA 7 KENT ST SUITE 4, BROOKLINE, MA 02146 SN 0039-6257 J9 SURV OPHTHALMOL JI Surv. Ophthalmol. PD NOV-DEC PY 1995 VL 40 IS 3 BP 197 EP 206 DI 10.1016/S0039-6257(95)80026-3 PG 10 WC Ophthalmology SC Ophthalmology GA TH473 UT WOS:A1995TH47300002 PM 8599155 ER PT J AU OLEARY, MP FOWLER, FJ LENDERKING, WR BARBER, B SAGNIER, PP GUESS, HA BARRY, MJ AF OLEARY, MP FOWLER, FJ LENDERKING, WR BARBER, B SAGNIER, PP GUESS, HA BARRY, MJ TI A BRIEF MALE SEXUAL FUNCTION INVENTORY FOR UROLOGY SO UROLOGY LA English DT Article ID BENIGN PROSTATIC HYPERPLASIA; QUESTIONNAIRE; DYSFUNCTION; MEN AB Objectives. To develop a brief questionnaire to measure male sexual function. Methods. An initial set of questions was refined and reduced through cognitive testing and two serial validation studies. In each study, men were recruited from a sexual dysfunction clinic and a general medicine practice to complete the instrument. Test-retest reliabilities, internal consistencies, and construct validities were examined. Results. The final instrument covers sexual drive (two items), erection (three items), ejaculation (two items), perceptions of problems in each area (three items), and overall satisfaction (one item). Psychometric performance was generally very satisfactory, although self-assessments of ejaculate volume are problematic. Translations have been developed and pilot tested in a number of languages. Conclusions. The Brief Sexual Function Inventory may be useful for measuring male sexual function in practice and research. C1 HARVARD UNIV,SCH MED,DEPT SURG,BOSTON,MA 02115. UNIV MASSACHUSETTS,SURVEY RES CTR,BOSTON,MA 02125. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,CTR MED PRACTICES EVALUAT,BOSTON,MA 02114. PHASE V TECHNOL INC,WELLESLEY HILLS,MA. MERCK SHARP & DOHME LTD,RES LABS,BLUE BELL,PA. MERCK SHARP & DOHME LTD,RES LABS,PARIS,FRANCE. RP OLEARY, MP (reprint author), BRIGHAM & WOMENS HOSP,DIV UROL,45 FRANCIS ST,BOSTON,MA 02115, USA. FU AHRQ HHS [HS 08397] NR 23 TC 279 Z9 289 U1 3 U2 6 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0090-4295 J9 UROLOGY JI UROLOGY PD NOV PY 1995 VL 46 IS 5 BP 697 EP 706 DI 10.1016/S0090-4295(99)80304-5 PG 10 WC Urology & Nephrology SC Urology & Nephrology GA TE466 UT WOS:A1995TE46600018 PM 7495124 ER PT J AU ADAMS, JC AF ADAMS, JC TI SOUND STIMULATION INDUCES FOS-RELATED ANTIGENS IN CELLS WITH COMMON MORPHOLOGICAL PROPERTIES THROUGHOUT THE AUDITORY BRAIN-STEM SO JOURNAL OF COMPARATIVE NEUROLOGY LA English DT Article DE ONCOGENE; COCHLEAR NUCLEUS; OLIVOCOCHLEAR; INFERIOR COLLICULUS; STELLATE CELLS ID INFERIOR COLLICULUS; TRANSCRIPTION FACTORS; COCHLEAR NUCLEUS; RAT; EXPRESSION; CAT; PROJECTIONS; NEURONS; IMMUNOCYTOCHEMISTRY; IMMUNOREACTIVITY AB Cells within the auditory brainstem of cat that respond to sound by producing the transcription factor Fos or related proteins were identified by immunostaining with antisera against Fos and Zif/268. Within the cochlear nucleus, all antisera showed similar staining patterns, however, in the superior olive and inferior colliculus, staining patterns differed between antisera. Immunostained cells were characterized by their size, location, by the presence of perisomatic terminals that immunostained for glutamate decarboxylase or synaptophysin, or by electron microscopy. Most cell classes were not immunopositive. In the ventral cochlear nucleus, roughly 99% of Fos-positive cells had few perisomatic terminals. Within the superior olivary complex (SOC), the majority of immunopositive cells had few perisomatic terminals. Lateral olivocochlear cells were identified as Fos positive by their size, location, lack of perisomatic terminals, and positive costaining for acetylcholinesterase as evidenced by a novel reaction product. This report appears to be the first demonstration of these cells responding to sound stimulation. Within the inferior colliculus, bands of positive cells produced by tonal stimulation extended from the central nucleus throughout the dorsal cortex and the posterior pericentral region, a finding unexpected on the basis of previous electrophysiological recordings and anatomical studies of ascending inputs to the colliculus. Approximately 35% of Fos-positive cells in the inferior colliculus had plentiful perisomatic terminals. Results demonstrate a high degree of specificity of auditory cell types that respond to sound by producing Fos-like proteins and show that previously intractable physiological questions can be addressed by assaying for sound-induced production of these antigens. (C) 1995 Wiley-Liss, Inc. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,DEPT OTOL & LARYNGOL,BOSTON,MA 02114. FU NIDCD NIH HHS [DC00269] NR 34 TC 33 Z9 34 U1 0 U2 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC 605 THIRD AVE, NEW YORK, NY 10158-0012 SN 0021-9967 J9 J COMP NEUROL JI J. Comp. Neurol. PD OCT 30 PY 1995 VL 361 IS 4 BP 645 EP 668 DI 10.1002/cne.903610408 PG 24 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA TC357 UT WOS:A1995TC35700007 PM 8576420 ER PT J AU BAZZONI, G SHIH, DT BUCK, CA HEMLER, ME AF BAZZONI, G SHIH, DT BUCK, CA HEMLER, ME TI MONOCLONAL-ANTIBODY 9EG7 DEFINES A NOVEL BETA(1) INTEGRIN EPITOPE INDUCED BY SOLUBLE LIGAND AND MANGANESE, BUT INHIBITED BY CALCIUM SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID IIB-IIIA COMPLEX; CELL-ADHESION MOLECULE-1; PLATELET GPIIB-IIIA; FIBRONECTIN RECEPTOR; BETA-1 SUBUNIT; T-CELLS; AFFINITY MODULATION; FIBRINOGEN BINDING; CYTOPLASMIC DOMAIN; DIVALENT-CATIONS AB The monoclonal antibody 9EG7 has been previously found to recognize an epitope induced by manganese on the integrin beta(1) chain (Lenter, M., Uhlig, H., Hamann, A., Jeno, P., Imhof, B., and Vestweber, D. (1993) Proc. Natl. Acad. Sci. U.S.A. 90, 9051-9055). Here we show that treatment of beta(1) integrins with manganese or soluble integrin ligands (e.g. fibronectin and RGD peptide) induced the 9EG7 epitope. This epitope was also induced upon EGTA treatment to remove calcium, and the addition of calcium inhibited 9EG7 epitope induction by manganese or by Ligand. Further emphasizing the importance of the 9EG7 epitope, the 9EG7 antibody itself stimulated adhesion mediated by multiple beta(1) integrins, and conversely, ligands for alpha(2) beta(1), alpha(3) beta(1), alpha(4) beta(1), and alpha(5) beta(1) all stimulated 9EG7 expression. Together these results support a model whereby (i) calcium inhibits beta(1) integrin function because it prevents the appearance of a conformation favorable to ligand binding and (ii) manganese enhances beta(1) integrin function because it induces the same favorable conformation that is induced by adding Ligand, or removing calcium. Notably, other beta(1)-stimulating agents (magnesium and mAb TS2/16) did not induce 9EG7 expression unless ligand was also present. Thus, although 9EG7 may reliably detect the ligand-bound conformation of beta(1) integrins, its expression does not always correlate with integrin ''activation.'' Finally, mouse/chicken beta(1) chimeric molecules were used to map the 9EG7 epitope to beta(1) residues 495-602 within the cysteine-rich region, and antibody cross-blocking studies showed that the 9EG7 epitope is distinct from all previously defined human beta(1) epitopes. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. WISTAR INST ANAT & BIOL,PHILADELPHIA,PA 19104. FU NCI NIH HHS [CA19144]; NHLBI NIH HHS [HLB47670]; NIGMS NIH HHS [GM38903] NR 70 TC 209 Z9 210 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 OCT 27 PY 1995 VL 270 IS 43 BP 25570 EP 25577 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600045 PM 7592728 ER PT J AU NAGARAJAN, S CHESLA, S COBERN, L ANDERSON, P ZHU, C SELVARAJ, P AF NAGARAJAN, S CHESLA, S COBERN, L ANDERSON, P ZHU, C SELVARAJ, P TI LIGAND-BINDING AND PHAGOCYTOSIS BY CD16 (FC-GAMMA RECEPTOR-III) ISOFORMS - PHAGOCYTIC SIGNALING BY ASSOCIATED ZETA-SUBUNITS AND GAMMA-SUBUNITS IN CHINESE-HAMSTER OVARY CELLS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID NATURAL-KILLER-CELLS; PROTEIN TYROSINE KINASES; CULTURED HUMAN-MONOCYTES; G-MEDIATED PHAGOCYTOSIS; RIII CD16; IGG FC; HUMAN-NEUTROPHILS; STRUCTURAL SIMILARITY; T-CELLS; EXPRESSION AB CD16, the low affinity Fc gamma receptor III for IgG (Fc gamma RIII), exists as a polypeptide-anchored form (Fc gamma RIIIA or CD16A) in human natural killer cells and macrophages and as a glycosylphosphatidylinositol-anchored form (Fc gamma RIIIB or CD16B) in neutrophils. CD16A requires association of the gamma subunit of Fc epsilon RI or the zeta subunit of the TCR-CDS complex for cell surface expression. The CD16B is polymorphic and the two alleles are termed NA1 and NA2. In this study, CD16A and the two alleles of CD16B have been expressed in Chinese hamster ovary (CHO) cells and their Ligand binding and phagocytic properties analyzed. The two allelic forms of CD16B showed a similar affinity toward human IgG1. However, the NA1 allele showed approximately S-fold higher affinity for the IgG3 than the NA2 allele. Although all three forms of CD16 efficiently bound rabbit IgG-coated erythrocytes (EA), only CD16A coexpressed with the gamma subunit phagocytosed EA. The phagocytosis mediated by CD16A expressed on CHO cells was independent of divalent cations but dependent on intact microfilaments. CHO cells expressing CD16A-gamma and CD16A-zeta chimeras also phagocytosed EA. The phagocytosis was specifically inhibited by tyrphostin-23, a tyrosine kinase inhibitor. In summary, our results demonstrate that glycosylphosphatidylinositol-anchored CD16B alleles differ from CD16A in their ability to mediate phagocytosis. Furthermore, since studies with other Fc gamma Rs have shown that CHO cells lack the phagocytic pathway mediated by the cytoplasmic domain of Fc gamma Rs, the phagocytosis of EA by CHO cells stably transfected with CD16A and CD16A-subunit chimera provides an ideal system to dissect the phagocytic signaling pathways mediated by these Fc gamma R-associated subunits. C1 EMORY UNIV,SCH MED,DEPT PATHOL & LAB MED,ATLANTA,GA 30322. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. GEORGIA INST TECHNOL,SCH MECH ENGN,ATLANTA,GA 30332. RI Zhu, Cheng/A-5724-2011 FU NCI NIH HHS [CA 53595]; NIAID NIH HHS [AI30631] NR 72 TC 46 Z9 46 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 OCT 27 PY 1995 VL 270 IS 43 BP 25762 EP 25770 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB466 UT WOS:A1995TB46600075 PM 7592758 ER PT J AU SCHMAHMANN, JD PANDYA, DN AF SCHMAHMANN, JD PANDYA, DN TI PREFRONTAL CORTEX PROJECTIONS TO THE BASILAR PENS IN RHESUS-MONKEY - IMPLICATIONS FOR THE CEREBELLAR CONTRIBUTION TO HIGHER FUNCTION SO NEUROSCIENCE LETTERS LA English DT Article DE FRONTAL LOBE; PENS; CEREBELLUM; CONNECTIONS; ANATOMY; BEHAVIOR; COGNITION ID SUPERIOR TEMPORAL SULCUS; FRONTAL EYE FIELD; BASIS PONTIS; CORTICOPONTINE PROJECTION; CONNECTIONS; ORGANIZATION; THALAMUS; MACAQUE; NUCLEI AB The feedforward limb of the cerebrocerebellar system is directed largely through the corticopontine pathway. We determined the extent to which higher order corticopontine projections are derived from prefrontal associative cortices by injecting anterograde tracers into multiple prefrontal regions in rhesus monkeys. Mast prefrontopontine projections were derived from the dorsolateral and dorsomedial convexities, including areas 8A, 46 dorsal, 9, and 10; and lighter projections arose from medial and ventrolateral cortices. These findings strengthen the observation that the cerebrocerebellar system incorporates associative cerebral regions, and they enhance the notion that the cerebellum participates in the organization of cognitive function. C1 HARVARD UNIV,SCH MED,BOSTON,MA. VET HOSP,ENRM,BEDFORD,MA. HARVARD UNIV,BETH ISRAEL HOSP,NEUROL UNIT,BOSTON,MA 02215. RP SCHMAHMANN, JD (reprint author), MASSACHUSETTS GEN HOSP,DEPT NEUROL,FRUIT ST,BOSTON,MA 02114, USA. FU PHS HHS [16841] NR 34 TC 155 Z9 156 U1 1 U2 3 PU ELSEVIER SCI PUBL IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0304-3940 J9 NEUROSCI LETT JI Neurosci. Lett. PD OCT 27 PY 1995 VL 199 IS 3 BP 175 EP 178 DI 10.1016/0304-3940(95)12056-A PG 4 WC Neurosciences SC Neurosciences & Neurology GA TE691 UT WOS:A1995TE69100004 PM 8577391 ER PT J AU MENG, QC BALCELLS, E DELLITALIA, L DURAND, J OPARIL, S AF MENG, QC BALCELLS, E DELLITALIA, L DURAND, J OPARIL, S TI SENSITIVE METHOD FOR QUANTITATION OF ANGIOTENSIN-CONVERTING ENZYME (ACE) ACTIVITY IN TISSUE SO BIOCHEMICAL PHARMACOLOGY LA English DT Article DE ANGIOTENSIN-CONVERTING ENZYME; HIGH PERFORMANCE LIQUID CHROMATOGRAPHY; ANGIOTENSIN I; ANGIOTENSIN II; RENIN-ANGIOTENSIN SYSTEM ID MYOCARDIAL-INFARCTION; ASSAY; SERUM AB A novel sensitive and specific method for the measurement of tissue angiotensin-converting enzyme (ACE) activity utilizing HPLC is described. ACE activity was determined in detergent-extracted canine hearts utilizing the synthetic ACE-specific substrate hippuryl histidyl leucine (HHL), both in the presence and the absence of the site-specific inhibitor captopril. Tissue ACE activity was quantitated from the moles of hippuric acid (HA) formed, in time-fixed assays, utilizing HPLC separation of HA from HHL and UV-spectrophotometry for quantitation of HA as in the standard Cushman and Cheung assay (Cushman DW and Cheung HS, Biochem Pharmacol 20: 1637-1648, 1971). Separation of HA from HHL was performed by reverse phase HPLC on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M aqueous ammonium phosphate buffer, pH 6.8. After the standard liquid/liquid extraction procedure with ethyl acetate, HPLC analysis revealed the presence of unreacted substrate, HHL, in amounts comparable to the product of interest, HA, in the final assay; moreover, the amount of HA formed did not fall completely to zero in the presence of captopril. Regional studies of canine cardiac ACE activity utilizing the HPLC-based assay and the standard assay method showed a significantly higher ACE activity in the right ventricle compared with the left ventricle (2.37 +/- 0.7 vs 1.24 +/- 0.18 mU/g, P < 0.05 [N = 6], respectively) in the HPLC-based assay, but no difference in right and left ventricular ACE activities by the standard assay (0.25 +/- 0.08 vs 0.31 +/- 0.09 mU/g [N = 6], respectively). Kinetic studies utilizing the HPLC-based assay coupled with the use of captopril showed K-m (1.34 +/- 0.08 mM) and V-max (36.8 +/- 11.5 x 10(-10) M/min) values in agreement with those in the literature. Our results demonstrate that the application of HPLC to the standard Cushman and Cheung assay improves the sensitivity and specificity of the standard assay and enables the use of much smaller amounts (similar to 4 vs similar to 400 mg for the Cushman and Cheung assay) of tissue for ACE activity assay. C1 UNIV ALABAMA,DEPT MED,DIV CARDIOVASC DIS,VASC BIOL & HYPERTENS PROGRAM,BIRMINGHAM,AL 35294. UNIV ALABAMA,BIRMINGHAM VET AFFAIRS MED CTR,BIRMINGHAM,AL 35294. FU NHLBI NIH HHS [HL47081, HL37722, HL07457] NR 20 TC 47 Z9 47 U1 1 U2 5 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 OCT 26 PY 1995 VL 50 IS 9 BP 1445 EP 1450 DI 10.1016/0006-2952(95)02038-1 PG 6 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TG549 UT WOS:A1995TG54900017 PM 7503795 ER PT J AU POMBO, CM KEHRL, JH SANCHEZ, I KATZ, P AVRUCH, J ZON, LI WOODGETT, JR FORCE, T KYRIAKIS, JM AF POMBO, CM KEHRL, JH SANCHEZ, I KATZ, P AVRUCH, J ZON, LI WOODGETT, JR FORCE, T KYRIAKIS, JM TI ACTIVATION OF THE SAPK PATHWAY BY THE HUMAN STE20 HOMOLOG GERMINAL CENTER KINASE SO NATURE LA English DT Article AB EUKARYOTIC cells respond to different extracellular stimuli by recruiting homologous signalling pathways that use members of the MEKK, MEK and ERK families of protein kinases. The MEKK-->MEK-->ERK core pathways of Saccharomyces cerevisiae may themselves be regulated by members of the STE20 family of protein kinases(1,2). Here we report specific activation of the mammalian stress-activated protein kinase (SAPK) pathway by germinal centre kinase (GCK; ref. 3), a human STE20 homologue(3,4). SAPKs, members of the ERK family, are activated in situ by inflammatory stimuli, including tumour-necrosis factor (TNF) and interleukin-1, and phosphorylate and probably stimulate the transactivation function of c-Jun(5-7). Although GCK is found in many tissues, its expression in lymphoid follicles is restricted to the cells of the germinal centre, where it may participate in B-cell differentiation(3). Activation of the SAPK pathway by GCK illustrates further the striking, conservation of eukaryotic signalling mechanisms and defines the first physiological function of a mammalian Ste20. C1 MASSACHUSETTS GEN HOSP E,DIABET RES LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP E,CARDIOL UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. NIAID,IMMUNOREGULAT LAB,BETHESDA,MD 20892. GEORGETOWN UNIV,MED CTR,DEPT MED,WASHINGTON,DC 20007. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. CHILDRENS HOSP,DIV HEMATOL ONCOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. PRINCESS MARGARET HOSP,ONTARIO CANC INST,TORONTO,ON M4X 1K9,CANADA. RI Woodgett, Jim/F-1087-2010 OI Woodgett, Jim/0000-0003-3731-5797 NR 23 TC 198 Z9 200 U1 0 U2 5 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 26 PY 1995 VL 377 IS 6551 BP 750 EP 754 DI 10.1038/377750a0 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB469 UT WOS:A1995TB46900062 PM 7477268 ER PT J AU SWARTZ, MN AF SWARTZ, MN TI MITOCHONDRIAL TOXICITY - NEW ADVERSE DRUG EFFECTS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Editorial Material RP SWARTZ, MN (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 12 TC 55 Z9 55 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 OCT 26 PY 1995 VL 333 IS 17 BP 1146 EP 1148 DI 10.1056/NEJM199510263331710 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA TA372 UT WOS:A1995TA37200010 PM 7565955 ER PT J AU BOE, SO SODROSKI, J HELLAND, DE FARNET, CM AF BOE, SO SODROSKI, J HELLAND, DE FARNET, CM TI DNA END-JOINING IN EXTRACTS FROM HUMAN-CELLS SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article ID MAMMALIAN-CELLS; MECHANISMS; INVITRO; INTEGRATION; BREAKS AB DNA end-joining is a central feature of several DNA recombination processes. A DNA end-joining activity present in extracts prepared from cells of the human SupT1 lymphocyte cell line was characterised. Joining of blunt ends and ends having complementary single-strand extensions (SSEs) were precise with no insertion or deletion of substrate base pairs. DNA sequencing analysis showed that molecules having non complementary ends of the same polarity, or molecules having one blunt end and one end with a SSE, were joined without loss of nucleotide sequences in the double-stranded region of the substrate molecule. The joining patterns observed have several features that are consistent with DNA end-joining activities previously observed in vitro in extracts from Xenopus eggs and in vivo in mammalian cells and yeast. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HUMAN RETROVIROL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV BERGEN,BIOTECHNOL LAB,N-5020 BERGEN,NORWAY. OI Farnet, Chris/0000-0003-4927-198X FU NIAID NIH HHS [AI 24845] NR 16 TC 16 Z9 17 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD OCT 24 PY 1995 VL 215 IS 3 BP 987 EP 993 DI 10.1006/bbrc.1995.2561 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TA982 UT WOS:A1995TA98200029 PM 7488071 ER PT J AU DRYJA, TP FINN, JT PENG, YW MCGEE, TL BERSON, EL YAU, KW AF DRYJA, TP FINN, JT PENG, YW MCGEE, TL BERSON, EL YAU, KW TI MUTATIONS IN THE GENE ENCODING THE ALPHA-SUBUNIT OF THE ROD CGMP-GATED CHANNEL IN AUTOSOMAL RECESSIVE RETINITIS-PIGMENTOSA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID FUNCTIONAL EXPRESSION; CATION CHANNEL; ONE FORM; DNA; POLYMORPHISMS; SEQUENCE AB Mutations in the genes encoding two proteins of the retinal rod phototransduction cascade, opsin and the beta subunit of rod cGMP phosphodiesterase, cause retinitis pigmentosa (RP) in some families. Here we report defects in a third member of this biochemical pathway in still other patients with this disease. We screened 94 unrelated patients with autosomal dominant RP and 173 unrelated patients with autosomal recessive RP for mutations in the gene encoding the cu subunit of the rod cGMP-gated cation channel. Five mutant sequences cosegregated with disease among four unrelated families with autosomal recessive RP. Two of these were nonsense mutations early in the reading Frame (Glu76End and Lys139End) and one was a deletion encompassing most if not all of the transcriptional unit; these three alleles would not be expected to encode a functional channel. The remaining two mutations were a missense mutation (Ser316Phe) and a frameshift [Arg654(1-bp del)] mutation truncating the last 32 aa in the C terminus. The latter two mutations were expressed in vitro and found to encode proteins that were predominantly retained inside the cell instead of being targeted to the plasma membrane. We conclude that the absence or paucity of functional cGMP-gated cation channels in the plasma membrane is deleterious to rod photoreceptors and is an uncommon cause of RP. C1 HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,TAYLOR SMITH LAB,BOSTON,MA 02114. JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROSCI,BALTIMORE,MD 21205. JOHNS HOPKINS UNIV,SCH MED,HOWARD HUGHES MED INST,BALTIMORE,MD 21205. RP DRYJA, TP (reprint author), HARVARD UNIV,MASSACHUSETTS EYE & EAR INFIRM,SCH MED,BERMAN GUND LAB STUDY RETINAL DEGENERAT,BOSTON,MA 02114, USA. FU NEI NIH HHS [EY00169, EY06837, EY08683] NR 23 TC 191 Z9 193 U1 0 U2 5 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 24 PY 1995 VL 92 IS 22 BP 10177 EP 10181 DI 10.1073/pnas.92.22.10177 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TB467 UT WOS:A1995TB46700050 PM 7479749 ER PT J AU WINANDY, S WU, P GEORGOPOULOS, K AF WINANDY, S WU, P GEORGOPOULOS, K TI A DOMINANT MUTATION IN THE IKAROS GENE LEADS TO RAPID DEVELOPMENT OF LEUKEMIA AND LYMPHOMA SO CELL LA English DT Article ID MATURE T-CELLS; RETINOBLASTOMA; MICE; LYMPHOCYTES; SELECTION; GLD; REARRANGEMENT; AUTOIMMUNITY; COMMITMENT; SUICIDE AB The Ikaros gene is essential for lymphoid lineage specification. As previously reported, mice homozygous fora mutation in the Ikaros DNA-binding domain fail to generate mature lymphocytes as well as their earliest described progenitors. In addition, our studies with mice heterozygous for this mutation establish the Ikaros gene as an essential regulator of T cell proliferation. Thymocytes display augmented TCR-mediated proliferative responses, and peripheral T cells are autoproliferative. A general lymphoproliferation precedes the T cell leukemia and lymphoma that rapidly develop in all heterozygotes. The first step toward leukemic transformation occurs within the maturing thymocyte population and is demarcated by clonal expansions and loss of the single Ikaros wild-type allele. From these studies, we propose that within developing and mature T lymphocytes, distinct thresholds of Ikaros activity are required to regulate proliferation. A decrease in Ikaros activity below the first threshold causes the rapid accumulation of T lymphoblasts, whereas a further decrease leads to neoplastic transformation. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CUTANEOUS BIOL RES CTR,BOSTON,MA 02129. FU NIAID NIH HHS [R01-AI33062-02] NR 35 TC 294 Z9 297 U1 0 U2 2 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 20 PY 1995 VL 83 IS 2 BP 289 EP 299 DI 10.1016/0092-8674(95)90170-1 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TA965 UT WOS:A1995TA96500015 PM 7585946 ER PT J AU POUYANI, T SEED, B AF POUYANI, T SEED, B TI PSGL-1 RECOGNITION OF P-SELECTIN IS CONTROLLED BY A TYROSINE SULFATION CONSENSUS AT THE PSGL-1 AMINO-TERMINUS SO CELL LA English DT Article ID GRANULE MEMBRANE-PROTEIN; ENDOTHELIAL VONWILLEBRAND-FACTOR; WEIBEL-PALADE BODIES; ACTIVATED PLATELETS; NEUTROPHIL ADHESION; CELL-ADHESION; CARBOHYDRATE LIGAND; GLYCOPROTEIN LIGAND; MOLECULAR-CLONING; HOMING RECEPTOR AB P-selectin binding to neutrophils requires a specific protein, P-selectin glycoprotein ligand 1 (PSGL-1), as well as sialyl-Lewis X (sLe(x)) glycan determinants. We have found that a short segment near the amino terminus nus of PSGL-1 that contains a tyrosine sulfation consensus is essential for P-selectin adhesion and that addition of the amino-terminal segment to some but not all mucin-like molecules confers on those molecules the ability to bind P-selectin. PSGL-1 synthesized in the presence of sulfation inhibitors binds P-selectin weakly, and within the amino-terminal 20 residues, mutation of the tyrosines to phenylalanine abolishes binding. Rolling of HL-60 cells on P-selectin-coated coverslips is strongly attenuated by treatment of cells with an inhibitor of sulfation. C1 MASSACHUSETTS GEN HOSP,DEPT MOLEC BIOL,BOSTON,MA 02114. RP POUYANI, T (reprint author), HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114, USA. FU NIDDK NIH HHS [DK43031] NR 60 TC 322 Z9 329 U1 2 U2 14 PU CELL PRESS PI CAMBRIDGE PA 50 CHURCH ST CIRCULATION DEPT, CAMBRIDGE, MA 02138 SN 0092-8674 J9 CELL JI Cell PD OCT 20 PY 1995 VL 83 IS 2 BP 333 EP 343 DI 10.1016/0092-8674(95)90174-4 PG 11 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TA965 UT WOS:A1995TA96500019 PM 7585950 ER PT J AU PATTI, ME SUN, XJ BRUENING, JC ARAKI, E LIPES, MA WHITE, MF KAHN, CR AF PATTI, ME SUN, XJ BRUENING, JC ARAKI, E LIPES, MA WHITE, MF KAHN, CR TI 4PS/INSULIN RECEPTOR SUBSTRATE (IRS)-2 IS THE ALTERNATIVE SUBSTRATE OF THE INSULIN-RECEPTOR IN IRS-1-DEFICIENT MICE SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Note ID PHOSPHATIDYLINOSITOL 3-KINASE; SIGNALING COMPLEXES; INTACT-CELLS; PROTEIN; IRS-1; ASSOCIATION; RAT; PHOSPHORYLATION; 3'-KINASE; MUSCLE AB Insulin receptor substrate-1 (IRS-1) is the major cytoplasmic substrate of the insulin and insulin-like growth factor (IGF)-1 receptors. Transgenic mice lacking IRS-1 are resistant to insulin and IGF-1, but exhibit significant residual insulin action which corresponds to the presence of an alternative high molecular weight substrate in liver and muscle. Recently, Sun et al. (Sun, X.-J, Wang, L. M., Zhang, Y., Yenush, L. P., Myers, M. G., Jr., Glasheen, E., Lane, W. S., Pierce, J, H., and White, M. F. (1995) Nature 377, 173-177) purified and cloned 4PS, the major substrate of the IL-4 receptor-associated tyrosine kinase in myeloid cells, which has significant structural similarity to IRS-1. To determine if 4PS is the alternative substrate of the insulin receptor in IRS-1-deficient mice, we performed immunoprecipitation, immunoblotting, and phosphatidylinositol (PI) 3-kinase assays using specific antibodies to 4PS. Following insulin stimulation, 4PS is rapidly phosphorylated in liver and muscle, binds to the p85 subunit of PI 3-kinase, and activates the enzyme. Insulin stimulation also results in the association of 4PS with Grb 2 in both liver and muscle. In IRS-1-deficient mice, both the phosphorylation of 4PS and associated PI 3-kinase activity are enhanced, without an increase in protein expression. Immunodepletion of 4PS from liver and muscle homogenates removes most of the phosphotyrosine-associated PI 3-kinase activity in IRS-1-deficient mice. Thus, 4PS is the primary alternative substrate, i.e. IRS-2, which plays a major role in physiologic insulin signal transduction via both PI 3-kinase activation and Grb 2/Sos association. In IRS-1-deficient mice, 4PS/IRS 2 provides signal transduction to these two major pathways of insulin signaling. C1 HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,DIV RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. FU NIDDK NIH HHS [DK33201, DK43808] NR 33 TC 180 Z9 181 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 OCT 20 PY 1995 VL 270 IS 42 BP 24670 EP 24673 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500013 PM 7559579 ER PT J AU RODRIGUEZ, CG CUNDELL, DR TUOMANEN, EI KOLAKOWSKI, LF GERARD, C GERARD, NP AF RODRIGUEZ, CG CUNDELL, DR TUOMANEN, EI KOLAKOWSKI, LF GERARD, C GERARD, NP TI THE ROLE OF N-GLYCOSYLATION FOR FUNCTIONAL EXPRESSION OF THE HUMAN PLATELET-ACTIVATING-FACTOR RECEPTOR - GLYCOSYLATION IS REQUIRED FOR EFFICIENT MEMBRANE TRAFFICKING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID SIGNAL TRANSDUCTION; ADRENERGIC-RECEPTOR; RABBIT PLATELET; HORMONE-BINDING; CLONING; PROTEIN; SITES; CELLS; LEUKOCYTES; ANTIGEN AB Streptococcus pneumoniae has been shown to utilize the platelet activating factor receptor for binding and invasion of host cells (Cundell, D. R., Gerard, N. P., Gerard, C., Idanpaan-Heikkila, I., and Tuomanen, E. I. (1995) Nature, in press). Because bacterial binding is in part carbohydrate dependent, and the human platelet activating factor (PAF) receptor bears a single N-linked glycosylation sequence in the second extracellular loop, we undertook studies to determine the role of this epitope in PAF receptor function. Binding of pneumococci to COS cells transfected with the human PAF receptor is greatly reduced for a receptor mutant that bears no N-linked glycosylation site. Immunohistochemical and binding analyses show decreased expression of the non-glycosylated molecule on the cell membrane relative to the wild type receptor; however, metabolic labeling and immunopurification indicate it is synthesized intracellularly at a level similar to the native molecule. A mutant receptor encoding a functional glycosylation site at the NH2 terminus is better expressed at the cell surface compared with the non-glycosylated form, indicating that trafficking to the cell surface is facilitated by glycosylation, but its location is relatively unimportant. The binding affinity for PAF is not significantly effected by the presence or location of the carbohydrate, and variations in cell surface expression have little influence on signal transduction, as the nonglycosylated PAF receptor is equally effective for activation of phospholipase C as the native molecule. These data are supportive of pneumococcal binding on protein moiety(ies) of the PAF receptor and indicate that N-glycosylation facilitates expression of the protein on the cell membrane. C1 HARVARD UNIV,BETH ISRAEL HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,CHILDRENS HOSP,SCH MED,INA SUE PERLMUTTER LAB,BOSTON,MA 02215. HARVARD UNIV,CHILDRENS HOSP,SCH MED,DEPT PEDIAT,BOSTON,MA 02215. HARVARD UNIV,WOMENS HOSP,SCH MED,BOSTON,MA 02215. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02215. HARVARD UNIV,SCH MED,THORNDIKE LAB,BOSTON,MA 02215. ROCKEFELLER UNIV,MOLEC INFECT DIS LAB,NEW YORK,NY 10021. NR 39 TC 33 Z9 34 U1 0 U2 0 PU AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 SN 0021-9258 J9 J BIOL CHEM JI J. Biol. Chem. PD OCT 20 PY 1995 VL 270 IS 42 BP 25178 EP 25184 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TB465 UT WOS:A1995TB46500087 ER PT J AU PACKARD, BZ LEE, SS REMOLDODONNELL, E KOMORIYA, A AF PACKARD, BZ LEE, SS REMOLDODONNELL, E KOMORIYA, A TI A SERPIN FROM HUMAN TUMOR-CELLS WITH DIRECT LYMPHOID IMMUNOMODULATORY ACTIVITY - MITOGENIC STIMULATION OF HUMAN TUMOR-INFILTRATING LYMPHOCYTES SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article DE TUMOR-INFILTRATING LYMPHOCYTE; SERPIN; IMMUNOTHERAPY; IMMUNOSURVEILLANCE; CANCER; (HUMAN) ID ELASTASE INHIBITOR; CARCINOMA ANTIGEN; CRYSTAL-STRUCTURE; REACTIVE CENTER; OVALBUMIN; CANCER AB A serum-free supernatant from an epidermal carcinoma cell line has previously been shown to contain mitogenic activity for human tumor infiltrating lymphocytes in culture [1]. From this conditioned medium we have now purified to homogeneity, as determined by SDS-PAGE analysis, a ca. 45 kDa protein which stimulates [H-3]thymidine incorporation into the DNA of these human T-lymphocytes, Amino acid composition data and immunoreactivity of the purified protein as well as sequence analyses of 7 tryptic fragments obtained therefrom suggest a strong similarity with human monocyte/neutrophil elastase inhibitor, which is a member of the serine protease inhibitor (serpin) superfamily, We have previously identified and purified from the same conditioned medium a 36 kDa protein with myeloid immunomodulatory activity [2]. Taken together, these two reports support the role of tumor-derived soluble factors in tumor immunosurveillance. C1 US FDA,CBER,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PEDIAT,BOSTON,MA 02115. RP PACKARD, BZ (reprint author), ONCOLUMMUNIN INC,335 PAINT BRANCH DR,COLLEGE PK,MD 20742, USA. FU NHLBI NIH HHS [HL41579] NR 44 TC 10 Z9 11 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4889 J9 BBA-MOL CELL RES JI Biochim. Biophys. Acta-Mol. Cell Res. PD OCT 19 PY 1995 VL 1269 IS 1 BP 41 EP 50 DI 10.1016/0167-4889(95)00113-7 PG 10 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TB499 UT WOS:A1995TB49900007 PM 7578269 ER PT J AU MILLER, JB AF MILLER, JB TI DEVELOPMENTAL BIOLOGY - MAKING ONE-CELL FROM 2 SO NATURE LA English DT Editorial Material ID FUSION; MYOTUBES; PROTEIN RP MILLER, JB (reprint author), MASSACHUSETTS GEN HOSP,NEUROMUSCULAR LAB,BOSTON,MA 02129, USA. NR 17 TC 6 Z9 6 U1 0 U2 1 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 19 PY 1995 VL 377 IS 6550 BP 575 EP 576 DI 10.1038/377575a0 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TA275 UT WOS:A1995TA27500024 PM 7566164 ER PT J AU BORIES, JC WILLERFORD, DM GREVIN, D DAVIDSON, L CAMUS, A MARTIN, P STEHELIN, D ALT, FW AF BORIES, JC WILLERFORD, DM GREVIN, D DAVIDSON, L CAMUS, A MARTIN, P STEHELIN, D ALT, FW TI INCREASED T-CELL APOPTOSIS AND TERMINAL B-CELL DIFFERENTIATION-INDUCED BY INACTIVATION OF THE ETS-1 PROTOONCOGENE SO NATURE LA English DT Article ID DNA-BINDING; TRANSCRIPTION FACTORS; GENE ENHANCER; MICE; ACTIVATION; THYMOCYTES; SEQUENCE AB THE Ets-1 proto-oncogene is a member of a transcription factor family characterized by homology to the v-ets oncogene(1-4). In adult mice, Ets-1 is expressed predominantly in lymphoid cells where it has been implicated in regulating transcription of lymphocyte-specific genes(5-7). Following T-cell activation, the specific DNA binding activity of Ets-1 is inactivated by transient phosphorylation, suggesting a function in the transition from the resting to activated state(8,9). Ets-1 has also been suggested to cooperate with the AP-1 transcription factor complex to mediate cellular growth factor responses(4). Here we show, by using RAG-2-deficient blastocyst complementation(10), that Ets-1 deficiency has dramatic, but different, effects on development and function of T- and B-lineage cells, Ets-1-deficient T cells were present in reduced numbers and were highly susceptible to cell death in vitro. In contrast, Ets-1-deficient B cells were present in normal numbers but a large proportion were IgM plasma cells, Our data demonstrate that Ets-1 is essential for maintenance of the normal pool of resting T- and B-lineage cells. C1 HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02115. CTR BLOOD RES,BOSTON,MA 02115. HOP ST LOUIS,INSERM,U93,F-75475 PARIS,FRANCE. INST PASTEUR,MOLEC ONCOL LAB,CNRS,URA 1160,F-59019 LILLE,FRANCE. INST PASTEUR,UNITE BIOL DEV,CNRS,URA 1960,F-75724 PARIS,FRANCE. RP BORIES, JC (reprint author), CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115, USA. RI Camus, Anne/P-1515-2014 NR 24 TC 238 Z9 245 U1 1 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 19 PY 1995 VL 377 IS 6550 BP 635 EP 638 DI 10.1038/377635a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA TA275 UT WOS:A1995TA27500054 PM 7566176 ER PT J AU BRUGGE, WR MARK, EJ SHEPARD, JAO PODOLSKY, DK MONCURE, AC AF BRUGGE, WR MARK, EJ SHEPARD, JAO PODOLSKY, DK MONCURE, AC TI A 78-YEAR-OLD WOMAN WITH INCREASING DYSPHAGIA AND ODYNOPHAGIA - CROHNS-DISEASE OF THE ESOPHAGUS SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Discussion ID BARRETTS ESOPHAGUS; ADENOCARCINOMA; TUBERCULOSIS; LYMPHOMA; LESIONS; MUCOSA C1 HARVARD UNIV,SCH MED,CAMBRIDGE,MA 02138. RP BRUGGE, WR (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 31 TC 1 Z9 1 U1 0 U2 0 PU MASS MEDICAL SOC PI BOSTON PA 10 SHATTUCK, BOSTON, MA 02115 SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD OCT 19 PY 1995 VL 333 IS 16 BP 1066 EP 1072 PG 7 WC Medicine, General & Internal SC General & Internal Medicine GA RZ340 UT WOS:A1995RZ34000008 ER PT J AU YAO, R COOPER, GM AF YAO, R COOPER, GM TI REGULATION OF THE RAS SIGNALING PATHWAY BY GTPASE-ACTIVATING PROTEIN IN PC12 CELLS SO ONCOGENE LA English DT Article DE RAS; GAP; PC12 CELLS ID NERVE GROWTH-FACTOR; NIH 3T3 CELLS; MAP KINASE; SACCHAROMYCES-CEREVISIAE; COMPLEX-FORMATION; THREONINE KINASE; MAMMALIAN-CELLS; FACTOR RECEPTOR; GENE-PRODUCT; HA-RAS AB We have investigated the role of Pas GTPase-activating protein (GAP) in NGF-induced neuronal differentiation by overexpressing both wild-type and membrane-targeted GAP in PC12 cells. Extension of neurites in response to NGF was completely blocked in cells expressing the highest level of membrane-targeted GAP and significantly inhibited in cells expressing either wild-type GAP or lower levels of membrane-targeted GAP. Overexpression of membrane-targeted GAP similarly inhibited induction of differentiation by src, but not by ras or raf oncogenes, indicating that GAP inhibits differentiation of PC12 cells by downregulating Ras function. GAP overexpression also inhibited stimulation of mitogen-activated protein (MAP) kinase and induction of immediate-early genes in response to NGF. In cells expressing wild-type GAP or lower levels of membrane-targeted GAP, the initial activation of MAP kinase and immediate-early gene expression were only partially inhibited. However, GAP expression in these cells resulted in substantial inhibition of sustained MAP kinase activity following NGF treatment, consistent with the inhibition of neurite extension in these cell lines. These results indicate that GAP acts as a negative regulation, rather than an effector, of Ras signaling in PC12 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 [CA18689] NR 58 TC 18 Z9 19 U1 0 U2 1 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 19 PY 1995 VL 11 IS 8 BP 1607 EP 1614 PG 8 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA TC535 UT WOS:A1995TC53500019 PM 7478585 ER PT J AU NI, RZ TOMITA, Y TOKUNAGA, F LIANG, TJ NODA, C ICHIHARA, A TANAKA, K AF NI, RZ TOMITA, Y TOKUNAGA, F LIANG, TJ NODA, C ICHIHARA, A TANAKA, K TI MOLECULAR-CLONING OF 2 TYPES OF CDNA-ENCODING SUBUNIT RC6-I OF RAT PROTEASOMES SO BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION LA English DT Article DE CDNA CLONING; MULTICATALYTIC PROTEINASE COMPLEX; PROTEASOME; SUBUNIT RC6-I ID MULTICATALYTIC PROTEINASE; HEPATOMA-CELLS; COMPONENT; LIVER; ACID; COMPLEXES; SEQUENCE AB A new subunit. named RC6-I, of the rat 20 S proteasome was purified and the partial amino acid sequences of several peptide fragments obtained by digestion with lysyl-endopeptidase were determined by Edman degradation. Amplification of cDNAs encoding RC6-I by the polymerase chain reaction (PCR) technique revealed two types of cDNA, tentatively designated as RC6-IL and RC6-IS in order of size. The nucleotide sequences of the two cDNAs are identical except that RC6-IL contains an insertion of Is nucleotides in the coding region compared with RC6-IS. The polypeptide predicted from the open reading frame of RC6-IS cDNA consists of 248 amino acid residues with a calculated molecular weight of 27 783. These values are consistent with those obtained by protein chemical analyses. Computer-assisted homology analysis showed that RC6-I belongs to the alpha-type subfamily of the proteasome gene family, which shows similarity to the alpha-subunit of the archaebacterium Thermoplasma acidophilum proteasome, and that the 18 nucleotide insert, encoding six amino acid residues, VVASVS, appears to be unique to RC6-IL, because this motif has not been conserved in any other alpha-type subunit. By reverse transcription (RT)-PCR analysis, the mRNAs for both RC6-IL, and RC6-IS were found in all the rat tissues examined. These results suggest that proteasomes are present as a heterogeneous population, possibly for acquisition of diversity of functions. C1 UNIV TOKUSHIMA,INST ENZYME RES,TOKUSHIMA 770,JAPAN. HIMEJI INST TECHNOL,FAC SCI,HIMEJI,HYOGO 67812,JAPAN. MASSACHUSETTS GEN HOSP,DEPT MED,GI UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. NR 26 TC 13 Z9 14 U1 0 U2 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-4781 J9 BBA-GENE STRUCT EXPR JI Biochim. Biophys. Acta-Gene Struct. Expression PD OCT 17 PY 1995 VL 1264 IS 1 BP 45 EP 52 DI 10.1016/0167-4781(95)00113-U PG 8 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA TB191 UT WOS:A1995TB19100011 PM 7578256 ER PT J AU WALD, TG SHULT, P KRAUSE, P MILLER, BA DRINKA, P GRAVENSTEIN, S AF WALD, TG SHULT, P KRAUSE, P MILLER, BA DRINKA, P GRAVENSTEIN, S TI A RHINOVIRUS OUTBREAK AMONG RESIDENTS OF A LONG-TERM-CARE FACILITY SO ANNALS OF INTERNAL MEDICINE LA English DT Article DE RHINOVIRUS; NURSING HOMES; RESPIRATORY TRACT INFECTIONS; DISEASE OUTBREAKS; LUNG DISEASES, OBSTRUCTIVE ID ILLNESS; INFECTIONS; PRECIPITANTS; VIRUSES; ASTHMA AB Objective: To describe the epidemiology of and clinical findings associated with a rhinovirus outbreak that occurred among institutionalized elderly persons. Design: Retrospective review of medical records and nursing surveillance reports. Setting: A 685-bed, long-term care facility for veterans and their spouses. Patients: 33 persons from whom rhinovirus was cultured. Measurements: Throat and nasopharyngeal virus culture; review of medical records to determine under-lying diseases, signs and symptoms of respiratory illness, illness duration, and interventions during illness; and review of nursing surveillance reports to determine room locations of ill persons. Results: Between 14 August and 2 September 1993, the number of respiratory illnesses increased. Throat and nasopharyngeal virus cultures were taken from 67 ill residents; 33 cultures yielded rhinovirus, and no other respiratory virus was isolated. Geographic clustering of persons infected with rhinovirus was observed. Of those persons with rhinovirus infections, 100% had upper respiratory symptoms, 34% had gastrointestinal symptoms, 71% had systemic symptoms, 66% had lower respiratory symptoms (including productive cough), and 52% had new abnormalities on lung auscultation. The 17 persons with rhinovirus infection who had chronic obstructive pulmonary disease had more severe illnesses: Five (29%) required glucocorticoid or bronchodilator therapy for illness-associated bronchospasm; 2 required transfer out of the facility; 1 developed a radiographically documented infiltrate; and 1 died of respiratory failure. Conclusions: Rhinovirus may cause epidemic, clinically important respiratory illness in nursing home residents. A large proportion of residents may become ill, and infection may be severe in persons with underlying lung disease. C1 UNIV WISCONSIN,SCH MED,INST AGING,MADISON,WI 53706. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. UNIV WISCONSIN,WISCONSIN STATE LAB HYG,MADISON,WI 53706. WISCONSIN VET HOME,KING,WI 54946. RI Gravenstein, Stefan/G-1681-2011 FU NIA NIH HHS [AG00548, AG09632, AG00213] NR 18 TC 68 Z9 68 U1 0 U2 1 PU AMER COLL PHYSICIANS PI PHILADELPHIA PA INDEPENDENCE MALL WEST 6TH AND RACE ST, PHILADELPHIA, PA 19106-1572 SN 0003-4819 J9 ANN INTERN MED JI Ann. Intern. Med. PD OCT 15 PY 1995 VL 123 IS 8 BP 588 EP 593 PG 6 WC Medicine, General & Internal SC General & Internal Medicine GA RY828 UT WOS:A1995RY82800004 PM 7677299 ER PT J AU FINE, HA AF FINE, HA TI TREATMENT OF PRIMARY CENTRAL-NERVOUS-SYSTEM LYMPHOMA - STILL MORE QUESTIONS THAN ANSWERS SO BLOOD LA English DT Editorial Material ID HIGH-DOSE METHOTREXATE; NON-HODGKINS-LYMPHOMA; PRIMARY CNS LYMPHOMA; SURVIVAL; BRAIN; THERAPY RP FINE, HA (reprint author), HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,DIV CANC PHARMACOL,BOSTON,MA 02115, USA. NR 16 TC 28 Z9 28 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 OCT 15 PY 1995 VL 86 IS 8 BP 2873 EP 2875 PG 3 WC Hematology SC Hematology GA RZ071 UT WOS:A1995RZ07100001 PM 7579377 ER PT J AU NICHOLS, KE RE, GG YAN, YX GARVIN, AJ HABER, DA AF NICHOLS, KE RE, GG YAN, YX GARVIN, AJ HABER, DA TI WT1 INDUCES EXPRESSION OF INSULIN-LIKE GROWTH-FACTOR-2 IN WILMS-TUMOR CELLS SO CANCER RESEARCH LA English DT Note ID FACTOR-A-CHAIN; GENE-PRODUCT; PROMOTER ACTIVITY; SUPPRESSOR WT1; LOCUS; TRANSCRIPTION; REPRESSION; DELETION AB The Wilms' tumor suppressor gene WT1 encodes a zinc finger transcription factor, whose expression inhibits the growth of the RM1 Wilms' tumor cell line, Transient transfection of WT1 constructs into 3T3 or 293 cells results in transcriptional repression of a number of cotransfected promoters containing the early growth response gene 1 consensus sequence, We now show that WT1 has properties of a transcriptional activator in RM1 cells, an effect that may be associated with the presence of a mutated p53 gene in these cells. Stable transfection of wild-type WT1 into RM1 cells results in induction of endogenous insulin-like growth factor 2 (IGF2) but not of other previously postulated WT1-target genes. The induction of IGF2 is dramatically enhanced by WT1 mutants encoding an altered transactivation domain. We conclude that IGF2 is a potentially physiological target gene for WT1 and that its induction may contribute to the growth-stimulating effects of WT1 variants. C1 MASSACHUSETTS GEN HOSP,CTR CANC,GENET MOLEC LAB,BOSTON,MA 02129. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29425. FU NCI NIH HHS [CA 58596, CA 37887] NR 24 TC 37 Z9 38 U1 0 U2 1 PU AMER ASSOC CANCER RESEARCH PI PHILADELPHIA PA PUBLIC LEDGER BLDG, SUITE 816, 150 S. INDEPENDENCE MALL W., PHILADELPHIA, PA 19106 SN 0008-5472 J9 CANCER RES JI Cancer Res. PD OCT 15 PY 1995 VL 55 IS 20 BP 4540 EP 4543 PG 4 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900010 PM 7553624 ER PT J AU BAXTER, LT ZHU, H MACKENSEN, DG BUTLER, WF JAIN, RK AF BAXTER, LT ZHU, H MACKENSEN, DG BUTLER, WF JAIN, RK TI BIODISTRIBUTION OF MONOCLONAL-ANTIBODIES - SCALE-UP FROM MOUSE TO HUMAN USING A PHYSIOLOGICALLY-BASED PHARMACOKINETIC MODEL SO CANCER RESEARCH LA English DT Article ID B-CELL LYMPHOMA; INTERSTITIAL HYPERTENSION; MICROVASCULAR PERMEABILITY; NEOPLASTIC TISSUES; DELIVERY SYSTEM; NATURES POISONS; CANCER-THERAPY; TUMORS; TRANSPORT; MACROMOLECULES AB The efficacy of a novel diagnostic or therapeutic agent depends on its selective localization in a target tissue, Biodistribution studies are expensive and difficult to carry out in humans, but such data can be obtained easily in rodents. We have developed a physiologically based pharmacokinetic model for scaling up data from mice to humans, the first such model for genetically engineered macromolecules that bind to their targets in vivo, such as mAbs, The mathematical model uses physiological parameters including organ volumes, blood flow rates, and vascular permeabilities; the compartments (organs) are connected anatomically, This allows the use of scale-up techniques to predict antibody distribution in humans. The model was tested with data obtained in human patients for the biodistribution of a mAb against carcinoembryonic antigen. The model was further tested for a two-step protocol: bifunctional antibodies and radiolabeled hapten, which compared favorably with data in both mice and humans. The model was useful for optimization of treatment parameters, such as dose and time interval of injections, binding affinities, and choice of molecular carrier, This framework may be applicable to other genetically engineered molecules (e.g., growth factors, antisense oligonucleotides, and gene-carrying vectors). C1 HARVARD UNIV, SCH MED, BOSTON, MA 02114 USA. MIT, RADIOL SCI PROGRAM, CAMBRIDGE, MA 02139 USA. HYBRITECH INC, SAN DIEGO, CA 92121 USA. RP BAXTER, LT (reprint author), MASSACHUSETTS GEN HOSP, DEPT RADIAT ONCOL, STEELE LAB, BOSTON, MA 02114 USA. FU NCI NIH HHS [R35-CA-56591] NR 58 TC 108 Z9 110 U1 2 U2 10 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 OCT 15 PY 1995 VL 55 IS 20 BP 4611 EP 4622 PG 12 WC Oncology SC Oncology GA RZ069 UT WOS:A1995RZ06900024 PM 7553638 ER PT J AU ZHANG, CH ROBERTSON, MJ SCHLOSSMAN, SF AF ZHANG, CH ROBERTSON, MJ SCHLOSSMAN, SF TI A TRIPLET OF NUCLEASE PROTEINS (NP(42-50)) IS ACTIVATED IN HUMAN JURKAT CELLS UNDERGOING APOPTOSIS SO CELLULAR IMMUNOLOGY LA English DT Article ID CALCIUM-DEPENDENT ENDONUCLEASE; FAS ANTIGEN; SURFACE ANTIGEN; DEATH; DEOXYRIBONUCLEASE; PURIFICATION; LYMPHOCYTES; IDENTIFICATION; THYMOCYTES; INDUCTION AB Activation of a triplet of nuclear proteins (NP42-50) was observed in human Jurkat T cell line following treatment with an antibody to CD95 (Fas/Apo-1), a cell surface molecule involved in apoptotic cell death. The nuclease activity, corresponding to a triplet of proteins observed at approximately 42, 45, and 50 kDa in size, was extractable, heat-stable, and detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis containing deoxyribonucleic acids (SDS-PAGE-DNA) assay. The NP42-50 activity requires the presence of Mg2+/Ca2+ and is insensitive to inactivation by heating at 80 degrees C for 5 min. Zinc effectively inhibited the enzymatic activity of NP42-50 on SDS-PAGE-DNA and also protected Jurkat cells from the CD95-mediated apoptosis in cell cultures. The nuclease activation, however, was not a unique pathway for the CD95-mediated cell death. The apoptosis induced by arabino-furanosyl cytosine, a chemotherapeutic agent, also activated the NP42-50 nuclease activity in Jurkat cells, suggesting that a similar cascade of subsequent events in apoptosis may occur in most instances although many different signals can initiate apoptotic cell death in various cell types. The nuclease identified by this study appears to be distinguishable from DNase I or DNase II by its molecular characteristics and its enzymatic requirements. The NP42-50, with respect to the nuclease activity closely associated with apoptotic cell death, may serve as a candidate for the endonuclease(s) involved in the cleavage of DNA into fragments during apoptosis. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. RP ZHANG, CH (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 01730]; NIAID NIH HHS [AI 33485, AI 12069] NR 28 TC 28 Z9 32 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD OCT 15 PY 1995 VL 165 IS 2 BP 161 EP 167 DI 10.1006/cimm.1995.1201 PG 7 WC Cell Biology; Immunology SC Cell Biology; Immunology GA RX555 UT WOS:A1995RX55500001 PM 7553879 ER PT J AU PIGNATA, C PRASAD, KVS HALLEK, M DRUKER, B RUDD, CE ROBERTSON, MJ RITZ, J AF PIGNATA, C PRASAD, KVS HALLEK, M DRUKER, B RUDD, CE ROBERTSON, MJ RITZ, J TI PHOSPHORYLATION OF SRC FAMILY LCK TYROSINE KINASE FOLLOWING INTERLEUKIN-12 ACTIVATION OF HUMAN NATURAL-KILLER-CELLS SO CELLULAR IMMUNOLOGY LA English DT Article ID LYMPHOCYTE MATURATION FACTOR; STIMULATORY FACTOR NKSF; GROWTH-FACTOR RECEPTOR; SIGNAL TRANSDUCTION; HETERODIMERIC CYTOKINE; CYTOLYTIC ACTIVITY; PHOSPHOLIPASE-C; T-CELLS; IL-12; PROLIFERATION AB Interleukin-12 (IL-12) is a heterodimeric cytokine that augments the cytolytic activity of human NK cells and T cells but has little mitogenic activity on resting lymphocytes. The intracellular signaling pathways involved in NK cell activation by IL-12 have not been fully characterized. In the present studies we found that IL-12 induces tyrosine phosphorylation of a 56-kDa protein, identified in Western blot experiments as p56(lck), in resting NK cells. IL-12 was active in the range of 0.1 to 1000 U/ml, with maximal activity between 10 and 100 U/ml (30 and 300 pM). The maximal effect was noted 5 min after stimulation and was almost completely inhibited by genistein. IL-12 induced similar effects in resting and IL-2-activated NK cells. Following IL-12 stimulation of resting NK cells, immunoprecipitated lck kinase exhibited increased in vitro autophosphorylation activity 5 and 10 min after activation. Several additional substrates were phosphorylated in vitro following IL-12 stimulation, including proteins of 70 and 110 kDa. These studies indicate that lck tyrosine kinase is involved in the IL-12 signaling pathway in human NK cells. As the primary functional effect of IL-12 on resting NK cells is the enhancement of cytolytic activity and secretory function rather than cell proliferation, these findings suggest that lck tyrosine kinase is involved in these signaling pathways in human NK cells. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV HEMATOL MALIGNANCIES,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DIV TUMOR IMMUNOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RI Pignata, Claudio/O-2466-2013; Ritz, Jerome/C-7929-2009 OI Pignata, Claudio/0000-0003-1568-9843; Ritz, Jerome/0000-0001-5526-4669 FU NCI NIH HHS [CA-41619, CA-01730] NR 49 TC 27 Z9 27 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD OCT 15 PY 1995 VL 165 IS 2 BP 211 EP 216 DI 10.1006/cimm.1995.1207 PG 6 WC Cell Biology; Immunology SC Cell Biology; Immunology GA RX555 UT WOS:A1995RX55500007 PM 7553885 ER PT J AU SOLOMON, KR CHAN, M FINBERG, RW AF SOLOMON, KR CHAN, M FINBERG, RW TI EXPRESSION OF GPI-ANCHORED COMPLEMENT REGULATORY PROTEINS CD55 AND CD59 DIFFERENTIATES 2 SUBPOPULATIONS OF HUMAN CD56(+)CD3(-) LYMPHOCYTES (NK CELLS) SO CELLULAR IMMUNOLOGY LA English DT Article ID NATURAL-KILLER-CELLS; DECAY-ACCELERATING FACTOR; LARGE GRANULAR LYMPHOCYTES; FC-RECEPTOR FUNCTIONS; TYROSINE KINASES; ACTIVATION; MEMBRANE; MOLECULES; ANTIGENS; LEU-11 AB CD55 and CD59 are both glycosylphosphatidylinositol (GPI)-anchored complement regulatory proteins found on the surface of most hemopoietic cells. Using three-color cytofluorographic analysis with antibodies recognizing CD56, CD3, and CD59 or CD55 we determined that CD56(+)CD)3(-) lymphocytes (NK cells) expressed both CD55 and CD59 but at lower levels than CD3(+) lymphocytes. Since the CD56(+)CD3(-) lymphocyte population is heterogeneous, we examined expression of CD55 and CD59 on selected CD56(+)CD3(-) lymphocyte populations by depleting peripheral blood leukocytes of T cells, B cells, and monocytes. Dual staining of the selected CD56(+)CD3(-) cells, which were >95% CD56(+), permitted the distinction of two subpopulations: a major CD16(bright)CD56(dim)CD55(dim)CD59(dim) subpopulation and a minor CD16(dim/neg)CD56(bright)CD55(bright)CD59(bright) subpopulation. Treatment with phosphatidylinositol-specific phospholipase C released both the CD55 and CD59 antigens from the surface of CD56(+)CD3(-) cells, indicating that both are GPI-anchored, as they are on other lymphocytes. CD56(+)CD3(-) cell subpopulations were individually isolated by anti-CD55 or anti-CD16 negative selection and were functionally compared to the parent CD56(+)CD3(-) cell population. The CD16(bright)CD56(dim)CD55(dim)CD59(dim) cells killed NK targets well but did not proliferate well in response to rIL-2, whereas CD16(dim/neg)CD56(bright)CD55(bright)CD59(bright) cells proliferated well in response to rIL-2 but did not kill NK targets efficiently. We conclude that all CD56(+)CD3(-) cells express some levels of the GPI-anchored proteins, CD55 and CD59, and that two CD56(+)CD3(-) subpopulations with different functional characteristics can be distinguished by the level of expression of these two antigens. (C) 1995 Academic Press, Inc. C1 HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02115. RP SOLOMON, KR (reprint author), CHILDRENS HOSP,DANA FARBER CANC INST,INFECT DIS LAB,BOSTON,MA 02115, USA. RI Finberg, Robert/E-3323-2010 NR 22 TC 10 Z9 11 U1 0 U2 1 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD OCT 15 PY 1995 VL 165 IS 2 BP 294 EP 301 DI 10.1006/cimm.1995.1217 PG 8 WC Cell Biology; Immunology SC Cell Biology; Immunology GA RX555 UT WOS:A1995RX55500017 PM 7553895 ER PT J AU KOELLING, TM MEYER, GS FIFER, MA AF KOELLING, TM MEYER, GS FIFER, MA TI OUTCOME FOLLOWING MITRAL-VALVE REPLACEMENT IN PATIENTS WITH MITRAL-STENOSIS AND LOW LEFT-VENTRICULAR ELECTION FRACTION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 93 EP 93 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000090 ER PT J AU BREZINSKI, ME TEARNEY, GJ BOUMA, BE BOPPART, SA HEE, MR SWANSON, EA SOUTHERN, JF FUJIMOTO, JG AF BREZINSKI, ME TEARNEY, GJ BOUMA, BE BOPPART, SA HEE, MR SWANSON, EA SOUTHERN, JF FUJIMOTO, JG TI HIGH-RESOLUTION IMAGING OF PLAQUE MORPHOLOGY WITH OPTICAL COHERENCE TOMOGRAPHY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. MIT,BOSTON,MA. RI Boppart, Stephen/C-7338-2009 NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 103 EP 103 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000105 ER PT J AU HEIN, KD NISHIO, Y AIELLO, LP FEENER, EP KING, GL AF HEIN, KD NISHIO, Y AIELLO, LP FEENER, EP KING, GL TI CHARACTERIZATION OF GLYCOGEN-PHOSPHORYLASE EXPRESSION IN DIABETIC RAT AORTA SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,JOSLIN DIABET CTR,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 533 EP 533 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000528 ER PT J AU LIPSHULTZ, SE SWANSON, KA LIPSITZ, SR DILLER, L AF LIPSHULTZ, SE SWANSON, KA LIPSITZ, SR DILLER, L TI ABNORMAL HUMAN NEURAL CREST DEVELOPMENT IS ASSOCIATED WITH CONGENITAL CARDIOVASCULAR MALFORMATIONS SO CIRCULATION LA English DT Meeting Abstract C1 CHILDRENS HOSP,BOSTON,MA. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 599 EP 599 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000594 ER PT J AU KUSHWAHA, S ZERVOS, G SEMIGRAN, M FIFER, MA ALPERT, N FISCHMAN, A DEC, GW GEWIRTZ, H AF KUSHWAHA, S ZERVOS, G SEMIGRAN, M FIFER, MA ALPERT, N FISCHMAN, A DEC, GW GEWIRTZ, H TI TEMPORAL ALTERATIONS IN RESTING END MAXIMAL MYOCARDIAL BLOOD-FLOW FOLLOWING CARDIAC TRANSPLANTATION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 626 EP 626 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000626 ER PT J AU BREZINSKI, ME TEARNEY, GJ WEISSMAN, NJ BOPPART, SA BOUMA, BE HEE, MD WEYMAN, AE SWANSON, EA SOUTHERN, JF FUJIMOTO, JG AF BREZINSKI, ME TEARNEY, GJ WEISSMAN, NJ BOPPART, SA BOUMA, BE HEE, MD WEYMAN, AE SWANSON, EA SOUTHERN, JF FUJIMOTO, JG TI ASSESSING ATHEROSCLEROTIC PLAQUE MORPHOLOGY, COMPARISON OF OPTICAL COHERENCE TOMOGRAPHY AND INTRAVASCULAR ULTRASOUND SO CIRCULATION LA English DT Meeting Abstract C1 MIT,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Boppart, Stephen/C-7338-2009 NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 705 EP 705 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000699 ER PT J AU MORENO, PR BERNARDI, V LOPEZCUELLAR, J MCMELLON, C GOLD, HK PALACIOS, IF FUSTER, V NEMERSON, Y FALLON, JT AF MORENO, PR BERNARDI, V LOPEZCUELLAR, J MCMELLON, C GOLD, HK PALACIOS, IF FUSTER, V NEMERSON, Y FALLON, JT TI MACROPHAGE CORONARY ATHEROSCLEROTIC CONTENT IS PREDICTOR FOR RESTENOSIS AFTER CORONARY INTERVENTION SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. MT SINAI MED CTR,MT SINAI SCH MED,NEW YORK,NY 10029. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 766 EP 766 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000760 ER PT J AU WALKER, PG WALTON, SP YOGANATHAN, AP LEVINE, RA AF WALKER, PG WALTON, SP YOGANATHAN, AP LEVINE, RA TI 3-DIMENSIONAL INTEGRATION OF MITRAL INFLOW FROM DIGITIZED DOPPLER COLOR-FLOW MAPPING - IN-VITRO VALIDATION SO CIRCULATION LA English DT Meeting Abstract C1 GEORGIA INST TECHNOL,ATLANTA,GA 30332. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. RI Walton, S. Patrick/A-7007-2008 NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 923 EP 923 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48000916 ER PT J AU LEE, JS ADRIE, C JACOB, HJ ROBERTS, JD ZAPOL, WM BLOCH, KD AF LEE, JS ADRIE, C JACOB, HJ ROBERTS, JD ZAPOL, WM BLOCH, KD TI CHRONIC INHALATION OF NITRIC-OXIDE INHIBITS NEOINTIMA FORMATION AFTER BALLOON ARTERIAL INJURY IN RATS SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1105 EP 1105 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001099 ER PT J AU YAO, ZH MIZUMURA, T MEI, DA GROSS, GJ AF YAO, ZH MIZUMURA, T MEI, DA GROSS, GJ TI BLOCKADE OF K-ATP CHANNELS ABOLISHES THE ACUTE MEMORY OF ISCHEMIC PRECONDITIONING (PC) IN ANESTHETIZED DOGS SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. MED COLL WISCONSIN,MILWAUKEE,WI 53226. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1200 EP 1200 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001194 ER PT J AU PRABHU, SD MURRAY, DR LELEUX, J FREEMAN, GL AF PRABHU, SD MURRAY, DR LELEUX, J FREEMAN, GL TI EFFECT OF RYANODINE ON LEFT-VENTRICULAR CONTRACTION AND RELAXATION IN CLOSED-CHEST DOGS - INSIGHTS INTO INTRACELLULAR CALCIUM HANDLING SO CIRCULATION LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX 78284. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1214 EP 1214 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001208 ER PT J AU PRABHU, SD LELEUX, J MURRAY, DR FREEMAN, GL AF PRABHU, SD LELEUX, J MURRAY, DR FREEMAN, GL TI EFFECT OF RYANODINE ON THE LEFT-VENTRICULAR SYSTOLIC AND DIASTOLIC FORCE-FREQUENCY RELATION IN CLOSED-CHEST DOGS SO CIRCULATION LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,SAN ANTONIO,TX 78284. AUDIE L MURPHY VET AFFAIRS HOSP,SAN ANTONIO,TX. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1215 EP 1215 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001209 ER PT J AU LENG, JA GILON, D WEISSMAN, NJ ROSE, GA WEYMAN, AE PICARD, MH AF LENG, JA GILON, D WEISSMAN, NJ ROSE, GA WEYMAN, AE PICARD, MH TI INSIGHTS INTO THE MECHANISM OF INCOMPLETE MITRAL LEAFLET CLOSURE FROM DOBUTAMINE STRESS ECHOCARDIOGRAPHY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1301 EP 1301 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001294 ER PT J AU PADIAL, LR OLIVER, A SAGIE, A WEYMAN, AE AF PADIAL, LR OLIVER, A SAGIE, A WEYMAN, AE TI PROGRESSION OF AORTIC REGURGITATION ASSESSED BY 2-D ECHOCARDIOGRAPHY IN 127 PATIENTS - LEFT-VENTRICULAR SIZE AND FUNCTION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1304 EP 1304 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001297 ER PT J AU GILON, D BUONANNO, FS KISTLER, JP LEAVITT, M MARSHALL, JE WEYMAN, AE LEVINE, RA AF GILON, D BUONANNO, FS KISTLER, JP LEAVITT, M MARSHALL, JE WEYMAN, AE LEVINE, RA TI MITRAL-VALVE PROLAPSE AND STROKE - LACK OF SIGNIFICANT ASSOCIATION IN YOUNG-PATIENTS STUDIED OVER A DECADE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1351 EP 1351 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001343 ER PT J AU ISSELBACHER, EM SILVER, MT EAGLE, KA PICARD, MH AF ISSELBACHER, EM SILVER, MT EAGLE, KA PICARD, MH TI EVALUATING PATIENTS WITH POSSIBLE BACTERIAL-ENDOCARDITIS - A PREDICTIVE RULE TO IDENTIFY PATIENTS IN WHOM TRANSTHORACIC ECHOCARDIOGRAPHY MAY BE OF LOW UTILITY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1703 EP 1703 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001692 ER PT J AU REUE, K COHEN, RD SLAVIN, BG AF REUE, K COHEN, RD SLAVIN, BG TI IMPAIRED FAT STORAGE AND ABERRANT EXPRESSION OF ADIPOCYTE DIFFERENTIATION MARKERS IN FATTY LIVER DYSTROPHY MUTANT MICE SO CIRCULATION LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. UNIV SO CALIF,LOS ANGELES,CA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1712 EP 1712 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001701 ER PT J AU MOROOKA, H BONYENTRE, JV POMBO, C KYRIAKIS, J FORCE, T AF MOROOKA, H BONYENTRE, JV POMBO, C KYRIAKIS, J FORCE, T TI ISCHEMIA AND REPERFUSION TARGET ATF-2 AND C-JUN TO CAMP RESPONSE ELEMENTS AND TO AN AP-1 SITE FROM THE C-JUN PROMOTER BY ACTIVATING AN ATF-2 KINASE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1766 EP 1766 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001755 ER PT J AU KHARBANDA, S HAIDER, N PANDEY, P KHAW, BA KUFE, DW NARULA, J AF KHARBANDA, S HAIDER, N PANDEY, P KHAW, BA KUFE, DW NARULA, J TI BRIEF EPISODES OF HYPOXIA INDUCE INTENSE BUT TRANSIENT EXPRESSION OF STRESS-ACTIVATED PROTEIN-KINASES IN CULTURED CARDIOMYOCYTES SO CIRCULATION LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1767 EP 1767 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001756 ER PT J AU BLOCH, KD FILIPPOV, G AF BLOCH, KD FILIPPOV, G TI REGULATION OF SOLUBLE GUANYLATE-CYCLASE, A NITRIC-OXIDE RECEPTOR, DURING PULMONARY DEVELOPMENT SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1785 EP 1785 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001774 ER PT J AU LEWANDOWSKI, ED YU, X WHITE, LT DAMICO, LA AF LEWANDOWSKI, ED YU, X WHITE, LT DAMICO, LA TI POSTISCHEMIC HEARTS DISPLAY REDUCED METABOLITE EXCHANGE BETWEEN MITOCHONDRIAL AND CYTOSOLIC COMPARTMENTS SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1845 EP 1845 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001833 ER PT J AU GRIMES, RY YOGANATHAN, AP LEVINE, RA AF GRIMES, RY YOGANATHAN, AP LEVINE, RA TI DYNAMICS OF SYSTOLIC PULMONARY VENOUS FLOW SO CIRCULATION LA English DT Meeting Abstract C1 GEORGIA INST TECHNOL,ATLANTA,GA 30332. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1890 EP 1890 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001878 ER PT J AU CANNISTRA, LB DAVIDOFF, R PICARD, MH DEMPSEY, A OMALLEY, CJ BALADY, GJ AF CANNISTRA, LB DAVIDOFF, R PICARD, MH DEMPSEY, A OMALLEY, CJ BALADY, GJ TI EFFECT OF EXERCISE TRAINING AFTER MYOCARDIAL-INFARCTION ON LEFT-VENTRICULAR REMODELING RELATIVE TO INFARCT SIZE SO CIRCULATION LA English DT Meeting Abstract C1 BOSTON UNIV,MED CTR,BOSTON,MA 02215. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1900 EP 1900 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001888 ER PT J AU TEARNEY, GJ BOUMA, BE BREZINSKI, ME BOPPART, SA HEE, MR SWANSON, EA SOUTHERN, JF FUJIMOTO, JG AF TEARNEY, GJ BOUMA, BE BREZINSKI, ME BOPPART, SA HEE, MR SWANSON, EA SOUTHERN, JF FUJIMOTO, JG TI IMAGING OF PLAQUE MICROSTRUCTURE WITH OPTICAL COHERENCE TOMOGRAPHY, INFLUENCE OF THE SOURCE ON RESOLUTION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSSETS GEN HOSP,CAMBRIDGE,MA. MIT,CAMBRIDGE,MA. RI Boppart, Stephen/C-7338-2009 NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1913 EP 1913 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003851 ER PT J AU ROSE, GA WEISSMAN, NJ GUERRERO, JL SVIZZERO, TA WEYMAN, E PICARD, MH AF ROSE, GA WEISSMAN, NJ GUERRERO, JL SVIZZERO, TA WEYMAN, E PICARD, MH TI IMPORTANCE OF THE RATE OF THICKENING IN THE MYOCARDIAL RESPONSE TO DOBUTAMINE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1963 EP 1963 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001950 ER PT J AU ROSE, GA WEISSMAN, NJ FOSTER, GPF PICARD, MH AF ROSE, GA WEISSMAN, NJ FOSTER, GPF PICARD, MH TI COMPARISON OF ARBUTAMINE TO DOBUTAMINE STRESS ECHOCARDIOGRAPHY IN HUMANS SO CIRCULATION 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 HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 1964 EP 1964 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001951 ER PT J AU PADIAL, LR OLIVER, A SAGIE, A LEVINE, RA AF PADIAL, LR OLIVER, A SAGIE, A LEVINE, RA TI PROGRESSION OF AORTIC ROOT SITE IN PATIENTS WITH CHRONIC AORTIC REGURGITATION - AN ECHOCARDIOGRAPHIC STUDY IN 127 PATIENTS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 1988 EP 1988 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48001975 ER PT J AU LEE, E GRODZINSKY, AJ LIBBY, P CLINTON, SK LARK, MW LEE, RT AF LEE, E GRODZINSKY, AJ LIBBY, P CLINTON, SK LARK, MW LEE, RT TI MONOCYTES INDUCE METALLOPROTEINASE SECRETION BY CULTURED HUMAN VASCULAR SMOOTH-MUSCLE CELLS THROUGH INTERLEUKIN-1 SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 2 Z9 2 U1 0 U2 2 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2025 EP 2025 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002012 ER PT J AU SATLER, CA VESELY, MR WALSH, E WONG, JCL GINSBURG, GS JACOB, H AF SATLER, CA VESELY, MR WALSH, E WONG, JCL GINSBURG, GS JACOB, H TI MAPPING A GENE FOR HEREDITARY LONG QT SYNDROME TO CHROMOSOME 7Q35-36 SO CIRCULATION LA English DT Meeting Abstract C1 CHILDRENS HOSP,DEPT CARDIOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 2073 EP 2073 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002058 ER PT J AU LEE, MY JIANG, L GILON, D BRILI, S HANDSCHUMACHER, MD KING, MEE GUERRERO, JL MARELLI, AJ AF LEE, MY JIANG, L GILON, D BRILI, S HANDSCHUMACHER, MD KING, MEE GUERRERO, JL MARELLI, AJ TI EFFECT OF RIGHT-VENTRICULAR DISTORTION ON ACCURACY OF LEFT-VENTRICULAR VOLUME MEASUREMENT - COMPARISON OF 2-DIMENSIONAL AND 3-DIMENSIONAL ECHOCARDIOGRAPHY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2110 EP 2110 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002093 ER PT J AU NEUBAUER, S HORN, M GODDE, M HARRE, K PABST, T NEWELL, JB PETERS, W HAHN, D ERTL, G KOCHSIEK, K AF NEUBAUER, S HORN, M GODDE, M HARRE, K PABST, T NEWELL, JB PETERS, W HAHN, D ERTL, G KOCHSIEK, K TI THE MYOCARDIAL CREATINE-PHOSPHATE ATP RATIO, MEASURED BY 31P-MR SPECTROSCOPY, AS A PREDICTOR OF MORTALITY IN PATIENTS WITH DILATED CARDIOMYOPATHY SO CIRCULATION LA English DT Meeting Abstract C1 UNIV WURZBURG,DEPT MED,W-8700 WURZBURG,GERMANY. UNIV WURZBURG,DEPT RADIOL,W-8700 WURZBURG,GERMANY. MASSACHUSETTS GEN HOSP,CTR CARDIAC COMP,BOSTON,MA 02114. RI Neubauer, Stefan/B-8448-2011 NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2131 EP 2131 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002114 ER PT J AU FEINSTEIN, S PASCOE, R PICARD, M MULVAGH, S BLOCK, R OSTOIC, T BRODSKY, L DEVRIES, S AF FEINSTEIN, S PASCOE, R PICARD, M MULVAGH, S BLOCK, R OSTOIC, T BRODSKY, L DEVRIES, S TI HARMONIC IMAGING IN PATIENTS FOLLOWING INTRAVENOUS CONTRAST INJECTIONS - PRELIMINARY DATA SO CIRCULATION LA English DT Meeting Abstract C1 UNIV ILLINOIS,CHICAGO,IL. MAYO CLIN,ROCHESTER,MN. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2209 EP 2209 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002192 ER PT J AU WEISSMAN, NJ FOSTER, GP ROSE, GA PICARD, MH AF WEISSMAN, NJ FOSTER, GP ROSE, GA PICARD, MH TI EFFECTS OF PROLONGING PEAK DOBUTAMINE DOSE DURING DOBUTAMINE STRESS ECHOCARDIOGRAPHY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2281 EP 2281 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002264 ER PT J AU CONNOLLY, ES WINFREE, CJ SPRINGER, TA GUTIERREZRAMOS, JC NAKA, Y YAN, SD LIAO, H STERN, DM SOLOMON, RA PINSKY, DJ AF CONNOLLY, ES WINFREE, CJ SPRINGER, TA GUTIERREZRAMOS, JC NAKA, Y YAN, SD LIAO, H STERN, DM SOLOMON, RA PINSKY, DJ TI DETRIMENTAL ROLE OF NEUTROPHIL ADHESION IN STROKE - A STUDY OF NEUTROPHIL DEFICIENT AND HOMOZYGOUS NULL ICAM-1 MICE SO CIRCULATION LA English DT Meeting Abstract C1 COLUMBIA UNIV,NEW YORK,NY. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2305 EP 2305 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002288 ER PT J AU JANSSENS, SP NONG, ZX BLOCH, KD GERARD, RD ZOLDHELYI, P COLLEN, D AF JANSSENS, SP NONG, ZX BLOCH, KD GERARD, RD ZOLDHELYI, P COLLEN, D TI ADENOVIRUS-MEDIATED TRANSFER OF THE HUMAN CONSTITUTIVE NITRIC-OXIDE SYNTHASE GENE TO HYPOXIC RAT LUNGS SO CIRCULATION LA English DT Meeting Abstract C1 CATHOLIC UNIV LEUVEN,CARDIAC UNIT,LOUVAIN,BELGIUM. CATHOLIC UNIV LEUVEN,CTR MOLEC & VASC BIOL,LOUVAIN,BELGIUM. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA 02129. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2391 EP 2391 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002373 ER PT J AU LEE, JS DICHEK, DA GIMBRONE, MA ROSENZWEIG, A AF LEE, JS DICHEK, DA GIMBRONE, MA ROSENZWEIG, A TI CYTOKINE ACTIVATION INHIBITS ADENOVIRUS-MEDIATED GENE-TRANSFER SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2395 EP 2395 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002377 ER PT J AU SATLER, CA PLUMMER, MH FAN, MX ZURAKOWSKI, D WALSH, E JACOB, H GINSBURG, GS AF SATLER, CA PLUMMER, MH FAN, MX ZURAKOWSKI, D WALSH, E JACOB, H GINSBURG, GS TI CLINICAL SEVERITY INCREASES IN SUCCESSIVE GENERATIONS OF FAMILIAL LQT SYNDROME SO CIRCULATION LA English DT Meeting Abstract C1 CHILDRENS HOSP,DEPT CARDIOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,CVRC,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2473 EP 2473 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002455 ER PT J AU LIN, LF OEUN, S LIU, L HOUNG, AK REED, GL AF LIN, LF OEUN, S LIU, L HOUNG, AK REED, GL TI MOLECULAR-BASIS OF THE INHIBITION OF STREPTOKINASE FUNCTION BY AMICAR SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2647 EP 2647 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002629 ER PT J AU ABASCAL, VM PATEL, AR WEYMAN, AE DAVIDOFF, R AF ABASCAL, VM PATEL, AR WEYMAN, AE DAVIDOFF, R TI LEFT ATRIAL REMODELING - DILATATION WITH ELONGATION SO CIRCULATION LA English DT Meeting Abstract C1 BOSTON UNIV,MED CTR,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2826 EP 2826 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002807 ER PT J AU GILON, D BUONANNO, FS JOFFE, M LEVINE, RA AF GILON, D BUONANNO, FS JOFFE, M LEVINE, RA TI PATENT FORAMEN OVALE - RECONSIDERATION OF ITS FREQUENT ASSOCIATION WITH ACUTE ISCHEMIC NEUROLOGIC EVENTS IN THE YOUNG SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2848 EP 2848 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002829 ER PT J AU FOSTER, GP GUERRERO, JL WEISSMAN, NJ ROSE, GA WEYMAN, AE LEVINE, RA AF FOSTER, GP GUERRERO, JL WEISSMAN, NJ ROSE, GA WEYMAN, AE LEVINE, RA TI INTRACARDIAC ECHOCARDIOGRAPHY - A NEW TECHNIQUE FOR DIRECT QUANTITATION OF THE REGURGITANT ORIFICE AREA IN AORTIC-INSUFFICIENCY - VALIDATION IN PULSATILE FLOW SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2850 EP 2850 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002831 ER PT J AU HELMAN, DN HILGENBERG, AD TORCHIANA, DF DAGGETT, WM VIAHAKES, GJ AF HELMAN, DN HILGENBERG, AD TORCHIANA, DF DAGGETT, WM VIAHAKES, GJ TI COMPLICATED AORTIC ENDOCARDITIS - RESULTS OF RADICAL TREATMENT SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2933 EP 2933 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002913 ER PT J AU LIN, LF OEUN, S LIU, L HOUNG, AK REED, GL AF LIN, LF OEUN, S LIU, L HOUNG, AK REED, GL TI MUTATIONAL STUDIES OF STREPTOKINASE IDENTIFY AMINO-ACID-RESIDUES CRITICAL TO GENERATION OF A FUNCTIONAL SK-PLASMINOGEN ACTIVATOR COMPLEX SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2984 EP 2984 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002964 ER PT J AU LIU, L LIN, LF OEUN, S HOUNG, AK MAGGINI, L CLEMENT, CY REED, GL AF LIU, L LIN, LF OEUN, S HOUNG, AK MAGGINI, L CLEMENT, CY REED, GL TI RECOMBINANT STREPTOKINASES RESISTANT TO CLEAVAGE AND INACTIVATION BY PLASMIN SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 2985 EP 2985 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48002965 ER PT J AU YU, X WHITE, LT DOUMEN, C LANOUE, KF ALPERT, NM LEWANDOWSKI, ED AF YU, X WHITE, LT DOUMEN, C LANOUE, KF ALPERT, NM LEWANDOWSKI, ED TI ENZYMATIC RATES AND SUBCELLULAR COMPARTMENTATION INFLUENCE C-13 RECYCLING AS DETECTED BY DYNAMIC C-13 NMR OF INTACT HEARTS SO CIRCULATION LA English DT Meeting Abstract C1 PENN STATE UNIV,MILTON S HERSHEY MED CTR,HERSHEY,PA 17033. HARVARD UNIV,SCH MED,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3031 EP 3031 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003011 ER PT J AU OCALLAGHAN, PA SOSASUAREZ, G MCGOVERN, BA RUSKIN, JN GARAN, H AF OCALLAGHAN, PA SOSASUAREZ, G MCGOVERN, BA RUSKIN, JN GARAN, H TI LONG-TERM SAFETY AND EFFICACY OF RADIOFREQUENCY CATHETER ABLATION FOR VENTRICULAR-TACHYCARDIA SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3276 EP 3276 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003254 ER PT J AU WONG, JCL VESELY, MR FAN, MX ZURAKOWSKI, D GINSBURG, GS WALSH, E JACOB, H SATLER, CA AF WONG, JCL VESELY, MR FAN, MX ZURAKOWSKI, D GINSBURG, GS WALSH, E JACOB, H SATLER, CA TI GENETIC CONFIRMATION OF A CLINICAL DIAGNOSTIC SCORING SYSTEM FOR AUTOSOMAL-DOMINANT LONG QT SYNDROME (LQTS) SO CIRCULATION LA English DT Meeting Abstract C1 CHILDRENS HOSP,DEPT CARDIOL,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,CARDIOVASC RES CTR,BOSTON,MA. NR 1 TC 0 Z9 0 U1 0 U2 0 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3394 EP 3394 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003372 ER PT J AU STAFFORD, RS BLUMENTHAL, D AF STAFFORD, RS BLUMENTHAL, D TI PATTERNS OF LIPID-LOWERING MEDICATION USE BY PATIENTS VISITING US PHYSICIANS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,HLTH POLICY & RES DEV UNIT,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3409 EP 3409 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003387 ER PT J AU HOPMEYER, J HANDSCHUMACHER, MD GILON, D GUERRERO, JL WALKER, PG YOGANATHAN, AP LEVINE, RA AF HOPMEYER, J HANDSCHUMACHER, MD GILON, D GUERRERO, JL WALKER, PG YOGANATHAN, AP LEVINE, RA TI IMPROVING THE ACCURACY OF FLOW CONVERGENCE CALCULATIONS OF MITRAL REGURGITATION - IN-VIVO APPLICATION OF THE HEMI-ELLIPTIC FORMULA USING DIGITAL DOPPLER MAPS SO CIRCULATION LA English DT Meeting Abstract C1 GEORGIA INST TECHNOL,ATLANTA,GA 30332. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3457 EP 3457 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003435 ER PT J AU JIANG, L HANDSCHUMACHER, MD LEE, MY GILON, D BRILI, S ADAMS, MS KING, ME WEYMAN, AE LEVINE, RA AF JIANG, L HANDSCHUMACHER, MD LEE, MY GILON, D BRILI, S ADAMS, MS KING, ME WEYMAN, AE LEVINE, RA TI 3-DIMENSIONAL RECONSTRUCTION OF THE TRICUSPID ANNULUS - IS IT NONPLANAR SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3461 EP 3461 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003439 ER PT J AU FOSTER, GP ZARICH, SW FITZPATRICK, PJ SHUBROOKS, SJ LEVINE, RA AF FOSTER, GP ZARICH, SW FITZPATRICK, PJ SHUBROOKS, SJ LEVINE, RA TI A NEW METHOD FOR QUANTIFYING THE REGURGITANT ORIFICE AREA IN AORTIC-INSUFFICIENCY USING INTRACARDIAC ECHOCARDIOGRAPHY - COMPARISON WITH CLINICAL STANDARDS SO CIRCULATION LA English DT Meeting Abstract C1 DEACONESS HOSP,BOSTON,MA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3462 EP 3462 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003440 ER PT J AU FOSTER, GP ROSE, GA GUERRERO, JL WEISSMAN, NJ LEVINE, RA AF FOSTER, GP ROSE, GA GUERRERO, JL WEISSMAN, NJ LEVINE, RA TI QUANTITATION OF THE REGURGITANT ORIFICE AREA IN AORTIC-INSUFFICIENCY USING THE CONTINUITY EQUATION - IN-VITRO VALIDATION SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3463 EP 3463 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003441 ER PT J AU HAIDER, N NARULA, J HAJJAR, RJ DISALVO, T SEMIGRAN, MJ DEC, GW KHAW, BA AF HAIDER, N NARULA, J HAJJAR, RJ DISALVO, T SEMIGRAN, MJ DEC, GW KHAW, BA TI APOPTOSIS IN HUMAN EXPLANTED CARDIOMYOPATHIC HEARTS SUGGESTS PROGRAMMED PROGRESSION OF DILATED CARDIOMYOPATHY SO CIRCULATION LA English DT Meeting Abstract C1 NORTHEASTERN UNIV,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 1 Z9 1 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3479 EP 3479 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003457 ER PT J AU MORENO, PR BERNARDI, V MCMELLON, C FALLON, JT PALACIOS, IP GOLD, HI AF MORENO, PR BERNARDI, V MCMELLON, C FALLON, JT PALACIOS, IP GOLD, HI TI IS SMOOTH-MUSCLE CELL-PROLIFERATION GREATER IN RESTENOTIC TISSUE FROM DIRECTIONAL CORONARY ATHERECTOMY THAN IN RESTENOTIC TISSUE FROM PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA. MT SINAI MED CTR,NEW YORK,NY 10029. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3485 EP 3485 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003463 ER PT J AU SAGER, PT KOH, SW NGUYEN, T AF SAGER, PT KOH, SW NGUYEN, T TI BETA-ADRENERGIC STIMULATION ACCELERATES HUMAN ACTION-POTENTIAL ACCOMMODATION SO CIRCULATION LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA. NR 0 TC 1 Z9 1 U1 1 U2 1 PU AMER HEART ASSOC PI DALLAS PA 7272 GREENVILLE AVENUE, DALLAS, TX 75231-4596 SN 0009-7322 J9 CIRCULATION JI Circulation PD OCT 15 PY 1995 VL 92 IS 8 SU S BP 3499 EP 3499 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003477 ER PT J AU GARABEDIAN, HD SVIZZERO, TA GUERRERO, JL PENA, LC LOVE, TW LEINBACH, RC GOLD, HK AF GARABEDIAN, HD SVIZZERO, TA GUERRERO, JL PENA, LC LOVE, TW LEINBACH, RC GOLD, HK TI A NEW DOSING STRATEGY FOR TNK VARIANT OF TISSUE-PLASMINOGEN ACTIVATOR ELIMINATES HEPARIN AND REDUCES BLEEDING WITHOUT LOSS OF THROMBOLYTIC EFFICACY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GENENTECH INC,S SAN FRANCISCO,CA 94080. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3554 EP 3554 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003532 ER PT J AU GARABEDIAN, HD GUERRERO, JL SVIZZERO, TA SCHWALL, RH BUNTING, S LEINBACH, RC GOLD, HK AF GARABEDIAN, HD GUERRERO, JL SVIZZERO, TA SCHWALL, RH BUNTING, S LEINBACH, RC GOLD, HK TI RECOMBINANT HEPATOCYTE GROWTH-FACTOR ACCELERATES ENDOTHELIAL-CELL REGROWTH IN-VIVO FOLLOWING ARTERIAL INJURY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. GENENTECH INC,S SAN FRANCISCO,CA 94080. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3604 EP 3604 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003582 ER PT J AU YU, X WHITE, LT LEWANDOWSKI, ED AF YU, X WHITE, LT LEWANDOWSKI, ED TI CYTOSOLIC REDOX STATE DRIVES CARBON FLUX ACROSS THE MITOCHONDRIAL-MEMBRANE AS SHOWN BY C-13 NMR OF INTACT HEARTS SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3709 EP 3709 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003685 ER PT J AU SAGER, PT AF SAGER, PT TI FREQUENCY-DEPENDENT ELECTROPHYSIOLOGIC EFFECTS OF DOFETILIDE IN HUMANS SO CIRCULATION LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3727 EP 3727 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003703 ER PT J AU MATHIER, MA ROSE, GA FIFER, MA CASTANO, HH DINSMORE, RE DEC, GW PALACIOS, IF SEMIGRAN, MJ AF MATHIER, MA ROSE, GA FIFER, MA CASTANO, HH DINSMORE, RE DEC, GW PALACIOS, IF SEMIGRAN, MJ TI ENDOTHELIUM-DEPENDENT CORONARY VASODILATION IS IMPAIRED AT BOTH THE EPICARDIAL AND MICROCIRCULATORY LEVEL IN ACUTE-ONSET IDIOPATHIC DILATED CARDIOMYOPATHY SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3784 EP 3784 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003760 ER PT J AU MIYAMOTO, MI MATHIER, MA COCKRILL, BA KACMAREK, R ZAPOL, WM FIFER, MA SEMIGRAN, MJ AF MIYAMOTO, MI MATHIER, MA COCKRILL, BA KACMAREK, R ZAPOL, WM FIFER, MA SEMIGRAN, MJ TI NITROPRUSSIDE BUT NOT INHALED NITRIC-OXIDE IMPROVES RIGHT-VENTRICULAR RELAXATION IN PATIENTS WITH PRIMARY PULMONARY-HYPERTENSION AND RIGHT-VENTRICULAR FAILURE SO CIRCULATION LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3806 EP 3806 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003782 ER PT J AU CLEMENT, CY MAGGINI, L HOUNG, AK OEUN, S LEE, WS REED, GL AF CLEMENT, CY MAGGINI, L HOUNG, AK OEUN, S LEE, WS REED, GL TI PLT24N, A NOVEL PLATELET ACTIVATION PROTEIN - ISOLATION, MOLECULAR-CLONING, AND CHARACTERIZATION SO CIRCULATION LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH PUBL HLTH,BOSTON,MA. NR 0 TC 0 Z9 0 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 OCT 15 PY 1995 VL 92 IS 8 SU S BP 3867 EP 3867 PG 1 WC Cardiac & Cardiovascular Systems; Peripheral Vascular Disease SC Cardiovascular System & Cardiology GA TB480 UT WOS:A1995TB48003843 ER PT J AU WITHERS, HR PETERS, LJ TAYLOR, JMG OWEN, JB MORRISON, WH SCHULTHEISS, TE KEANE, T OSULLIVAN, B VANDYK, J GUPTA, N WANG, CC JONES, CU DOPPKE, KP MYINT, S THOMPSON, M PARSONS, JT MENDENHALL, WM DISCHE, S AIRD, EGA HENK, JM BIDMEAD, MAM SVOBODA, V CHON, Y HANLON, AL PETERS, TL HANKS, GE AF WITHERS, HR PETERS, LJ TAYLOR, JMG OWEN, JB MORRISON, WH SCHULTHEISS, TE KEANE, T OSULLIVAN, B VANDYK, J GUPTA, N WANG, CC JONES, CU DOPPKE, KP MYINT, S THOMPSON, M PARSONS, JT MENDENHALL, WM DISCHE, S AIRD, EGA HENK, JM BIDMEAD, MAM SVOBODA, V CHON, Y HANLON, AL PETERS, TL HANKS, GE TI LOCAL-CONTROL OF CARCINOMA OF THE TONSIL BY RADIATION-THERAPY - AN ANALYSIS OF PATTERNS OF FRACTIONATION IN 9 INSTITUTIONS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CARCINOMA OF TONSIL; RADIATION THERAPY; DOSE-FRACTIONATION; GROWTH KINETICS; OUTCOME ANALYSIS; ACCELERATED TUMOR GROWTH; RADIATION DOSE RESPONSE ID SQUAMOUS-CELL CARCINOMA; DOSE FRACTIONATION; TUMOR-CONTROL; HYPERFRACTIONATED RADIOTHERAPY; CONVENTIONAL FRACTIONATION; ACCELERATED FRACTIONATION; OROPHARYNGEAL CARCINOMA; TREATMENT TIME; ORAL CAVITY; NECK-CANCER AB Purpose: To investigate the importance to outcome of treatment, for squamous cell carcinomas of the tonsillar fossa, of dose per fraction, overall treatment duration, and total dose. Methods and Materials: A collaborative retrospective study was undertaken in nine centers that used widely different dose-fractionation patterns for external beam radiation therapy. Results: There were 676 eligible cases treated only with photon beams during the years 1976-1985. The probability of local control (of the tonsillar fossa primary) was influenced by both T-stage and N-stage. Significant treatment parameters were total dose and overall treatment duration, but not dose per fraction. Over the range of about 40 to 90% and for a constant overall treatment duration, local tumor control probability increased by nearly 2% for each 1 Gy increase in total dose. For a constant total dose there was a decrease in the probability of local control associated with prolongation of overall treatment duration, presumed to result from accelerated regrowth of surviving tumor clonogens during the course of treatment, If it is assumed that accelerated regrowth occurred at a constant rate and began within 9 days of the start of treatment, an average of 0.53 Gy extra dose per day's extension of treatment would be required to maintain a constant probability of local control. Correspondingly, the probability of local control from a constant dose would be lowered by an average of at least 1% for each day's extension of treatment duration. However, the data are slightly more consistent with an average delay of as Long as 30 days before onset of accelerated repopulation, with a consequent increase to an average of 0.73 Gy per day for the value of the compensatory dose. The alpha/beta ratio for this tumor is high enough that the effect of fraction size on the probability of local control can be ignored; a precise estimate is not possible because the best value for beta was close to zero. After accounting for the significant variables studied (treatment time, T-stage, N-stage), the dose-response curves for tumor control were still shallow, suggesting that there are additional causes for heterogeneity of responses among these tumors. Conclusions: Total dose is important to treatment outcome: After accounting for other treatment variables, there is about a 2% per Gy increase in probability of tumor control over the ranges of control commonly achieved. Overall treatment duration is important: There is at least a 1% per day decrease in tumor control probability if delivery of a constant total dose is prolonged, requiring a compensatory increase in dose by 0.5-0.7 Gy per day to achieve a constant rate of tumor control. Fraction size is not, of itself, an important factor in the response of primary carcinoma of the tonsil. If a tumor has demonstrated a capacity for metastatic spread to lymph nodes, a higher total dose should be considered to achieve control rates at the primary site equivalent to those in node negative patients. Even after accounting for variables such as tumor stage, total dose, and overall treatment duration, there is sufficient heterogeneity in other undocumented determinants of tumor control to cause the tumor control probability curve to be a shallow function of dose. C1 UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90024. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. PRINCESS MARGARET HOSP,TORONTO,ON M4X 1K9,CANADA. CHRISTIE HOSP,MANCHESTER,LANCS,ENGLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CLATTERBRIDGE HOSP,LIVERPOOL,MERSEYSIDE,ENGLAND. UNIV FLORIDA,GAINESVILLE,FL 32611. ROYAL MARSDEN HOSP,LONDON SW3 6JJ,ENGLAND. MT VERNON HOSP,NORTHWOOD HA6 2RN,MIDDX,ENGLAND. PORTSMOUTH HOSP,PORTSMOUTH,HANTS,ENGLAND. AMER COLL RADIOL,PHILADELPHIA,PA. RP WITHERS, HR (reprint author), UNIV CALIF LOS ANGELES,MED CTR,DEPT RADIAT ONCOL,10833 LE CONTE AVE,LOS ANGELES,CA 90024, USA. FU NCI NIH HHS [CA-31612, CA-45216, N01-CM87275] NR 54 TC 104 Z9 104 U1 1 U2 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 549 EP 562 DI 10.1016/0360-3016(95)00228-Q PG 14 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300001 PM 7558943 ER PT J AU WITHERS, HR PETERS, LJ TAYLOR, JMG OWEN, JB MORRISON, WH SCHULTHEISS, TE KEANE, T OSULLIVAN, B VANDYK, J GUPTA, N WANG, CC JONES, CU DOPPKE, KP MYINT, S THOMPSON, M PARSONS, JT MENDENHALL, WM DISCHE, S AIRD, EGA HENK, M BIDMEAD, MAM SVOBODA, V CHON, Y HANLON, AL PETERS, TL HANKS, GE AF WITHERS, HR PETERS, LJ TAYLOR, JMG OWEN, JB MORRISON, WH SCHULTHEISS, TE KEANE, T OSULLIVAN, B VANDYK, J GUPTA, N WANG, CC JONES, CU DOPPKE, KP MYINT, S THOMPSON, M PARSONS, JT MENDENHALL, WM DISCHE, S AIRD, EGA HENK, M BIDMEAD, MAM SVOBODA, V CHON, Y HANLON, AL PETERS, TL HANKS, GE TI LATE NORMAL TISSUE SEQUELAE FROM RADIATION-THERAPY FOR CARCINOMA OF THE TONSIL - PATTERNS OF FRACTIONATION STUDY OF RADIOBIOLOGY SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE DOSE FRACTIONATION; COMPLICATIONS; CARCINOMA OF TONSIL; FIELD SIZE; MANDIBULAR NECROSIS ID INCOMPLETE REPAIR; RADIOTHERAPY; IRRADIATION; RESPONSES; TOLERANCE; KINETICS; MODEL AB Purpose: To evaluate the influence of dose fractionation and other factors on the development of late complications in mandibular bone, muscle, and mucosa of the oral cavity after external beam radiation therapy for carcinoma of the tonsil. Methods and Materials: A retrospective analysis was made of the results in 676 patients treated with a spectrum of fractionation regimens in nine centers during the years 1976-1985. Only severe (Grades 3-4) late complications were analyzed. Results: With more than 5 years follow-up, it was found that total dose was a factor for all three types of complications, but that in other respects, the radiobiology of late-(>3 months) developing mucosal ulcerations was different from that for mandibular necrosis and muscle injury. Dose per fraction was a significant factor for bone and muscle (estimated alpha/beta values of 0.85 Gy and 3.1 Gy, respectively). By contrast, mucosa showed no influence on response from change in fraction size over the range of approximately 1.0-3.5 Gy. Complications in bone and muscle were not related to overall treatment duration, whereas there was a significant inverse relationship for mucosa breakdown. The rate of development of complications was fastest in mucosa and slowest in bone. The appearance of complications by 4 years after treatment was about 80% of those developing by 8 years in the mucosa, 66% in muscle, and about 50% in bone. The high alpha beta ratio, inverse relationship with overall treatment duration, and faster development of mucosal complications suggests that they may develop as a consequence of earlier mucosal injury. As anticipated, adequate retrospective analysis of acute complications could not be made even when objective criteria such as weight loss, unplanned delays in completing treatment, or hospitalization during treatment were the measures. Field size was a significant factor for mandible complications, but not for muscle or mucosa. Conclusion: The radiobiological characteristics of bone and muscle were those characteristic of other late-responding tissues, whereas late sequelae in mucosa had radiobiological parameters similar to those for acute responses. Field size was a significant factor for bone complications but not for others. C1 UNIV CALIF LOS ANGELES,JONSSON COMPREHENS CANC CTR,LOS ANGELES,CA 90095. UNIV TEXAS,MD ANDERSON CANC CTR,HOUSTON,TX. PRINCESS MARGARET HOSP,TORONTO,ON M4X 1K9,CANADA. CHRISTIE HOSP,MANCHESTER,LANCS,ENGLAND. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CLATTERBRIDGE HOSP,LIVERPOOL,MERSEYSIDE,ENGLAND. UNIV FLORIDA,GAINESVILLE,FL 32611. MT VERNON HOSP,NORTHWOOD HA6 2RN,MIDDX,ENGLAND. ROYAL MARSDEN HOSP,LONDON SW3 6JJ,ENGLAND. PORTSMOUTH HOSP,PORTSMOUTH,HANTS,ENGLAND. AMER COLL RADIOL,PHILADELPHIA,PA. RP WITHERS, HR (reprint author), UNIV CALIF LOS ANGELES,MED CTR,DEPT RADIAT ONCOL,10833 LE CONTE AVE,LOS ANGELES,CA 90095, USA. OI Schultheiss, Timothy/0000-0002-8984-196X FU NCI NIH HHS [CA-31612, CA-45216, N01-CM87275] NR 16 TC 74 Z9 75 U1 0 U2 4 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 563 EP 568 DI 10.1016/0360-3016(95)00229-R PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300002 PM 7558944 ER PT J AU FAGUNDES, MA HUG, EB LIEBSCH, NJ DALY, W EFIRD, J MUNZENRIDER, JE AF FAGUNDES, MA HUG, EB LIEBSCH, NJ DALY, W EFIRD, J MUNZENRIDER, JE TI RADIATION-THERAPY FOR CHORDOMAS OF THE BASE OF SKULL AND CERVICAL-SPINE - PATTERNS OF FAILURE AND OUTCOME AFTER RELAPSE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE CHORDOMA; BASE OF SKULL; CERVICAL SPINE; PROTON THERAPY; RADIATION ID LOCAL-CONTROL; CRANIAL BASE; CHONDROSARCOMA; ULTRASTRUCTURE; CARCINOMA; TUMORS AB Purpose: To determine the patterns of failure and outcome following relapse of chordomas of the base of skull and cervical spine. Methods and Materials: Between November 1975 and October 1993, 204 patients were treated for chordoma of the base of skull or cervical spine, of which 63 have developed relapse. These 63 patients constitute the main focus of this study. Forty-five patients presented with base of skull and 18 with cervical spine tumors. All patients received combined proton and photon beam radiation. The median prescribed dose was 70.1 cobalt-Gray equivalent (CGE) (range 66.6-77.4). There were 25 males and 38 females, with a median age of 41 years (range 7-66). Median follow-up was 54 months (range 8-158). Results: Sixty-three of the 204 patients treated (31%) had treatment failure. Among the 63 patients who relapsed, 60 (95%) experienced local recurrence, and in 49 patients (78%), this was the only site of failure. Two of 63 patients (3%) developed regional lymph node relapse and 3 of 63 (5%) developed surgical pathway recurrence (1 left neck, 1 palate and 1 nasal cavity). Thirteen of 204 patients relapsed in distant sites, accounting for 20% (13 of 63) of all patients with recurrence in this series. The most common metastatic sites were lungs and bones presenting in 7 of 13 and 6 of 13 patients, respectively. Only 2 of 13 patients failed with isolated distant metastasis. The actuarial 3- and 5-year survival rates after local relapse (60 patients) were 44 and 5%, respectively. Following distant failure (13 patients), the 3- and 5-year survival rates were 25 and 12%, respectively. After any relapse (63 patients) the corresponding survival rates were 43 and 7%. Following local relapse, 49 of 60 patients underwent salvage therapy consisting of subtotal resection in most patients (46 of 49). The remaining 11 of 60 patients received supportive care only. Salvage therapy resulted in stable or improved status without subsequent disease progression in 7 of 49 (14%), stable or improved status with subsequent disease progression in 26 of 49 (53%), and progressive disease in 16 of 49 patients (33%). The actuarial 2- and 5-year overall survival rates following relapse for the 49 patients who underwent salvage treatment were 63 and 6%, which favorably compared to the a-year survival rate of 21% for those who received supportive care only (p = 0.001). Conclusion: Local relapse is the predominant type of treatment failure for chordomas of the base of skull and cervical spine. Salvage treatment may relieve symptoms; however, most patients will ultimately succumb to their disease. Poor long-term survival rates following relapse emphasize the importance of a combined treatment approach with experienced surgeons and radiation oncologists at the time of primary treatment. For most patients, only permanent local tumor control will offer a chance of cure. C1 HARVARD UNIV,CYCLOTRON LAB,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA. RP FAGUNDES, MA (reprint author), NEW ENGLAND MED CTR,DEPT RADIAT ONCOL,750 WASHINGTON ST,BOSTON,MA 02111, USA. NR 30 TC 100 Z9 102 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 579 EP 584 DI 10.1016/0360-3016(95)02014-3 PG 6 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300004 PM 7558946 ER PT J AU WILLERS, H HUG, EB SPIRO, IJ EFIRD, JT ROSENBERG, AE WANG, CC AF WILLERS, H HUG, EB SPIRO, IJ EFIRD, JT ROSENBERG, AE WANG, CC TI ADULT SOFT-TISSUE SARCOMAS OF THE HEAD AND NECK TREATED BY RADIATION AND SURGERY OR RADIATION ALONE - PATTERNS OF FAILURE AND PROGNOSTIC FACTORS SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE SOFT TISSUE SARCOMA; HEAD AND NECK; ANGIOSARCOMA; PROGNOSTIC FACTORS; LOCAL CONTROL AB Purpose: To analyze our experience treating soft tissue sarcomas of the head and neck in adults, and to identify patterns of failure and prognostic factors. Methods and Materials: The records of 57 patients with Stage MO disease treated by radiation with or without surgery between 1972 and 1993 were reviewed. Median follow-up time was 4.3 years (range, 1.1-16.8 years). A group of potential prognostic factors was evaluated, including age at diagnosis, sex, initial tumor presentation (primary vs. recurrent), grade, T-stage, direct tumor extension, tumor depth, duration of treatment, and radiation dose. Results: The subset of angiosarcomas (11 out of 57 patients) had a considerably adverse effect on treatment outcome for the total group of sarcomas, with actuarial 5-year overall survival (OS), locoregional control (LRC), and freedom from distant metastasis (FDM) rates being 31%, 24%, and 42%, respectively. In contrast, for the remaining 46 patients with other histopathological tumor types, OS, LRC, and FDM rates were significantly higher (74%, 69%, and 83%, respectively). For this group of patients, significant prognostic factors identified by uni- and multivariate analysis included tumor grade as a predictor of OS and T-stage as a predictor of LRC (p less than or equal to 0.050). Those patients who experienced a locoregional recurrence were at a significantly increased risk of dying (p = 0.004 in a multivariate model). All 17 patients without direct tumor extension to neurovascular structures, bone, contiguous organs, or skin remained free from distant failure. In contrast, 27% of 29 patients with direct extension had developed distant metastases at 5 years. In multivariate analysis, the absence of direct extension was a positive predictor of FDM (p = 0.007) and of OS (p = 0.034). Conclusions: 1) Angiosarcomas of the head and neck have a considerably poorer prognosis than other soft tissue sarcomas of this site. 2) In addition to tumor grade and size, direct tumor extension may be a useful additional staging parameter. 3) High rates of locoregional failure in the head and neck area, a potential cause of morbidity and death, indicate a need for improved treatment strategies. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIAT ONCOL,BOSTON,MA 02114. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,CYCLOTRON LAB,BOSTON,MA 02114. UNIV HAMBURG,INST BIOPHYS & RADIOBIOL,W-2000 HAMBURG,GERMANY. NR 26 TC 39 Z9 42 U1 0 U2 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 585 EP 593 DI 10.1016/0360-3016(95)00256-X PG 9 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300005 PM 7558947 ER PT J AU PALTA, JR BIGGS, PJ HAZLE, JD HUQ, MS DAHL, RA OCHRAN, TG SOEN, J DOBELBOWER, RR MCCULLOUGH, EC AF PALTA, JR BIGGS, PJ HAZLE, JD HUQ, MS DAHL, RA OCHRAN, TG SOEN, J DOBELBOWER, RR MCCULLOUGH, EC TI INTRAOPERATIVE ELECTRON-BEAM RADIATION-THERAPY - TECHNIQUE, DOSIMETRY, AND DOSE SPECIFICATION - REPORT OF TASK-FORCE 48 OF THE RADIATION-THERAPY COMMITTEE, AMERICAN-ASSOCIATION-OF-PHYSICISTS-IN-MEDICINE SO INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS LA English DT Article DE RADIOTHERAPY; SURGERY; INTRAOPERATIVE CARE; ELECTRONS; NEOPLASMS ID INTRA-OPERATIVE RADIOTHERAPY; RECURRENT COLORECTAL-CANCER; APPLICATOR SYSTEM; ADVANCED-CARCINOMA; IRRADIATION; ACCELERATOR; MEVATRON-80; EXPERIENCE; PARAMETERS; PROSPECTS AB Intraoperative radiation therapy (IORT) is a treatment modality whereby a large single dose of radiation is delivered to a surgically open, exposed cancer site. Typically, a beam of megavoltage electrons is directed at an exposed tumor or tumor bed through a specially designed applicator system. In the last few years, IORT facilities have proliferated around the world. The IORT technique and the applicator systems used at these facilities vary greatly in sophistication and design philosophy. The IORT beam characteristics vary for different designs of applicator systems. It is necessary to document the existing techniques of IORT, to detail the dosimetry data required for accurate delivery of the prescribed dose, and to have a uniform method of dose specification for cooperative clinical trials. The specific charge to the task group includes the following: (a) identify the multidisciplinary IORT team, (b) outline special considerations that must be addressed by an IORT program, (c) review currently available IORT techniques, (d) describe dosimetric measurements necessary for accurate delivery of prescribed dose, (e) describe dosimetric measurements necessary in documenting doses to the surrounding normal tissues, (f) recommend quality assurance procedures for IORT, (g) review methods of treatment documentation and verification, and (h) recommend methods of dose specification and recording for cooperative clinical trials. C1 MASSACHUSETTS GEN HOSP,DEPT RADIAT MED,BOSTON,MA 02114. UNIV TEXAS,MD ANDERSON CANC CTR,DEPT DIAGNOST RADIOL,HOUSTON,TX. THOMAS JEFFERSON UNIV,DEPT RADIAT ONCOL,PHILADELPHIA,PA. MAYO CLIN,ROCHESTER,MN. PARIS REG CANC CTR,PARIS,TX. HINSDALE HOSP,HINSDALE,IL. MED COLL OHIO,DEPT RADIAT THERAPY,TOLEDO,OH 43699. RP PALTA, JR (reprint author), UNIV FLORIDA,HLTH SCI CTR,DEPT RADIAT ONCOL,POB 100385,GAINESVILLE,FL 32610, USA. NR 66 TC 44 Z9 45 U1 0 U2 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD, ENGLAND OX5 1GB SN 0360-3016 J9 INT J RADIAT ONCOL JI Int. J. Radiat. Oncol. Biol. Phys. PD OCT 15 PY 1995 VL 33 IS 3 BP 725 EP 746 DI 10.1016/0360-3016(95)00280-C PG 22 WC Oncology; Radiology, Nuclear Medicine & Medical Imaging SC Oncology; Radiology, Nuclear Medicine & Medical Imaging GA TA483 UT WOS:A1995TA48300023 PM 7558965 ER PT J AU GRANT, EP MICHALEK, MT GOLDBERG, AL ROCK, KL AF GRANT, EP MICHALEK, MT GOLDBERG, AL ROCK, KL TI RATE OF ANTIGEN DEGRADATION BY THE UBIQUITIN-PROTEASOME PATHWAY INFLUENCES MHC CLASS-I PRESENTATION SO JOURNAL OF IMMUNOLOGY LA English DT Article ID MAJOR HISTOCOMPATIBILITY COMPLEX; TOXIC LYMPHOCYTES-T; MULTICATALYTIC PROTEINASE COMPLEX; SHORT-LIVED PROTEIN; N-END RULE; MULTIUBIQUITIN CHAIN; PROTEOLYTIC SYSTEM; INFECTED CELLS; GENE; RETICULOCYTES AB The effect on MHC class I Ag presentation of enhancing a protein's rate of degradation by the ubiquitin-proteasome pathway was investigated, In extracts of mouse B-lymphoblasts and reticulocytes, as in rabbit reticulocytes, proteins with acidic or basic N-termini are conjugated to ubiquitin and degraded by the 26S proteasome very rapidly, We found that the rate of MHC class I presentation of microinjected beta-galactosidase was enhanced when this antigenic protein was modified with such a destabilizing amino-terminal residue, This enhanced presentation was inhibited by blocking potential ubiquitination sites on the protein through methylation of amino groups and by peptide aldehyde inhibitors of the proteasome. Furthermore, in B lymphoblast cell extracts, the rapid degradation of these beta-galactosidase constructs required ATP and ubiquitin and was blocked by inhibitors of proteasomes. Their rates of degradation in extracts correlated with their rates of class I Ag presentation in vivo. These results indicate that ubiquitin conjugation is a key rate-limiting step in Ag presentation and provide further evidence for a critical role of ubiquitin and the 26S proteasome in generating MHC class I-presented peptides. C1 DANA FARBER CANC INST,DIV LYMPHOCYTE BIOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. NR 59 TC 123 Z9 126 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 OCT 15 PY 1995 VL 155 IS 8 BP 3750 EP 3758 PG 9 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100009 PM 7561079 ER PT J AU YOKOTA, K MURATA, N SAIKI, O SHIMIZU, M SPRINGER, TA KISHIMOTO, T AF YOKOTA, K MURATA, N SAIKI, O SHIMIZU, M SPRINGER, TA KISHIMOTO, T TI HIGH AVIDITY STATE OF LEUKOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 ON RHEUMATOID SYNOVIAL-FLUID T-LYMPHOCYTES SO JOURNAL OF IMMUNOLOGY LA English DT Article ID ADHESION RECEPTORS; ARTHRITIS PATIENTS; CLINICAL-FEATURES; ENDOTHELIAL-CELLS; PERIPHERAL-BLOOD; MOLECULE ICAM-1; HELPER-INDUCER; IMMUNE-SYSTEM; LFA-1; EXPRESSION AB The integrin LFA-1 (CD11a/CD18) is a cell surface adhesion molecule required for leukocyte extravasation and subsequent immune and inflammatory responses. Rapid transition between nonadherent and adherent states of LFA-1 is of key importance to Ag-specific recognition of T lymphocytes. In this paper, LFA-1-mediated adhesiveness of peripheral blood (PB) and synovial fluid (SF) T lymphocytes to affinity-purified ICAM-1-coated plates was studied in patients with rheumatoid arthritis (RA) and in patients with non-RA panels, including osteoarthritis, ankylosing spondylitis, erythema nodosum, pseudogout, and pustulosis. LFA-1-mediated adhesiveness of SF T lymphocytes was not observed in any of the 10 non-RA patients studied, although cross-linking of the TCR on lymphocytes from these patients rapidly converted LFA-1 to an adhesive state. In contrast, SF T lymphocytes from 10 of 12 RA patients exhibited LFA-1-mediated adhesiveness without a requirement for cross-linking of the TCR. No difference was seen in the cell surface density of LFA-1 between non-RA and RA T lymphocytes, suggesting that the difference in adhesiveness was due to a high avidity state of LFA-1 on SF T lymphocytes in RA. Furthermore, exposure of PB T lymphocytes, which showed a low avidity state of LFA-1, to whole SF from RA patients that was depleted of T lymphocytes could induce a high avidity state of LFA-1 in vitro. Cellfree SF from RA patients also could stimulate adhesiveness, although to a lesser extent. These data suggest the existence of a LFA-1-activating environment that is selectively found in SF from RA patients. C1 OSAKA UNIV,SCH MED,DEPT MED 3,SUITA,OSAKA 565,JAPAN. OSAKA MINAMI NATL HOSP,DIV RHEUMATOL,KAWACHIANAGANO,OSAKA 586,JAPAN. HARVARD UNIV,SCH MED,CTR BLOOD RES,BOSTON,MA 02115. RI Kishimoto, Tadamitsu/C-8470-2009 NR 48 TC 17 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 OCT 15 PY 1995 VL 155 IS 8 BP 4118 EP 4124 PG 7 WC Immunology SC Immunology GA RY581 UT WOS:A1995RY58100055 ER PT J AU RUSSELL, PS CHASE, CM COLVIN, RB AF RUSSELL, PS CHASE, CM COLVIN, RB TI CORONARY ATHEROSCLEROSIS IN TRANSPLANTED MOUSE HEARTS .4. EFFECTS OF TREATMENT WITH MONOCLONAL-ANTIBODIES TO INTERCELLULAR-ADHESION MOLECULE-1 AND LEUKOCYTE FUNCTION-ASSOCIATED ANTIGEN-1 SO TRANSPLANTATION LA English DT Article ID VCAM-1 EXPRESSION; CARDIAC ALLOGRAFT; REJECTION AB Atherosclerotic lesions in the coronary arteries of transplanted mouse hearts manifest high expression of ICAM-1 (CD54), especially on endothelial surfaces, and of LFA-1 (CD11a) on migratory mononuclear cells. The possible participation of cellular adhesion systems in the evolution of these complex lesions was suggested by the increased expression of intercellular adhesion molecule-1 (ICAM-1) and leukocyte function-associated antigen-1 (LFA-1) and also by our previous studies with this experimental system, In our studies, we have found that administration of a monoclonal antibody (mAb) to gamma-interferon will greatly suppress coronary changes, and gamma-interferon is known to stimulate the formation of these adhesion molecules. The present experiments were to evaluate how administration to murine heart transplant recipients of mAbs against ICAM-1, LFA-1, or both affected the development of coronary atherosclerosis, It was found that treatment with either mAb alone did not alter the severity of coronary atherosclerosis, but that both mAbs given together can significantly suppress lesion formation at 30 days compared with controls (P<0.044). Continuing treatment was even more effective when extended to 60 days (P<0.003). The mAbs to ICAM-1 and LFA-1 bound their targets in vivo (primarily endothelium and mononuclear cells, respectively), but complete, long-term saturation of combining sites was not attained, even with very high doses. No appreciable reduction in arterial endothelial ICAM-1 expression was evident. It is concluded that the ICAM-1/LFA-1 system is of central importance in the evolution of accelerated coronary atherosclerosis. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RP RUSSELL, PS (reprint author), MASSACHUSETTS GEN HOSP,DEPT SURG,TRANSPLANTAT UNIT,WHITE 515,BOSTON,MA 02114, USA. FU NHLBI NIH HHS [R01-HL43340] NR 19 TC 34 Z9 34 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0041-1337 J9 TRANSPLANTATION JI Transplantation PD OCT 15 PY 1995 VL 60 IS 7 BP 724 EP 729 DI 10.1097/00007890-199510150-00019 PG 6 WC Immunology; Surgery; Transplantation SC Immunology; Surgery; Transplantation GA RZ968 UT WOS:A1995RZ96800019 PM 7570984 ER PT J AU YU, K BAYONA, W KALLEN, CB HARDING, HP RAVERA, CP MCMAHON, G BROWN, M LAZAR, MA AF YU, K BAYONA, W KALLEN, CB HARDING, HP RAVERA, CP MCMAHON, G BROWN, M LAZAR, MA TI DIFFERENTIAL ACTIVATION OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS BY EICOSANOIDS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RETINOID-X RECEPTOR; FATTY-ACIDS; ADIPOCYTE DIFFERENTIATION; NUCLEAR RECEPTOR; RESPONSE ELEMENT; THYROID-HORMONE; GENE-EXPRESSION; MOUSE SKIN; CELLS; TRANSCRIPTION AB Peroxisome proliferator-activated receptors (PPARs) are nuclear hormone receptors that regulate gene transcription in response to peroxisome proliferators and fatty acids. PPARs also play an important role in the regulation of adipocyte differentiation. It is unclear, however, what naturally occurring compounds activate each of the PPAR subtypes. To address this issue, a screening assay was established using heterologous fusions of the bacterial tetracycline repressor to several members of the peroxisome proliferator-activated receptor (PPAR) family. This assay was employed to compare the activation of PPAR family members by known PPAR activators including peroxisome proliferators and fatty acids. Interestingly, the activation of PPARs by fatty acids was partially inhibited by the cyclooxygenase inhibitor indomethacin, which prevents prostaglandin synthesis. Indeed, prostaglandins PGA1 and 2, PGD1 and 2, and PGJ2-activated PPARs, while a number of other prostaglandins had no effect. We also screened a variety of hydroxyeicosatetraenoic acids (HETEs) for the ability to activate PPARs. 8(S)-HETE, but not other (S)-HETEs, was a strong activator of PPAR alpha. Remarkably, PPAR activation by 8(S)-HETE was stereoselective. In addition, 8(S)-HETE was able to induce differentiation of 3T3-L1 preadipocytes. These results indicate that PPARs are differentially activated by naturally occurring eicosanoids and related molecules. C1 UNIV PENN,SCH MED,DEPT MED,DIV ENDOCRINOL DIABET & METAB,PHILADELPHIA,PA 19104. UNIV PENN,SCH MED,DEPT GENET,PHILADELPHIA,PA 19104. SANDOZ PHARMACEUT CORP,SANDOZ RES INST,PRECLIN RES,ONCOL RES PROGRAM,E HANOVER,NJ 07936. DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. OI Kallen, Caleb/0000-0002-4156-6719 FU NIDDK NIH HHS [DK45586] NR 57 TC 547 Z9 552 U1 1 U2 7 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 OCT 13 PY 1995 VL 270 IS 41 BP 23975 EP 23983 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700021 PM 7592593 ER PT J AU ENGELAND, K ANDREWS, NC MATHEYPREVOT, B AF ENGELAND, K ANDREWS, NC MATHEYPREVOT, B TI MULTIPLE PROTEINS INTERACT WITH THE NUCLEAR INHIBITORY PROTEIN REPRESSOR ELEMENT IN THE HUMAN INTERLEUKIN-3 PROMOTER SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID COLONY-STIMULATING FACTOR; HUMAN IL-3; TRANSCRIPTION FACTOR; GENE-EXPRESSION; MESSENGER-RNA; CELLS; IDENTIFICATION; INDUCTION; REQUIRES; REGION AB T cell expression of interleukin 3 (IL-3) is directed by positive and negative cis-acting DNA elements clustered within 300 base pairs of the transcriptional start site, A strong repressor element, termed nuclear inhibitory protein (NIP), was previously mapped to a segment of the IL-3 promoter between nucleotides -271 and -250. Functional characterization of this element demonstrates that it can mediate repression when linked in cis to a heterologous promoter, DNA binding experiments were carried out to characterize the repressor activity, Using varying conditions, three distinct complexes were shown to interact specifically with the NIP region, al though only one correlates with repressor activity, Complex 1 results from binding of a ubiquitous polypeptide that recognizes the 3' portion of this sequence and is not required for repression, Complex 2 corresponds to binding of transcription factor (upstream stimulatory factor) to an E-box motif in the 5' portion of the NIP region, DNA binding specificity of complex 3 overlaps with that of upstream stimulatory factor but is clearly distinct, To determine which of the latter two complexes represents NIP activity, we incorporated small alterations into the NIP site of an IL-3 promoter-linked reporter construct and examined their effects on NIP-mediated repression, Functional specificity for repression matches the DNA binding specificity of complex 3; both repressor activity and complex 3 binding require the consensus sequence CTCACNTNC. C1 HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT PEDIAT ONCOL,BOSTON,MA 02115. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. CHILDRENS HOSP,HOWARD HUGHES MED INST,BOSTON,MA 02115. OI Andrews, Nancy/0000-0003-0243-4462 FU NIDDK NIH HHS [R01 DK41758] NR 29 TC 16 Z9 16 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 OCT 13 PY 1995 VL 270 IS 41 BP 24572 EP 24579 PG 8 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA TA217 UT WOS:A1995TA21700104 PM 7592676 ER PT J AU YE, B AKAMATSU, M SHOELSON, SE WOLF, G GIORGETTIPERALDI, S YAN, XJ ROLLER, PP BURKE, TR AF YE, B AKAMATSU, M SHOELSON, SE WOLF, G GIORGETTIPERALDI, S YAN, XJ ROLLER, PP BURKE, TR TI L-O-(2-MALONYL)TYROSINE - A NEW PHOSPHOTYROSYL MIMETIC FOR THE PREPARATION OF SRC-HOMOLOGY-2 DOMAIN INHIBITORY PEPTIDES SO JOURNAL OF MEDICINAL CHEMISTRY LA English DT Article ID TYROSINE-PHOSPHORYLATED PEPTIDES; SOLID-PHASE SYNTHESIS; SH2 DOMAIN; BIOREVERSIBLE PROTECTION; BINDING; METHYLPHOSPHONATE; BIOACTIVATION; RECOGNITION; STABILITY; P56(LCK) AB Inhibition of Src homology 2 (SH2) domain-binding interactions affords one potential means of modulating protein-tyrosine kinase-dependent signaling. Small phosphotyrosyl (pTyr)-containing peptides are able to bind to SH2 domains and compete with larger pTyr peptides or native pTyr-containing protein ligands. Such pTyr-containing peptides are limited in their utility as SH2 domain inhibitors in vivo due to their hydrolytic lability to protein-tyrosine phosphatases (PTPs) and the poor cellular penetration of the ionized phosphate moiety. An important aspect of SH2 domain inhibitor design is the creation of pTyr mimetics which are stable to PTPs and have reasonable bioavailability. To date, most PTP-resistant pTyr mimetics which bind to SH2 domains are phosphonates such as (phosphonomethyl)phenylalanine (Pmp, 2), [(monofluorophosphono)methyl]phenylalanine (FPmp, 3) or [(difluorophosphono)-methyl]-phenylalanine (F(2)Pmp, 4). Herein we report the incorporation of a new non-phosphorus-containing pTyr mimetic, L-O-(2-malonyl)tyrosine (L-OMT, 5), into SH2 domain inhibitory peptides using the protected analogue L-N-alpha-Fmoc-O'-(O '', O ''-di-tert-butyl-2-malonyl)tyrosine (6) and solid-phase peptide synthesis techniques. Five OMT-containing peptides were prepared against the following SH2 domains: the PI-3 kinase C-terminal p85 SH2 domain (Ac-D-(L-OMT)-V-P-M-L-amide, 10, IC50 = 14.2 mu M), the Src SH2 domain (Ac-Q-(L-OMT)-E-E-I-P-amide, 11, IC50 = 25 mu M, and Ac-Q-(L-OMT)-(L-OMT)-E-I-P-amide, 14, IC50 = 23 mu M), the Grb2 SH2 domain (Ac-N-(L-OMT)-V-N-I-E-amide, 12, IC50 = 120 mu M), and the N-terminal SH-PTP2 SH2 domain (Ac-L-N-(L-OMT)-I-D-L-D-L-V-amide, 13, IC50 = 22.0 mu M). These results show that peptides 10, 11, 13, and 14 have reasonable affinity for their respective SH2 domains, with the IC50 value for the SH-PTPB SH2 domain-directed peptide 13 being equivalent to that previously observed for the corresponding F(2)Pmp-containing peptide. OMT may afford a new structural starting point for the development of novel and useful SH2 domain inhibitors. C1 NCI,DIV CANC TREATMENT,MED CHEM LAB,DEV THERAPEUT PROGRAM,BETHESDA,MD 20892. HARVARD UNIV,SCH MED,JOSLIN DIABET CTR,BOSTON,MA 02215. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02215. RI Burke, Terrence/N-2601-2014 NR 45 TC 73 Z9 75 U1 0 U2 9 PU AMER CHEMICAL SOC PI WASHINGTON PA PO BOX 57136, WASHINGTON, DC 20037-0136 SN 0022-2623 J9 J MED CHEM JI J. Med. Chem. PD OCT 13 PY 1995 VL 38 IS 21 BP 4270 EP 4275 DI 10.1021/jm00021a016 PG 6 WC Chemistry, Medicinal SC Pharmacology & Pharmacy GA TA407 UT WOS:A1995TA40700016 PM 7473554 ER PT J AU WALSH, JH PETERSON, WL AF WALSH, JH PETERSON, WL TI THE TREATMENT OF HELICOBACTER-PYLORI INFECTION IN THE MANAGEMENT OF PEPTIC-ULCER DISEASE SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Review ID RANDOMIZED CONTROLLED TRIAL; DOUBLE-BLIND TRIAL; RAPID UREASE TEST; DUODENAL-ULCER; CAMPYLOBACTER-PYLORI; TRIPLE THERAPY; METRONIDAZOLE RESISTANCE; BREATH TEST; ANTIMICROBIAL AGENTS; BISMUTH SUBCITRATE C1 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED,LOS ANGELES,CA 90024. UNIV TEXAS,SW MED SCH,DEPT INTERNAL MED,DALLAS,TX 75230. VET AFFAIRS MED CTR,MED SERV,DALLAS,TX. RP WALSH, JH (reprint author), UNIV CALIF LOS ANGELES,W LOS ANGELES VET AFFAIRS MED CTR,CTR GASTROENTER BIOL,LOS ANGELES,CA 90073, USA. FU NIDDK NIH HHS [DK 17294, DK 41301] NR 94 TC 361 Z9 368 U1 1 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 OCT 12 PY 1995 VL 333 IS 15 BP 984 EP 991 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA RY586 UT WOS:A1995RY58600008 PM 7666920 ER PT J AU NEUMANN, HPH ENG, C MULLIGAN, LM GLAVAC, D ZAUNER, I PONDER, BAJ CROSSEY, PA MAHER, ER BRAUCH, H AF NEUMANN, HPH ENG, C MULLIGAN, LM GLAVAC, D ZAUNER, I PONDER, BAJ CROSSEY, PA MAHER, ER BRAUCH, H TI CONSEQUENCES OF DIRECT GENETIC TESTING FOR GERMLINE MUTATIONS IN THE CLINICAL MANAGEMENT OF FAMILIES WITH MULTIPLE ENDOCRINE NEOPLASIA, TYPE-II SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID VONHIPPEL-LINDAU DISEASE; RET PROTOONCOGENE; PHEOCHROMOCYTOMAS; FEATURES AB Objective.-Multiple endocrine neoplasia, type II (MEN-II) is an autosomal dominant disorder characterized by tumors of thyroid C cells and pheochromocytoma. Recently, germline mutations in the RET proto-oncogene have been identified in patients with MEN-II. The aims of this study were (1) to define the mutations in clinically diagnosed MEN-II families, (2) to compare the results of genetic and biochemical testing, and (3) to evaluate the impact of mutation analyses for the members of these families. Design.-Register-based survey study of clinically affected and unaffected members of MEN-II families. Setting.-Register of families from Germany and Spain with pheochromocytomas. Two research laboratories at Cambridge University in the United Kingdom. Patients.-We investigated consenting affected and unaffected members belonging to a series of 10 families who met the clinical criteria for MEN-II. Main Outcome Measures.-(1) Presence or absence of germline mutation in the RET proto-oncogene in affected and unaffected members of the 10 families, and (2) in the absence of RET mutation in a given family, presence or absence of germline mutation in the von Hippel-Lindau (VHL) gene, which is the susceptibility gene involved in a closely related syndrome, von Hippel-Lindau disease. Results.-In eight of these families, RET mutations were identified. The specific mutations were detected in all affected members. The remaining two families without RET mutations were subsequently shown to have a mutation within the VHL gene. The VHL mutations were identified in both families and represent a previously undescribed base change, After identification of the mutation, premorbid genetic testing was performed in all MEN-II and VHL families, resulting in detection of asymptomatic carriers in the MEN-II families. Clinically, the two VHL families differed from the eight MEN-II families by the presence of a C-cell tumor in only one individual from each family and extra-adrenal pheochromocytoma in three of nine affected individuals in the two families combined. Conclusions.-The diagnosis of MEN-II should be confirmed by molecular genetic analysis and the diagnosis of VHL syndrome should be considered for families with an absence of RET mutations and a preponderance of pheochromocytomas. C1 UNIV CAMBRIDGE,DEPT PATHOL,CRC,HUMAN CANC GENET RES GRP,CAMBRIDGE,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. QUEENS UNIV,DEPT PAEDIAT,KINGSTON,ON,CANADA. QUEENS UNIV,DEPT PATHOL,KINGSTON,ON K7L 3N6,CANADA. TECH UNIV MUNICH,DEPT PATHOL,W-8000 MUNICH,GERMANY. NATL INST CHEM,LJUBLJANA,SLOVENIA. UNIV CAMBRIDGE,DEPT PATHOL,MOLEC GENET GRP,CAMBRIDGE,ENGLAND. UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT CLIN GENET,CAMBRIDGE,ENGLAND. RP NEUMANN, HPH (reprint author), UNIV FREIBURG,DEPT HYPERTENS & NEPHROL,HUGSTETTER STR 55,D-79106 FREIBURG,GERMANY. RI MAHER, EAMONN/A-9507-2008; OI MAHER, EAMONN/0000-0002-6226-6918; Eng, Charis/0000-0002-3693-5145 NR 21 TC 66 Z9 68 U1 1 U2 2 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 SN 0098-7484 J9 JAMA-J AM MED ASSOC JI JAMA-J. Am. Med. Assoc. PD OCT 11 PY 1995 VL 274 IS 14 BP 1149 EP 1151 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA RY056 UT WOS:A1995RY05600030 PM 7563486 ER PT J AU BROOKER, DR KOZAK, CA KLEYMAN, TR AF BROOKER, DR KOZAK, CA KLEYMAN, TR TI EPITHELIAL SODIUM-CHANNEL GENES SCNN1B AND SCNN1G ARE CLOSELY LINKED ON DISTAL MOUSE CHROMOSOME-7 SO GENOMICS LA English DT Note ID SKELETAL-MUSCLE; ALPHA-SUBUNIT; ISOFORMS; BRAIN AB The chromosomal localizations of Scnn1b and Scnn1g, genes corresponding to the beta- and gamma-subunits, respectively, of an epithelial non-voltage-gated amiloride-sensitive sodium channel, were determined by analyses of two sets of multilocus crosses using probes generated by polymerase chain reaction and a mouse kidney cortical collecting tubule cell line (M1). Scnn1b and Scnn1g were determined to be closely linked on distal mouse chromosome 7, showing no recombination with Zp2, whereas the gene for the alpha-subunit, Scnn1a, was confirmed to map to distal mouse chromosome 6. (C) 1995 Academic Press, Inc. C1 UNIV PENN,DEPT MED,DIV RENAL,PHILADELPHIA,PA 19104. UNIV PENN,DEPT PHYSIOL,PHILADELPHIA,PA 19104. VET AFFAIRS MED CTR,PHILADELPHIA,PA 19104. NIAID,BETHESDA,MD 20892. FU NIDDK NIH HHS [DK07006] NR 26 TC 7 Z9 7 U1 0 U2 0 PU ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS PI SAN DIEGO PA 525B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 SN 0888-7543 J9 GENOMICS JI Genomics PD OCT 10 PY 1995 VL 29 IS 3 BP 784 EP 786 PG 3 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA TA966 UT WOS:A1995TA96600033 PM 8575777 ER PT J AU WEISS, MJ ORKIN, SH AF WEISS, MJ ORKIN, SH TI TRANSCRIPTION FACTOR GATA-1 PERMITS SURVIVAL AND MATURATION OF ERYTHROID PRECURSORS BY PREVENTING APOPTOSIS SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE ERYTHROPOIESIS; EMBRYONIC STEM CELLS; IN VITRO DIFFERENTIATION ID PORPHOBILINOGEN DEAMINASE GENE; ERYTHROPOIETIN RECEPTOR; CELL-DEATH; DIFFERENTIATION; P53; EXPRESSION; PROMOTER AB The transcription factor GATA-1 recognizes a consensus motif present in regulatory regions of numerous erythroid-expressed genes. Mouse embryonic stem cells lacking GATA-1 cannot form mature red blood tells in vivo. in vitro differentiation of GATA-1(-) embryonic stem cells gives rise to a population of committed erythroid precursors that exhibit developmental arrest and death. We show here that the demise of GATA-1(-) erythroid cells is accompanied by several features characteristic of apoptosis. This process occurs despite normal expression of all known GATA target genes examined, including the erythropoietin receptor, and independent of detectable accumulation of the tumor suppressor protein p53. Thus, in addition to its established role in regulating genes that define the erythroid phenotype, GATA-1 also supports the viability of red cell precursors by suppressing apoptosis. These results illustrate the multifunctional nature of GATA-1 and suggest a mechanism by which other hematopoietic transcription factors may ensure the development of specific lineages. C1 HARVARD UNIV,SCH MED,HOWARD HUGHES MED INST,BOSTON,MA 02115. RP WEISS, MJ (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,CHILDRENS HOSP,DEPT PEDIAT,DIV HEMATOL ONCOL,BOSTON,MA 02115, USA. RI Weiss, Mitchell/A-1245-2013 FU NHLBI NIH HHS [K08 HL03364-01] NR 45 TC 236 Z9 241 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9623 EP 9627 DI 10.1073/pnas.92.21.9623 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200040 PM 7568185 ER PT J AU KAHANA, JA SCHNAPP, BJ SILVER, PA AF KAHANA, JA SCHNAPP, BJ SILVER, PA TI KINETICS OF SPINDLE POLE BODY SEPARATION IN BUDDING YEAST SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SACCHAROMYCES-CEREVISIAE; MITOTIC SPINDLE; CYTOPLASMIC DYNEIN; CAENORHABDITIS-ELEGANS; KINETOCHORES; ORIENTATION; MOVEMENT; PLAQUES AB In the budding yeast Saccharomyces cerevisiae, the spindle pole body (SPB) serves as the microtubule-organizing center and is the functional analog of the centrosome of higher organisms. By expressing a fusion of a yeast SPB-associated protein to the Aequorea victoria green fluorescent protein, the movement of the SPBs in living yeast cells undergoing mitosis was observed by fluorescence microscopy. The ability to visualize SPBs in vivo has revealed previously unidentified mitotic events. During anaphase, the mitotic spindle has four sequential activities: alignment at the mother-daughter junction, fast elongation, translocation into the bud, and slow elongation. These results indicate that distinct forces act upon the spindle at different times during anaphase. C1 HARVARD UNIV, SCH MED, DEPT BIOL CHEM & MOLEC PHARMACOL, BOSTON, MA 02115 USA. DANA FARBER CANC INST, BOSTON, MA 02115 USA. HARVARD UNIV, SCH MED, DEPT CELL BIOL, BOSTON, MA 02115 USA. NR 23 TC 120 Z9 124 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9707 EP 9711 DI 10.1073/pnas.92.21.9707 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200057 PM 7568202 ER PT J AU HASSON, T HEINTZELMAN, MB SANTOS-SACCHI, J COREY, DP MOOSEKER, MS AF HASSON, T HEINTZELMAN, MB SANTOS-SACCHI, J COREY, DP MOOSEKER, MS TI EXPRESSION IN COCHLEA AND RETINA OF MYOSIN VIIA, THE GENE-PRODUCT DEFECTIVE IN USHER SYNDROME TYPE 1B SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID PIGMENT EPITHELIUM; HAIR; DYSTROPHY; RAT AB Myosin VIIa is a newly identified member of the myosin superfamily of actin-based motors. Recently, the myosin VIIa gene was identified as the gene defective in shaker-1, a recessive deafness in mice [Gibson, F., Walsh, J., Mburu, P., Varela, A., Brown, K. A., Antonio, M., Beisel, K. W., Steel, K. P. & Brown, S. D. M. (1995) Nature (London) 374, 62-64], and in human Usher syndrome type 1B, an inherited disease characterized by congenital deafness, vestibular dysfunction, and retinitis pigmentosa [Well, D., Blanchard, S., Kaplan, J., Guilford, P., Gibson, F., Walsh, J., Mburu, P., Varela, A., Levilliers, J., Weston, M. D., Kelley, P. M., Kimberling, W. J., Wagenaar, M., Levi-Acobas, F., Larget-Piet, D., Munnich, A., Steel, K. P., Brown, S. D. M. & Petit, C. (1995) Nature (London) 374, 60-61]. To understand the normal function of myosin VIIa and how it could cause these disease phenotypes when defective, we generated antibodies specific to the tail portion of this unconventional myosin. We found that myosin VIIa was expressed in cochlea, retina, testis, lung, and kidney. In cochlea, myosin VIIa expression was restricted to the inner and outer hair cells, where it was found in the apical stereocilia as well as the cytoplasm. In the eye, myosin VIIa was expressed by the retinal pigmented epithelial cells, where it was enriched within the apical actin-rich domain of this cell type. The cell-specific localization of myosin VIIa suggests that the blindness and deafness associated with Usher syndrome is due to lack of proper myosin VIIa function within the cochlear hair cells and the retinal pigmented epithelial cells. C1 YALE UNIV, DEPT CELL BIOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT SURG OTOLARYNGOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT NEUROBIOL, NEW HAVEN, CT 06520 USA. YALE UNIV, DEPT PATHOL, NEW HAVEN, CT 06520 USA. HARVARD UNIV, MASSACHUSETTS GEN HOSP, SCH MED, HOWARD HUGHES MED INST, BOSTON, MA 02114 USA. HARVARD UNIV, SCH MED, PROGRAM NEUROSCI, BOSTON, MA 02114 USA. RP HASSON, T (reprint author), YALE UNIV, DEPT BIOL, POB 6666, NEW HAVEN, CT 06520 USA. OI Corey, David/0000-0003-4497-6016 FU NIDCD NIH HHS [R01 DC000273]; NIDDK NIH HHS [DK25387, DK34989, DK38979] NR 24 TC 305 Z9 311 U1 2 U2 10 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9815 EP 9819 DI 10.1073/pnas.92.21.9815 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200079 PM 7568224 ER PT J AU NILAVER, G MULDOON, LL KROLL, RA PAGEL, MA BREAKEFIELD, XO DAVIDSON, BL NEUWELT, EA AF NILAVER, G MULDOON, LL KROLL, RA PAGEL, MA BREAKEFIELD, XO DAVIDSON, BL NEUWELT, EA TI DELIVERY OF HERPESVIRUS AND ADENOVIRUS TO NUDE RAT INTRACEREBRAL TUMORS AFTER OSMOTIC BLOOD-BRAIN-BARRIER DISRUPTION SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID SIMPLEX VIRUS MUTANTS; INVIVO GENE-TRANSFER; VECTOR; MOUSE AB The delivery of viral vectors to the brain for treatment of intracerebral tumors is most commonly accomplished by stereotaxic inoculation directly into the tumor. However, the small volume of distribution by inoculation may limit the efficacy of viral therapy of large or disseminated tumors. We have investigated mechanisms to increase vector delivery to intracerebral xenografts of human LX-1 small-cell lung carcinoma tumors in the nude rat. The distribution of Escherichia coli lacZ transgene expression from primary viral infection was assessed after delivery of recombinant virus by intratumor inoculation or intracarotid infusion with or without osmotic disruption of the blood-brain barrier (BBB). These studies used replication-compromised herpes simplex virus type 1 (HSV; vector RH105) and replication-defective adenovirus (AdRSVlacZ), which represent two of the most commonly proposed viral vectors for tumor therapy. Transvascular delivery of both viruses to intracerebral tumor was demonstrated when administered intraarterially (i.a.) after osmotic BBB disruption (n = 9 for adenovirus; n = 7 for HSV), while no virus infection was apparent after i.a. administration without BBB modification (n = 8 for adenovirus; n = 4 for HSV). The thymidine kinase-negative HSV vector infected dumps of tumor cells as a result of its ability to replicate selectively in dividing cells. Osmotic BBB disruption in combination with i.a. administration of viral vectors may offer a method of global delivery to treat disseminated brain tumors. C1 OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT CELL BIOL & ANAT,PORTLAND,OR 97201. OREGON HLTH SCI UNIV,DEPT BIOCHEM & MOLEC BIOL,DIV NEUROSURG,PORTLAND,OR 97201. VET ADM MED CTR,PORTLAND,OR 97201. HARVARD UNIV,SCH MED,PROGRAM NEUROSCI,DEPT NEUROL,BOSTON,MA 02129. HARVARD UNIV,SCH MED,CTR CANC,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP EAST,BOSTON,MA 02129. UNIV IOWA,COLL MED,DEPT INTERNAL MED,IOWA CITY,IA 52242. FU NCI NIH HHS [CA31770]; NINDS NIH HHS [NS24279, NS33618] NR 23 TC 92 Z9 92 U1 0 U2 1 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9829 EP 9833 DI 10.1073/pnas.92.21.9829 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200082 PM 7568227 ER PT J AU HU, ED TONTONOZ, P SPIEGELMAN, BM AF HU, ED TONTONOZ, P SPIEGELMAN, BM TI TRANSDIFFERENTIATION OF MYOBLASTS BY THE ADIPOGENIC TRANSCRIPTION FACTORS PPAR-GAMMA AND C/EBP-ALPHA SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID DNA-BINDING PROTEINS; DIFFERENTIATED STATE; NEGATIVE REGULATOR; PRADER-WILLI; CELL-LINES; 5-AZACYTIDINE; ACTIVATION; EXPRESSION; MUSCLE; MULTIPLE AB Skeletal muscle and adipose tissue development often has a reciprocal relationship in vivo, particularly in myodystrophic states. We have investigated whether determined myoblasts with no inherent adipogenic potential can be induced to transdifferentiate into mature adipocytes by the ectopic expression of two adipogenic transcription factors, PPAR gamma and C/EBP alpha. When cultured under optimal conditions for muscle differentiation, murine G8 myoblasts expressing PPAR gamma and C/EBP alpha show markedly reduced levels of the myogenic basic helix-loop-helix proteins MyoD, myogenin, MRF4, and myf5 and are completely unable to differentiate into myotubes. Under conditions permissive for adipogenesis including a PPAR activator, these cells differentiate into mature adipocytes that express molecular markers characteristic of this lineage. Our results demonstrate that a developmental switch between these two related but highly specialized cell types can be controlled by the expression of key adipogenic transcription factors. These factors have an ability to inhibit myogenesis that is temporally and functionally separate from their ability to stimulate adipogenesis. C1 HARVARD UNIV,SCH MED,DEPT CELL BIOL,BOSTON,MA 02115. RP HU, ED (reprint author), HARVARD UNIV,SCH MED,DANA FARBER CANC INST,44 BINNEY ST,BOSTON,MA 02115, USA. FU NIDDK NIH HHS [DK31405] NR 46 TC 473 Z9 488 U1 1 U2 15 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD OCT 10 PY 1995 VL 92 IS 21 BP 9856 EP 9860 DI 10.1073/pnas.92.21.9856 PG 5 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RZ072 UT WOS:A1995RZ07200087 PM 7568232 ER PT J AU ALBANESE, C JOHNSON, J WATANABE, G EKLUND, N VU, D ARNOLD, A PESTELL, RG AF ALBANESE, C JOHNSON, J WATANABE, G EKLUND, N VU, D ARNOLD, A PESTELL, RG TI TRANSFORMING P21(RAS) MUTANTS AND C-ETS-2 ACTIVATE THE CYCLIN D1 PROMOTER THROUGH DISTINGUISHABLE REGIONS SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID CELL-SPECIFIC INHIBITOR; STIMULATING FACTOR-I; C-JUN ACTIVITY; SIGNAL TRANSDUCTION; TRANSCRIPTIONAL ACTIVATION; PROTEIN-KINASE; SACCHAROMYCES-CEREVISIAE; G0-TO-G1 TRANSITION; MOUSE FIBROBLASTS; NUCLEAR-PROTEIN AB Several different oncogenes and growth factors promote G(1) phase progression, Cyclin D1, the regulatory subunit of several cyclin dependent kinases, is required for, and capable of shortening, the G(1) phase of the cell cycle. The present study demonstrates that transforming mutants of p21(ras) (Ras Val-12, Ras Leu-61) induce the cyclin D1 promoter in human trophoblasts (JEG-3), mink lung epithelial (Mv1.Lu), and in Chinese hamster ovary fibroblast cell lines, Site-directed mutagenesis of AP-l-like sequences at -954 abolished p21(ras)-dependent activation of cyclin D1 expression. The AP-l-like sequences were also required for activation of the cyclin D1 promoter by c-Jun. In electrophoretic mobility shift assays using nuclear extracts from cultured cells and primary tissues, several AP-1 proteins (c-Jun, JunB, JunD, and c-Fos) bound the cyclin D1 -954 region. Cyclin D1 promoter activity was stimulated by overexpression of mitogen-activated protein kinase (p41(MAPK)) or c-Ets-2 through the proximal 22 base pairs. Expression of plasmids encoding either dominant negative MAPK (p41(MAPKi)) Or dominant negatives of ETS activation (Ets-LacZ), antagonized MAPK dependent induction of cyclin D1 promoter activity. Epidermal growth factor induction of cyclin D1 transcription, through the proximal promoter region, was antagonized by either p41(MAPKi) or Ets-LacZ, suggesting that ETS functions downstream of epidermal growth factor and MAPK in the context of the cyclin D1 promoter. The activation of cyclin D1 transcription by p21(ras) provides evidence for cross-talk between the p21(ras) and cell cycle regulatory pathways. C1 NORTHWESTERN UNIV,SCH MED,DIV ENDOCRINOL METAB & MOLEC MED,CHICAGO,IL 60611. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,ENDOCRINE ONCOL UNIT,BOSTON,MA 02114. FU NCI NIH HHS [CA55909, KO8 CA 620008-01] NR 90 TC 699 Z9 704 U1 0 U2 14 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 OCT 6 PY 1995 VL 270 IS 40 BP 23589 EP 23597 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY909 UT WOS:A1995RY90900053 PM 7559524 ER PT J AU LUO, ZJ ZHANG, XF RAPP, U AVRUCH, J AF LUO, ZJ ZHANG, XF RAPP, U AVRUCH, J TI IDENTIFICATION OF THE 14.3.3-ZETA DOMAINS IMPORTANT FOR SELF-ASSOCIATION AND RAF BINDING SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID EUKARYOTIC PROTEINS; KINASE; PURIFICATION; EXPRESSION; P21(RAS); FAMILY AB The 14.3.3 zeta protein is a ubiquitous and abundant arachidonate-selective acyltransferase and putative phospholipase A(2), which self assembles into dimers and binds to c-Raf-1 and other polypeptides in vitro and in intact cells. The 14.3.3 polypeptides endogenous to Sf9 cells associate in situ with both active and inactive recombinant Raf and copurify at a fairly reproducible molar ratio that is probably 1. Purified baculoviral recombinant Raf, despite its preassociated 14.3.3 polypeptide, binds additional recombinant 14.3.3 zeta polypeptide in vitro, in a saturable and specific reaction, forming a complex that is resistant to 1 M LiCl. A two-hybrid analysis indicates that 14.3.3 zeta binds primarily to Raf noncatalytic sequences distinct from those that bind Ras-GTP, and in vitro 14.3.3 zeta binds to Raf without inhibiting the Ras-Raf association or Raf catalyzed MEK phosphorylation. Deletion analysis of 14.3.3 zeta (1-245) indicates that the 14.3.3 domain responsible for binding to Raf extends over the carboxyl-terminal 100 amino acids, whereas 14.3.3 dimerization is mediated by amino-terminal sequences. As with Ras, the 14.3.3 zeta polypeptide does not activate purified Raf directly in vitro. Moreover, expression of recombinant 14.3.3 zeta in COS cells beyond the substantial level of endogenous 14.3.3 pro tein does not alter endogenous Raf kinase, as judged by the activity of a cotransfected Erk-1 reporter. Coexpression of recombinant 14.3.3 with recombinant Myc-tagged Raf in COS cells does increase substantially the Myc-Raf kinase activity achieved during transient expression, which is attributable primarily to an increased level of Myc-Raf polypeptide, without alteration of Myc-Raf specific activity or the activation that occurs in response to epidermal growth factor or 12-O-tetradecanoylphorbol-13-acetate. Nevertheless, evidence that 14.3.3 actively participates in Raf activation in situ is provided by the finding that although full-length 14.3.3 zeta binds active Raf in situ, truncated versions of 14.3.3, some of which bind Raf polypeptide in situ nearly as well as full-length 14.3.3 zeta, are recovered in association only with inactive Raf polypeptides. Thus, 14.3.3 polypeptides bind tightly to one or more sites on c-Raf. Overexpression of 14.3.3 zeta enhances the expression of recombinant Raf, perhaps by stabilizing the Raf polypeptide. In addition, Raf polypeptides bound to truncated 14.3.3 polypeptides are unable to undergo activation in situ, indicating that 14.3.3 participates in the process of Raf activation by mechanisms that remain to be elucidated. C1 MASSACHUSETTS GEN HOSP EAST,DIABET RES LABS,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP EAST,MED SERV,BOSTON,MA 02129. HARVARD UNIV,SCH MED,DEPT MED,BOSTON,MA 02129. UNIV WURZBURG,INST MED STRAHLENKUNDE & ZELLFORSCH,D-97078 WURZBURG,GERMANY. NR 25 TC 83 Z9 84 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 OCT 6 PY 1995 VL 270 IS 40 BP 23681 EP 23687 PG 7 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA RY909 UT WOS:A1995RY90900066 PM 7559537 ER PT J AU KUROKAWA, R SODERSTROM, M HORLEIN, A HALACHMI, S BROWN, M ROSENFELD, MG GLASS, CK AF KUROKAWA, R SODERSTROM, M HORLEIN, A HALACHMI, S BROWN, M ROSENFELD, MG GLASS, CK TI POLARITY-SPECIFIC ACTIVITIES OF RETINOIC ACID RECEPTORS DETERMINED BY A CO-REPRESSOR SO NATURE LA English DT Article ID BINDING PROTEIN; DIRECT REPEAT; HORMONE; RAR AB RETINOIC acid receptors (RARs) and retinoid-X receptors (RXRs) activate or repress transcription by binding as heterodimers to DNA-response elements that generally consist of two direct repeat half-sites of consensus sequence AGGTCA (reviewed in ref. 1). On response elements consisting of direct repeats spaced by five base pairs (DR + 5 elements), RAR/RXR heterodimers activate transcription in response to RAR-specific ligands, such as all-trans-retinoic acid (RA)(2). In contrast, on elements consisting of direct repeats spaced by one base pair (DR + 1 elements), RAR/RXR heterodimers exhibit little or no response to activating ligands and repress RXR-dependent transcription(3). Here we show that ligand-dependent transactivation by RAR on DR + 5 elements requires the dissociation of a new nuclear receptor co-repressor, N-CoR, and recruitment of the putative co-activators p140 and p160 (refs 4, 5). Surprisingly, on DR + 1 elements, N-CoR remains associated with RAR/RXR heterodimers even in the presence of RAR ligands, resulting in constitutive repression. These observations indicate that DNA-response elements can allosterically regulate RAR-co-repressor interactions to determine positive or negative regulation of gene expression. C1 UNIV CALIF SAN DIEGO,DEPT MED,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DIV ENDOCRINOL & METAB,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,DIV CELLULAR & MOLEC MED,LA JOLLA,CA 92093. UNIV CALIF SAN DIEGO,HOWARD HUGHES MED INST,LA JOLLA,CA 92093. DANA FARBER CANC INST,DIV NEOPLAST DIS MECHANISMS,BOSTON,MA 02115. RI Soderstrom, Mats/C-4005-2009; OI Soderstrom, Mats/0000-0003-3927-4394; Brown, Myles/0000-0002-8213-1658 NR 21 TC 463 Z9 464 U1 0 U2 2 PU MACMILLAN MAGAZINES LTD PI LONDON PA 4 LITTLE ESSEX STREET, LONDON, ENGLAND WC2R 3LF SN 0028-0836 J9 NATURE JI Nature PD OCT 5 PY 1995 VL 377 IS 6548 BP 451 EP 454 DI 10.1038/377451a0 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA RY190 UT WOS:A1995RY19000056 PM 7566126 ER PT J AU RODABAUGH, KJ BIGGS, RB QURESHI, JA BARRETT, AJ WELCH, WR BELL, DA BERKOWITZ, RS MOK, SC AF RODABAUGH, KJ BIGGS, RB QURESHI, JA BARRETT, AJ WELCH, WR BELL, DA BERKOWITZ, RS MOK, SC TI DETAILED DELETION MAPPING OF CHROMOSOME 9P AND P16 GENE ALTERATIONS IN HUMAN BORDERLINE AND INVASIVE EPITHELIAL OVARIAN-TUMORS SO ONCOGENE LA English DT Article DE BORDERLINE OVARIAN TUMOR; OVARIAN CANCER; CHROMOSOME 9P; LOSS OF HETEROZYGOSITY; P16 GENE ID UNIFOCAL ORIGIN; CARCINOMAS; HETEROZYGOSITY; CANCER AB We used PCR amplification of tandem repeats to study the pattern of allelic loss in borderline and invasive ovarian epithelial tumors using 12 primer pairs to generate a detailed deletion map of chromosome 9p. In the invasive ovarian carcinomas, there were three regions displaying high frequency of loss of heterozygosity (LOH) ranging from 31-38%. In contrast, LOH was a rare event among the borderline ovarian tumors, with one region revealing a rate of 20% and the remaining regions only 0-8% LOH. Therefore, allelic loss does not seem to be important for the development of borderline ovarian tumors. We also examined p16 gene expression and mutations in ovarian cancer cell lines and invasive and borderline ovarian tumor tissues. Southern blot analysis revealed no losses of the p16 gene in either the invasive or borderline ovarian tumors. However, the ovarian carcinoma cell lines showed a 50% homozygous deletion rate, SSCP analysis detected a mobility shift in only one (borderline) tumor. Since the primary invasive ovarian tumors did not show any deletions or mutations, it appears that p16 does not play a role in the pathogenesis of these tumors. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT OBSTET GYNECOL & REPROD BIOL,GYNECOL ONCOL LAB,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. FU NCI NIH HHS [R01CA63381] NR 27 TC 44 Z9 45 U1 0 U2 0 PU STOCKTON PRESS PI BASINGSTOKE PA HOUNDMILLS, BASINGSTOKE, HANTS, ENGLAND RG21 2XS SN 0950-9232 J9 ONCOGENE JI Oncogene PD OCT 5 PY 1995 VL 11 IS 7 BP 1249 EP 1254 PG 6 WC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Oncology; Cell Biology; Genetics & Heredity GA RY967 UT WOS:A1995RY96700004 PM 7478544 ER PT J AU STROMINGER, JL WILEY, DC AF STROMINGER, JL WILEY, DC TI THE CLASS-I AND CLASS-II PROTEINS OF THE HUMAN MAJOR HISTOCOMPATIBILITY COMPLEX SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID MOLECULES; ANTIGEN; PEPTIDE; HLA-A2 C1 DANA FARBER CANC INST,DIV TUMOR VIROL,BOSTON,MA 02115. CHILDRENS HOSP,HOWARD HUGHES MED INST,DEPT MED,MOLEC MED LAB,BOSTON,MA. RP STROMINGER, JL (reprint author), HARVARD UNIV,DEPT MOLEC & CELLULAR BIOL,CAMBRIDGE,MA 02138, USA. NR 16 TC 9 Z9 9 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 OCT 4 PY 1995 VL 274 IS 13 BP 1074 EP 1076 DI 10.1001/jama.274.13.1074 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA RX108 UT WOS:A1995RX10800036 PM 7563464 ER PT J AU GOLDHIRSCH, A WOOD, WC SENN, HJ GLICK, JH GELBER, RD AF GOLDHIRSCH, A WOOD, WC SENN, HJ GLICK, JH GELBER, RD TI MEETING HIGHLIGHTS - INTERNATIONAL CONSENSUS PANEL ON THE TREATMENT OF PRIMARY BREAST-CANCER SO JOURNAL OF THE NATIONAL CANCER INSTITUTE LA English DT Editorial Material ID SURGICAL ADJUVANT BREAST; TAMOXIFEN; THERAPY; CHEMOTHERAPY; TUMORS C1 EMORY UNIV,SCH MED,ATLANTA,GA. KANTONSSPITAL,MED KLIN C,ST GALLEN,SWITZERLAND. UNIV PENN,CTR CANC,PHILADELPHIA,PA 19104. DANA FARBER CANC INST,DIV BIOSTAT,BOSTON,MA 02115. RP GOLDHIRSCH, A (reprint author), OSPED CIVICO,INT BREAST CANC STUDY GRP,CH-6900 LUGANO,SWITZERLAND. NR 16 TC 150 Z9 151 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 OCT 4 PY 1995 VL 87 IS 19 BP 1441 EP 1445 DI 10.1093/jnci/87.19.1441 PG 5 WC Oncology SC Oncology GA RW694 UT WOS:A1995RW69400007 PM 7674331 ER PT J AU ENGLERT, C HOU, X MAHESWARAN, S BENNETT, P NGWU, C RE, GG GARVIN, AJ ROSNER, MR HABER, DA AF ENGLERT, C HOU, X MAHESWARAN, S BENNETT, P NGWU, C RE, GG GARVIN, AJ ROSNER, MR HABER, DA TI WT1 SUPPRESSES SYNTHESIS OF THE EPIDERMAL GROWTH-FACTOR RECEPTOR AND INDUCES APOPTOSIS SO EMBO JOURNAL LA English DT Article DE APOPTOSIS; EPIDERMAL GROWTH FACTOR RECEPTOR; WILMS TUMOR; WT1 ID WILMS-TUMOR GENE; FACTOR-A-CHAIN; S1 NUCLEASE; CELL-DEATH; KIDNEY DEVELOPMENT; UROGENITAL SYSTEM; PROMOTER ACTIVITY; SUPERCOILED DNA; EXPRESSION; PRODUCT AB The Wilms tumor suppressor gene WT1 encodes a developmentally regulated transcription factor that is mutated in a subset of embryonal tumors. To test its functional properties, we developed osteosarcoma cell lines expressing WT1 under an inducible tetracycline-regulated promoter. Induction of WT1 resulted in programmed cell death. This effect, which was differentially mediated by the alternative splicing variants of WT1, was independent of p53, WT1-mediated apoptosis was associated with reduced synthesis of the epidermal growth factor receptor (EGFR), but not of other postulated WT1-target genes, and it was abrogated by constitutive expression of EGFR, WT1 repressed transcription from the EGFR promoter, binding to two TC-rich repeat sequences. In the developing kidney, EGFR expression in renal precursor cells declined with the onset of WT1 expression. Repression of EGFR and induction of apoptosis by WT1 provide a potential mechanism that may contribute to its critical role in normal kidney development and to the immortalization of tumor cells with inactivated WT1 alleles. C1 MASSACHUSETTS GEN HOSP,MOLEC GENET LAB,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. UNIV CHICAGO,BEN MAY INST,DEPT MOLEC GENET & CELL BIOL,CHICAGO,IL 60637. MED UNIV S CAROLINA,DEPT PATHOL & LAB MED,CHARLESTON,SC 29325. FU NCI NIH HHS [CA58596, CA35541, CA 37887] NR 83 TC 284 Z9 288 U1 0 U2 1 PU OXFORD UNIV PRESS UNITED KINGDOM PI OXFORD PA WALTON ST JOURNALS DEPT, OXFORD, ENGLAND OX2 6DP SN 0261-4189 J9 EMBO J JI Embo J. PD OCT 2 PY 1995 VL 14 IS 19 BP 4662 EP 4675 PG 14 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA TA216 UT WOS:A1995TA21600003 PM 7588596 ER PT J AU HENG, JE MOSCARITOLO, K DREYER, EB AF HENG, JE MOSCARITOLO, K DREYER, EB TI NMDA SENSITIVITY IS NEURITE ENHANCED SO NEUROREPORT LA English DT Article DE N-METHYL-D-ASPARTATE; RETINAL GANGLION CELLS; NEURITES; EXCITOTOXICITY; GLUTAMATE; AXONS; CELL DEATH ID GLUTAMATE RECEPTOR SUBUNIT; RAT-BRAIN; NERVOUS-SYSTEM; NEUROTOXICITY; LOCALIZATION; ANTIBODIES; DROSOPHILA; ASPARTATE; OUTGROWTH; LESIONS AB GLUTAMATE toxicity in retinal ganglion cells has been well documented both in vitro and in vitro, and may play a role in both normal neuronal development and a variety of pathological states. Glutamate receptors are found on cell bodies and neuronal processes, both axons and dendrites. Other work has suggested that one or more of these locales may play a more pronounced role in glutamate-mediated toxicity. We now report that N-methyl-D-aspartate (NMDA) is more toxic to retinal ganglion cells with neurites. Cells without neurites were relatively unaffected by glutamate or NMDA. Cells with longer neurites or more neurite branch points were more likely to sustain NMDA-mediated neurotoxicity. These observations suggest that glutamate-mediated loss may be mediated through NMDA receptors found on neurites, rather than through a direct effect on the cell body. C1 MASSACHUSETTS EYE & EAR INFIRM,HOWE LAB,DEPT OPHTHALMOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. FU NEI NIH HHS [R01 EY10009] NR 29 TC 11 Z9 11 U1 0 U2 0 PU RAPID SCIENCE PUBLISHERS PI LONDON PA 2-6 BOUNDARY ROW, LONDON, ENGLAND SE1 8NH SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD OCT 2 PY 1995 VL 6 IS 14 BP 1890 EP 1892 DI 10.1097/00001756-199510020-00016 PG 3 WC Neurosciences SC Neurosciences & Neurology GA RX808 UT WOS:A1995RX80800016 PM 8547591 ER PT J AU TORCHILIN, VP AF TORCHILIN, VP TI TARGETING OF DRUGS AND DRUG CARRIERS WITHIN THE CARDIOVASCULAR-SYSTEM SO ADVANCED DRUG DELIVERY REVIEWS LA English DT Review DE DRUG TARGETING; CIRCULATION; LUNG; HEART; THROMBOSIS; ATHEROSCLEROSIS; MYOCARDIAL INFARCTION; LUNG CANCER; TARGETED THROMBOLYTIC THERAPY; TARGETED IMAGING; MONOCLONAL ANTIBODY; LIPOSOME ID SINGLE-CHAIN UROKINASE; TISSUE PLASMINOGEN-ACTIVATOR; ANGIOTENSIN-CONVERTING ENZYME; CELL LUNG-CANCER; BISPECIFIC MONOCLONAL-ANTIBODY; LOW-DENSITY LIPOPROTEINS; EXPERIMENTAL MYOCARDIAL-INFARCTION; INHIBITS PLATELET-AGGREGATION; MYOSIN-SPECIFIC ANTIBODY; ISCHEMIC-HEART-DISEASE AB The targeting of pharmaceuticals within the cardiovascular system is reviewed. The delivery of both diagnostic and therapeutic agents is discussed with the use of different soluble and particulate carriers, including liposomes, microspheres, and cells. Targeting of pharmaceuticals to pathological areas of the vascular bed involves diagnostics and treatment of thromboses, atherosclerosis, and different malignancies, Special emphasis is put on the targeted diagnostics (visualization) of thromboses and targeted thrombolytic therapy. Antibody-mediated and magnetically driven delivery of thrombolytic enzymes is discussed. Targeting of atherosclerotic lesions with specific antibody-based diagnostic preparations is considered. The interaction of particulate carriers (liposomes) with endothelial cells is analyzed. Lung-targeted delivery can be performed via both respiratory and circulatory routes. A brief description of aerosolized preparations is presented. Drug and carrier targeting to lung-specific antigens is described with a special emphasis on lung malignancy targeting. Principal systems for drug targeting to compromised myocardium are reviewed, with a primary impact on those based on anti-cardiac myosin antibodies, Targeted visualization of myocardial infarction and myocarditis is discussed, Possible use of liposomes, immunoliposomes and long-circulating (immuno)liposomes for targeting of pharmaceuticals to the heart is also considered. RP TORCHILIN, VP (reprint author), MASSACHUSETTS GEN HOSP EAST,CTR IMAGING & PHARMACEUT RES,149 13TH ST,BOSTON,MA 02129, USA. NR 242 TC 33 Z9 34 U1 0 U2 12 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0169-409X J9 ADV DRUG DELIVER REV JI Adv. Drug Deliv. Rev. PD OCT PY 1995 VL 17 IS 1 BP 75 EP 101 DI 10.1016/0169-409X(95)00042-6 PG 27 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA TH265 UT WOS:A1995TH26500007 ER PT J AU PRESTON, DB YOUNG, EW KOCH, PB FORTI, EM AF PRESTON, DB YOUNG, EW KOCH, PB FORTI, EM TI THE NURSES ATTITUDES ABOUT AIDS SCALE (NAAS) - DEVELOPMENT AND PSYCHOMETRIC ANALYSIS SO AIDS EDUCATION AND PREVENTION LA English DT Article ID BEHAVIOR AB This article describes the development and psychometric evaluation of the Nurses' Attitudes About AIDS Scale (NAAS). Based on a review of the literature on attitude theory and measurement and on HIV/AIDS, 273 items were developed for inclusion in the scale. Content validity was established by a panel of ten nurses in current practice, six experts in AIDS education and adult health nursing, and one expert in attitude and scaling theory and measurement. On this basis, 60 items were selected and pilot tested for face validity on 33 practicing nurses, Responses from a purposive sample of 731 working RNs were evaluated. A factor analysis yielded a single homosexuality factor explaining 53% of the variance in the 21-item measure, This subscale was labeled attitudes about people with AIDS. Alpha reliability coefficient was .96. Two subscales were identified in the AIDS dimension: attitudes about nursing care concerns (12 items; alpha =.83) and attitudes about social-professional concerns (8 items; alpha =.72), These subscales explained 38.5% of the variance. Additional evidence of construct validity as well as predictive validity were established. C1 MASSACHUSETTS GEN HOSP,INST HLTH PROFESS,BOSTON,MA 02114. RP PRESTON, DB (reprint author), PENN STATE UNIV,DEPT HLTH EDUC & NURSING,UNIVERSITY PK,PA 16802, USA. NR 22 TC 11 Z9 11 U1 1 U2 2 PU GUILFORD PRESS PI NEW YORK PA 72 SPRING STREET, NEW YORK, NY 10012 SN 0899-9546 J9 AIDS EDUC PREV JI Aids Educ. Prev. PD OCT PY 1995 VL 7 IS 5 BP 443 EP 454 PG 12 WC Education & Educational Research; Public, Environmental & Occupational Health SC Education & Educational Research; Public, Environmental & Occupational Health GA RY815 UT WOS:A1995RY81500006 PM 8672396 ER PT J AU BIRD, DA SZCZEPIORKOWSKI, ZM TRACE, VC LAPOSATA, M AF BIRD, DA SZCZEPIORKOWSKI, ZM TRACE, VC LAPOSATA, M TI LOW-DENSITY-LIPOPROTEIN RECONSTITUTED WITH FATTY-ACID ETHYL-ESTERS AS A PHYSIOLOGICAL VEHICLE FOR ETHYL-ESTER DELIVERY TO INTACT-CELLS SO ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH LA English DT Article DE LIPIDS; ETHANOL; LIPOPROTEINS; FATTY ACIDS; HEPG2 CELLS ID ETHANOL; DEGRADATION; METABOLITES AB Fatty acid ethyl esters (FAEEs), esterification products of ethanol and fatty acids, have been found selectively in the organs damaged by ethanol abuse, and on that basis have been implicated as contributors to ethanol-induced organ damage. To directly assess the cytotoxic potential of FAEEs with intact cells in a physiological system, solubility must be achieved for these highly nonpolar lipids in aqueous medium. After ethanol ingestion, FAEEs can be found within low-density lipoproteins (LDLs). Therefore, to achieve solubility with FAEEs bound to a naturally occurring lipid carrier, we developed a method for FAEE solubilization and delivery to cells in culture. We synthesized radiolabeled FAEEs and incorporated them into human LDL particles that bind to LDL receptors and deliver FAEEs to intact cells. Ethyl palmitate acid ethyl oleate were incorporated into LDLs yielding molar ratios of FAEEs to LDLs of 2,153 +/- 249 and 4,208 +/- 403, respectively. LDL reconstituted with FAEE had the same electrophoretic mobility on agarose gel electrophoresis as native LDL, indicating that the reconstituted LDL (rLDL) was not oxidatively modified. Quantitative analysis of the solubilization of FAEEs in aqueous medium was investigated by adding FAEEs to tissue culture medium either directly or reconstituted in LDL at a concentration of 27 mu M. The percentage of FAEE quantitated was 40.0 +/- 2.5% and 89.3 +/- 0.6% for FAEEs added directly and in rLDLs, respectively. After sterile filtration of these two media, the percentage of FAEE that remained was 11.8 +/- 1.3% (direct addition) and 74.9 +/- 1.3% (addition within rLDL), further demonstrating that the LDL particle did solubilize the FAEE. There was a linear relationship between the amount of rLDL in the medium and the amount of FAEE incorporated into the cells. Finally, native LDL (1:21 for rLDL:native LDL) was shown to decrease the uptake of ethyl oleate rLDL by HepG2 cells by 23.1 +/- 3.1%, indicating the involvement of a receptor in rLDL uptake. Use of LDL reconstituted with FAEE as a solubilized farm of the ester will permit in vivo and in vitro studies assessing the physiological and pathological roles of these potentially toxic ethanol metabolites. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,CLIN LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. RI Szczepiorkowski, Zbigniew/A-1359-2007 OI Szczepiorkowski, Zbigniew/0000-0003-2357-9564 FU NIDDK NIH HHS [R01 DK37454, R01 DK43159] NR 19 TC 14 Z9 14 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0145-6008 J9 ALCOHOL CLIN EXP RES JI Alcoholism (NY) PD OCT PY 1995 VL 19 IS 5 BP 1265 EP 1270 DI 10.1111/j.1530-0277.1995.tb01610.x PG 6 WC Substance Abuse SC Substance Abuse GA TA738 UT WOS:A1995TA73800026 PM 8561300 ER PT J AU BROWN, JH DELUCA, SA AF BROWN, JH DELUCA, SA TI THE RADIOLOGY OF RHEUMATOID-ARTHRITIS SO AMERICAN FAMILY PHYSICIAN LA English DT Article AB Rheumatoid arthritis is a connective tissue disorder of unknown etiology that can involve any synovial-lined joint in the body. The most frequently involved joints are the small joints of the hands and feet, the wrists, knees and elbows, and the glenohumeral and acromioclavicular joints. The radiographic hallmarks of rheumatoid arthritis are swelling of the soft tissue, osteoporosis, narrowing of the joint spaces and marginal erosions. The unique combination of osteoporosis, marginal erosions and relatively minimal reactive bone formation help distinguish rheumatoid arthritis from other inflammatory arthritides. RP BROWN, JH (reprint author), MASSACHUSETTS GEN HOSP,BOSTON,MA 02114, USA. NR 0 TC 7 Z9 7 U1 0 U2 4 PU AMER ACAD FAMILY PHYSICIANS PI KANSAS CITY PA 8880 WARD PARKWAY, KANSAS CITY, MO 64114-2797 SN 0002-838X J9 AM FAM PHYSICIAN JI Am. Fam. Physician PD OCT PY 1995 VL 52 IS 5 BP 1372 EP 1380 PG 9 WC Primary Health Care; Medicine, General & Internal SC General & Internal Medicine GA RY414 UT WOS:A1995RY41400017 PM 7572560 ER PT J AU SIU, SC LEVINE, RA RIVERA, JM XIE, SW LETHOR, JP HANDSCHUMACHER, MD WEYMAN, AE PICARD, MH AF SIU, SC LEVINE, RA RIVERA, JM XIE, SW LETHOR, JP HANDSCHUMACHER, MD WEYMAN, AE PICARD, MH TI 3-DIMENSIONAL ECHOCARDIOGRAPHY IMPROVES NONINVASIVE ASSESSMENT OF LEFT-VENTRICULAR VOLUME AND PERFORMANCE SO AMERICAN HEART JOURNAL LA English DT Article ID CROSS-SECTIONAL ECHOCARDIOGRAPHY; 3-DIMENSIONAL ECHOCARDIOGRAPHY; 2-DIMENSIONAL ECHOCARDIOGRAPHY; QUANTIFYING VOLUME; MATHEMATIC MODELS; RECONSTRUCTION; VALIDATION AB To calculate left ventricular (LV) volume by two-dimensional echocardiography (2DE), assumptions must be made about ventricular symmetry and geometry. Three-dimensional echocardiography (3DE) can quantitate LV volume without these limitations, yet its incremental value over 2DE is unknown. The purpose of this study was to compare the accuracy of LV volume determination by 3DE to standard 2DE methods. To compare the accuracy of 3DE with standard 2DE algorithms for quantitating LV volume, 28 excised canine ventricles of known volume and varying shapes (15 symmetric and 13 aneurysmal) and 10 instrumented dogs prepared so that instantaneous ventricular volume could be measured were examined by 2DE (bullet and biplane Simpson's formulas) and again by 3DE. In both excised and beating hearts, 3DE was more accurate in quantitating volume than either 2DE method (excised: error = 0.6 +/- 3.2, 2.5 +/- 10.7, and 4.0 +/- 8.5 ml by 3D, bullet, and Simpson's, respectively; beating: error = -0.5 +/- 3.5, -0.3 +/- 9.6, and -7.6 +/- 8.0 mi by 3DE, bullet, and Simpson's, respectively). This difference in accuracy between 3DE and 2DE methods was especially apparent in asymmetric ventricles distorted by ischemia or right ventricular volume overload. Stroke volume and ejection fraction calculated by 3DE also demonstrated better agreement with actual values than the bullet or Simpson methods with less variability (ejection fraction: error = -0.2% +/- 5.1%, 7.7% +/- 8.5%, and 6.8% +/- 12.3% by 3DE, bullet, and Simpson's, respectively). In both in vitro and in vivo settings, 3DE provides improved accuracy for LV volume and performance than current 2DE algorithms. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CARDIAC ULTRASOUND LAB,CARDIAC UNIT,BOSTON,MA 02114. FU NHLBI NIH HHS [HL-38176] NR 25 TC 48 Z9 50 U1 0 U2 2 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 OCT PY 1995 VL 130 IS 4 BP 812 EP 822 DI 10.1016/0002-8703(95)90082-9 PG 11 WC Cardiac & Cardiovascular Systems SC Cardiovascular System & Cardiology GA RX471 UT WOS:A1995RX47100019 PM 7572591 ER PT J AU QUINTANILLAMARTINEZ, L ZUKERBERG, LR FERRY, JA HARRIS, NL AF QUINTANILLAMARTINEZ, L ZUKERBERG, LR FERRY, JA HARRIS, NL TI EXTRAMEDULLARY TUMORS OF LYMPHOID OR MYELOID BLAST - THE ROLE OF IMMUNOHISTOLOGY IN DIAGNOSIS AND CLASSIFICATION SO AMERICAN JOURNAL OF CLINICAL PATHOLOGY LA English DT Article DE IMMUNOHISTOCHEMISTRY; MYELOID SARCOMA; ACUTE LEUKEMIA; LYMPHOBLASTIC LYMPHOMA; MIXED LINEAGE ID ACUTE LYMPHOBLASTIC-LEUKEMIA; MIXED-LINEAGE LEUKEMIA; EMBEDDED TISSUE-SECTIONS; T-CELL; GRANULOCYTIC SARCOMA; ANTIGEN EXPRESSION; CLINICAL IMPORTANCE; CD3 ANTIGEN; CHILDHOOD; MARKER AB The diagnosis of primitive hematologic malignancies in extramedullary sites (lymphoblastic lymphoma of T- or B-cell type and myeloid sarcoma) on paraffin-embedded tissue sections is difficult and often impossible because of the primitive morphology of the neoplastic cells. The authors studied 21 extramedullary tumors of lymphoid or myeloid blasts. They used a panel of 22 antibodies on frozen sections and 9 antibodies on paraffin sections to determine the spectrum of immunophenotypes and to develop a practical panel for diagnosis. All but two of the cases could be classified as lymphoid or myeloid using immunohistologic analysis, Thirteen cases were classified as lymphoblastic lymphoma/acute lymphoblastic leukemia (LBL/ALL); 10 were classified as precursor T (CD7+, CD3+/-, CD45+) and 3 as precursor B-cell (CD19+/- CD10+ CD45-) type. Five cases were classified as myeloid sarcoma (CD13+ myeloperoxidase+, lysozyme+). Two LBL/ALL coexpressed either CD33 (1 case) or CD15 (1 case), and one myeloid sarcoma coexpressed TdT and CD7. One case appeared to be truly mixed lineage, coexpressing CD3 with myeloperoxidase and lysozyme, and two cases expressed no lineage-specific antigens. There were clinical differences between the three major tumor types, and within the category of T-precursor LBL/ALL, classification according to stage of thymocyte differentiation was associated with distinctive clinical features. In conclusion, the spectrum of immunophenotypes detected on frozen section was similar to that reported by flow cytometry on peripheral blood and bone marrow specimens. The most useful antigens on frozen sections were CD7 and CD3 (T cell), CD10 and CD19 (B cell), and CD13 (myeloid). TdT was coexpressed by one myeloid sarcoma and was undetectable in 40% of LBL/ALL. On paraffin sections, myeloperoxidase and lysozyme were reliable markers of myeloid lineage, but none of the markers used on paraffin sections distinguished between LBL/ALL of T- and B-precursor types. Both B-LBL/ALL and myeloid sarcomas were often CD45- on paraffin sections, which may be a obstacle in determining the diagnosis. These distinctions appear to have clinical relevance. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NR 60 TC 32 Z9 34 U1 0 U2 2 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0002-9173 J9 AM J CLIN PATHOL JI Am. J. Clin. Pathol. PD OCT PY 1995 VL 104 IS 4 BP 431 EP 443 PG 13 WC Pathology SC Pathology GA RZ475 UT WOS:A1995RZ47500013 PM 7572794 ER PT J AU REBBECK, TR WALKER, A HOSKINS, K PHELAN, C NAROD, SA GARBER, JE WEBER, BL AF REBBECK, TR WALKER, A HOSKINS, K PHELAN, C NAROD, SA GARBER, JE WEBER, BL TI MODIFICATION OF FAMILIAL BREAST-CANCER PENETRANCE BY GLUTATHIONE-S-TRANSFERASE GENOTYPES SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV PENN,PHILADELPHIA,PA 19104. MCGILL UNIV,MONTREAL,PQ,CANADA. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 19 EP 19 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700021 ER PT J AU LEGARE, RD HO, CY OTTERUD, B VARVIL, T SAXENA, R GALLAGHER, M DEHART, D KOHLER, S LI, F LEPPERT, M GILLILAND, DG AF LEGARE, RD HO, CY OTTERUD, B VARVIL, T SAXENA, R GALLAGHER, M DEHART, D KOHLER, S LI, F LEPPERT, M GILLILAND, DG TI A FAMILIAL PLATELET DISORDER WITH PROPENSITY TO DEVELOP ACUTE MYELOID-LEUKEMIA IS LINKED TO HUMAN-CHROMOSOME 21Q22.1-22.2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,BOSTON,MA 02115. UNIV UTAH,DEPT HUMAN GENET,SALT LAKE CITY,UT. UNIV UTAH,HOWARD HUGHES MED INST,SALT LAKE CITY,UT. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 109 EP 109 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700109 ER PT J AU MURTHY, AE GUSELLA, JF AF MURTHY, AE GUSELLA, JF TI IDENTIFICATION OF NOVEL GENES WHOSE PRODUCTS MAY INTERACT WITH MERLIN SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 113 EP 113 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700111 ER PT J AU AGOSTI, CG XU, L PINNEY, D BEAUCHAMP, R HOBBS, W GUSELLA, J RAMESH, V AF AGOSTI, CG XU, L PINNEY, D BEAUCHAMP, R HOBBS, W GUSELLA, J RAMESH, V TI CELLULAR-LOCALIZATION OF ENDOGENOUS AND EPITOPE-TAGGED NF2 PROTEIN MERLIN SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 114 EP 114 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700114 ER PT J AU MUNROE, DJ BRIC, E PELLETIER, J MORGENBESSER, S PRAWITT, D LOEBBERT, R SAIT, S NOWAK, N HIGGINS, M PETRUZZI, MJ DASGUPTA, S WINTERPACHT, A ZABEL, BU SHOWS, TB BUCKLER, A HOUSMAN, DE AF MUNROE, DJ BRIC, E PELLETIER, J MORGENBESSER, S PRAWITT, D LOEBBERT, R SAIT, S NOWAK, N HIGGINS, M PETRUZZI, MJ DASGUPTA, S WINTERPACHT, A ZABEL, BU SHOWS, TB BUCKLER, A HOUSMAN, DE TI A SMALL REGION ON 11P15.5 THAT IS HOMOZYGOUSLY DELETED IN WILMS-TUMORS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MIT,CTR CANC RES,CAMBRIDGE,MA 02139. MCGILL UNIV,CTR CANC,MONTREAL,PQ H3G 1Y6,CANADA. ROSWELL PK CANC INST,BUFFALO,NY 14263. UNIV MAINZ,CHILDRENS HOSP,W-6500 MAINZ,GERMANY. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 116 EP 116 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700118 ER PT J AU HENSKE, EP NEUMANN, HPH SCHEITHAUER, BW SHORT, MP HERBST, EW KWIATKOWSKI, DJ AF HENSKE, EP NEUMANN, HPH SCHEITHAUER, BW SHORT, MP HERBST, EW KWIATKOWSKI, DJ TI FREQUENT CHROMOSOME 16P13 LOSS OF HETEROZYGOSITY IN TUBEROUS SCLEROSIS ANGIOMYOLIPOMAS SUPPORTS A TUMOR-SUPPRESSOR ROLE FOR TSC2 BUT NOT TSC1 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. UNIV FREIBURG,FREIBURG,GERMANY. MAYO CLIN & MAYO FDN,ROCHESTER,MN 55905. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 117 EP 117 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700116 ER PT J AU SEBOUN, E OKSENBERG, J LATHROP, M GOODKIN, DE RIMMLER, J HAINES, JL FIZAMES, C LINCOLN, R PERICAKVANCE, MA GUSELLA, JF ROSES, AD WEISSENBACH, J HAUSER, SL AF SEBOUN, E OKSENBERG, J LATHROP, M GOODKIN, DE RIMMLER, J HAINES, JL FIZAMES, C LINCOLN, R PERICAKVANCE, MA GUSELLA, JF ROSES, AD WEISSENBACH, J HAUSER, SL TI MULTIPLE-SCLEROSIS AND INSULIN-DEPENDENT DIABETES-MELLITUS SHARE SUSCEPTIBILITY LOCI SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 GENETHON,F-91002 EVRY,FRANCE. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. HOP ST LOUIS,F-75010 PARIS,FRANCE. DUKE UNIV,DURHAM,NC. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RI Hauser, Stephen/J-2978-2016 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 181 EP 181 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700181 ER PT J AU STOTLER, CJ LAWRENCE, N RUTTER, M DEAVEN, L MCCORMICK, MK BUCKLER, AJ AF STOTLER, CJ LAWRENCE, N RUTTER, M DEAVEN, L MCCORMICK, MK BUCKLER, AJ TI TRANSCRIPTION AND PHYSICAL MAPPING OF HUMAN-CHROMOSOME-12 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. LOS ALAMOS NATL LAB,LOS ALAMOS,NM. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 291 EP 291 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700291 ER PT J AU MYERS, SM ENG, C PONDER, BAJ MULLIGAN, LM AF MYERS, SM ENG, C PONDER, BAJ MULLIGAN, LM TI CHARACTERIZATION OF RET PROTOONCOGENE 3' SPLICING VARIANTS AND POLYADENYLATION SITES - A NOVEL C-TERMINAL FOR RET SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 QUEENS UNIV,DEPT PATHOL,KINGSTON,ON K7L 3N6,CANADA. QUEENS UNIV,DEPT PEDIAT,KINGSTON,ON K7L 3N6,CANADA. UNIV CAMBRIDGE,ADDENBROOKES HOSP,CRC HUMAN CANC GENET RES GRP,CAMBRIDGE CB2 2QQ,ENGLAND. HARVARD UNIV,SCH MED,DANA FARBER CANC INST,DEPT MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 389 EP 389 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700389 ER PT J AU ALLINGHAM, RR DAMII, KF SPEER, MC PRITCHARD, M HAINES, JL PERICAKVANCE, MA AF ALLINGHAM, RR DAMII, KF SPEER, MC PRITCHARD, M HAINES, JL PERICAKVANCE, MA TI THE UTILITY OF INTRAOCULAR-PRESSURE AS A QUANTITATIVE TRAIT FOR GENETIC-LINKAGE ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 441 EP 441 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700441 ER PT J AU DELBONO, EA GWIAZDA, JE HAINES, JL WIGGS, JL AF DELBONO, EA GWIAZDA, JE HAINES, JL WIGGS, JL TI ANALYSIS OF PEDIGREES AFFECTED BY JUVENILE-ONSET MYOPIA - EVIDENCE FOR AUTOSOMAL-DOMINANT INHERITANCE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT OPHTHALMOL,BOSTON,MA 02111. MIT,DEPT BRAIN & COGNIT SCI,BOSTON,MA. MASSACHUSETTS GEN HOSP,DEPT MOLEC NEUROGENET,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 473 EP 473 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700475 ER PT J AU CHEN, ZY KRAMM, CM BATTINELLI, EM LI, F SCHUBACK, DE COREY, DP AF CHEN, ZY KRAMM, CM BATTINELLI, EM LI, F SCHUBACK, DE COREY, DP TI NEURON-SPECIFIC EXPRESSION OF THE NORRIE DISEASE GENE (NDP) IN THE CENTRAL-NERVOUS-SYSTEM SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP EAST,MOLEC NEUROGENET LAB,BOSTON,MA 02129. MASSACHUSETTS GEN HOSP EAST,HOWARD HUGHES MED INST,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 747 EP 747 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700747 ER PT J AU CROOP, JM LUX, M FLETCHER, JA TILLER, GE AF CROOP, JM LUX, M FLETCHER, JA TILLER, GE TI THE HUMAN HOMOLOG OF THE DROSOPHILA WHITE GENE MAPS NEAR A POTENTIAL LOCUS FOR BIPOLAR AFFECTIVE-DISORDER ON CHROMOSOME 21Q22.3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DANA FARBER CANC INST,BOSTON,MA 02115. HARVARD UNIV,SCH MED,BOSTON,MA. VANDERBILT UNIV,SCH MED,NASHVILLE,TN 37212. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 807 EP 807 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700807 ER PT J AU LONG, KR MORROW, B KUCHERLAPATI, R MCCORMICK, MK BUCKLER, AJ TROFATTER, JA AF LONG, KR MORROW, B KUCHERLAPATI, R MCCORMICK, MK BUCKLER, AJ TROFATTER, JA TI LOCALIZATION OF A NOVEL CLATHRIN HEAVY-CHAIN GENE TO THE DIGEORGE-SYNDROME REGION OF HUMAN-CHROMOSOME-22 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA. ALBERT EINSTEIN COLL MED,BRONX,NY. NR 0 TC 0 Z9 0 U1 0 U2 3 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 832 EP 832 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700834 ER PT J AU MITCHISON, HM MUNROE, PB ORAWE, AM TASCHNER, PEM KREMMIDIOTIS, G LENSINK, I MEINCKE, LI DARIGO, KL DEVOS, N GARDINER, RM CALLEN, DF BREUNING, MH LERNER, TI DOGGETT, NA MOLE, SE AF MITCHISON, HM MUNROE, PB ORAWE, AM TASCHNER, PEM KREMMIDIOTIS, G LENSINK, I MEINCKE, LI DARIGO, KL DEVOS, N GARDINER, RM CALLEN, DF BREUNING, MH LERNER, TI DOGGETT, NA MOLE, SE TI BATTEN-DISEASE .3. GENOMIC STRUCTURE OF A CANDIDATE FOR CLN3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UCL, SCH MED, DEPT PAEDIAT, LONDON W1N 8AA, ENGLAND. LEIDEN UNIV, DEPT GENET, LEIDEN, NETHERLANDS. WOMENS & CHILDRENS HOSP, DEPT CYTOGENET & MOLEC GENET, ADELAIDE, SA, AUSTRALIA. LOS ALAMOS NATL LAB, DIV LIFE SCI, LOS ALAMOS, NM USA. MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET UNIT, BOSTON, MA USA. RI Callen, David/G-1975-2012 NR 0 TC 0 Z9 0 U1 0 U2 0 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 836 EP 836 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700836 ER PT J AU MUDD, SH LEVY, HL TANGERMAN, A BOUJET, C BUIST, N DAVIDSONMUNDT, A HUDGINS, L OYANAGI, K NAGAO, M WILSON, WG AF MUDD, SH LEVY, HL TANGERMAN, A BOUJET, C BUIST, N DAVIDSONMUNDT, A HUDGINS, L OYANAGI, K NAGAO, M WILSON, WG TI ISOLATED PERSISTENT HYPERMETHIONINEMIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID METHIONINE ADENOSYLTRANSFERASE DEFICIENCY; TRANSAMINATION; BALANCES; PATHWAY; HUMANS; DEFECT AB New information has been obtained on 30 patients with isolated persistent hypermethioninemia, most of them previously unreported. Biopsies to confirm the presumptive diagnosis of partially deficient activity of ATP: L-methionine S-adenosyltransferase (MAT; E.C.2.5.1.6) in liver were not performed on most of these patients. However, none showed the clinical findings or the extreme elevations of serum folate previously described in other patients with isolated hypermethioninemia considered not to have hepatic MAT deficiency. Patients ascertained on biochemical grounds had no neurological abnormalities, and 27/30 had IQs or Bayley development-index scores within normal limits or were judged to have normal mental development. Methionine transamination metabolites accumulated abnormally only when plasma methionine concentrations exceeded 300-350 mu M and did so more markedly after 0.9 years of age. Data were obtained on urinary organic acids as well as plasma creatinine concentrations. Patterns of inheritance of isolated hypermethioninemia were variable. Considerations as to the optimal management of this group of patients are discussed. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02114. HARVARD UNIV,CHILDRENS HOSP,SCH MED,BOSTON,MA 02115. UNIV NIJMEGEN HOSP,DIV GASTROINTESTINAL & LIVER DIS,6500 HB NIJMEGEN,NETHERLANDS. CHU GRENOBLE,BIOCHIM METAB & EXPLORAT NUTR LAB,F-38043 GRENOBLE,FRANCE. OREGON HLTH SCI UNIV,CTR CHILD DEV & REHABIL,PORTLAND,OR 97201. UNIV COLORADO,CHILDRENS HOSP,HLTH SCI CTR,DENVER,CO 80218. UNIV ARIZONA,HLTH SCI CTR,MARICOPA MED CTR,PHOENIX,AZ. ODORI CHILDRENS CLIN,SAPPORO,HOKKAIDO,JAPAN. NATL OTARU HOSP,OTARU,HOKKAIDO,JAPAN. UNIV VIRGINIA,CHILDRENS MED CTR,CHARLOTTESVILLE,VA 22903. RP MUDD, SH (reprint author), NIMH,DIRP,LGCB,BLDG 36,ROOM 3D-06,36 CONVENT DR,MSC 4094,BETHESDA,MD 20892, USA. NR 42 TC 56 Z9 56 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. 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PD OCT PY 1995 VL 57 IS 4 SU S BP 970 EP 970 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700969 ER PT J AU ROGUS, JJ HAINES, JL PERICAKVANCE, MA HARRINGTON, DP AF ROGUS, JJ HAINES, JL PERICAKVANCE, MA HARRINGTON, DP TI AN EXTENSION OF THE WEIGHTED PAIRWISE CORRELATION STATISTIC (WPC) TO TEST FOR LINKAGE IN THE PRESENCE OF GENE-ENVIRONMENT INTERACTION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DUKE UNIV,MED CTR,DURHAM,NC. DANA FARBER CANC INST,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 974 EP 974 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68700974 ER PT J AU BERGER, R MEZEY, E CLANCY, K HARTA, G BROWN, RH BROWNSTEIN, M PATTERSON, D AF BERGER, R MEZEY, E CLANCY, K HARTA, G BROWN, RH BROWNSTEIN, M PATTERSON, D TI ALDEHYDE OXIDASE AND XANTHINE DEHYDROGENASE AS CANDIDATE GENES FOR ALS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 ELEANOR ROOSEVELT INST,DENVER,CO. NIH,BETHESDA,MD. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV COLORADO,HLTH SCI CTR,DENVER,CO. RI Brownstein, Michael/B-8609-2009 NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1072 EP 1072 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701071 ER PT J AU HAINES, JL SEBOUN, E RIMMLER, J GOODKIN, DE LINCOLN, R BAZYK, A LEE, A OKSENBERG, J GUSELLA, JF ROSES, AD HAUSER, SL PERICAKVANCE, MA AF HAINES, JL SEBOUN, E RIMMLER, J GOODKIN, DE LINCOLN, R BAZYK, A LEE, A OKSENBERG, J GUSELLA, JF ROSES, AD HAUSER, SL PERICAKVANCE, MA TI A COMPLETE GENOMIC SCREEN FOR MULTIPLE-SCLEROSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA. GENETHON,PARIS,FRANCE. DUKE UNIV,MED CTR,DURHAM,NC. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA. RI Hauser, Stephen/J-2978-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1105 EP 1105 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701105 ER PT J AU HAYNES, C SPEER, MC PEEDIN, M ROSES, AD HAINES, JL VANCE, JM PERICAKVANCE, MA AF HAYNES, C SPEER, MC PEEDIN, M ROSES, AD HAINES, JL VANCE, JM PERICAKVANCE, MA TI PEDIGENE - A COMPREHENSIVE DATA MANAGEMENT-SYSTEM TO FACILITATE EFFICIENT AND RAPID DISEASE GENE-MAPPING SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DIV NEUROL,DURHAM,NC 27710. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1106 EP 1106 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701106 ER PT J AU KIM, DJ ROGUS, JJ SIDDIQUE, T DENG, HX HENTATI, A PERICAKVANCE, MA HAINES, JL AF KIM, DJ ROGUS, JJ SIDDIQUE, T DENG, HX HENTATI, A PERICAKVANCE, MA HAINES, JL TI MEIOTIC BREAKPOINT MAPPING ON CHROMOSOME-2 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH PUBL HLTH,BOSTON,MA 02115. NORTHWESTERN UNIV,SCH MED,CHICAGO,IL 60611. DUKE UNIV,SCH MED,DURHAM,NC. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1121 EP 1121 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701121 ER PT J AU LIU, AWY DELGADOESCUETA, AV GEE, MN ZHAO, HZ SPELLMAN, JM MEDINA, MT ALONSO, ME CORDOVA, S DONNADIEU, FR PECK, R SPARKES, RS AF LIU, AWY DELGADOESCUETA, AV GEE, MN ZHAO, HZ SPELLMAN, JM MEDINA, MT ALONSO, ME CORDOVA, S DONNADIEU, FR PECK, R SPARKES, RS TI JUVENILE MYOCLONIC EPILEPSY IN CHROMOSOME 6P12-11 - RECOMBINATIONS NARROW INTO 6CM REGION AND LOCUS HETEROGENEITY SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV CALIF LOS ANGELES,COMPREHENS EPILEPSY PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,W LOS ANGELES DVA MED CTR,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. UNIV CALIF LOS ANGELES,DEPT MED,LOS ANGELES,CA 90024. NATL INST NEUROL & NEUROSURG,MEXICO CITY,DF,MEXICO. NATL AUTONOMOUS UNIV TEGUCIGALPA,TEGUCIGALPA,HONDURAS. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1131 EP 1131 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701132 ER PT J AU MCINTOSH, I CLOUGH, MV PETERS, K GREENSPAN, D KWIATKOWSKI, DJ MCCORMICK, MK FRANCOMANO, CA AF MCINTOSH, I CLOUGH, MV PETERS, K GREENSPAN, D KWIATKOWSKI, DJ MCCORMICK, MK FRANCOMANO, CA TI NAIL-PATELLA SYNDROME - REFINED LINKAGE TO MARKERS ON 9Q34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 JOHNS HOPKINS UNIV,SCH MED,CTR GENET MED,BALTIMORE,MD. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. KAISER PERMANENTE,SACRAMENTO,CA. UNIV WISCONSIN,SCH MED,MADISON,WI. BRIGHAM & WOMENS HOSP,BOSTON,MA 02115. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1135 EP 1135 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701134 ER PT J AU PERICAKVANCE, MA CONNEALLY, PM GASKELL, PC SMALL, GW SAUNDERS, AM YAMAOKA, L ROBINSON, C TERMINASSIAN, M LOCKE, PA PRITCHARD, M HAYNES, CS GROWDON, J TANZI, RE GUSELLA, JF ROSES, AD HAINES, JL AF PERICAKVANCE, MA CONNEALLY, PM GASKELL, PC SMALL, GW SAUNDERS, AM YAMAOKA, L ROBINSON, C TERMINASSIAN, M LOCKE, PA PRITCHARD, M HAYNES, CS GROWDON, J TANZI, RE GUSELLA, JF ROSES, AD HAINES, JL TI THE SEARCH FOR ADDITIONAL LATE-ONSET ALZHEIMER-DISEASE GENES - A COMPLETE GENOMIC SCREEN SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN 46204. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1150 EP 1150 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701148 ER PT J AU ROSES, AD DEVLIN, B CONNEALLY, PM SMALL, GW SAUNDERS, AM PRITCHARD, M LOCKE, PA HAINES, JL PERICAKVANCE, MA RISCH, N AF ROSES, AD DEVLIN, B CONNEALLY, PM SMALL, GW SAUNDERS, AM PRITCHARD, M LOCKE, PA HAINES, JL PERICAKVANCE, MA RISCH, N TI MEASURING THE GENETIC CONTRIBUTION OF APOE IN LATE-ONSET ALZHEIMER-DISEASE (AD) SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. CARNEGIE MELLON UNIV,PITTSBURGH,PA 15213. INDIANA UNIV,MED CTR,INDIANAPOLIS,IN. UNIV CALIF LOS ANGELES,LOS ANGELES,CA. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. STANFORD UNIV,STANFORD,CA 94305. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1163 EP 1163 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701163 ER PT J AU SARRATOSA, JM DELGADOESCUETA, AV POSADA, I SHIH, S DRURY, I BERCIANO, J ZABALA, JA ANTUNEZ, MC SPARKES, RS AF SARRATOSA, JM DELGADOESCUETA, AV POSADA, I SHIH, S DRURY, I BERCIANO, J ZABALA, JA ANTUNEZ, MC SPARKES, RS TI A GENE FOR PROGRESSIVE MYOCLONUS EPILEPSY OF THE LAFORA TYPE MAPS TO CHROMOSOME 6Q SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,CALIF COMPREHENS EPILEPSY PROGRAM,LOS ANGELES,CA. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. HOSP DOCE OCTUBRE,DEPT NEUROL,MADRID,SPAIN. UNIV MICHIGAN HOSP,DEPT NEUROL,ANN ARBOR,MI 48109. HOSP MARQUES VALDECILLA,DEPT NEUROL,SANTANDER,SPAIN. CLIN PUERTA HIERRO,NEUROL SERV,MADRID,SPAIN. HOSP UNIV VIRGEN ARRIXACA,NEUROL SERV,MURCIA,SPAIN. UNIV CALIF LOS ANGELES,DEPT MED,DIV MED GENET,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1167 EP 1167 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701168 ER PT J AU KOLODNY, EH SOSA, MAG BATTISTINI, S SARTORATO, EL YERETSIAN, J MACFARLANE, H GUSELLA, J DEGASPERI, R AF KOLODNY, EH SOSA, MAG BATTISTINI, S SARTORATO, EL YERETSIAN, J MACFARLANE, H GUSELLA, J DEGASPERI, R TI MOLECULAR-GENETICS OF LATE-ONSET KRABBE DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 NYU,SCH MED,DEPT NEUROL,NEW YORK,NY 10016. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,BOSTON,MA 02115. RI Battistini, Stefania/N-2596-2015 OI Battistini, Stefania/0000-0003-2887-7624 NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1250 EP 1250 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701249 ER PT J AU NANCE, MA RAABE, WA MIDANI, H DAVID, WS MEGNA, L PERICAKVANCE, MA HAINES, JL AF NANCE, MA RAABE, WA MIDANI, H DAVID, WS MEGNA, L PERICAKVANCE, MA HAINES, JL TI CONFIRMATION LINKAGE OF FAMILIAL SPASTIC PARAPARESIS TO CHROMOSOME 2P21 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 VET ADM MED CTR,DEPT NEUROL,MINNEAPOLIS,MN. HENNEPIN CTY MED CTR,DEPT NEUROL,MINNEAPOLIS,MN. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. DUKE UNIV,MED CTR,DURHAM,NC. NR 0 TC 1 Z9 1 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1281 EP 1281 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701282 ER PT J AU RIMMLER, J HAUSER, SL GOODKIN, DE SEBOUN, E LINCOLN, R BAZYK, A ALPER, C OKSENBERG, J GUSELLA, JF ROSES, AD PERICAKVANCE, MA HAINES, JL AF RIMMLER, J HAUSER, SL GOODKIN, DE SEBOUN, E LINCOLN, R BAZYK, A ALPER, C OKSENBERG, J GUSELLA, JF ROSES, AD PERICAKVANCE, MA HAINES, JL TI LINKAGE OF MULTIPLE-SCLEROSIS TO THE HLA REGION ON CHROMOSOME SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 DUKE UNIV,MED CTR,DURHAM,NC. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA 94143. GENETHON,PARIS,FRANCE. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. CTR BLOOD RES,BOSTON,MA 02115. RI Hauser, Stephen/J-2978-2016 NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1307 EP 1307 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701307 ER PT J AU TANZI, RE ROMANO, D SHERRINGTON, R PETTINGELL, W ROGAEV, E LIANG, Y SCHMIDT, S ROGAEVA, E CROWLEY, A LEVESQUE, G MURRELL, J IKEZA, M CHI, H FRASER, P ROMMENS, G BUCKLER, A STGEORGEHYSLOP, P WASCO, W AF TANZI, RE ROMANO, D SHERRINGTON, R PETTINGELL, W ROGAEV, E LIANG, Y SCHMIDT, S ROGAEVA, E CROWLEY, A LEVESQUE, G MURRELL, J IKEZA, M CHI, H FRASER, P ROMMENS, G BUCKLER, A STGEORGEHYSLOP, P WASCO, W TI ISOLATION OF CANDIDATE GENES FOR THE MAJOR EARLY-ONSET FAMILIAL ALZHEIMERS-DISEASE LOCUS ON CHROMOSOME-14 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,GENET & AGING LAB,BOSTON,MA. UNIV TORONTO,TORONTO,ON,CANADA. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1326 EP 1326 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701323 ER PT J AU TASCHNER, PEM MITCHISON, HM KREMMIDIOTIS, G ORAWE, A MUNROE, PB DEVOS, N BOUSTANY, RM LENSINK, I MEINCKE, LJ ANDERSON, JW DARIGO, KL JARVELA, IE BUCKLER, AJ GUSELLA, JF HAINES, JL GARDINER, RM SUTHERLAND, GR DOGGETT, NA CALLEN, DF MOLE, SE LERNER, TJ BREUNING, MH AF TASCHNER, PEM MITCHISON, HM KREMMIDIOTIS, G ORAWE, A MUNROE, PB DEVOS, N BOUSTANY, RM LENSINK, I MEINCKE, LJ ANDERSON, JW DARIGO, KL JARVELA, IE BUCKLER, AJ GUSELLA, JF HAINES, JL GARDINER, RM SUTHERLAND, GR DOGGETT, NA CALLEN, DF MOLE, SE LERNER, TJ BREUNING, MH TI BATTEN-DISEASE .2. GENOMIC ALTERATIONS IN CLN3 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 LEIDEN UNIV, DEPT HUMAN GENET, 2300 RA LEIDEN, NETHERLANDS. UCL, SCH MED, DEPT PAEDIAT, LONDON W1N 8AA, ENGLAND. WOMENS & CHILDRENS HOSP, DEPT CYTOGENET & MOLEC GENET, ADELAIDE, SA, AUSTRALIA. MASSACHUSETTS GEN HOSP, MOLEC NEUROGENET UNIT, BOSTON, MA USA. LOS ALAMOS NATL LAB, DIV LIFE SCI, LOS ALAMOS, NM USA. RI Mole, Sara/C-2024-2008; Sutherland, Grant/D-2606-2012; Callen, David/G-1975-2012 NR 0 TC 0 Z9 0 U1 0 U2 1 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1328 EP 1328 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701327 ER PT J AU WILSON, PJ SHORT, MP BOVE, C JOZWIAK, S KWIATKOWSKI, DJ RAMESH, V HAINES, JL AF WILSON, PJ SHORT, MP BOVE, C JOZWIAK, S KWIATKOWSKI, DJ RAMESH, V HAINES, JL TI IDENTIFICATION OF MUTATIONS IN THE TSC2 GENE USING SINGLE-STRAND CONFORMATIONAL POLYMORPHISM ANALYSIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. CHILDRENS HLTH CTR,DIV CHILD NEUROL,WARSAW,POLAND. BRIGHAM & WOMENS HOSP,DIV EXPTL MED,BOSTON,MA 02115. NR 0 TC 0 Z9 0 U1 0 U2 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1345 EP 1345 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701344 ER PT J AU HASSON, T RAMAKRISHNAN, M HEINTZELMAN, MB SCHWARTZ, M SANTOS-SACCHI, J CHEN, ZY COREY, DP MOOSEKER, MS AF HASSON, T RAMAKRISHNAN, M HEINTZELMAN, MB SCHWARTZ, M SANTOS-SACCHI, J CHEN, ZY COREY, DP MOOSEKER, MS TI EXPRESSION IN COCHLEA AND RETINA OF MYOSIN-VIIA, THE GENE DEFECTIVE IN USHER SYNDROME TYPE 1B SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 YALE UNIV, DEPT BIOL, NEW HAVEN, CT USA. YALE UNIV, DEPT CELL BIOL, NEW HAVEN, CT USA. YALE UNIV, DEPT SURG OTOLARYNGOL, NEW HAVEN, CT USA. YALE UNIV, DEPT NEUROBIOL, NEW HAVEN, CT USA. MASSACHUSETTS GEN HOSP, DEPT NEUROL, BOSTON, MA 02114 USA. HARVARD UNIV, HOWARD HUGHES MED INST, SCH MED, BOSTON, MA USA. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1396 EP 1396 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701396 ER PT J AU JACKSON, CE RIMMLER, JB ROBINSON, LC JOHNSON, CC DHONDT, E PRITCHARD, ML HAINES, JL PERICAKVANCE, MA AF JACKSON, CE RIMMLER, JB ROBINSON, LC JOHNSON, CC DHONDT, E PRITCHARD, ML HAINES, JL PERICAKVANCE, MA TI LACK OF APOLIPOPROTEIN E-4 [APOE-4] EFFECT IN LATE-ONSET ALZHEIMER-DISEASE [AD] IN THE AMISH POPULATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HENRY FORD HOSP,DETROIT,MI. DUKE UNIV,MED CTR,DURHAM,NC. MASSACHUSETTS GEN HOSP,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1404 EP 1404 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701403 ER PT J AU PRALEA, M MATTOX, CL HAINES, JL SCHUMAN, JS WIGGS, JL AF PRALEA, M MATTOX, CL HAINES, JL SCHUMAN, JS WIGGS, JL TI GENETIC-ANALYSIS OF JUVENILE GLAUCOMA - PHENOTYPIC COMPARISON OF PEDIGREES GENETICALLY LINKED TO 1Q21-Q31 WITH THOSE AFFECTED PEDIGREES NOT GENETICALLY LINKED TO THE CHROMOSOME-1 LOCUS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 TUFTS UNIV NEW ENGLAND MED CTR,DEPT OPHTHALMOL,BOSTON,MA. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1443 EP 1443 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701441 ER PT J AU REHM, H GUTIERREZESPELETA, G SIMS, KB GARCIA, R JIMENEZ, G PRIEST, JM KEATS, BJB MORTON, CC AF REHM, H GUTIERREZESPELETA, G SIMS, KB GARCIA, R JIMENEZ, G PRIEST, JM KEATS, BJB MORTON, CC TI NORRIE GENE MUTATION IN A COSTA-RICAN KINDRED WITH A NOVEL PHENOTYPE INCLUDING PERIPHERAL VASCULAR-DISEASE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT GENET,BOSTON,MA 02115. HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,BOSTON,MA 02115. UNIV COSTA RICA,ESCUELA BIOL,SAN JOSE,COSTA RICA. MASSACHUSETTS GEN HOSP,CTR NEUROSCI,BOSTON,MA. HOSP MEXICO,SAN JOSE,COSTA RICA. LOUISIANA STATE UNIV,MED CTR,DEPT BIOMETRY & GENET,NEW ORLEANS,LA 70112. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1446 EP 1446 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701445 ER PT J AU SINGH, I KREMSER, K GHOSH, B SINGH, AK PAI, GS AF SINGH, I KREMSER, K GHOSH, B SINGH, AK PAI, GS TI ABNORMALITY IN TRANSLATIONAL REGULATION OF CATALASE IN DISORDERS OF PEROXISOMAL BIOGENESIS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MED UNIV S CAROLINA,DEPT PEDIAT,CHARLESTON,SC 29425. RALPH H JOHNSON VET AFFAIRS MED CTR,DEPT PATHOL,CHARLESTON,SC. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1454 EP 1454 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701455 ER PT J AU CUTONE, S RUTTER, M OZELIUS, L MURRELL, J BUCKLER, A MCCORMICK, MK AF CUTONE, S RUTTER, M OZELIUS, L MURRELL, J BUCKLER, A MCCORMICK, MK TI PHYSICAL MAPPING OF HUMAN-CHROMOSOME SEGMENT 9Q34 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1495 EP 1495 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701496 ER PT J AU KELLEY, PM HASSON, T OVERBECK, LD WESTON, MD CHEN, Z ORTEN, DJ COREY, DP MOOSEKER, MS SUMEGI, J KIMBERLING, WJ AF KELLEY, PM HASSON, T OVERBECK, LD WESTON, MD CHEN, Z ORTEN, DJ COREY, DP MOOSEKER, MS SUMEGI, J KIMBERLING, WJ TI A PHYSICAL MAP OF THE USHER IB MYOSIN-VII REGION ON CHROMOSOME 11Q SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 BOYS TOWN NATL RES HOSP,DEPT GENET,OMAHA,NE 68131. YALE UNIV,DEPT BIOL,NEW HAVEN,CT. MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV NEBRASKA,MED CTR,DEPT PATHOL & MICROBIOL,OMAHA,NE 68182. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1517 EP 1517 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701516 ER PT J AU LUCENTE, D SHEA, D BUCKLER, A RUTTER, M MCCORMICK, MK AF LUCENTE, D SHEA, D BUCKLER, A RUTTER, M MCCORMICK, MK TI EXON CONTENT MAP OF THE REGION OF CHROMOSOME-21 AROUND LOCUS D21S55 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MOLEC NEUROGENET UNIT,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT GENET,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1527 EP 1527 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701527 ER PT J AU MCCORMICK, MK MCINTOSH, I RUTTER, M FRANCOMANO, C CUTONE, S AF MCCORMICK, MK MCINTOSH, I RUTTER, M FRANCOMANO, C CUTONE, S TI POSITIONAL CLONING OF THE NAIL-PATELLA SYNDROME GENE SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,DEPT NEUROL,MOLEC NEUROGENET UNIT,BOSTON,MA 02129. HARVARD UNIV,SCH MED,BOSTON,MA 02129. JOHNS HOPKINS UNIV,SCH MED,CTR MED GENET,BALTIMORE,MD 21205. NIH,NATL CTR HUMAN GENOME RES,MED GENET BRANCH,BETHESDA,MD 20892. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1530 EP 1530 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701529 ER PT J AU MURRELL, J CUTONE, S VU, D RUTTER, M LONG, K LAWRENCE, N STOTLER, C MCCORMICK, MK BUCKLER, A AF MURRELL, J CUTONE, S VU, D RUTTER, M LONG, K LAWRENCE, N STOTLER, C MCCORMICK, MK BUCKLER, A TI PHYSICAL AND TRANSCRIPTION MAP OF A 2.5 MB REGION OF HUMAN-CHROMOSOME 9Q34 SPANNING THE TUBEROUS SCLEROSIS COMPLEX-1 CANDIDATE REGION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET LAB,BOSTON,MA 02114. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1542 EP 1542 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701541 ER PT J AU SAINZ, J SERRATOSA, JM SHIH, S DELGADOESCUETA, AV AF SAINZ, J SERRATOSA, JM SHIH, S DELGADOESCUETA, AV TI CONSTRUCTION OF A 7 CM YAC CONTIG WITHIN THE REGION OF THE JUVENILE MYOCLONIC EPILEPSY GENE ON CHROMOSOME 6P12-P11 SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 W LOS ANGELES VET AFFAIRS MED CTR,CALIF COMPREHENS EPILEPSY PROGRAM,LOS ANGELES,CA 90073. UNIV CALIF LOS ANGELES,DEPT NEUROL,LOS ANGELES,CA 90024. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1563 EP 1563 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701563 ER PT J AU SLAUGENHAUPT, SA LIEBERT, CB MULL, J MACCORMACK, K LEBEL, A OLEARY, K LUCENTE, D MCCORMICK, MK BUCKLER, AJ MAAYAN, C AXELROD, F BLUMENFELD, A GUSELLA, JF AF SLAUGENHAUPT, SA LIEBERT, CB MULL, J MACCORMACK, K LEBEL, A OLEARY, K LUCENTE, D MCCORMICK, MK BUCKLER, AJ MAAYAN, C AXELROD, F BLUMENFELD, A GUSELLA, JF TI EVALUATION OF CANDIDATE GENES FOR FAMILIAL DYSAUTONOMIA SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02115. HADASSAH UNIV HOSP,IL-91120 JERUSALEM,ISRAEL. NYU,MED CTR,NEW YORK,NY 10016. NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1569 EP 1569 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701569 ER PT J AU GULLEY, ML PULITZER, DR EAGAN, PA CHO, CG SCHNEIDER, BG AF GULLEY, ML PULITZER, DR EAGAN, PA CHO, CG SCHNEIDER, BG TI EPSTEIN-BARR-VIRUS IS AN EARLY EVENT IN GASTRIC CARCINOGENESIS AND IS INDEPENDENT OF BCL2 EXPRESSION AND P53 ACCUMULATION SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 UNIV TEXAS,HLTH SCI CTR,DEPT PATHOL,SAN ANTONIO,TX. AUDIE L MURPHY MEM VET ADM MED CTR,SAN ANTONIO,TX. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1749 EP 1749 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701748 ER PT J AU CHAN, P SHULTS, CW TANNER, CM FINK, JS KURTH, M MAREK, KL ELMER, LW AF CHAN, P SHULTS, CW TANNER, CM FINK, JS KURTH, M MAREK, KL ELMER, LW TI USE OF A CLINICAL-TRIALS POPULATION IN GENETIC RESEARCH SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 PARKINSONS INST,PARKINSON STUDY GRP,SUNNYVALE,CA. UNIV CALIF SAN DIEGO,LA JOLLA,CA 92093. MASSACHUSETTS GEN HOSP,BOSTON,MA 02114. BARROW NEUROL INST,PHOENIX,AZ 85013. YALE UNIV,NEW HAVEN,CT. UNIV MICHIGAN,ANN ARBOR,MI 48109. NR 1 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 1835 EP 1835 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701835 ER PT J AU CARSIQUE, R PHAMDINH, D BOESPFLUGTANGUY, O GOODKIN, DE LATHROP, M RIMMLER, J HAINES, JL OKSENBERG, J FIZAMES, C LINCOLN, R PERICAKVANCE, MA GUSELLA, JF ROSES, AD WEISSENBACH, J DAUTIGNY, A HAUSER, SL SEBOUN, E AF CARSIQUE, R PHAMDINH, D BOESPFLUGTANGUY, O GOODKIN, DE LATHROP, M RIMMLER, J HAINES, JL OKSENBERG, J FIZAMES, C LINCOLN, R PERICAKVANCE, MA GUSELLA, JF ROSES, AD WEISSENBACH, J DAUTIGNY, A HAUSER, SL SEBOUN, E TI GENETIC SUSCEPTIBILITY TO MULTIPLE-SCLEROSIS - THE ROLE OF MAG, MBP, MOG, OMGP AND PLP SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 GENETHON,F-91002 EVRY,FRANCE. CNRS,URA 1488,F-75005 PARIS,FRANCE. FAC MED CLERMONT FERRAND,INSERM,U384,CLERMONT FERRAND,FRANCE. UNIV CALIF SAN FRANCISCO,SAN FRANCISCO,CA. HOP ST LOUIS,F-75010 PARIS,FRANCE. DUKE UNIV,DURHAM,NC. MASSACHUSETTS GEN HOSP,MOLEC NEUROGENET UNIT,BOSTON,MA. RI Hauser, Stephen/J-2978-2016 NR 0 TC 0 Z9 0 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 OCT PY 1995 VL 57 IS 4 SU S BP 1872 EP 1872 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68701871 ER PT J AU BOVE, C MACCOLLIN, M SHORT, MP ADAMS, D AF BOVE, C MACCOLLIN, M SHORT, MP ADAMS, D TI ADVISABILITY OF TESTING CHILDREN AND ADOLESCENTS PRESYMTOMATICALLY FOR NFII - FAMILIES AND NURSES PERCEPTIONS SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 MASSACHUSETTS GEN HOSP,NF CLIN,BOSTON,MA. BOSTON COLL NURSING,BOSTON,MA. NR 0 TC 0 Z9 0 U1 0 U2 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 S WOODLAWN AVE, CHICAGO, IL 60637 SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 1995 VL 57 IS 4 SU S BP 2017 EP 2017 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA RW687 UT WOS:A1995RW68702016 ER PT J AU HAY, ED ZUK, A AF HAY, ED ZUK, A TI TRANSFORMATIONS BETWEEN EPITHELIUM AND MESENCHYME - NORMAL, PATHOLOGICAL, AND EXPERIMENTALLY-INDUCED SO AMERICAN JOURNAL OF KIDNEY DISEASES LA English DT Review DE CADHERINS; EPITHELIUM; EPITHELIAL MESENCHYMAL TRANSFORMATION; HEPATIC GROWTH FACTOR SCATTER FACTOR; INTEGRINS; KIDNEY DEVELOPMENT; MDCK CELLS; MESENCHYME; MESENCHYMAL-EPITHELIAL TRANSFORMATION; NIDOGEN; POLYCYSTIC KIDNEY DISEASE; RENAL MALIGNANCY ID POLYCYSTIC KIDNEY-DISEASE; HEPATOCYTE GROWTH-FACTOR; CELL-ADHESION MOLECULES; E-CADHERIN; SCATTER FACTOR; EXTRACELLULAR-MATRIX; COLLAGEN GELS; MONOCLONAL-ANTIBODY; SURFACE POLARITY; LENS EPITHELIUM AB In this review, we define the two major tissue types, epithelium and mesenchyme, and we describe the transformations (transdifferentiations) of epithelium to mesenchyme (EMT) and mesenchyme to epithelium (MET) that occur during embryonic development, The differentiation of the metanephric blastema provides a striking example of MET, Differentiation of metanephric epithelium is promoted by matrix molecules and receptors (nidogen, laminins, alpha 6 integrins), hepatic growth factor/scatter factor, and products of the genes wnt-1, wnt-4, and Pax-2, Transformation of MDCK epithelium to mesenchyme-like cells is promoted in vitro by antibodies to E-cadherin, products of v-src, v-ras, and v-mos, and by manipulation of the epithelium on collagen gels. Suspension in collagen gel, transforming growth factors, and c-fos have also been shown to promote EMT in epithelia. We present studies from our laboratory showing that alpha 5 beta 1 integrin has a role in the EMT of lens epithelium that is brought about by suspension in collagen gel, Our laboratory has also shown that transfection with the E-cadherin gene induces embryonic corneal fibroblasts to undergo MET and that this MET is enhanced by interaction of the differentiating epithelium with living fibroblasts, This review calls attention to the roles that EMT and MET might have in kidney pathologies and urges further study of the involvement of these phenomena in renal development, renal injury, and renal malignancy. (C) 1995 by the National Kidney Foundation, Inc. C1 HARVARD UNIV, MASSACHUSETTS GEN HOSP,SCH MED,DEPT MED,RENAL UNIT, BOSTON, MA USA. RP HAY, ED (reprint author), HARVARD UNIV, SCH MED, DEPT CELL BIOL, 220 LONGWOOD AVE, BOSTON, MA 02115 USA. FU NEI NIH HHS [R01 EY09721]; NIDDK NIH HHS [P01-DK38452, R01 DK46768] NR 104 TC 282 Z9 295 U1 1 U2 8 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 OCT PY 1995 VL 26 IS 4 BP 678 EP 690 DI 10.1016/0272-6386(95)90610-X PG 13 WC Urology & Nephrology SC Urology & Nephrology GA RY619 UT WOS:A1995RY61900021 PM 7573028 ER PT J AU RASKIN, P GANDA, OP SCHWARTZ, S WILLARD, D ROSENSTOCK, J LODEWICK, PA CRESSMAN, MD PHILLIPSON, B WEINER, B MCGOVERN, ME NORTON, JM CUCINOTTA, GG BEHOUNEK, BD AF RASKIN, P GANDA, OP SCHWARTZ, S WILLARD, D ROSENSTOCK, J LODEWICK, PA CRESSMAN, MD PHILLIPSON, B WEINER, B MCGOVERN, ME NORTON, JM CUCINOTTA, GG BEHOUNEK, BD TI EFFICACY AND SAFETY OF PRAVASTATIN IN THE TREATMENT OF PATIENTS WITH TYPE-I OR TYPE-II DIABETES-MELLITUS AND HYPERCHOLESTEROLEMIA SO AMERICAN JOURNAL OF MEDICINE LA English DT Article ID CORONARY HEART-DISEASE; CHOLESTEROL LEVELS; SERUM-LIPIDS; LIPOPROTEIN; HYPERLIPIDEMIA; RISK; APOLIPOPROTEINS; ATHEROGENESIS; HYPERTENSION; DYSLIPIDEMIA AB PURPOSE: Patients with type I and type II diabetes mellitus have an increased risk of coronary heart disease. In many diabetics, hypercholesterolemia is present and further exacerbates this risk. We investigated the efficacy and safety of pravastatin in the treatment of patients with type I or type II diabetes mellitus and hypercholesterolemia. PATIENTS AND METHODS: In this 24-week, multicenter, double-blind, placebo-controlled study, 94 patients (45 men, 49 women), 18 to 70 years of age, with type I or type II diabetes mellitus and hypercholesterolemia (fasting plasma low-density lipoprotein cholesterol [LDL-C] levels > 150 mg/dL and above the 75th percentile for the US population by age and gender) were randomized to receive pravastatin 20 mg hs or matching placebo. Two patients were randomized to treatment with drug for every 1 randomized to placebo. The dose could be doubled after 10 weeks, and cholestyramine or colestipol could be added after 18 weeks, as needed, to attempt to lower the LDL-C levels to below the 50th percentile for the US population. RESULTS: Significant reductions in LDL-C (-27.6%), total cholesterol (-22.1%), very-low-density lipoprotein cholesterol (-22.6%), and triglycerides (-12.8%) (P less than or equal to 0.001 versus placebo for all reductions), and significant increases in high-density lipoprotein cholesterol (4.4%) (P less than or equal to 0.05 versus placebo) were noted in the pravastatin treatment group (average dose 29.5 mg) at 16 weeks. The beneficial lipid-lowering effects of pravastatin were maintained throughout the 24 weeks of the study. Pravastatin was well tolerated, and the frequency of side effects was similar in the pravastatin and placebo groups. No clinically significant changes in the control of diabetes, as assessed by fasting blood glucose levels and glycosylated hemoglobin measurements, were seen during this study. CONCLUSION: The results of this study demonstrate that pravastatin is well tolerated and effective in lowering total cholesterol and LDL-C in patients with type I or type II diabetes mellitus and hypercholesterolemia. C1 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,PRINCETON,NJ 08543. UNIV TEXAS,HLTH SCI CTR,DEPT INTERNAL MED,DALLAS,TX 75235. JOSLIN DIABET CTR,BOSTON,MA 02215. DIABET & GLANDULAR DIS CLIN,SAN ANTONIO,TX. MED CTR PRINCETON,PRINCETON,NJ. DALLAS DIABET & ENDOCRINE CTR,DALLAS,TX. LARCHMONT MED CTR,MT LAUREL,NJ. CLEVELAND CLIN,DIV RES,CLEVELAND,OH 44106. PROVIDENCE HOSP,PORTLAND,OR. UNIV MASSACHUSETTS,SCH MED,DIV CARDIOVASC MED,WORCESTER,MA. NR 44 TC 22 Z9 22 U1 0 U2 1 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9343 J9 AM J MED JI Am. J. Med. PD OCT PY 1995 VL 99 IS 4 BP 362 EP 369 DI 10.1016/S0002-9343(99)80182-X PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA RY611 UT WOS:A1995RY61100006 PM 7573090 ER PT J AU SORENSEN, AG WRAY, SH WEISSKOFF, RM BOXERMAN, JL DAVIS, TL CARAMIA, F KWONG, KK STERN, CE BAKER, JR BREITER, H GAZIT, IE BELLIVEAU, JW BRADY, TJ ROSEN, BR AF SORENSEN, AG WRAY, SH WEISSKOFF, RM BOXERMAN, JL DAVIS, TL CARAMIA, F KWONG, KK STERN, CE BAKER, JR BREITER, H GAZIT, IE BELLIVEAU, JW BRADY, TJ ROSEN, BR TI FUNCTIONAL MR OF BRAIN ACTIVITY AND PERFUSION IN PATIENTS WITH CHRONIC CORTICAL STROKE SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE BRAIN, INFARCTION; MAGNETIC RESONANCE, FUNCTIONAL ID CONTRAST; VISION AB PURPOSE: (1) To determine whether functional MR can reliably map functional deficits in patients with stroke in the primary visual cortex; (2) to determine whether functional MR can reliably map perfusion deficits; and (3) to determine whether functional MR can give any additional diagnostic information beyond conventional MR. METHODS: Seven patients who had had a stroke in their primary visual system were examined using two functional MR techniques: (1) dynamic susceptibility contrast imaging, and (2) cortical activation mapping during full-field visual stimulation. Maps of relative cerebral blood volume and activation were created and compared with visual field examinations and conventional T2-weighted images on a quadrant-by-quadrant basis in five of these patients. RESULTS: Visual field mapping matched with both T2-weighted conventional images and activation mapping of 16 of 18 quadrants. In two quadrants, the activation maps detected abnormalities that were present on the visual field examination but not present on the T2-weighted images nor on the relative cerebral blood volume maps, which may indicate abnormal function without frank infarction. In addition, the activation maps demonstrated decreased activation in extrastriate cortex and had normal T2 signal and relative cerebral blood volume but was adjacent to infarcted primary cortex, mapping in vivo how stroke in one location can affect the function of distant tissue. CONCLUSION: Functional MR techniques can accurately map functional and perfusion deficits and thereby provide additional clinically useful information. Additional studies will be needed to determine the prognostic utility of functional MR in stroke patients. C1 MASSACHUSETTS GEN HOSP,CTR NMR,BOSTON,MA 02114. MASSACHUSETTS GEN HOSP,NEUROVISUAL DISORDERS UNIT,BOSTON,MA 02114. RP SORENSEN, AG (reprint author), MASSACHUSETTS GEN HOSP,DEPT RADIOL,GRAY 2 NEURORADIOL,BOSTON,MA 02114, USA. FU NCI NIH HHS [P01-CA48729, R01-CA40303]; NHLBI NIH HHS [R01-HL39810] NR 19 TC 23 Z9 23 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 OCT PY 1995 VL 16 IS 9 BP 1753 EP 1762 PG 10 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA RZ932 UT WOS:A1995RZ93200001 PM 8693971 ER PT J AU GONZALEZ, RG FISCHMAN, AJ GUIMARAES, AR CARR, CA STERN, CE HALPERN, EF GROWDON, JH ROSEN, BR AF GONZALEZ, RG FISCHMAN, AJ GUIMARAES, AR CARR, CA STERN, CE HALPERN, EF GROWDON, JH ROSEN, BR TI FUNCTIONAL MR IN THE EVALUATION OF DEMENTIA - CORRELATION OF ABNORMAL DYNAMIC CEREBRAL BLOOD-VOLUME MEASUREMENTS WITH CHANGES IN CEREBRAL METABOLISM ON POSITRON EMISSION TOMOGRAPHY WITH FLUDEOXYGLUCOSE F-18 SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article DE DEMENTIA; MAGNETIC RESONANCE, FUNCTIONAL; POSITRON EMISSION TOMOGRAPHY ID ALZHEIMERS-DISEASE; HIPPOCAMPAL; DIAGNOSIS; FLOW AB PURPOSE: To determine whether magnetic susceptibility functional MR imaging of cerebral blood volumes provides information similar to fludeoxyglucose F 18 positron emission tomography (PET) brain images in patients undergoing evaluation for dementia. METHODS: Ten subjects were studied with both PET and functional MR. Clinical diagnoses included probable Alzheimer disease (n = 5), possible Alzheimer disease (n = 1), Pick disease (n = 2), and primary progressive aphasia (n = 2). The studies were quantitatively evaluated by coregistration of PET and functional MR images followed by regression analyses of corresponding regions of interest. Qualitatively, each brain was categorized into eight regions, and each was classified as normal or abnormal by visual inspection. RESULTS: Correlation coefficients between registered functional MR and PET images were excellent (mean, r = 0.58) in most of the cerebrum. Significant correlations were observed in 72 of 74 brain sections. Qualitatively, 16 brain regions were judged to be abnormal by both MR imaging and PET; 46 regions were normal by both; 10 regions were abnormal by PET only; and 8 regions were abnormal only by functional MR. The concordance between functional MR and PET was 78%, which was highly significant. CONCLUSION: Cerebral blood volumes images derived from magnetic susceptibility (functional MR) provide information similar to fludeoxyglucose F 18 PET images in demented patients undergoing evaluation for dementia. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR IMAGING & PHARMACEUT RES,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DIV NEURORADIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,PET LAB,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT RADIOL,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,MASSACHUSETTS ALZHEIMERS DIS RES CTR,BOSTON,MA 02115. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,DEPT NEUROL,BOSTON,MA 02115. RP GONZALEZ, RG (reprint author), MASSACHUSETTS GEN HOSP,CTR NMR,BLDG 149,13TH ST,2ND FL,RM 2301,BOSTON,MA 02129, USA. FU NIA NIH HHS [AG10679] NR 19 TC 69 Z9 69 U1 0 U2 2 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD OCT PY 1995 VL 16 IS 9 BP 1763 EP 1770 PG 8 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA RZ932 UT WOS:A1995RZ93200002 PM 8693972 ER PT J AU CURTIN, HD AF CURTIN, HD TI NORTH-AMERICAN-SKULL-BASE-SOCIETY 6TH ANNUAL-MEETING SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Editorial Material RP CURTIN, HD (reprint author), MASSACHUSETTS EYE & EAR INFIRM,DEPT RADIOL,243 CHARLES ST,BOSTON,MA 02114, 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 OCT PY 1995 VL 16 IS 9 BP 1922 EP 1922 PG 1 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA RZ932 UT WOS:A1995RZ93200027 ER PT J AU XIAO, S RENSHAW, A CIBAS, ES HUDSON, TJ FLETCHER, JA AF XIAO, S RENSHAW, A CIBAS, ES HUDSON, TJ FLETCHER, JA TI NOVEL FLUORESCENCE IN-SITU HYBRIDIZATION APPROACHES IN SOLID TUMORS - CHARACTERIZATION OF FROZEN SPECIMENS, TOUCH PREPARATIONS, AND CYTOLOGICAL PREPARATIONS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID MOLECULAR CYTOGENETIC ANALYSIS; HUMAN-MALIGNANT MESOTHELIOMA; INSITU HYBRIDIZATION; INTERPHASE CYTOGENETICS; CHROMOSOME-ABERRATIONS; BLADDER-CANCER; CELLS; AMPLIFICATION; METAPHASE; HETEROGENEITY AB Fluorescence in situ hybridization has emerged as an extremely important tool for detection and characterization of nonrandom chromosome aberrations in cancer, Fluorescence in situ hybridization assays have been very reliable ill cytogenetic tumor preparations, but have been more unpredictable in archival, paraffin-embedded specimens, We describe novel approaches for detection of chromosome aberrations in frozen tumor specimens, touch preparations, and cytological preparations., These approaches are both simple and reproducible, with minimal case-to-case variation in hybridization efficiency or hybridization signal quality, We demonstrate potential applications of these novel approaches by evaluating: I) significance of normal karyotypes in malignant peripheral nerve sheath tumors; 2) p15/p16 copy number in prostate cancer; and 3) clonal chromosome 3p deletion in cytological preparations of pleural fluid from patients with mesothelioma. C1 BRIGHAM & WOMENS HOSP,DEPT PATHOL,BOSTON,MA 02115. CHILDRENS HOSP,DEPT PATHOL,BOSTON,MA. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,WHITEHEAD INST BIOL SCI,CTR GENOME RES,CAMBRIDGE,MA 02139. DANA FARBER CANC INST,DIV PEDIAT ONCOL,BOSTON,MA 02115. FU NCI NIH HHS [1K11CA01498-05]; NINDS NIH HHS [P20 NS31110] NR 50 TC 45 Z9 46 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1995 VL 147 IS 4 BP 896 EP 904 PG 9 WC Pathology SC Pathology GA RZ182 UT WOS:A1995RZ18200004 PM 7573365 ER PT J AU DELAMONTE, SM NG, SC HSU, DW AF DELAMONTE, SM NG, SC HSU, DW TI ABERRANT GAP-43 GENE-EXPRESSION IN ALZHEIMERS-DISEASE SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID GROWTH-ASSOCIATED PROTEIN; AXONALLY TRANSPORTED PROTEINS; CALMODULIN-BINDING-PROTEIN; GOLDFISH OPTIC-NERVE; FETAL-RAT BRAIN; MESSENGER-RNA; KINASE-C; NEUROFIBRILLARY TANGLES; REGENERATION; NEURONS AB GAP-43 is a growth-associated phosphoprotein expressed at high levels in neurons during development, axonal regeneration, and neuritic sprouting. GAP-43 gene expression in mature neurons is probably functionally important for the structural remodeling of synapses as required for learning and establishing new memory. The widespread aberrant neuritic growth accompanied by impaired synaptic plasticity in Alzheimer's disease (AD) suggests that abnormal GAP-43 gene expression may contribute to the cascade of neurodegeneration. In the present study, end-state AD brains exhibited reduced neuronal expression but increased glial cell levels of GAP-43 mRNA and protein. Glial cell localization of GAP-43 gene expression was confirmed by in situ hybridization of cerebral tissue, Northern blot analysis of microdissected cerebral white matter, and independent analysis of astrocytoma cell lines and primary malignant astrocytomas. In addition, in AD, GAP-43 immunoreactivity was translocated from the cytosol to membranes of swollen neuritic (dendritic) and glial cell processes throughout cerebral cortex and white matter. Downregulated and aberrant neuronal GAP-43 gene expression appears to reflect an important molecular lesion that precedes and progresses with the widespread synaptic disconnection and dementia in AD. At the same time, the presence of similar neuronal abnormalities in Pick's disease, diffuse Lewy body disease, Parkinson's disease, and Down syndrome suggests common mechanisms in the respective cascades of neurodegeneration. Finally, the finding of aberrantly increased glial cell GAP-43 gene expression in AD exposes a previously unrecognized neurodegenerative changes that may account for axonal loss and white matter atrophy detected early in the course of disease. C1 HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,NEUROPATHOL LAB,ALZHEIMERS DIS RES CTR,BOSTON,MA. HARVARD UNIV,MASSACHUSETTS GEN HOSP,SCH MED,CTR CANC,BOSTON,MA. FU NINDS NIH HHS [R01-NS29793] NR 59 TC 44 Z9 44 U1 0 U2 2 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1995 VL 147 IS 4 BP 934 EP 946 PG 13 WC Pathology SC Pathology GA RZ182 UT WOS:A1995RZ18200008 PM 7573369 ER PT J AU NICKELEIT, V ZAGACHIN, L NISHIKAWA, K PETERS, JH HYNES, RO COLVIN, RB AF NICKELEIT, V ZAGACHIN, L NISHIKAWA, K PETERS, JH HYNES, RO COLVIN, RB TI EMBRYONIC FIBRONECTIN ISOFORMS ARE SYNTHESIZED IN CRESCENTS IN EXPERIMENTAL AUTOIMMUNE GLOMERULONEPHRITIS SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID TRANSFORMING GROWTH-FACTOR; BASEMENT-MEMBRANE DISEASE; MESSENGER-RNA PRECURSORS; FACTOR-BETA; MONOCLONAL-ANTIBODIES; EXPRESSION; PROTEIN; CELLS; RAT; INTERLEUKIN-1 AB Crescents are a severe and stereotyped glomerular response to injury that occur in several forms of glomerulonephritis that progress to renal failure The key pathogenetic step that leads to glomerular scarring is unknown, but fibronectin (FN), the clotting system, macrophages, and proliferating parietal epithelial cells are known to participate. This study tons designed to determine whether FN is synthesized locally, and in what molecular isoform, and whether cytokines known to promote FN synthesis are present in the crescent. Rats immunized with bovine glomerular basement membrane develop cellular crescents by 14 days and fibrous crescents and glomerulosclerosis by 35 days, In situ hybridization was performed with oligonucleotides specific for sequences common to all FN isoforms (total FN) or sequences specific for the alternatively spliced segments (EIIIA, EIIIB, and V). Throughout the time period (14, 21, and 35 days) all crescents and glomerular tufts contained cells with strong ISH signals for total and V+ mRNA, with the strongest signals present in large cellular crescents at tiny 21, lit contrast, EIIIA(+) and EIIIB(+) mRNAs showed maximal abundance within sclerosing crescents at 35 days, Protein deposition of EIIIA(+), EIIIB(+), and V+ FN isoforms was confirmed by immunofluorescence with segment-specific FN antibodies, Transforming growth factor-beta and interleukin-1 beta both known to promote FN synthesis, were found in cellular crescents (days 14 and 21) and were still present, but greatly, diminished, ii, the sclerotic phase (day 35), In summary, EIIIA(-), EIIIB(-), and V+ FN mRNA plasma isoforms predominate in cellular crescents, whereas hi the fibrosing stage, mainly, the oncofetal EIIIA(+), EIIIB(+), and V+ isoforms are synthesized and accumulate. C1 MASSACHUSETTS GEN HOSP,DEPT PATHOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA. MIT,HOWARD HUGHES MED INST,CAMBRIDGE,MA. MIT,CTR CANC RES,DEPT BIOL,CAMBRIDGE,MA 02139. FU NCI NIH HHS [R37CA20822]; NHLBI NIH HHS [P01HL41484]; NIDDK NIH HHS [DK-36807] NR 45 TC 26 Z9 26 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1995 VL 147 IS 4 BP 965 EP 978 PG 14 WC Pathology SC Pathology GA RZ182 UT WOS:A1995RZ18200011 PM 7573372 ER PT J AU BUSAM, KJ BERWICK, M BLESSING, K FANDREY, K KANG, S KARAOLI, T FINE, J COCHRAN, AJ WHITE, WL RIVERS, J ELDER, DE WEN, DRP HEYMAN, BH BARNHILL, RL AF BUSAM, KJ BERWICK, M BLESSING, K FANDREY, K KANG, S KARAOLI, T FINE, J COCHRAN, AJ WHITE, WL RIVERS, J ELDER, DE WEN, DRP HEYMAN, BH BARNHILL, RL TI TUMOR VASCULARITY IS NOT A PROGNOSTIC FACTOR FOR MALIGNANT-MELANOMA OF THE SKIN SO AMERICAN JOURNAL OF PATHOLOGY LA English DT Article ID VIII-RELATED ANTIGEN; BREAST-CARCINOMA; UVEAL MELANOMA; ANGIOGENESIS; METASTASIS; PROGRESSION; THICKNESS; LESIONS; CANCER; LECTIN AB Tumor vascularity has been proposed as a prognostic indicator for a number of solid tumors. Although a correlation between microvessel number and metastatic behavior has also been suggested for cutaneous melanoma, the small number of cases studied to date allows, one to draw only preliminary conclusions In this study, we have assessed tumor vascularity in cutaneous melanoma by comparing 60 cases of metastasizing and non-metastasizing tumors matched for tumor thickness, age, sex, and anatomic site. Ulex europaeus agglutinin I appeared to be the most suitable vascular marker for this study. Our results indicate that there was no statistically significant difference between the two groups with regard to tumor vascularity. Even after identifying 15 cases of thin (<1.0 mm thick) melanoma, there was no significant difference in the number of microvessels between metastatizing and non-metastasizing tumors. Comparison of patterns of vascular microarchitecture also failed to discriminate between the two groups. Thus, our results indicate that tumor vascularity may not be an independent prognostic factor for cutaneous melanoma. C1 HARVARD UNIV,BRIGHAM & WOMENS HOSP,SCH MED,DEPT PATHOL,DIV DERMATOPATHOL,BOSTON,MA 02115. MEM SLOAN KETTERING CANC CTR,NEW YORK,NY. UNIV ABERDEEN,ABERDEEN,SCOTLAND. YALE UNIV,CANC PREVENT RES UNIT,NEW HAVEN,CT. UNIV CALIF LOS ANGELES,SCH MED,LOS ANGELES,CA. WAKE FOREST UNIV,BOWMAN GRAY SCH MED,WINSTON SALEM,NC. UNIV BRITISH COLUMBIA,VANCOUVER,BC,CANADA. UNIV PENN,SCH MED,PHILADELPHIA,PA. MASSACHUSETTS GEN HOSP,BOSTON,MA. RI Berwick, Marianne/E-9608-2010; OI Berwick, Marianne/0000-0001-5062-2180 FU NCI NIH HHS [P01-CA42101] NR 29 TC 91 Z9 91 U1 0 U2 0 PU AMER SOC INVESTIGATIVE PATHOLOGY, INC PI BALTIMORE PA 428 EAST PRESTON ST, BALTIMORE, MD 21202-3993 SN 0002-9440 J9 AM J PATHOL JI Am. J. Pathol. PD OCT PY 1995 VL 147 IS 4 BP 1049 EP 1056 PG 8 WC Pathology SC Pathology GA RZ182 UT WOS:A1995RZ18200018 PM 7573350 ER PT J AU BONINI, JA COLCA, JR DAILEY, C WHITE, M HOFMANN, C AF BONINI, JA COLCA, JR DAILEY, C WHITE, M HOFMANN, C TI COMPENSATORY ALTERATIONS FOR INSULIN SIGNAL-TRANSDUCTION AND GLUCOSE-TRANSPORT IN INSULIN-RESISTANT DIABETES SO AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM LA English DT Article DE INSULIN RECEPTOR SUBSTRATE-1; PHOSPHATIDYLINOSITOL 3-KINASE; GROWTH FACTOR RECEPTOR-BOUND PROTEIN 2; SYP; RECEPTOR ID 3T3-L1 ADIPOCYTES; NCK PROTEIN; EXPRESSION; PHOSPHORYLATION; IRS-1; TRANSLOCATION; RNA AB Insulin binding activates the receptor tyrosine kinase toward the insulin receptor substrate-1 (IRS-1). Phosphorylated IRS-1 then interacts with the p85 alpha subunit of phosphatidylinositol S-kinase (PI3K), Nck, growth factor receptor-bound protein 2 (GRB2), and Syp, thus branching insulin's signal for both mitogenic and metabolic responses. To determine whether the expression of these proteins is altered in insulin resistance, the levels of these proteins were compared in adipose and liver tissues of nondiabetic mice and obese insulin-resistant diabetic KKA(y) mice. IR and PI3K p85 alpha protein levels were significantly lower in KKA(y) mice than in control nondiabetic mice, whereas IRS-1 protein levels were not altered. In contrast, the protein levels of GRB2, Nck, Syp, and GLUT-1 were dramatically elevated in KKA(y) fat, with less striking changes in liver. Treatment of diabetic animals with pioglitazone, an insulin-sensitizing antihyperglycemic agent, partially corrected the expression of some of these proteins. Taken together, these findings suggest that the insulin-resistant diabetic condition is characterized by changes in expression of insulin signal transduction components that may be associated with altered glucose metabolism. C1 LOYOLA UNIV, STRITCH SCH MED, DEPT MOLEC & CELLULAR BIOCHEM, MAYWOOD, IL 60153 USA. HINES VET AFFAIRS HOSP, RES SERV, HINES, IL 60141 USA. LOYOLA UNIV, MED CTR, INST SHOCK TRAUMA, MAYWOOD, IL 60153 USA. UPJOHN CO, METAB DIS RES, KALAMAZOO, MI 49001 USA. JOSLIN DIABET CTR, DIV RES, BOSTON, MA 02215 USA. NR 28 TC 30 Z9 31 U1 0 U2 0 PU AMER PHYSIOLOGICAL SOC PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0193-1849 J9 AM J PHYSIOL-ENDOC M JI Am. J. Physiol.-Endocrinol. Metab. PD OCT PY 1995 VL 269 IS 4 BP E759 EP E765 PG 7 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA TA573 UT WOS:A1995TA57300022 PM 7485492 ER PT J AU NIERENBERG, AA MCLEAN, NE ALPERT, JE WORTHINGTON, JJ ROSENBAUM, JF FAVA, M AF NIERENBERG, AA MCLEAN, NE ALPERT, JE WORTHINGTON, JJ ROSENBAUM, JF FAVA, M TI EARLY NONRESPONSE TO FLUOXETINE AS A PREDICTOR OF POOR 8-WEEK OUTCOME SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID DEPRESSION; THERAPY; TRIAL AB Objective: The purpose of this study was to quantify the proportion of patients who show no response to a fixed dose of fluoxetine after 2, 4, and 6 weeks of treatment and then respond by week 8. Method: In an open trial, 143 outpatients who met DSM-III-R criteria for major depressive disorder were treated with a regimen of fluoxetine, 20 mg/day. The authors analyzed the proportion of patients who had less than a 20% decrease from baseline in their scores on the Hamilton Rating Scale for Depression after 2, 4, and 6 weeks and who went on to have a 50% or greater reduction by week 8. A last-observation-carried-forward strategy was used to calculate conditional probabilities of 8-week response. Kaplan-Meier survival analysis was used to estimate probabilities of response at week 8 given degrees of response at week 2. Results: Eighty-two subjects (57.3%) who started the trial responded by week 8. Of those subjects who showed no improvement at weeks 2, 4, and 6, the proportions of responders at week 8 were 36.4%, 18.9%, and 6.5%, respectively. The Kaplan-Meier estimate of 8-week response given nonresponse at week 2 was 0.45. Conclusions: The proportion of patients with no response to antidepressant treatment by 4 or 6 weeks who responded by week 8 was substantially less than that for subjects who had at least a partial response. Nonresponse as early as week 2 predicted 8-week outcome. RP NIERENBERG, AA (reprint author), MASSACHUSETTS GEN HOSP,CLIN PSYCHOPHARMACOL UNIT,DEPRESS RES PROGRAM,WACC 815,15 PARKMAN ST,BOSTON,MA 02114, USA. OI Alpert, Jonathan/0000-0002-4332-908X FU NIMH NIH HHS [MH-48483] NR 15 TC 140 Z9 141 U1 2 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 OCT PY 1995 VL 152 IS 10 BP 1500 EP 1503 PG 4 WC Psychiatry SC Psychiatry GA RX730 UT WOS:A1995RX73000014 PM 7573590 ER PT J AU FAN, CM WHITMAN, GJ CHEW, FS AF FAN, CM WHITMAN, GJ CHEW, FS TI XANTHOGRANULOMATOUS PYELONEPHRITIS SO AMERICAN JOURNAL OF ROENTGENOLOGY LA English DT Note C1 MASSACHUSETTS GEN HOSP,DEPT RADIOL,BOSTON,MA 02114. HARVARD UNIV,SCH MED,BOSTON,MA 02114. 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 OCT PY 1995 VL 165 IS 4 BP 1008 EP 1008 PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA RW138 UT WOS:A1995RW13800055 PM 7676950 ER PT J AU MYERS, GA HARMS, BA STARLING, JR AF MYERS, GA HARMS, BA STARLING, JR TI MANAGEMENT OF PARAESOPHAGEAL HERNIA WITH A SELECTIVE APPROACH TO ANTIREFLUX SURGERY SO AMERICAN JOURNAL OF SURGERY LA English DT Article ID GASTROESOPHAGEAL REFLUX; INTRATHORACIC STOMACH; HIATAL-HERNIA AB BACKGROUND: The role of an antireflux procedure in the management of paraesophageal hernia is controversial. To address this issue, we reviewed our experience with selective use of antireflux procedures in patients with pure paraesophageal hernia (type II; n = 26) and those with a partial sliding component (type III; n = 11). PATIENTS AND METHODS: Surgical repair was performed on diagnosis in all 37 patients. Competency of the lower esophageal sphincter was evaluated on the basis of reflux symptoms, and objectively, with endoscopy in 21 patients and 24-hour esophageal pH studies in 17 patients. Repair included an antireflux procedure in 11 patients, as indicated by reflux disease. RESULTS: Preoperatively, 80% of both type II and type III patients reported obstructive symptoms. Reflux symptoms were present in 27% of patients-19% of type II and 45% of type III patients. Endoscopy revealed esophagitis in 5 cases, and 24-hour pH studies indicated significant reflux in 3 of 17 patients. There were no operative deaths and 1 recurrence. Symptoms improved in 92% of patients after surgery. Medically manageable reflux was identified in 2 patients. CONCLUSIONS: Frequent obstructive symptoms and the potential for gastric volvulus indicate elective repair of paraesophageal hernia on diagnosis. Significant gastroesophageal reflux is less common, especially in type II patients, and excellent symptomatic results are obtained with selective application of an antireflux procedure. C1 UNIV WISCONSIN,DEPT SURG,MADISON,WI 53792. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. NR 14 TC 42 Z9 44 U1 0 U2 0 PU CAHNERS PUBL CO PI NEW YORK PA 249 WEST 17 STREET, NEW YORK, NY 10011 SN 0002-9610 J9 AM J SURG JI Am. J. Surg. PD OCT PY 1995 VL 170 IS 4 BP 375 EP 380 DI 10.1016/S0002-9610(99)80307-9 PG 6 WC Surgery SC Surgery GA RW931 UT WOS:A1995RW93100013 PM 7573732 ER PT J AU ALBORESSAAVEDRA, J YOUNG, RH AF ALBORESSAAVEDRA, J YOUNG, RH TI TRANSITIONAL-CELL NEOPLASMS (CARCINOMAS AND INVERTED PAPILLOMAS) OF THE UTERINE CERVIX - A REPORT OF 5 CASES SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE UTERINE CERVIX; TRANSITIONAL CELL CARCINOMA; INVERTED TRANSITIONAL CELL PAPILLOMA ID ADENOID CYSTIC CARCINOMA; OVARIAN BRENNER TUMORS; ECTOCERVICAL EPITHELIUM; ADENOCARCINOMA; METASTASES AB We report five transitional cell neoplasms of the uterine cervix: three infiltrating high-grade transitional cell carcinomas and two inverted transitional cell papillomas. The patients with TCCs were aged 34, 73, and 81 years, two presented with vaginal bleeding and the third with a large cystic ovarian mass. The three transitional cell carcinomas had a superficial noninvasive papillary component. Two tumors metastasized, one to the pelvic lymph nodes, the other to the ovary. The two patients with metastasis are alive after radical hysterectomy or total abdominal hysterectomy and chemotherapy, but follow-up is short. The third patient is currently receiving radiotherapy. Microscopically, the transitional cell carcinomas were similar to those originating in the urinary bladder or ovary. The inverted transitional cell papillomas were discovered in the cervixes of young adult women, one of whom had atypical squamous cells on a cervical smear at her presentation. The second patient had a slightly raised lesion in the cervix noted when routine smears were obtained. The microscopic features of the inverted transitional cell papillomas were similar to those of the corresponding tumor of the urinary bladder. It is important to separate transitional cell carcinomas from other papillary cancers of the cervix to delineate their clinical and pathological features and establish the prognostic differences, if any, from squamous cell carcinoma. Inverted transitional cell papilloma of the cervix represents a hitherto undescribed benign neoplasm arising at this site. These cases illustrate that cervical epithelium, which is known to undergo benign transitional cell metaplasia, may also give rise to benign and malignant transitional cell neoplasms C1 MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. RP ALBORESSAAVEDRA, J (reprint author), UNIV TEXAS,SW MED CTR,DEPT PATHOL,DIV ANAT PATHOL,5323 HARRY HINES BLVD,DALLAS,TX 75235, USA. NR 41 TC 41 Z9 43 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQ, PHILADELPHIA, PA 19106 SN 0147-5185 J9 AM J SURG PATHOL JI Am. J. Surg. Pathol. PD OCT PY 1995 VL 19 IS 10 BP 1138 EP 1145 DI 10.1097/00000478-199510000-00004 PG 8 WC Pathology; Surgery SC Pathology; Surgery GA RX226 UT WOS:A1995RX22600004 PM 7573672 ER PT J AU CLEMENT, PB YOUNG, RH KEH, P OSTOR, AG SCULLY, RE AF CLEMENT, PB YOUNG, RH KEH, P OSTOR, AG SCULLY, RE TI MALIGNANT MESONEPHRIC NEOPLASMS OF THE UTERINE CERVIX - A REPORT OF 8 CASES, INCLUDING 4 WITH A MALIGNANT SPINDLE-CELL COMPONENT SO AMERICAN JOURNAL OF SURGICAL PATHOLOGY LA English DT Article DE CERVIX; MESONEPHRIC; ADENOCARCINOMA; MALIGNANT MESONEPHRIC MIXED TUMOR; SARCOMATOID CARCINOMA; CARCINOSARCOMA ID PROBABLE WOLFFIAN ORIGIN; FEMALE ADNEXAL TUMOR; CLINICOPATHOLOGICAL ANALYSIS; ENDOMETRIOID ADENOCARCINOMA; OVARIAN-TUMORS; HYPERPLASIA; VAGINA; CARCINOMAS AB Eight mesonephric adenocarcinomas of the uterine cervix, four of which had a malignant spindle-cell component, occurred in women aged 34 to 71 (median 43, mean 54.5) years, bringing to 14 the number of cervical mesonephric carcinomas in the literature. The tumors with a malignant spindle-cell component (''malignant mesonephric mixed tumors'') are, with one possible exception, the first reported examples at this site. The patients, almost all of whom presented with vaginal bleeding, underwent hysterectomy; five also had a pelvic lymph node dissection. The tumors were all stage IB, although microscopic lymph node metastases were found in two cases. Gross examination revealed an invasive cervical mass in each case. On microscopic examination, seven tumors were adjacent to mesonephric hyperplasia, which in five cases was florid and focally atypical; in the remaining case, occasional non-neoplastic mesonephric tubules were found only within the tumor. The adenocarcinomas typically exhibited a variety of patterns, including a ductal pattern resembling endometrioid adenocarcinoma, a small tubular pattern, a retiform pattern, a solid pattern, and a sex-cord-like pattern. These disparate patterns frequently caused diagnostic difficulty. The spindle-cell component generally resembled endometrial stromal sarcoma or a nonspecific spindle-cell sarcoma; one tumor also contained multiple foci of osteosarcoma and another, a single chondroid focus. Immunohistochemical staining for a variety of antigens failed to reveal a distinctive profile, although all the carcinomas were immunoreactive for vimentin. Follow-up in six cases revealed three patients to be alive without evidence of recurrence at postoperative intervals of 2 to 3 years. Recurrent tumor developed in a fourth patient 1 year after hysterectomy; she was treated with chemotherapy and was alive and free of disease at 2 years. Another patient had intra-abdominal recurrences (including liver metastases) at 9 and 11 years and was alive with tumor at 13 years. Death at 8.5 months in a final patient was probably due to an independent stage IIc ovarian clear-cell carcinoma. These and prior observations in the literature suggest that malignant mesonephric tumors of the cervix may be more indolent than their mullerian counterparts, from which they should be distinguished. Mesonephric carcinomas in this site should also be distinguished from florid mesonephric hyperplasia, with which they are usually associated. C1 UNIV BRITISH COLUMBIA,VANCOUVER,BC,CANADA. MASSACHUSETTS GEN HOSP,JAMES HOMER WRIGHT PATHOL LABS,BOSTON,MA 02114. HARVARD UNIV,SCH MED,DEPT PATHOL,BOSTON,MA 02115. NORTHWESTERN UNIV HOSP,DEPT PATHOL,CHICAGO,IL. ROYAL HOSP WOMEN,DEPT PATHOL,MELBOURNE,VIC,AUSTRALIA. RP CLEMENT, PB (reprint author), VANCOUVER HOSP & HLTH SCI CTR,DEPT PATHOL,910 W 10TH,ROOM 1302,VANCOUVER,BC V5Z 4E3,CANADA. NR 43 TC 57 Z9 58 U1 0 U2 2 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 OCT PY 1995 VL 19 IS 10 BP 1158 EP 1171 DI 10.1097/00000478-199510000-00006 PG 14 WC Pathology; Surgery SC Pathology; Surgery GA RX226 UT WOS:A1995RX22600006 PM 7573674 ER PT J AU CONNELLY, TJ AHERN, C CORONADO, R AF CONNELLY, TJ AHERN, C CORONADO, R TI KETAMINE, AT CLINICAL CONCENTRATIONS, DOES NOT ALTER THE FUNCTION OF CARDIAC SARCOPLASMIC-RETICULUM CALCIUM-RELEASE CHANNELS SO ANESTHESIA AND ANALGESIA LA English DT Article ID VENTRICULAR MYOCARDIUM; MUSCLE; MECHANISM; MEMBRANE; BINDING; RAT AB In the absence of sympathetically mediated stimulation, ketamine depresses myocardial contractility. This results from a decrease in the availability of intracellular Ca2+ for excitation-contraction coupling. Although sites of action other than the Ca2+ release channel of sarcoplasmic reticulum have been implicated, ketamine-induced alterations in Ca2+ efflux from the sarcoplasmic reticulum remain contentious. The purpose of the present study was to identify interactions of ketamine with the calcium release channel using sarcoplasmic reticulum enriched vesicles from porcine left ventricle. Ketamine did not alter [H-3]ryanodine binding at concentrations of 1 mM or less, while binding was almost completely inhibited at 10 mM. Gating and conductance of SR Ca2+ channels studied in planar bilayers was not altered by clinical concentrations of ketamine over the range of physiologic cytoplasmic free Ca2+ concentrations. Channel inactivation was observed at 10 mM ketamine, well in excess of clinical concentrations. These findings indicate that clinical concentrations of ketamine do not alter the function of the Ca2+ release channel. Alterations in intracellular Ca2+ homeostasis that result in depression of myocardial contractility must therefore result from effects at other sites along the excitation-contraction coupling pathway. C1 UNIV WISCONSIN,DEPT ANESTHESIOL,MADISON,WI. UNIV WISCONSIN,DEPT PHYSIOL,MADISON,WI. WILLIAM S MIDDLETON MEM VET ADM MED CTR,MADISON,WI. NR 23 TC 5 Z9 6 U1 0 U2 0 PU WILLIAMS & WILKINS PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 SN 0003-2999 J9 ANESTH ANALG JI Anesth. Analg. PD OCT PY 1995 VL 81 IS 4 BP 849 EP 854 DI 10.1097/00000539-199510000-00033 PG 6 WC Anesthesiology SC Anesthesiology GA RX477 UT WOS:A1995RX47700033 PM 7574022 ER PT J AU LELL, W COMUNALE, M MADDI, R LEUNG, J FRIEDMAN, A STARR, N PATAFIO, O MOHIUDDEN, S ADKINS, M STANLEY, T BELLOWS, W ROACH, G REEVES, J DAMBRA, M WAHR, J MARSHALL, K SIEGEL, L FABIAN, J SPIESS, B GRADMAN, A AGGARWAL, A MATHEW, J MANGANO, DT HOLLENBERG, M ZIOLA, K GOLDMAN, M RADULESCU, A JAIN, U ALOCOZY, MN ALOKOZAI, BD PINZON, S NGO, L GRAHAM, S BROWNER, W LI, E AF LELL, W COMUNALE, M MADDI, R LEUNG, J FRIEDMAN, A STARR, N PATAFIO, O MOHIUDDEN, S ADKINS, M STANLEY, T BELLOWS, W ROACH, G REEVES, J DAMBRA, M WAHR, J MARSHALL, K SIEGEL, L FABIAN, J SPIESS, B GRADMAN, A AGGARWAL, A MATHEW, J MANGANO, DT HOLLENBERG, M ZIOLA, K GOLDMAN, M RADULESCU, A JAIN, U ALOCOZY, MN ALOKOZAI, BD PINZON, S NGO, L GRAHAM, S BROWNER, W LI, E TI EFFECTS OF ACADESINE ON THE INCIDENCE OF MYOCARDIAL-INFARCTION AND ADVERSE CARDIAC OUTCOMES AFTER CORONARY-ARTERY BYPASS GRAFT-SURGERY SO ANESTHESIOLOGY LA English DT Article DE HEART, ACADESINE, ADENOSINE, ADENOSINE-REGULATING AGENT, MYOCARDIAL INFARCTION, MYOCARDIAL INJURY, MYOCARDIAL ISCHEMIA, PERIOPERATIVE CARDIAC MORBIDITY, VENTRICULAR FUNCTION; SURGERY, CORONARY ARTERY BYPASS GRAFT ID ADENOSINE REGULATING AGENT; AICA-RIBOSIDE; ANGINA-PECTORIS; ISCHEMIC DAMAGE; MB RELEASE; CK-MB; REPERFUSION; PROTECTION; RECOVERY; INJURY AB Background: Acadesine (AICA riboside) (5-amino-1-[beta-D-ribofuranosy]imidazole-4-carboxamide) is a purine nucleoside analog belonging to a new class of agents generally termed adenosine regulating agents (ARAs) that increase the availability of adenosine locally in ischemic tissues, The effects of acadesine on the incidence of fatal and nonfatal myocardial infarction (MI) and on the incidence of all adverse cardiovascular outcomes (cardiac death, MI, congestive heart failure, Life-threatening dysrhythmia, or cerebrovascular accident) was investigated in patients undergoing coronary artery bypass graft (CABG) surgery. Methods: In 20 medical centers in the United States participating in the Multicenter Study of Perioperative Ischemia (McSPI), 633 patients undergoing CABG surgery were randomized in a double-blind fashion to receive either placebo (n = 212), low-dose acadesine (0.05 mg . kg(-1) . min(-1), n = 214), or high-dose acadesine (0.1 mg . kg(-1) . min(-1), n = 207) by intravenous infusion starting 15 min before anesthetic induction and continuing for 7 h, as well as added to the cardioplegic solution (final concentration of 5 mu g/ml for those patients receiving acadesine). Anesthesia was standardized, and perioperative hemodynamics were to be strictly controlled, Twelve-lead electrocardiograms (ECGs), CK-MB isoenzyme concentrations, and autopsy were used to assess the occurrence of MI. Results: There was a similar incidence of adverse events in the acadesine groups and the placebo group, with the exception that serum uric acid transiently increased in the high-dose acadesine group. The incidence of perioperative MI, using the prespecified MI criterion (ECG Q wave, CK-MB elevation, or autopsy evidence), was not different between groups (24% versus 26% versus 21% [P = 0.574]), nor was the incidence of all cardiovascular outcomes (30% versus 30% versus 22% [P = 0.151]). After completion of the study, a post hoc analysis also was performed using the more specific definition of MI (ECG Q wave and CK-MB elevation, or autopsy evidence), and the incidence of MI was lower (P = 0.018, alpha = 0.017, corrected for multiple comparisons), as were adverse cardiovascular outcomes (P = 0.002) and CVA (P = 0.02) for patients treated with 0.1 mg . kg(-1) . min(-1) acadesine. In patients with Q-wave infarction, the high-dose acadesine group had a lower peak median CK-MB (P = 0.042) and area under the CK-MB curve (P = 0.021). No differences were found in the incidence or characteristics of MI (Holter or transesophageal echocardiography). Conclusions The results of this trial did not demonstrate a statistically significant difference between acadesine and placebo using the prespecified criterion for MI. Of interest are the results of the post hoc analysis, using the more specific criterion for MI, which indicate that acadesine may reduce the incidence of larger Q-wave infarctions after coronary artery bypass surgery. A second trial is underway to evaluate this contention. C1 UNIV ALABAMA,TUSCALOOSA,AL 35487. HARVARD UNIV,BETH ISRAEL HOSP,BOSTON,MA 02215. HARVARD UNIV,BRIGHAM & WOMENS HOSP,BOSTON,MA 02215. UNIV CALIF SAN FRANCISCO,VET ADM MED CTR,SAN FRANCISCO,CA. CEDARS SINAI MED CTR,SAN FRANCISCO,CA. CLEVELAND CLIN,CLEVELAND,OH 44106. CORNELL UNIV,ITHACA,NY 14853. CREIGHTON UNIV,OMAHA,NE 68178. DUKE UNIV,DURHAM,NC 27706. KAISER PERMANENTE MED CTR,SAN DIEGO,CA 92120. HARVARD UNIV,MASSACHUSETTS GEN HOSP,BOSTON,MA. UNIV MICHIGAN,ANN ARBOR,MI 48109. NYU,NEW YORK,NY 10016. STANFORD UNIV,STANFORD,CA 94305. VIRGINIA COMMONWEALTH UNIV,MED COLL VIRGINIA,RICHMOND,VA 23298. UNIV WASHINGTON,SEATTLE,WA 98195. WESTERN PENN HOSP,PITTSBURGH,PA 15224. MED COLL WISCONSIN,MILWAUKEE,WI 53226. YALE UNIV,NEW HAVEN,CT 06520. DEBORAH HEART & LUNG CTR,BROWNS MILLS,NJ 08015. OI Siegel, Lawrence/0000-0002-8456-7551 NR 67 TC 23 Z9 24 U1 0 U2 0 PU LIPPINCOTT-RAVEN PUBL PI PHILADELPHIA PA 227 EAST WASHINGTON SQUARE, PHILADELPHIA, PA 19106 SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD OCT PY 1995 VL 83 IS 4 BP 658 EP 673 PG 16 WC Anesthesiology SC Anesthesiology GA RY955 UT WOS:A1995RY95500006 ER EF